BEGIN:VCALENDAR VERSION:2.0 PRODID:-//CERN//INDICO//EN BEGIN:VEVENT SUMMARY:The role of Natural Killer cells in the development of a primary t umour mass and metastasis formation DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-34@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Victoria Gershuny (University of Arizona)\nIn recent years\, advances in cancer research have shown that the body’s immune r esponse to tumour cells plays a significant role in fighting cancer growth . Although the immune system is intrinsically capable of destroying tumour cells\, tumours and their microenvironment have an ability to suppress th e immune response. Whereas the roles of some immune cells have been greatl y studied\, the role of Natural Killer (NK) cells is less clear. Despite t he fact that studies have shown that NK cells are not very effective at pe netrating the tumour environment and play a minimal role in the direct ki lling of tumour cells in a tumour mass\, studies with NK cell immunotherap ies in humans have shown great success. The leading cause of death for can cer is not primary tumour growth\, but instead metastasis formation. In mi ce\, depleting NK cells has shown to prevent metastasis formation. In orde r to understand the complex interplay between the primary tumour\, the met astases\, and the immune system\, it is necessary to develop a model of tu mour growth that includes these immune subpopulations and their interactio ns with the tumour and with each other. Here\, such a model is presented\ , consisting of 17 coupled ordinary differential equations and one stochas tic ODE that capture the complex interplay between CD4+ and CD8+ T cells\, regulatory T cells\, NK cells\, dendritic cells\, MDSCs\, and both immuno stimulatory (IL-2\, IFN-gamma) and immunosuppressive (IL-10\, TGF-beta) cy tokines or factors\, the primary tumour\, circulating tumour cells\, and t umour metastases. All parameters are estimated from experimental data. The model shows that one of the main immune components contributing to the pr evention of metastasis formation is killing of circulating tumour cells by NK cells. For tumours with high antigen expression on their surface\, T c ells play the primary role in preventing metastasis formation\, however ci rculating tumour cells with low antigen expression are eradicated mostly b y NK cells. With this model\, it is possible to replicate experimental dat a of metastasis formation under NK cell depletion. Implications for consid ering immunologic effects of standard chemotherapy combinations\, in parti cular FOLFOX for colorectal cancer\, are discussed.\n\nhttps://conferences .maths.unsw.edu.au/event/2/contributions/34/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/34/ END:VEVENT BEGIN:VEVENT SUMMARY:Metapopulation epidemic model fitted to spatiotemporal spread of r ubella in Japan\, 2012-13 DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-64@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hiroshi Nishiura (Hokkaido University)\n*Background: * Japan experienced a nationwide rubella epidemic from 2012 to 2013\, most ly in urban prefectures with large population sizes. The present study aim ed to capture the spatiotemporal patterns of rubella using a parsimonious metapopulation epidemic model and examine the potential usefulness of spat ial vaccination.\n\n*Methodology/Principal Findings:* A metapopulation epi demic model in discrete time and space was devised and applied to rubella notification data from 2012 to 2013. Linearly approximating growth pattern s in six different time periods using the particle Markov chain Monte Carl o method yielded estimates of effective reproduction numbers of 1.37 (95% CrI: 1.12\, 1.77) and 1.37 (95% CrI: 1.24\, 1.48) in Tokyo and Osaka group s\, respectively\, during the growing phase of the epidemic in 2013. The r ubella epidemic in 2012 involved substantial uncertainties in its paramete r estimates and forecasts. We examined multiple scenarios of spatial vacci nation with coverages of 1%\, 3% and 5% for all of Japan to be distributed in different combinations of prefectures. Scenarios indicated that vaccin ating the top six populous urban prefectures (i.e.\, Tokyo\, Kanagawa\, Os aka\, Aichi\, Saitama and Chiba) could potentially be more effective than random allocation. However\, greater uncertainty was yielded by initial se eds of infectious individuals\, initial fraction susceptible and stochasti city.\n\n*Conclusions:* While the forecast in 2012 was accompanied by broa d uncertainties\, a narrower uncertainty bound of parameters and reliable forecast were achieved during the greater rubella epidemic in 2013. By bet ter capturing the underlying epidemic dynamics\, possibly with age-depende nt and prefecture-specific susceptibility distributions\, spatial vaccinat ion could potentially be substantially discriminated from random vaccinati on.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/64/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/64/ END:VEVENT BEGIN:VEVENT SUMMARY:Positive equilibria of weakly reversible power law kinetic systems with linear independent interactions DTSTART;VALUE=DATE-TIME:20180711T053000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-47@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Editha Jose (University of the Philippines Los Banos )\nIn this talk\, we present our results on power law kinetic systems whos e kinetic order vectors (which we call “interactions”) are reactant-de termined (i.e. reactions with the same reactant complex have identical kin etic order vectors) and are linear independent per linkage class. In parti cular\, we focus on its subset called PL-TLK systems. Our main result stat es that any weakly reversible PL-TLK system has a complex balanced equilib rium. We can consider this result as a “Higher Deficiency Theorem” for such systems since in our previous work\, we derived analogues of the Def iciency Zero and the Deficiency One Theorems for mass action kinetics (MAK ) systems for them\, thus covering the “Low Deficiency” case. On the o ther hand\, our result can also be viewed as a “Weak Reversibility Theor em” (WRT) in the sense that the statement “any weakly reversible syste m with a kinetics from the given set has a positive equilibrium” holds. According to the work of Deng et al. and more recently of Boros\, such a W RT holds for MAK systems. However\, we show that a WRT does not hold for t wo proper MAK supersets: the set PL-NIK of non-inhibitory power law kineti cs (i.e. all kinetic orders are non-negative) and the set PL-FSK of factor span surjective power law kinetics (i.e. different reactants imply differ ent interactions).\n\nhttps://conferences.maths.unsw.edu.au/event/2/contri butions/47/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/47/ END:VEVENT BEGIN:VEVENT SUMMARY:Patch dynamics for fluid flow through long narrow tubes DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-159@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Judy Bunder (University of Adelaide)\nPatch dynamics is a numerical multiscale solver which constructs a macroscale solution o f a microscale system by solving the original microscale problem\, but onl y within discrete patches. These patches are spread across the domain of t he system and are separated by the desired macroscale spacing\, thus provi ding a description of the system at the macroscale. The space between the patches is unsimulated\, which reduces the size of the problem and permits a reduction in computational time. For the patches to accurately capture the macroscale behaviour of the system\, the patches must be coupled acros s the unsimulated space. In developing patch dynamics\, one of the main ta sks is to ensure the patch coupling is both accurate and efficient. We con sider the example of the flow of fluid\, such as blood\, through a long na rrow tube with fixed obstructions. We show how to apply patch dynamics to obtain an accurate description of the fluid flow over long space and time scales.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/159 / LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/159/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical model of contractile ring-driven cytokinesis in a thr ee-dimensional domain DTSTART;VALUE=DATE-TIME:20180709T060000Z DTEND;VALUE=DATE-TIME:20180709T062000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-319@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Seunggyu Lee (National Institute for Mathematical Sc iences)\nIn this presentation\, a mathematical model of contractile ring-d riven cytokinesis is presented by using both phase-field and immersed-boun dary methods in a three-dimensional domain. It is one of the powerful hypo theses that cytokinesis happens driven by the contractile ring\; however\, there are only few mathematical models following the hypothesis\, to the author’s knowledge. I consider a hybrid method to model the phenomenon. First\, a cell membrane is represented by a zero-contour of a phase-field implicitly because of its topological change. Otherwise\, immersed-boundar y particles represent a contractile ring explicitly based on the author’ s previous work. Here\, the multi-component (or vector-valued) phase-field equation is considered to avoid the emerging of each cell membrane right after their divisions. Using a convex splitting scheme\, the governing equ ation of the phase-field method has unique solvability. The numerical conv ergence of contractile ring to cell membrane is proved. Several numerical simulations are performed to validate the proposed model.\n\nhttps://confe rences.maths.unsw.edu.au/event/2/contributions/319/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/319/ END:VEVENT BEGIN:VEVENT SUMMARY:No flows in vein: blood\, oxygen\, and pumping - oh my! DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-32@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Nick Battista (The College of New Jersey)\nFrom hear t tubes to respiratory breathing\, many organisms use valveless pumping me chanisms for internal flow transport. These pumping mechanisms were first seen in basal chordates\, e.g.\, tunicates\, where the drove through throu gh their open circulatory systems. As evolution took its course these pump ing techniques begun to be found in insect hearts and during first stage o f vertebrate heart development\, when the heart is nothing more than a val veless tube. However\, valveless pumping is not unique to only circulatory systems\; some anthropods\, such pycnogonids (sea spiders) use it for res piratory purposes as well. In this talk we will use fully-coupled fluid-st ructure interaction models to explore various valveless pumping techniques and their implications for internal flows produced across a variety of or ganisms and biological scales.\n\nhttps://conferences.maths.unsw.edu.au/ev ent/2/contributions/32/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/32/ END:VEVENT BEGIN:VEVENT SUMMARY:Extended logistic growth model for heterogeneous populations DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-380@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Wang Jin (School of Mathematical Sciences\, Queensla nd University of Technology)\nCell proliferation is the most important cel lular-level mechanism responsible for regulating cell population dynamics in living tissues. Modern experimental procedures show that the proliferat ion rates of individual cells can vary significantly within the same cell line. However\, in the mathematical biology literature cell proliferation is typically modelled using a classical logistic equation with a constant proliferation rate\, and this approach neglects variations in the prolifer ation rate. In this work we consider a discrete mathematical model of cell migration and cell proliferation\, modulated by volume exclusion (crowdin g) effects\, with variable rates of proliferation across the total populat ion. We refer to this variability as heterogeneity. Constructing the conti nuum limit of the discrete model leads to a generalisation of the classica l logistic growth model. Comparing numerical solutions of the model to ave raged data from discrete simulations shows that the new model captures the key features of the discrete process. Applying the extended logistic mode l to simulate a proliferation assay using rates from recent experimental l iterature shows that neglecting the role of heterogeneity can\, at times\, lead to misleading results.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/380/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/380/ END:VEVENT BEGIN:VEVENT SUMMARY:The emergence of neuromechanical resonance in jellyfish locomotion DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-157@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Alexander Hoover (Tulane University)\nIn order for a n organism to have an robust mode of locomotion\, the underlying neuromusc ular organization must be maneuverable in a changing environment. In jelly fish\, the activation and release of muscular tension is governed by the i nteraction of pacemakers with the underlying motor nerve net that communic ates with the musculature. This set of equally-spaced pacemakers located a t bell rim alter their firing frequency in response to environmental cues\ , forming a distributed mechanism to control the bell's muscular contracti on. When turning\, pacemakers induce an asymmetrically timed contraction w ith the bell musculature. In this work\, we explore the control of neuromu scular activation with a model jellyfish bell immersed in a viscous fluid and use numerical simulations to describe the interplay between active mus cle contraction\, passive body elasticity\, and fluid forces. The fully-co upled fluid structure interaction problem is solved using an adaptive and parallelized version of the immersed boundary method (IBAMR). This model i s then used to explore the interplay between the speed of neuromechanical activation\, fluid dynamics\, and the material properties of the bell.\n\n https://conferences.maths.unsw.edu.au/event/2/contributions/157/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/157/ END:VEVENT BEGIN:VEVENT SUMMARY:Dynamical conditions for the containment of HIV infection by CD8+ T Cells – a variable structure control approach DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-50@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Anet Jorim Norbert Anelone (Theoretical biology\, Ut recht University)\nIn the study of the Human Immunodeficiency Virus (HIV) infection dynamics\, the reproductive ratio is a well known tool which pro vides a steady-state condition to determine the outcome of the infection. This paper assesses the control of HIV by the immune response. Dynamical c onditions for the containment of HIV infection by the HIV-specific CD8+ T cell response are evaluated using a model of HIV dynamics in vivo in which HIV-infected cells are killed before they start producing new virion. The reachability paradigm from Variable Structure Control (VSC) theory is use d to formulate a dynamical condition for immunity. Simulation results show that this reachability condition effectively monitors the immunological r equirements to contain HIV. This work also suggests that the cytolytic kil ling mechanism of CD8+ T cells operates as a boundary layer control to con tain HIV infection. Together\, the findings indicate that in contrast to t he reproductive ratio\, the proposed VSC approach delivers a framework to assess the effects of nonlinear dynamics and uncertainty as well as provid ing a means to investigate immunotherapy strategies.\n\nhttps://conference s.maths.unsw.edu.au/event/2/contributions/50/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/50/ END:VEVENT BEGIN:VEVENT SUMMARY:Development and validation of a model of renal oxygen transport in the rat renal medulla DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-61@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Chang-Joon Lee (School of Engineering and Informatio n Technology\, Murdoch University\, Australia)\n*Background and Purpose:* Renal hypoxia is postulated to be a leading cause of acute kidney injury\, and the renal medulla is known to be most susceptible to hypoxia. The abi lity to accurately predict normal and abnormal oxygen states in terms of t issue oxygen tension (PO2) within the renal medulla is highly desirable\, as among other uses predicted medullary PO2 can be correlated with local t issue damage. In this study\, we have developed a computational model for blood and oxygen transport within the renal medulla to estimate medullary tissue PO2.\n\n*Materials and Methods:* A multiscale modelling approach wa s used to model the blood flow and oxygen transport within a realistic 3-D medullary geometry. At the macroscale level\, the blood flow in the medul lary vasa recta was modelled using a set of three\, coupled\, 3D porous me dia models\, each representing the blood flow in the descending vasa recta \, long ascending vasa recta\, and short ascending vasa recta. Another set of three advection-diffusion models\, each coupled with a blood flow mode l\, were employed to simultaneously represent the oxygen transport through out the whole medulla. In addition to the six top-level models\, four diff usive oxygen transport models were employed at the microscale level to des cribe the distribution of oxygen in two spatial dimensions across the rena l tissue surrounding the vasculature. Each low-level model represents a si ngle vascular bundle and associated tissue. The low-level models were loca ted in the outer and inner stripes\, near the base and near the tip of the inner medulla. The model predictions\, based on reported geometry\, model parameters\, boundary conditions and source-sink terms obtained from the literature on the rat kidney were found by iterating between the macroscal e and microscale sub-models until all ten sub-models were satisfied simult aneously. \n\n*Results & Discussion:* The model predictions were validated by simulating eight sets of published experimental data in rats (four set s of control groups and four sets of treatment groups\, reported in four i ndependent papers). These experiments examined the effects of acute hemodi lution\, acute renal ischemia/reperfusion (IR)\, and chronic administratio n (30 days) of dinitrophenol (DNP). For each validation test\, model param eters were altered according to experimental observations. Tissue and/or m icrovascular PO2 predicted by the model was then compared with that observ ed experimentally.\n\nAll model predictions for control groups were within ± 1 standard error of the mean (SEM) value observed experimentally. Most of the model predictions for treatment groups were also within ± 1 SEM\, except for later stages in the acute hemodilution experiment\, where the model predicted PO2 exceeded the measured PO2 by more than 7 SEM. Deviatio ns from the model predictions are probably due to unidentified external or intra-renal processes\, triggered by pathologic processes\, but not accou nted for in the model or measured in the experiments. \n \n*Conclusion:* T he validation tests confirmed that the proposed renal medullary PO2 model is robust and can accurately capture the behaviour of renal medullary oxyg enation in both normal and early pathologic states in the rat.\n\nhttps:// conferences.maths.unsw.edu.au/event/2/contributions/61/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/61/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal amplitude and frequency of breathing DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-36@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Faheem Zaidi (Institute of Natural and Mathematical Sciences\, Massey University\, Auckland\, New Zealand)\nPhysiological leve ls of oxygen and carbon dioxide in the blood are tightly regulated by vary ing the pattern of breathing\, but this can be achieved with different com binations of amplitude and frequency. Why a specific combination of amplit ude and frequency of breathing is observed remains a mystery. The aim of t his study is to explore the hypothesis that the particular combination rea lised is optimal with respect to some objective function. Several objectiv e functions have been suggested in the literature\, such as the rate of wo rk during inhalation\, the average force exerted by the respiratory muscle s\, and the weighted sum of volumetric acceleration and work during inhala tion\; all of these objective functions provide physiologically acceptable minima under normal conditions. Resolving this issue requires optimal sol utions of mathematical models that reflect more accurately the complex int eraction between lung mechanics and gas exchange\, but this in turn requir es the development of new computational methodologies. To help achieve thi s goal\, we constructed a simple mathematical model\, consisting of two pi ecewise linear differential equations\, that mimics gas exchange in the lu ngs. By using concepts from optimal control theory\, we found the necessa ry conditions that minimise a given objective function subject to several constraints\, such as satisfying the differential equations and maintainin g one of the variables at a given average value. We could then solve the optimal control problem both analytically and numerically. Our method can be extended to models with higher dimensions.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/36/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/36/ END:VEVENT BEGIN:VEVENT SUMMARY:Majority decisions by four or five members: rules that can be form ed and maintained in viral populations to exclude free riders. DTSTART;VALUE=DATE-TIME:20180710T010000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-49@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Shuhei Miyashita (Tohoku University)\nMost of the vi ral gene products are shared among a viral population in a host cell\, whi ch accumulates up to $10^6$ to $10^7$ genomes. High mutation rates in vira l genome replication bring genetic variety to the intracellular population \, and this makes the situation social: mutant genomes that do not code in tact gene products can survive as free riders\, by using the gene products from the other genomes in the intracellular population. We have previousl y shown that two plant RNA viruses\, Japanese soil-borne wheat mosaic viru s and tomato mosaic virus\, infect a host cell by 5-6 and ~4 genomes in av erage\, respectively\, and proposed that this cell infection by a limited number of genomes enhance stochastic separation of free riders from others \, resulting in exclusion of free riders from the whole population [1\,2]. Here we simulated the evolution of average number of viral genomes to inf ect a cell (multiplicity of infection\, or MOI\, in virology). The simulat ion showed that MOI evolves to 4-5 *in silico*. This result could be expla ined by a balance between exclusion of free riders by smaller MOI and avoi dance of stochastic failure of infection. Consistently\, our further exper iments showed that a tripartite plant RNA virus\, cucumber mosaic virus (C MV)\, also has MOIs of 3-5 for its multiple genomic segments in multiple h osts.\n \nThe MOI of 4-5 does enhance separation of free riders from other s\, but still allows their co-existence for a certain period of time. This requires “decisions” by viruses. The intracellular populations exclus ively consisting of free riders cannot infect new adjacent cells\, and tho se exclusively consisting of intact genomes will infect the adjacent cells at high probability\; those consisting of both free riders and intact gen omes need to decide whether to infect the adjacent cells\, depending on th e ratio of free riders in each intracellular population. Our simulations s howed that a majority-decision-like system\, where the cell-to-cell infect ion probability sharply changes between 0 and 1 at a certain threshold for the ratio of free riders\, can be favoured by plant viruses. The simulati on result was supported by a co-inoculation experiment of CMV variants tha t carry a functional cell-to-cell movement protein gene or a dysfunctional one.\n\n[1] Miyashita and Kishino (2010) “Estimation of the size of gen etic bottlenecks in cell-to-cell movement of soil-borne wheat mosaic virus and the possible role of the bottlenecks in speeding up selection of vari ations in trans-acting genes or elements.” *J Virol* 84(4) 1828-1837.\n[ 2] Miyashita\, Ishibashi\, Kishino and Ishikawa (2015) “Viruses roll the dice: the stochastic behavior of viral genome molecules accelerates viral adaptation at the cell and tissue levels.” *PLOS Biol* 13(3) e1002094.\ n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/49/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/49/ END:VEVENT BEGIN:VEVENT SUMMARY:Cell-free versus cell-to-cell viral transmission in a spatial stru cture DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-73@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Koichi Saeki (Utrecht University)\nViruses have two modes spread in a host body\, one is to release infectious particles from infected cells (cell-free) and the other is to infect directly from an inf ected cell to an adjacent cell (cell-to-cell). Since the mode of spread af fects the evolution of life history traits\, such as virulence\, it is imp ortant to reveal which mode is selected. Here we show the evolutionarily s table proportion of cell-free and cell-to-cell infection\, and how it depe nds on the spatial distribution of target cells. Using an epidemic model o n a 2D regular lattice\, we consider the infection dynamics by pair approx imation and check the evolutionarily stable strategy. We also conduct the Monte-Carlo simulation to observe evolutionary dynamics. We show that a hi gher cell-to-cell infection is selected as target cells become clustered. The selected strategy depends not only on the degree of clustering but als o the abundance of target cells per se.\n\nhttps://conferences.maths.unsw. edu.au/event/2/contributions/73/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/73/ END:VEVENT BEGIN:VEVENT SUMMARY:Topology-dependent density optima for efficient simultaneous netwo rk exploration DTSTART;VALUE=DATE-TIME:20180709T021000Z DTEND;VALUE=DATE-TIME:20180709T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-335@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Daniel Wilson (The University of Oxford)\nFrom the f oraging strategies of large organisms\, to T-cells hunting pathogens\, to proteins examining strands of DNA\, carefully optimised search processes a re a phenomenon that pervades throughout nature at many scales. Often thes e search processes do not proceed in isolation\, but instead many instance s proceed in parallel\, competing for space and resources. In this talk I shall discuss optimisation of search processes on networked topologies whe re the searchers interact with each other through competition for space. T aking the simple exclusion process as the fundamental model for spatial in teractions\, I consider search strategies that seek to minimise the averag e cover time for individuals that search in parallel. We will see that the optimal strategy is to implement parallel searching at an optimal density of searchers that depends heavily on the given network topology\, and tha t the optimal density can be well predicted by the spectral gap of the net work. These results are verified over a broad class of networks\, as well as real-world transport networks such as the London tube network. I will c onclude by considering an asymmetric search process that reveals unexpecte d changes in efficiency between classes of networks.\n\nhttps://conference s.maths.unsw.edu.au/event/2/contributions/335/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/335/ END:VEVENT BEGIN:VEVENT SUMMARY:What do spider monkeys\, Peruvian fishing boats and sulking albatr oss have in common? DTSTART;VALUE=DATE-TIME:20180712T060000Z DTEND;VALUE=DATE-TIME:20180712T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-199@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Alex James (University of Canterbury)\nLévy walks h ave dominated foraging theory since they were brought to our attention in the mid-nineties. However the path to enlightenment has not been smooth. I will take you on a brief history of Lévy foraging theory that has played out in the published literature. Are they the solution to finding your ke ys or an ecological version of the quaternion?\n\nhttps://conferences.math s.unsw.edu.au/event/2/contributions/199/ LOCATION:University of Sydney -/--Eastern Avenue Auditorium URL:https://conferences.maths.unsw.edu.au/event/2/contributions/199/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling for autophagosome formation DTSTART;VALUE=DATE-TIME:20180709T054000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-317@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yuji Sakai (The University of Tokyo)\nAutophagy is a n intracellular degradation process mediated by the autophagosome. The mem brane dynamics of autophagosome formation is unique and complicated\, whic h involves development of a small membrane cisterna into a cup-shaped stru cture and a double membrane spherical structure by closing the edge [1].\n \nIn this presentation\, we discuss the mechanism of autophagosome formati on from a physical point of view. A flat cisterna has a highly-curved rim\ , which is energetically unstable. As increasing the membrane surface\, th e rim area also increases. In order to reduce the energy\, the cisterna is spontaneously curled by decreasing the rim area. Accordingly\, a shape tr ansition occurs suddenly due to the first order transition [2]. \n\nHoweve r\, live-imaging experiments have shown that autophagosome formation takes place gradually and sudden closure of a flat membrane is not observed. We hypothesize the presence of protein(s) that stabilize the highly-curved r im\, which enables gradual enclosure. Indeed\, several autophagy proteins are present at the rim.\n\nThus\, we consider the effects of the rim-stabi lizing proteins on the dynamics of autophagosome formation. We show that t he proteins localize at the highly-curved rim and stabilize it. As a resul t\, intermediate cup-shape states appear and the closing dynamics becomes moderate similar to that of autophagosome formation *in vivo*.\n\n[1] Mizu shima 2017\, PMID28186333\n[2] Knorr *et al*.\, 2012\, PMID22427874\n\nhtt ps://conferences.maths.unsw.edu.au/event/2/contributions/317/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/317/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling the evolution of sex-specific dominance in response to s exually antagonistic selection DTSTART;VALUE=DATE-TIME:20180711T010000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-12@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hamish Spencer (University of Otago)\nArguments abou t the evolutionary modification of genetic dominance have a long history i n genetics\, dating back over 100 years. Mathematical investigations have shown that modifiers of the level of dominance at the locus of interest ca n only spread at a reasonable rate if heterozygotes at that locus are comm on. One hitherto neglected scenario is that of sexually antagonistic selec tion\, which is ubiquitous in sexual species and can also generate the sta ble high frequencies of heterozygotes that would be expected to facilitate the spread of such modifiers.\n\nI will present a recursion-equation mode l that shows that sexually specific dominance modification is a potential outcome of sexually antagonistic selection. The model predicts that loci w ith higher levels of sexual conflict should exhibit greater differentiatio n between males and females in levels of dominance and that the strength o f antagonistic selection experienced by one sex should be proportional to the level of dominance modification. These predictions match the recent di scovery of a gene in Atlantic salmon\, in which sex-dependent dominance le ads to earlier maturation of males than females\, a difference that is str ongly favoured by selection. Finally\, I suggest that empiricists should b e alert to the possibility of there being numerous cases of sex-specific d ominance.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/1 2/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/12/ END:VEVENT BEGIN:VEVENT SUMMARY:Staged HIV transmission and treatment in a dynamic model with conc urrency DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-231@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Katharine Gurski (Howard University)\nHIV progressio n studies have asserted three stages: acute infection\, chronic infection\ , and AIDS. We develop a model with three stages and include an infection class with non-uniform Highly Active Anti-Retroviral Treatment leading to viral suppression. Capturing the incidence rate of HIV in minority U.S. wo men requires a model stratified by race/ethnicity and sexual behaviour in addition to assumptions of assortative partner choice and concurrent relat ionships. We include the effect of concurrency following the work of Watts and May (1992\, Math. Biosciences) who in a simple deterministic model al lowed for overlapping partnerships and infection from either a new sexual partner or a longtime partner who was uninfected at the start of the partn ership. This model was hampered by the assumption of a latent phase which generated a non-autonomous system. We present a new autonomous determinist ic model of the effect of concurrent sexual partnerships that allows for a n analytical study of disease transmission. We incorporate the effect of concurrency through the newly derived force of infection term in a mathema tical model of the transmission of HIV through sexual contact in a populat ion stratified by sexual behaviour and race/ethnicity. Time series analysi s\, as well as parameter sensitivity analysis\, determine which strategy h as the largest impact in the short and long term. Interventions focused on encouraging chronically infected into viral suppression\, as well as inte rventions focused on maintaining viral suppression have the largest impact on the long term dynamics\, and the latter having the largest impact on t he heterosexual community due to current racial disparity in treatment. Wh ile reducing concurrency likelihood and duration positively impacts the lo ng term dynamics\, left unchecked\, an increase in concurrency will signif icantly raise the values of the endemic equilibrium.\n\nhttps://conference s.maths.unsw.edu.au/event/2/contributions/231/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/231/ END:VEVENT BEGIN:VEVENT SUMMARY:Rational steady state parametrizations for biochemical reaction sy stems DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-53@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Matthew Johnston (San Jose State University)\nClassi cal results give structural conditions under which the steady state set of a (bio)chemical reaction system has a monomial parametrization. This prop erty has been studied extensively in the context of characterizing a mecha nism's capacity for mono- and multi-stationarity. In this talk\, we genera lize the existing structural framework and derive sufficient conditions fo r guaranteeing that the steady states have a rational parametrization. App lications include the EnvZ-OmpR osmoregularity pathway and the Shuttled WN T signalling pathway.\n\nhttps://conferences.maths.unsw.edu.au/event/2/con tributions/53/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/53/ END:VEVENT BEGIN:VEVENT SUMMARY:A transcriptional regulatory network of cell type specific gene ex pression in hematopoiesis DTSTART;VALUE=DATE-TIME:20180711T052000Z DTEND;VALUE=DATE-TIME:20180711T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-383@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jun Nakabayashi (Yokohama-city University)\nDuring d ifferentiation process\, cell type specific gene expression pattern is est ablished by orchestrate regulatory network of transcription factors (TFs). Resolving the structure of the transcriptional regulatory network (TRN) is promising way to understand the detailed mechanism of cell differentiat ion.\n\nHere I estimate a transcriptional regulatory network determining t he cell type specific gene expression pattern in hematopoiesis obtained fr om public database (GEO accession number GSE60101)[1]. Transcription fact ors upregulated in at least one cell type through hematopoiesis are identi fied as cell type specific transcription factors. It is simply assumed th at the expression of the transcription factor is regulated by transcriptio n factors of those binding motifs are enriched in its promoter region. A transcriptional regulatory network of cell type specific gene expression i s estimated based on the expression profile and distribution of enriched t ranscription factor binding motifs in the promoter regions. The network i s represented as a directional graph. And the structure of the network is analyzed based on graph theory. \n\nBranching process where two differen t cell types differentiate from one progenitor through hematopoiesis is es pecially focused in this study. Transcriptional regulatory networks of Co mmon Myeloid Progenitor (CMP) and Common Lymphoid Progenitor (CLP) specifi c gene expressions are constructed. To compare with these regulatory netw orks\, a regulatory network of hematopoietic stem cell is also constructed as a pluripotent cell.\n\nThrough the network analysis it is clarified th at the modular structure in the transcriptional regulatory network is deve loped through cell differentiation process. In CMP network TFs mainly reg ulated by Cebp family member is obviously clustered. Average expression l evels of TFs in this Cebp cluster gradually increase through granulocyte d ifferentiation. It is suggested that these TFs in Cebp cluster are myeloi d lineage signature TFs. On the other hand\, TFs mainly regulated by Lef1 are clustered in CLP network. Average expression levels of Lef1 cluster TFs increase in lymphoid lineage cells such as T cell and B cell. The net work analysis in this study suggests that development of the modular struc tures composed of specific cell lineage signature TFs are critical mechani sm determining cell fate.\n\n[1] Chromatin state dynamics during blood for mation. *Science* 2014 Aug 22\;345(6199):943-9\n\nhttps://conferences.mat hs.unsw.edu.au/event/2/contributions/383/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/383/ END:VEVENT BEGIN:VEVENT SUMMARY:A comparison of models of the glucose-insulin regulatory system fo r applications in circadian research DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-453@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ethan Ryan (School of Physics\, The University of Sy dney)\nCircadian clocks control 24-hour rhythms in the human body\, includ ing glucose and insulin dynamics. Glucose tolerance changes depending on t he time of day and misalignment between environmental stimuli such as ligh t and food and internal circadian clocks\, e.g.\, as observed in shiftwork \, is associated with metabolic disturbances and diabetes. The mechanisms of these are poorly understood. A number of mathematical models of circadi an clocks and those of glucose-insulin dynamics have been developed. Howev er\, no model accounts for the interaction between the two systems. Here w e examine and compare key existing models of glucose-insulin regulatory sy stem with the aim to select the most appropriate model for incorporation o f circadian rhythms.\n\nA large number of mathematical models designed to study glucose-insulin dynamics have been developed over the past few decad es and account for such key features as (i) ultradian oscillations\, (ii) response to glucose infusion\, and (iii) glucose homeostasis. The seminal model able to reproduce these oscillations was developed by Sturis *et al* . (1991) utilising a system of 6 ODEs. Since then\, a number of other mode ls have been adapted from this model\, aiming to either reformulate the St uris model—often as a system of DDEs—or to extend the model to allow o ther applications\, for example in the Intravenous Glucose Tolerance Test. However\, comparisons of the models with physiological experimental studi es have been relatively limited in scope. \n\nIn this work\, we compare th e qualitative and quantitative predictions of the Sturis *et al*. (1991)\, Tolić *et al*. (2000)\, and Li *et al*. (2006) models and two other mode ls with experimental results\, under constant glucose infusion. We show th e different parameter ranges in which the models display sustained ultradi an oscillations and how this corresponds to the expected behaviour in publ ished physiological studies. We also test the mean values\, amplitudes\, a nd frequencies of the simulated glucose and insulin concentrations against experimental studies. This sophisticated comparison of the models allows us to select the most appropriate model to incorporate circadian rhythms.\ n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/453/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/453/ END:VEVENT BEGIN:VEVENT SUMMARY:The effect of genomic imprinting on QST DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-13@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Anna Santure (University of Auckland)\nA gene is imp rinted when its level of expression is dependent on the sex of the parent it was inherited from. An unusual consequence of imprinting is that male a nd female additive genetic variances differ\, and so ignoring imprinting c an lead to misspecification of a number of evolutionary parameters\, inclu ding the predicted response to selection. QST - the differentiation of qua ntitative traits between populations - is a consequence of the combined ef fects of both neutral and selective forces acting across the metapopulatio n. QST is often compared to FST\, the differentiation across populations m easured at (presumably) neutral loci\, in order to determine the role of s election in shaping trait divergence between populations. Previous theoret ical work has demonstrated that properties of the genetic basis of a quant itative trait\, such as inbreeding\, dominance and epistasis\, can margina lly inflate or deflate QST\, although it is unlikely that any of these pro perties would be strong enough to “hide” the effects of strong selecti on. Here\, we assess the effects of imprinting on QST by exploring a two-p opulation model of migration\, inbreeding\, selection and imprinting. We s how that imprinting is unlikely to hide the effects of divergent selection \, lending further support to the general conclusion that strong selection is unlikely to be masked by inter- and intra-locus interactions. However\ , the magnitude of imprinting’s effect on QST is surprisingly large – ignoring imprinting\, and hence the differences between male and female ad ditive genetic variances\, will lead to considerable over-estimation of th e strength of selection.\n\nhttps://conferences.maths.unsw.edu.au/event/2/ contributions/13/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/13/ END:VEVENT BEGIN:VEVENT SUMMARY:A numerical simulation of an edge-based SEIR model on random netwo rks DTSTART;VALUE=DATE-TIME:20180709T064000Z DTEND;VALUE=DATE-TIME:20180709T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-313@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Cherrylyn Alota (University of the Philippines Dilim an / University of the Philippines Cebu)\nNetworks representing the spread of infectious diseases in populations have been widely studied. Here\, w e formulate an SEIR model using an edge-based approach on a static random network with arbitrary degree distribution. The corresponding basic reprod uction number and final epidemic size are computed. The SEIR model is used to investigate the stochasticity of the SEIR dynamics. Assuming exposed\ , infection and recovery each happen at constant rates\, stochastic simula tions of the SEIR dynamics are performed applying continuous-time Gillespi e's algorithm given a Poisson or a power law with exponential cut-off degr ee distributions. The resulting simulations match well with the numerical predictions of the SEIR model given the initial conditions. Final epidemi c size remains unchanged when the initial infecteds are varied. On the oth er hand\, varying the disease parameters of the SEIR model affects the tim e when the epidemic accelerates\, the peak of the epidemic\, and the final epidemic size. These results capture scenarios of an epidemic in a netwo rk implying control strategies in the disease transmissions.\n\nhttps://co nferences.maths.unsw.edu.au/event/2/contributions/313/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/313/ END:VEVENT BEGIN:VEVENT SUMMARY:Host-parasite co-evolution in space: it’s reproduction that real ly matters DTSTART;VALUE=DATE-TIME:20180710T020000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-74@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michael Boots (UC Berkeley)\nThe impact of spatial s tructure on evolutionary outcomes can be profound due to both ecological a nd genetic correlations. One of the best developed areas of spatial evolut ionary theory has focused on the coevolution of hosts and parasites. There are profound impacts of local as opposed to global infection on both para site and host evolutionary outcomes. Using a combination of pair approxima tions to apply approximate adaptive dynamics to spatial models and simulat ions we show the central importance of reproduction to the outcome. For ex ample spatial effects on the evolution of resistance arise to due less cos tly local reproduction rather than spatial epidemiological patterns\, the host spatial structure that is created by local reproduction has profound effects on parasite evolution even if transmission is mostly global and th e impact of disease on reproduction rates impacts ESS virulence. This high lights the importance of indirect spatial effects on the spatial evolution ary ecology of focal traits.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/74/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/74/ END:VEVENT BEGIN:VEVENT SUMMARY:Models for the spread of $\\textit{Wolbachia}$ in mosquito populat ions DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-370@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sarah Belet (Monash University)\nThe vector-borne De ngue fever poses a major health issue in tropic environments\, which inclu des areas such as far-north Queensland. Historically\, attempts at curtail ing the spread of dengue have focused on controlling the size and spread o f mosquito populations that carry the virus. Several factors make this an astronomically difficult task to accomplish on any reasonable scale\, howe ver\, and so more novel methods of suppressing dengue outbreaks are being explored. One such method is the introduction of bacteria called *Wolbachi a* into mosquito populations\, which prevents mosquitoes from passing on v iruses to humans. A *Wolbachia* invasion has strong potential to completel y saturate mosquito populations due to a mechanism called cytoplasmic inco mpatibility. The mathematical modelling problem here becomes twofold-first \, the task of inferring the position of mosquito populations\, and then t he modelling of *Wolbachia* spreading through these populations. Here\, we will be discussing the effects and mechanisms of *Wolbachia* in more deta il\, including the phenomenon of cytoplasmic incompatibility. Next\, recen t developments in modelling mosquito populations such as the use of semi a gent-based models will be outlined\, within the context of predicting the spread of *Wolbachia*.\n\nhttps://conferences.maths.unsw.edu.au/event/2/co ntributions/370/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/370/ END:VEVENT BEGIN:VEVENT SUMMARY:A model for epidemic dynamics in a community with visitor subpopul ation DTSTART;VALUE=DATE-TIME:20180709T091500Z DTEND;VALUE=DATE-TIME:20180709T093000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-233@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Emmanuel Dansu (Research Center for Pure and Applied Mathematics\, Graduate School of Information Sciences\, Tohoku University \, Sendai\, Japan)\nWith a five dimensional system of ordinary differentia l equations based on the SIR model\, we consider the dynamics of epidemics in a community which consists of residents and visitors/tourists over a s hort period of time. The total population size of the community is taken t o be constant\, ignoring its change due to any birth and death in the peri od under consideration. Also\, the resident and visitor populations are re spectively constant. We assume that every immigrating visitor is susceptib le and is likely to be infected during their stay in the community. Furthe rmore\, infected visitors can carry on their activities normally during th eir stay in the community thus still appearing like susceptible visitors. From the analysis of the model\, we obtained a threshold expected value of duration per visitor which determines whether an epidemic persists in the community or not. More so\, the basic reproduction numbers with respect t o the entire community as well as the resident and visitor populations are obtained and they can help us to formulate important public health polici es in order to contain epidemics in the community.\n\nhttps://conferences. maths.unsw.edu.au/event/2/contributions/233/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/233/ END:VEVENT BEGIN:VEVENT SUMMARY:Understanding the dynamics of reactivation from latency in macaque s infected with tagged simian immunodeficiency virus DTSTART;VALUE=DATE-TIME:20180711T063000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-142@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mykola Pinkevych (University of New South Wales Sydn ey)\nModern anti-retroviral therapy can effectively control HIV. However\ , the virus cannot be eradicated due to the presence of latently infected CD4+ cells that cause the reactivation of virus when a patient stops anti- retroviral treatment. \n\nThere is a lack of knowledge about the basic dyn amics of reactivation of latently infected cells and the interaction of vi rus with immunity. We combined mathematical modelling with a novel experi mental method of ‘barcoded’ viruses to quantify the contribution of in dividual latently infected cells. \n\nRhesus macaques were infected intrav enously with a sequence-tagged SIV-M virus with ~10\,000 different barcode s. Animals were treated with antiretroviral therapy for various times pri or to treatment interruption. After interruption serum samples were subjec ted to gene sequencing in order to identify the frequency of individual ba rcoded viruses.\n\nWe developed a mathematical model of growth of virus fr om different latently infected cells. Applying this model to experimental data we estimate that the frequency of reactivation from latency ranges fr om around 20 reactivations per day to 0.5 reactivations per day\, dependin g on the timing and duration of treatment. A single reactivated latent cel l can produce an average viral load equivalent to ~0.1-0.5 viral copies/ml of virus\, depending on assumptions about duration of drug action. \n\nWe have also studied the virological parameters that may predict reactivatio n rate. When comparing animals treated starting on day 4 and day 27 post-i nfection and find that monkeys treated on day 4 have 40-fold higher reacti vation rate per SIV DNA copy then monkeys treated on day 27. This differe nce cannot be simply explained by differences in immune activation or immu ne response. We analyse this by modelling the dynamics of DNA accumulation and viral-immune interactions. \n\nThe combination of mathematical modell ing of viral dynamics of barcoded virus provides a powerful tool to unders tand latency formation\, maintenance and reactivation in SIV / HIV.\n\nhtt ps://conferences.maths.unsw.edu.au/event/2/contributions/142/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/142/ END:VEVENT BEGIN:VEVENT SUMMARY:Estimating the basic reproduction number at the beginning of an ou tbreak DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-62@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sawitree Boonpatcharanon (York University)\nThe basi c reproduction number\, $R_0$\, is a key quantity allowing public health o fficials to track how quickly an outbreak spreads through a population. In this talk\, we compare several different estimators of $R_0$ assuming t hat only weekly data is available\, with a focus on the early stages of an outbreak. We compare four estimators: a variant on maximum likelihood\, incidence decay\, incidence decay with exponential adjustment\, and parti ally observed Markov process approaches. Our simulations concentrate on a flu epidemic\, and several different scenarios are considered. In particul ar\, we study also the setting of model misspecification\, when one model structure is fit to data generated by a different model. Benefits and draw backs of each $R_0$ estimator will be discusssed.\n\nhttps://conferences.m aths.unsw.edu.au/event/2/contributions/62/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/62/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling the migration of astrocytes during retinal development DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-5@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tracy Stepien (University of Arizona)\nRetinal vascu lature is essential for adequate oxygen supply to the inner layers of the retina\, the light sensitive tissue in the eye. In embryonic development\, formation of the retinal vasculature via angiogenesis is critically depen dent on prior establishment of a mesh of astrocytes\, which are a type of brain glial cell. Astrocytes emerge from the optic nerve head and then mi grate over the retinal surface as a proliferating cell population in a rad ially symmetric manner. Astrocytes begin as stem cells\, termed astrocyte precursor cells (APCs)\, then transition to immature perinatal astrocytes (IPAs) which eventually transition to mature astrocytes. We develop a pa rtial differential equation model describing the migration of astrocytes w here APCs and IPAs are represented as two subpopulations. Numerical simul ations are compared to experimental data to assist in elucidating the mech anisms responsible for the distribution of astrocytes.\n\nhttps://conferen ces.maths.unsw.edu.au/event/2/contributions/5/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/5/ END:VEVENT BEGIN:VEVENT SUMMARY:Visualising mitochondrial networks in a beating heart cell DTSTART;VALUE=DATE-TIME:20180711T053000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-94@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Adarsh Kumbhari (University of Sydney)\nMitochondria are specialised organelles that produce adenosine triphosphate (ATP)\, a molecule used by cells as an energy source. Mitochondria form dynamic netw orks that constantly undergo fission and fusion in response to increased A TP demand. There is a lack of high-resolution data tracking the reorganisa tion mitochondrial networks in a beating heart cell. We use an agent-based model to simulate a mitochondrial network reorganising in beating heart c ell. Our visualisation highlights how mitochondrial networks respond to a variety of stressors such as increased cellular respiration and localised hypoxia.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/94 / LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/94/ END:VEVENT BEGIN:VEVENT SUMMARY:Spatial and temporal analysis of FluTracking data and implications for influenza spread in Australia DTSTART;VALUE=DATE-TIME:20180710T005000Z DTEND;VALUE=DATE-TIME:20180710T011000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-291@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Dennis Liu (The University of Adelaide)\nModelling t he spread of influenza across Australia is of substantial public health co ncern. However\, there are many challenges in creating accurate models\, i ncluding how best to capture the spatial and temporal characteristics of t he disease spreading process\, and aligning with the actual contact proces s and mobility of individuals in the population. How influenza spreads spa tially\, whether by infecting neighbouring regions or through major domest ic centres via air traffic\, is of particular interest in building predict ive models. Recent work has suggested the spread of influenza in the Unite d States is dominated by work commutes rather than air traffic. In contras t\, influenza in Australia has been shown to have highly synchronized epid emics between major cities across large geographic distances and varying c limates.\n\nFluTracking is a participatory online health surveillance syst em for monitoring influenza-like-illness (ILI)\, with one of its principal aims to detect the onset of influenza in Australia. Since 2010\, there ar e over 10\,000 participants each year\, with participation continuing to i ncrease. In this work\, we analyse weekly reports from the FluTracking sys tem from May 2011 to October 2017 to infer spatial and temporal dynamics o f influenza in Australia. These dynamics could then be used as a starting point for building contact and contagion networks in models for epidemic f orecasting\, and lead to a greater understanding of the mechanisms behind the spread of influenza-like-illness in Australia.\n\nhttps://conferences. maths.unsw.edu.au/event/2/contributions/291/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/291/ END:VEVENT BEGIN:VEVENT SUMMARY:Inducing chondrogenesis in layered tissue engineering constructs w ith exogenous TGF-β DTSTART;VALUE=DATE-TIME:20180709T064000Z DTEND;VALUE=DATE-TIME:20180709T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-321@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mike Chen (University of Adelaide)\nThe differentiat ion of mesenchymal stem cells (MSCs) into chondrocytes (native cartilage c ells)\, or chondrogenesis\, is a key step in the tissue engineering of art icular cartilage. Chondrogenesis is regulated by transforming growth facto r-beta (TGF-β)\, a short-lived cytokine whose effect is prolonged by stor age in the extracellular matrix (ECM). Tissue engineering applications req uire the complete differentiation of an initial population of MSCs\, and t wo common strategies used to achieve this in vitro are (1) co-culture the MSCs with chondrocytes\, which constitutively produce TGF\; or (2) add exo genous TGF-β. We are motivated by recent experiments where a tissue engin eering construct is seeded with cells in spatially separated layers\, with a layer of MSCs lying below a layer of chondrocytes\, and is then stimula ted with exogenous TGF-β from above. \n\nTo investigate the efficacy of t his seeding strategy we develop a reaction-diffusion model for the interac tions between the TGF-β\, MSCs and chondrocytes. A feature of this model is that it describes the different forms TGF-β takes throughout its lifec ycle\, some of which are bound to the ECM (and so not diffusible)\, and th e process by which the TGF-β cytokine is cleaved from the molecular laten cy complex it is secreted with to become available to cell receptors. Usin g this model we demonstrate that the concentration of TGF-β required to i nduce chondrogenesis of the MSCs in the lower layer is not physically real istic for layers of equal depth (as used experimentally). We then suggest improvements to the current experimental protocols\, as well as compare th e use of the layered cell seeding strategy with a strategy where the initi al cell populations are well-mixed (which we have previously investigated with an ordinary differential equation model).\n\nhttps://conferences.math s.unsw.edu.au/event/2/contributions/321/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/321/ END:VEVENT BEGIN:VEVENT SUMMARY:Characterizing SHIV infection $\\textit{in vitro}$ and $\\textit{i n vivo}$ DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-29@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Shingo Iwami (Department of Biology\, Faculty of Sci ences\, Kyushu University\, Fukuoka 819-0395\, Japan)\nThe host range of h uman immunodeficiency virus (HIV) is quite narrow. Therefore\, analyzing H IV-1 pathogenesis *in vivo* has been limited owing to lack of appropriate animal model systems. To overcome this\, chimeric simian and human immunod eficiency viruses (SHIVs) that encode HIV-1 Env and are infectious to maca ques have been developed and used to investigate the pathogenicity of HIV- 1 *in vivo*. So far\, we have many SHIV strains that show different pathog enesis in macaque experiments. However\, dynamic aspects of SHIV infection have not been well understood. To fully understand the dynamic properties of SHIVs\, we focused on two representative strains — the highly pathog enic SHIV\, SHIV-KS661\, and the less pathogenic SHIV\, SHIV-#64 — and m easured the time-course of experimental data in cell culture and rhesus ma caque and analyzed them. I would like to discuss our quantitative results and future direction of this study.\n\nhttps://conferences.maths.unsw.edu. au/event/2/contributions/29/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/29/ END:VEVENT BEGIN:VEVENT SUMMARY:A computational simulation of vascular deformation when subject to internally and externally applied forces DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-262@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jessica Crawshaw (The University of Melbourne)\nThe walls of our blood vessels are under a constant mechanical load\, introduc ed by the blood pulsating through our vessels. Recent years have seen a su bstantial increase in the understanding of the interplay between the dynam ics of blood flow (haemodynamics) and vessel (vascular) morphology. Altera tions in the homeostatic distribution of mechanical forces exerted by bloo d on the vessel wall is correlated with various cardiovascular diseases\, including atherosclerosis and aneurysm development and rupture. Furthermor e\, alterations in the haemodynamic distribution have a notable effect on vascular development and remodelling. Experimental analysis of the effects of blood flow on the local vasculature is invasive and extremely difficul t to measure in real time. As such\, the development of computational mode ls to analyse the relationship between the local haemodynamics and the sur rounding vasculature is invaluable.\n\nIn this project we will develop a c omputational model to study how vessels deform when subject to internally and externally applied forces. Using the open source multicellular modelli ng software package\, Chaste\, we will employ a discretised approach to si mulate long time scale vascular wall deformation. A Voronoi tessellation-b ased model will be used to model vessel walls. This discretised model will enable us to examine how blood vessels deform when subject to internal an d external forces\, thus laying the foundations for future research examin ing vascular deformation due to haemodynamic pressure.\n\nhttps://conferen ces.maths.unsw.edu.au/event/2/contributions/262/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/262/ END:VEVENT BEGIN:VEVENT SUMMARY:Causes and potential consequences of conditional host dispersal: t he importance of spite in host populations DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-105@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ryosuke Iritani (UC Berkeley)\nSpatial structure owi ng to localized dispersal in hosts can have dramatic impacts upon the coev olutionary dynamics of hosts and parasites. The basic idea is that localiz ed dispersal in hosts can lead to localized transmission\, thereby selecti ng for costly resistance in hosts and lower virulence in parasites. Both o f these evolutionary forces are grounded on the altruism (i.e.\, costly to the actor but benefitial to recipients). From the viewpoints of the hosts \, however\, they can also utilize the pathogens to harm their neighbors ( biological weapon hypothesis)\, thereby gaining positive inclusive-fitness benefits overall. Despite this\, few studies looked at the causes and con sequences of host dispersal evolution. Here\, using mathematical models of inclusive fitness theory\, we show three understudied ideas. First\, diff erential costs of dispersal between susceptible and infected individuals c an modify the host population structure. Second\, if hosts can condition t heir dispersal propensity depending on the sickness (susceptible or infect ed)\, then the evolutionary dynamics of such conditional host dispersal ca n generate evolutionary bistabilities such that dispersal propensity biase s towards susceptible or infected individuals depending on the initial con ditions of the host populations. Finally\, we propose that such drasticall y different dispersal propensity could turn over the classic idea that spa tial structure can often favour increased resistance: rather\, differentia l costs of dispersal and/or conditional dispersal propensity in hosts coul d favour “spite” of the hosts\, which has been largely ignored aspects in spatially structured host-parasite dynamics. We overall highlight the neglected but profound aspects of host dispersal.\n\nhttps://conferences.m aths.unsw.edu.au/event/2/contributions/105/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/105/ END:VEVENT BEGIN:VEVENT SUMMARY:Differential priming and tolerance of monocytes challenged with ex ternal stimuli DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-378@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Stanca Ciupe ()\nCellular adaptation to varying sign al strengths has been observed in the innate immune cells responses to ext ernal and internal challenges. Monocytes persistently challenged with low levels of external stimulants\, can be skewed into a low-grade ‘primed ’ state\, while persistent challenges with high levels of external stimu lants will skew them into to a ‘tolerant’ state. Based on experimental and modelling studies\, we have identified a generic network motif\, comp osed of mutually competitive signals\, as a potential principle for bistab le and/or intermediate priming and tolerance responses. We use analytical and numerical techniques to identify the detailed mechanisms for the activ ation magnitude\, duration\, and potential transition between priming to t olerant states.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribut ions/378/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/378/ END:VEVENT BEGIN:VEVENT SUMMARY:Multiscale modelling of saliva secretion DTSTART;VALUE=DATE-TIME:20180712T010000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-104@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: James Sneyd (University of Auckland)\nThe parotid sa livary gland consists of groups of acinar cells all transporting water int o a lumen with a complex branched structure. In addition\, each acinar cel l itself has a complex spatial structure\, with heterogenous spatial distr ibutions of the channels that control water transport. The goal of our mod el is to determine the relationships between structure and function\, both at the level of individual acinar cells\, and at the level of the entire salivary gland. \n\nTo answer this question we have constructed an anatomi cally accurate model\, based on reconstruction of a z-series of optical sl ices through a group of acinar cells. Our model shows how the structure of each acinar cell is critical for an understanding of how water flow throu gh each cell is controlled\, and how the multicellular branching structure of the lumen can affect total fluid flow.\n\nhttps://conferences.maths.un sw.edu.au/event/2/contributions/104/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/104/ END:VEVENT BEGIN:VEVENT SUMMARY:A multi-layered screening model for computational identification o f leaf colour-related genes in rice plant DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-237@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Chang-Kug Kim ()\nRice field art is a large-scale ar t form in which people design rice fields using various kinds of ornamenta l rice plants with different leaf colours. Leaf colour-related genes play an important role in the study of chlorophyll biosynthesis\, chloroplast s tructure and function\, and anthocyanin biosynthesis. We performed whole-g enome resequencing and transcriptomic analysis of regulatory patterns and genetic diversity among different rice cultivars to discover new genetic m echanisms that promote enhanced levels of various leaf colours. We re-sequ enced the genomes of 10 rice leaf-colour varieties to an average depth of $40\\times$ depth and >95% coverage and performed 30 RNA-seq experiments u sing the 10 rice varieties sampled at three developmental stages. The sequ encing results yielded a total of $1\,814\\times10^6$ reads and identified an average of 713\,114 SNPs per rice variety. Based on our analysis of th e DNA variation and gene expression\, we selected 47 candidate genes. We u sed an integrated analysis of the whole-genome resequencing data and the R NA-seq data to divide the candidate genes into two groups: genes related t o macronutrient (i.e.\, magnesium and sulfur) transport and genes related to flavonoid pathways including anthocyanidin biosynthesis. We verified th e candidate genes with quantitative RT-PCR using transgenic T-DNA insertio n mutants. Our study demonstrates the potential of integrated screening me thods combined with genetic-variation and transcriptomic data to isolate g enes involved in complex biosynthetic networks and pathways.\n\nhttps://co nferences.maths.unsw.edu.au/event/2/contributions/237/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/237/ END:VEVENT BEGIN:VEVENT SUMMARY:Industrial bees: when agricultural intensification doesn't impact disease burden DTSTART;VALUE=DATE-TIME:20180710T011000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-282@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Carly Rozins ()\nThe intensification of farming indi sputably changes the ecology of agricultural infectious diseases with mode rn management practice impacting both host density and between-host contac ts. We typically assert that these changes result in higher disease burden s\, but there is relatively little specific modelling testing this idea. F or example\, the industrialisation of apiculture has been suggested to pla y a critical role in the increased losses of Apis mellifera colonies to in fectious diseases\, with specific apicultural practices (reflecting indust ry-wide intensification) implicated in higher disease burdens. Here we bui ld multi- honeybee colony models to examine how ‘apicultural intensifica tion’ in its most plausibly extreme case is predicted to impact honeybee pathogen epidemiology within apiary. Counter to the prevailing view\, our models predict that intensification\, captured though increased populatio n sizes\, changes in population network structure\, and increased between- colony transmission\, has little effect on disease burden across an apiary . Disease burdens\, and therefore impacts of intensification\, are critica lly determined by the R0 (reproductive ratio) of a given pathogen prior to intensification. The greatest impacts of intensification are found for di seases with initially low R0 values\, however such diseases cause little o verall disease burden and so impacts are universally minor. Importantly in this context\, the smallest impacts of intensification are found for dise ases with high R0 values\, which appear to be typical of important honeybe e diseases. Our findings highlight a lack of support for the hypothesis th at current and ongoing aspects of management intensification lead to highe r disease burdens in honeybees. More broadly\, our work demonstrates the n eed for specific models of agricultural systems and management practices i n order to understand the implications of management changes on disease bu rden.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/282/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/282/ END:VEVENT BEGIN:VEVENT SUMMARY:From crawlers to swimmers- mathematical and computational problems in cell motility DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-45@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hans Othmer (University of Minnesota)\nCell locomoti on is essential for early development\, angiogenesis\, tissue regeneration \, the immune response\, and wound healing in multicellular organisms\, an d plays a very deleterious role in cancer metastasis in humans. Locomotion involves the detection and transduction of extracellular chemical and mec hanical signals\, integration of the signals into an intracellular signal \, and the spatio-temporal control of the intracellular biochemical and m echanical responses that lead to force generation\, morphological changes and directed movement. We will discuss some of the mathematical and comp utational challenges that the integration of these processes poses and de scribe recent progress on some component processes.\n\nhttps://conference s.maths.unsw.edu.au/event/2/contributions/45/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/45/ END:VEVENT BEGIN:VEVENT SUMMARY:Geometric analysis of synchronization in neuronal networks with gl obal inhibition and coupling delays DTSTART;VALUE=DATE-TIME:20180709T093000Z DTEND;VALUE=DATE-TIME:20180709T094500Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-23@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hwayeon Ryu (University of Hartford)\nWe study synap tically coupled neuronal networks to identify the role of coupling delays in network's synchronized behaviours. We consider a network of excitable\, relaxation oscillator neurons where two distinct populations\, one excita tory and one inhibitory\, are coupled and interact with each other. The ex citatory population is uncoupled\, while the inhibitory population is tigh tly coupled. A geometric singular perturbation analysis yields existence a nd stability conditions for synchronization states under different firing patterns between the two populations\, along with formulas for the periods of such synchronous solutions. Our results demonstrate that the presence of coupling delays in the network promotes synchronization. Numerical simu lations are conducted to supplement and validate analytical results. We sh ow the results carry over to a model for spindle sleep rhythms in thalamoc ortical networks\, one of the biological systems which motivated our study . The analysis helps to explain how coupling delays in either excitatory o r inhibitory synapses contribute to producing synchronized rhythms.\n\nhtt ps://conferences.maths.unsw.edu.au/event/2/contributions/23/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/23/ END:VEVENT BEGIN:VEVENT SUMMARY:Zombies\, foxes and murder: experiences in learning and teaching q uantitative biology using technology DTSTART;VALUE=DATE-TIME:20180712T053000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-28@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Shelby Scott (University of Tennessee\, Knoxville)\n Since the publication of the National Research Council's Report *BIO2010*\ , efforts have increased to better integrate mathematics and biology at th e undergraduate level. Unfortunately\, similar efforts to introduce quanti tative biology at the secondary level have been seldom. This can lead to q uantitative achievement mismatch in students from different secondary back grounds. We believe that technology can be used in order to diminish this mismatch. Technology has become pervasive in the personal lives of seconda ry and undergraduate students\, but some instructors are hesitant to incor porate technology into pedagogy. In this work\, we review available resour ces for teaching quantitative biology with technology\, and anecdotally ex plore the effectiveness of learning with and teaching with these resources .\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/28/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/28/ END:VEVENT BEGIN:VEVENT SUMMARY:An age-dependent mathematical model and vaccination strategies for 2009 A/H1N1 influenza in the Republic of Korea DTSTART;VALUE=DATE-TIME:20180709T062000Z DTEND;VALUE=DATE-TIME:20180709T064000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-267@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Soyoung Kim (Konkuk University)\nIn this talk\, we w ill present a mathematical model of 2009 A/H1N1 influenza considering age structure in the Republic of Korea and suggest vaccination strategies for mitigating the epidemics. There were 750\,000 confirmed cases of 2009 A/H1 N1 influenza from May 2009 and August 2010. Because influenza viruses are spread through close contact\, contact pattern plays an important role fo r the disease spread. We developed an age-dependent SEIAR model. The total population is divided into five subgroups and age-specific transmission r ates are estimated based on laboratory confirmed data from Korea Centers f or Disease Control and Prevention (KCDC). Vaccination policies is importan t to minimize the number of infected individuals especially when the vacci ne supply is limited. Using mathematical model\, we could assess the impac t of the age-dependent vaccination priority on transmission dynamics.\n\nh ttps://conferences.maths.unsw.edu.au/event/2/contributions/267/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/267/ END:VEVENT BEGIN:VEVENT SUMMARY:Reaction diffusion approximation for nonlocal interactions DTSTART;VALUE=DATE-TIME:20180711T010000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-146@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yoshitaro Tanaka (FUTURE UNIVERSITY HAKODATE)\nRecen tly\, nonlocal interactions (spatial long range interactions) have attract ed attention in many fields. Mathematical treatment of nonlocal interactio n is mainly based on convolution with kernels. If the profile of a nonloca l interaction is detected by experiments\, we can easily investigate how p atterns are generated by numerical simulations. However\, nonlocal interac tions are often inconvenient for observing specific mechanisms behind the target phenomena. In response to this\, we proposed a new method that coul d convert nonlocal interactions into a reaction-diffusion system with auxi liary unknown variables. In this talk\, we will explain the method of appr oximation\, and how to determine the parameters of the reaction-diffusion system for the given kernel shape.\n\nhttps://conferences.maths.unsw.edu.a u/event/2/contributions/146/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/146/ END:VEVENT BEGIN:VEVENT SUMMARY:Search times of T Cells in the liver DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-202@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jonathan Manton (University of Melbourne)\nThe preve ntion of diseases such as malaria require certain T cells to find all path ogens in the liver within a certain period of time (e.g.\, within 48 hours \, which is the time required for liver-stage development of parasites in rodent malaria). This motivates the fundamental question of how many T cel ls are required to ensure complete coverage of the liver within a specifie d time\, to a high probability. After describing our existing results\, we will present our current thoughts and approaches. Explanations will be gi ven of how to model the liver sinusoids\, how to implement fast simulation s of T cell movement\, and various possibilities for how to model the move ment of T cells.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribu tions/202/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/202/ END:VEVENT BEGIN:VEVENT SUMMARY:Bistable dynamics in a model of SIV infection with antibody respon se DTSTART;VALUE=DATE-TIME:20180711T015000Z DTEND;VALUE=DATE-TIME:20180711T021000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-292@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jonathan Forde (Hobart and William Smith Colleges)\ nExperiments in rhesus macaques have shown that for simian immunodeficienc y virus the size of the viral inoculum and the infection stage of the dono r animal alter the likelihood of establishment of infection. In this study \, we postulate a role for the host and donor antibodies in explaining the dependence of infectiousness on donor infection stage. The resulting math ematical model exhibits bistable dynamics\, with viral clearance and persi stence dependent on initial conditions. We fit the model to temporal virus data using a censored data approach for measurements below the limit of d etection\, and make predictions about the minimal viral load in the inocul um required for persistent infection.\n\nhttps://conferences.maths.unsw.ed u.au/event/2/contributions/292/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/292/ END:VEVENT BEGIN:VEVENT SUMMARY:Thin-film modelling of multiphase collagen gel mechanics DTSTART;VALUE=DATE-TIME:20180709T062000Z DTEND;VALUE=DATE-TIME:20180709T064000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-318@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: James Reoch (The University of Adelaide)\nCells are often grown within collagen gels *in* *vitro* for applications in tissue e ngineering. The behaviour of these cells is regulated by their mechanical environment\; however\, the forces exerted by cells in turn affect the mec hanical behaviour of the gel. We aim to better understand the interactions between the cells and the gel using mathematical modelling.\n\n\n\nWe hav e developed a multiphase model for this system\, incorporating cells and t heir traction forces alongside chemical effects such as osmosis. To date\, we have modelled this problem in one-dimensional Cartesian and spherical coordinates\, mimicking experiments performed with spheres of collagen gel . However\, these gels are often produced in Petri dishes\, resulting in a thin disc. We have therefore transformed our model to examine this type o f geometry. In this presentation\, we will demonstrate how we can exploit thin-film approximations to reduce the two-dimensional system to a leading -order\, one-dimensional model. We will also discuss the equilibrium behav iour of this reduced thin-film system.\n\nhttps://conferences.maths.unsw.e du.au/event/2/contributions/318/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/318/ END:VEVENT BEGIN:VEVENT SUMMARY:Individually based stochastic model of influenza: an analysis of s chool closure DTSTART;VALUE=DATE-TIME:20180709T060000Z DTEND;VALUE=DATE-TIME:20180709T062000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-320@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Masayuki Kakehashi (Hiroshima University)\nIn this r esearch\, we proposed an infectious disease spread model of influenza whic h was individually based and stochastic. We first described the method to build a realistic model\, or to estimate realistic parameter values\, base d on observed data. An appropriate model has to be individually based and stochastic if we take advantage of small unit data (in this case\, every d ay class unit data). We also analysed the effect of different strategies o f school closure\, e.g.\, the criteria for implementing school closure and the duration of continuous school closure. \n\nThe data we used were the daily reported data of the numbers of cases of swine flu and the dates of school/class closure in each class of schools collected from September 20 09 to March 2010 in a city in Japan. Because the data were collected in ea ch class\, transmission rates could be estimated separately for within cla ss\, within-school and inter-school rates. Totally 21\,253 cases were repo rted out of 51\,871 students in 134 schools (elementary schools\, junior h igh schools\, high schools and kindergartens). To construct accurate model \, infected numbers must be estimated from case report data taking latent period into account\, which is deterministically impossible. To resolve th is difficulty\, we stochastically estimated and obtained data of infected numbers by ‘Monte Carlo back calculation’ and used in the analysis. Th e analysis was mainly carried out using data during September up to Decemb er to avoid the influence of vacations. The influence of humidity was also analysed using daily meteorological data of the area where data were coll ected. The analysis of total population using deterministic model was also carried out to obtain the overview of the flu spread. \n\nThe transmissio n rates of different levels were estimated by maximum likelihood method us ing detailed data reconstructed by Monte Carlo back calculation method. Th e rate within class was much larger (approximately 15 times larger) than w ithin school rate. The transition rate between schools was much smaller th an between classes of the same school. Stochastic variations of estimated parameters were also analysed. Optimal strategy of school closure was anal ysed in relation to the characteristics of flu. \n\nBy the analysis based on stochastic infectious disease spread model\, we could have presented po ssible variations of total number of cases and the size and timing of the epidemic peak. ‘Monte Carlo back calculation’ approach was concluded t o be useful in the analysis of effective preventive strategy against influ enza based on individually based stochastic model.\n\nhttps://conferences. maths.unsw.edu.au/event/2/contributions/320/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/320/ END:VEVENT BEGIN:VEVENT SUMMARY:Model-based assessment of gene drive strategies to control pest po pulations in agricultural systems DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-259@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mathieu Legros (CSIRO)\nAgricultural systems through out the world are threatened by a variety of pest species\, including inse cts\, pathogens and weeds. Conventional control methods often have limited success\, notably in the case of pesticide use due to the ubiquitous deve lopment of resistance. Novel control approaches are therefore needed to im prove management of these pest populations. Gene drive strategies\, based on the use of genetic constructs with biased inheritance to drive traits i nto target populations\, offer promising avenues for the development of su ch control methods\, facilitated by the advent of CRISPR-Cas molecular too ls. Implementation of such strategies in agrosystems\, with actively manag ed populations and strict socioeconomic constraints\, offers a specific se t of opportunities and challenges. Here we present a newly developed model ling framework design to study the outcome of these genetic control strate gies in a variety of agricultural systems. This framework is built as a mo dular toolset that can simulate a wide range of scenarios\, including a di versity of pest species\, in a biologically and ecologically detailed fash ion. We detail here the ability of this modelling tool to take into accoun t specific aspects of the life history\, ecology and genetics of the targe t organism. We introduce results demonstrating how genetic strategies can be used to control pesticide resistance. Finally\, we discuss the future a venues of research offered by this theoretical framework\, notably in term s of optimising implementation and deployment of genetic strategies in spe cific agrosystems\, as well as investigating potential approaches for spat ial and temporal containment of the associated genetic constructs.\n\nhttp s://conferences.maths.unsw.edu.au/event/2/contributions/259/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/259/ END:VEVENT BEGIN:VEVENT SUMMARY:Derivation of a fluid-type continuum model for contracting actomyo sin bundles. DTSTART;VALUE=DATE-TIME:20180711T020000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-87@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Dietmar Oelz (The University of Queensland)\nStartin g from a detailed physical model for the interplay of actin filaments\, my osin motor proteins and cross-linker proteins in a contracting cell divisi on ring\, we derive a continuum model as a short filament limit of the age nt based model. The model features highly nontrivial pattern formation and traveling wave solutions and explains the aggregation of actin and myosin predicted by the microscopic model as well as the scaling properties that cause the constant rate of contraction.\n\nhttps://conferences.maths.unsw .edu.au/event/2/contributions/87/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/87/ END:VEVENT BEGIN:VEVENT SUMMARY:Meta-population modelling to evaluate vaccination policy alternati ves vis-à-vis measles and rubella in China DTSTART;VALUE=DATE-TIME:20180711T010000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-39@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: John Glasser (Centers for Disease Control and Preven tion)\n*Background:* Measles and rubella are rash illnesses that typically afflicted young children in the pre-vaccination era\, but rubella usually is mild while measles may be severe. Because child deaths to which measle s contributes often have other proximate causes\, measles mortality is und er-ascertained. Rubella during the first trimester invariably causes misca rriages\, stillbirths and\, among livebirths\, congenital rubella syndrome (CRS)\, an array of individually severe afflictions that often co-occur. As childhood vaccines commonly include antigens to the viruses causing bot h diseases\, vaccination programs must be designed to attain disparate goa ls: prevent measles among young children and rubella among young women. By virtue of increasingly effective routine vaccination\, together with targ eted supplemental immunization activities (SIAs)\, health authorities in t he People’s Republic of China have reduced measles’ reproduction numbe r from about 18 to 2.3. Despite substantial residual susceptibility among young adults\, more in some province-level jurisdictions than others\, sus tained childhood immunization likely would eliminate measles eventually. B ecause routine vaccination against rubella began more recently\, residual susceptibility is concentrated among adolescents. Nonetheless\, childhood immunization has reduced rubella’s reproduction number from 7.6 to 1.2. To support global eradication efforts\, as well as expedite morbidity and mortality reductions in China\, we evaluated alternative SIAs via mechanis tic mathematical modelling. \n\n*Methods:* Our model Chinese population is stratified by immune status (susceptible to infection\; infected\, but no t yet infectious\; infectious\; and recovered or immunized)\, age (0\, 1-4 \, 5-9\, …\, 65+ years)\, and location (31 provinces\, municipalities or administrative regions). It includes a function by which contacts between members of different groups are a mixture of preferential and proportiona te with respect to age\, but decline exponentially with distance at age-de pendent rates. We estimated initial conditions and most parameters from re cent cross-sectional serological surveys\, disease surveillance and demogr aphic observations. Then we evaluated the effective reproduction numbers a nd their partial derivatives with respect to sub-population immunization r ates. Within regions\, these gradients identify province-level jurisdictio ns where vaccination would reduce the effective reproduction number the mo st. And within jurisdictions\, they identify age classes where vaccination would be most effective. We corroborated our analytical results by simula ting adolescent and young adult SIAs using a deterministic model with seas onally-forced person-to-person contact rates. And\, using a demographicall y-realistic stochastic model of a relatively small but representative popu lation\, we estimated the risk of rubella outbreaks\, burden of CRS\, and impact of adolescent vaccination. \n\n*Findings:* Measles’ gradients are more heterogeneous than rubella’s\, but generally indicate that vaccina ting young adults is the optimal strategy. Simulations corroborate this\, but indicate that a catch-up campaign among adolescent schoolchildren woul d accelerate elimination nonetheless\, with timing dependent on uptake. Mo reover\, this strategy is optimal for rubella\, which is woefully under-re ported\, especially among adults. Thus\, using measles-rubella or measles- mumps-rubella vaccine in SIAs during the first months of several consecuti ve school years would both accelerate measles elimination and avert impend ing outbreaks of rubella that\, because of the immune profile in China\, w ould greatly increase the incidence of CRS. Interpretation: These results are largely due to indirect effects (i.e.\, fewer infections than vaccinat ed people might otherwise cause)\, which meta-population models with reali stic mixing are uniquely capable of reproducing accurately.\n\nhttps://con ferences.maths.unsw.edu.au/event/2/contributions/39/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/39/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling of the Spread of MERS-CoV DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-107@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Qianying Lin (The Hong Kong Polytechnic University)\ nMiddle East Respiratory Syndrome Coronavirus (MERS-CoV) has been persiste nt in the Middle East region since 2012. Abundant scientific evidence show ed that dromedary camels are the primary host of the virus. Majority of hu man cases (i.e. 75% or 88%) are due to human-to-human transmission\, while the others are due to camel-to-human transmission. Mathematical modelling of MERS-CoV camel-to-camel transmission was lacking. Using the plug-and-p lay likelihood-based inference framework\, we fitted a susceptible-exposed -infectious-recovered-susceptible model of camels to the reported human ca ses with a constant proportion of human cases from camels (i.e. either 25% or 12%). We considered two scenarios: (i) the transmission rate among cam els is time-varying with a constant spill-over rate from camels to human\, or (ii) the spill-over rate is time-varying with a constant transmission rate among camels. Our estimated loss-of-immunity rate and prevalence of M ERS-CoV infections among camels largely matched previous serological or vi rological studies\, shedding light on this issue. We recommended including dromedary camels in animal surveillance and control of MERS-CoV in Saudi Arabia which could help reduce their sporadic introductions to humans.\n\n https://conferences.maths.unsw.edu.au/event/2/contributions/107/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/107/ END:VEVENT BEGIN:VEVENT SUMMARY:Cell adhesion and dynamic fibre redistribution within two-scale mo ving boundary cancer invasion DTSTART;VALUE=DATE-TIME:20180711T010000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-141@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Robyn Shuttleworth (University of Dundee)\nCancer ce ll invasion\, recognised as one of the hallmarks of cancer\, is a complex process involving the secretion of matrix-degrading enzymes that have the ability to degrade the surrounding extracellular matrix (ECM). Combined wi th cell proliferation\, migration\, and changes in cell-cell and cell-matr ix adhesion\, a tumour is able to spread into the surrounding tissue. We h ighlight the multiscale character of this process through a double feedbac k link between the cell-scale molecular processes and those occurring at t he tissue level. In order to gain a deeper understanding of the mechanics of cancer cell invasion\, we look to further investigate the surrounding m icroenvironment of a tumour.\n\nThe ECM is a key biological structure that not only provides structure and support to surrounding cells\, but also a cts as a platform on which the cells can communicate and exercise spatial movement. There are several other vital structures within the ECM\, howeve r we are going to focus primarily on fibrous proteins\, such as fibronecti n. These fibres are key players in the function of healthy cells\, contrib uting to many essential processes such as cell migration\, differentiation \, migration and proliferation. They also play a crucial role in tumour pr ogression with the ability to anchor cells to other components of the ECM. \n\nIn this work we consider the two-scale dynamic cross-talk between can cer cells and a two component ECM (consisting of both a fibrous and a non- fibrous phase). To that end\, we incorporate the dynamics interlinked macr o-micro cells-ECM interactions within inside the tumour support that contr ibutes simultaneously both to cell-adhesion and to the dynamic re-arrangem ent and restructuring of the ECM fibres. Furthermore\, this is embedded wi thin a multiscale moving boundary approach for the cancer cell population in the presence of cell-adhesion at the tissue scale and matrix degrading enzyme molecular processes and fibre redistribution considered at cell-sca le. Computational simulations will accompany the presentation of the overa ll modelling framework to examine the impact of different levels of adhesi on between cells in conjunction with the continuous ECM fibres restructuri ng on cancer invasion patterns.\n\nhttps://conferences.maths.unsw.edu.au/e vent/2/contributions/141/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/141/ END:VEVENT BEGIN:VEVENT SUMMARY:Predicting vegetation diversity & structure from ecological and ev olutionary first principles DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-154@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Daniel Falster (University of New South Wales)\nWalk ing through any forest\, one is struck by the variety of plant forms coexi sting. To explain vegetation structure and diversity\, models must allow f or multiple species to coexist\, and ultimately\, predict the outcome of c ommunity assembly in different environments. In this talk\, I describe how adaptive dynamics theory provides a new framework for predicting the mixt ures of species traits that are favoured in vegetation. Predictions are ge nerated by embedding trait-based coexistence and selection into models of forest dynamics\, mapping from physiological trade-offs in plant function to individual-level outcomes such as growth rates\, and ultimately populat ion-level demographics\, and fitness. Results thus far show how i) how key trait-based trade-offs enable different strategies to coexist via success ional niche differentiation\; ii) how joint consideration of multiple trai ts can produce forests of higher diversity than was previously thought pos sible\, and iii) how trait mixtures respond to environmental conditions. T o conclude\, I consider some major challenges in applying this approach to making large-scale predictions of forest structure.\n\nhttps://conference s.maths.unsw.edu.au/event/2/contributions/154/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/154/ END:VEVENT BEGIN:VEVENT SUMMARY:Joining forces: combining machine learning and mechanistic models to predict tumour cell density for glioblastoma patients DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-188@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kristin Swanson (Mayo Clinic)\nGlioblastoma is the m ost aggressive primary brain cancer\, with poor survival that can be large ly attributed to intra-tumoural heterogeneity. While these tumours are pr imarily monitored via contrast-enhanced (CE) T1-weighted and T2-weighted m agnetic resonance (MR) images\, these standard clinical images are known t o be non-specific in their correlation with tumour cell density. This lack of relationship makes it difficult to define the specific regions of inte rest to target for surgery and radiation. Previous efforts have shown some promise in better interpreting these images utilizing either machine lear ning (ML) or mechanistic modelling independently. But methods to harness t he strengths of both approaches are sorely needed to make clinically actio nable progress. \n\nHere we present a novel\, first-of-its-kind\, hybrid m odel which brings together a graph-based semi-supervised machine learning approach with a mechanistic partial differential equation model of gliobla stoma growth\, known as the Proliferation-Invasion (PI) model\, to generat e predictive tumour cell density maps with high accuracy. Our ML approach bridges cell density as quantified from image-localized biopsies with text ure analysis of multiparametric MR images. To incorporate the mechanistic model\, the PI model is first used to generate an independent prediction o f cell density which is then introduced into the ML algorithm through a La placian matrix\, which ensures regions with similar predictions from the P I model will have similar predictions in the final model. \n\nWe have appl ied our proposed ML-PI model framework to 18 patients with a total of 82 i mage localized biopsies. Each patient’s tumour was imaged with multi-par ametric MR images\, including T1-weighted\, CE T1-weighted\, T2-weighted\, dynamic contrast-enhanced (DCE) imaging\, diffusion weighted imaging (DWI )\, and diffusion tensor imaging (DTI). In this cohort\, our hybrid model was able to achieve higher accuracy in cell density prediction than eithe r of the independent models (ML or PI) alone\, with a mean accuracy predic tion error of 0.084 vs 0.227 for PI alone and 0.220 for ML alone. We hope that with more verification\, this tool can be used to not only guide spat ially localized therapies such as surgery and radiation\, but also help br oadly in the interpretation of images for glioblastoma patients.\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/188/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/188/ END:VEVENT BEGIN:VEVENT SUMMARY:Spike trains to force generation DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-455@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Katie Newhall (UNC Chapel Hill)\nThe field of neu romechanics\, which attempts to integrate neural control with muscl e activation and the resulting movement of an organism\, is an emerging f ield of organismal biology. Approaches from experimental biology\, robot ics\, and mathematics have now reached the point where their knowledge abo ut the different facets of (animal) locomotion can be combined and integra ted into realistic and useful models. This integration between fields ope ns up new questions and problems for researchers to solve. In this talk\, we explored the interface between neuron and muscle during the initial tr ansfer of information that generates muscle contraction. \n\nMuscle contra ction occurs when neuron action potentials stimulate the sarcoplasmic reti culum\, releasing calcium ions that then bind to muscle filaments\, allowi ng the myosin to contract the muscle. We will present a model that couple s spike-train activation to mass-action equations for calcium ions\, which in turn couples to the Hill model for muscle contraction force-velocity r elationship. This model allows for investigation of spike trains required to produce partial twitch response\, and total tetanic contraction.\n\nht tps://conferences.maths.unsw.edu.au/event/2/contributions/455/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/455/ END:VEVENT BEGIN:VEVENT SUMMARY:What is the likely impact of group A Streptococcus vaccines on thr oat and skin infections across different populations? DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-57@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Patricia Campbell (Peter Doherty Institute for Infec tion and Immunity\, The University of Melbourne)\nSevere diseases arising as sequelae of superficial skin and throat infections with group A *Strept ococcus* (GAS) are important causes of morbidity and mortality worldwide. The observed high level of heterogeneity in GAS prevalence across various temporal and spatial settings suggests potentially complex dynamics of pop ulation transmission. One of the most visible indicators of heterogeneity is the different prevalence of skin and throat infections across populatio ns. \n\nSustained control of GAS infections in settings of poverty has fai led\, and an effective vaccine may be the most practical long-term strateg y to reduce the burden of GAS-related disease. Research into GAS vaccines has been ongoing for many decades\, and there are a number of vaccine cand idates currently at various stages of development. Those based on the M-pr otein\, the major virulence factor of GAS\, include multivalent vaccines t argeting the variable N-terminal of the M-protein\, and vaccines that cont ain antigens from the conserved C-repeat region. It is anticipated that th ese vaccines will provide varying levels of protection across populations depending on the match between circulating and vaccine strains. \n\nWe hav e developed a compartmental model of GAS transmission incorporating skin a nd throat infection separately and allowing for interaction between the tw o. To address the many uncertainties that exist around GAS transmission an d immunity\, we used the Metropolis-Hastings algorithm with informative pr iors to sample parameter space and simulate our model. We conducted three separate explorations to match epidemiologic attributes observed in popula tion settings with different combinations of skin and throat infection pre valence: 1) throat \n\nhttps://conferences.maths.unsw.edu.au/event/2/contr ibutions/57/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/57/ END:VEVENT BEGIN:VEVENT SUMMARY:Control of prokaryotic cell division by Turing patterns DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-149@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: James Walsh (UNSW)\nCell division requires the preci se placement of the division ring at mid-cell to ensure both daughter cell s are viable. However\, the mechanisms behind this localization remain poo rly characterized. There are a limited number of known ways to identify th e centre of the cell. One such mechanism is a Turing pattern. One intracel lular Turing pattern has been identified\, that produced by the Min protei n system. In *Escherichia coli*\, the Min protein system plays a role in e stablishing the division ring position. Membrane-bound Min proteins form a n oscillating spatial pattern where the proteins are concentrated at one p ole of the cell and then another\, leaving a barezone at the centre of the cell where the FtsZ ring will form. Based on molecular interactions of th e Min system\, we have formulated a mathematical model that reproduces Min patterning during cell growth and division. This model provides a platfor m to explore how the Min system functions and what characteristics are lik ely to be shared with other Turing patterning systems\, should they exist. We examine the general characteristics of Turing patterns produced by the Min system. In particular\, patterning approximates a harmonic of the cel l shape and selects the dominant harmonic in a predictable manner. This sh ows what alternative intracellular Turing patterning systems are likely to appear and how they would behave in relation to cell shape. The oscillati ons of the Min system are shown to be translated into a mid-cell localizat ion signal via the harmonics generated by non-linear interactions of the s ystem. We show that division plane orientation in the pleomorphic archeon *Haloferax volcanii* can be predicted from cell shape by assuming that it is dictated by a Turing mechanism. This work makes progress towards unders tanding how the Min system functions to regulate cell division. More gener ally it develops tools to identify alternative Turing patterning systems a nd to understand how patterning can be translated into localization signal s.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/149/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/149/ END:VEVENT BEGIN:VEVENT SUMMARY:Continuum mathematical models for cell migration incorporating cel l cycle dynamics DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T062000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-302@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sean Vittadello (Queensland University of Technology )\nFluorescent ubiquitination-based cell cycle indicator\, also known as F UCCI\, allows the visualisation of the G1 and S/G2/M cell cycle phases of individual cells. FUCCI consists of two fluorescent probes\, so that cells in the G1 phase fluoresce red and cells in the S/G2/M phase fluoresce gre en. FUCCI reveals real-time information about cell cycle dynamics of indiv idual cells\, and can be used to explore how the cell cycle relates to the location of individual cells\, local cell density\, and different cellula r microenvironments. In particular\, FUCCI is used in experimental studie s examining cell migration\, such as malignant invasion and wound healing. Here we present new mathematical models which can describe cell migration and cell cycle dynamics as indicated by FUCCI. The *fundamental* model de scribes the two cell cycle phases\, G1 and S/G2/M\, which FUCCI directly l abels. The *extended* model includes a third phase\, early S\, which FUCCI indirectly labels. We present experimental data from scratch assays using FUCCI-transduced melanoma cells\, and show that the predictions of spatia l and temporal patterns of cell density in the experiments can be describe d by the fundamental model. We obtain numerical solutions of both the fund amental and extended models\, which can take the form of travelling waves. These solutions are mathematically interesting because they are a combina tion of moving wavefronts and moving pulses. We derive and confirm a simpl e analytical expression for the minimum wave speed\, as well as exploring how the wave speed depends on the spatial decay rate of the initial condit ion.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/302/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/302/ END:VEVENT BEGIN:VEVENT SUMMARY:Ecological stability\, epidemiological stability and reservoirs of infection DTSTART;VALUE=DATE-TIME:20180711T063000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-63@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mick Roberts (Institute of Natural and Mathematical Sciences\, Massey University\, Auckland\, New Zealand)\nThe structure of a n ecosystem and the interaction of the species within it can determine whe ther a pathogen can persist. We have described a model for interacting spe cies that are hosts and non-hosts of a pathogen. The population densities of the ecosystem species can determine the value of the basic reproduction number\, $\\mathcal{R}_0$. We have defined concepts of ecological and epi demiological stability\, shown how changes in the ecosystem can change the dynamics of the pathogen\, and how the introduction or removal of a patho gen can lead to changes in the ecosystem structure. In particular\, the so -called dilution effect\, where an increase in biodiversity leads to a red uction in the prevalence of an infectious disease\, has been the subject o f speculation and controversy. We have found criteria for when the dilutio n effect is present\, or when the opposite (amplification) effect may occu r. Another concept often used informally in the literature is that of a re servoir of infection. Finding a robust definition of a reservoir is not st raightforward\, particularly as the presence of other species in an ecosys tem\, even non-host species\, can change the value of $\\mathcal{R}_0$.\n\ nCollaborative research with Hans Heesterbeek.\n\nhttps://conferences.math s.unsw.edu.au/event/2/contributions/63/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/63/ END:VEVENT BEGIN:VEVENT SUMMARY:Hamilton-Jacobi equations on networks and motion flow models DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-14@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Adriano Festa (INSA Rouen)\nAfter reviewing the basi cs about the relation between some motion flow models (pedestrians\, anima ls\, vehicles) and a class of Hamilton-Jacobi-Bellmann equations on Networ ks we introduce and discuss some numerical methods for the approximation o f the solution. Several tests are performed to illustrate the properties p reviously theoretically presented.\n\nhttps://conferences.maths.unsw.edu.a u/event/2/contributions/14/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/14/ END:VEVENT BEGIN:VEVENT SUMMARY:Statistical inference for parameters of biochemical networks DTSTART;VALUE=DATE-TIME:20180711T020000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-38@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Grzegorz Rempała (The Ohio State University)\nThe i nference for the reaction rates in chemical networks is often challenging due to intrinsic and extrinsic biological noise\, missing data and lack o f experimental reproducibility. The talk will provide an overview of some recent work on new efficient methods of rates estimation in stochastic biochemical networks both at molecular and population scales. Stochastic S IR and Michaelis Menten models will be used as examples to illustrate br oader points.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributio ns/38/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/38/ END:VEVENT BEGIN:VEVENT SUMMARY:Assessing physical control mechanisms in lung branching morphogene sis DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-98@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sharon R. Lubkin (North Carolina State University)\n We have developed several models of the physical control of branching morp hogenesis in the lung\, considering a variety of factors\, including trans port and mechanics. Simple models can explain complex phenomena\, though h ow reasonable a model initially seems is not necessarily correlated with i ts ultimate explanatory power. In this talk\, we will present a variety of models of branching morphogenesis\, and compare their implications.\n\nht tps://conferences.maths.unsw.edu.au/event/2/contributions/98/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/98/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling eco-evolutionary dynamics: an integrative overview DTSTART;VALUE=DATE-TIME:20180711T020000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-176@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ulf Dieckmann (Evolution and Ecology Program (EEP)\, International Institute for Applied Systems Analysis (IIASA))\nAnalyzing humankind’s interactions with our collective environment typically requi res understanding eco-evolutionary dynamics in complex adaptive systems. T his is especially important for mitigating anthropogenic impacts on the bi osphere\, managing the multifaceted services provided by ecosystems\, and shaping social interactions among agents utilizing these systems. Understa nding complex adaptive systems requires a marriage of ecological dynamics with evolutionary dynamics. This is because adaptations in living systems cannot be understood without accounting for the rich ecological and social embedding of populations and communities\; conversely\, predicting the fu ture of ecosystems\, especially when exposed to strong anthropogenic impac ts\, necessitates accounting for the prospect of rapid evolution\, both bi ological and cultural. Bridging the often still profound gap between theor ies and applications\, this presentation provides an integrative overview of modern modelling approaches linking ecological and evolutionary dynamic s in real-world complex adaptive systems.\n\nhttps://conferences.maths.uns w.edu.au/event/2/contributions/176/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/176/ END:VEVENT BEGIN:VEVENT SUMMARY:Physiologically based modelling of circadian dynamics of melatonin and its metabolite aMT6s DTSTART;VALUE=DATE-TIME:20180712T053000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-46@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Svetlana Postnova (School of Physics\, University of Sydney\, Sydney\, Australia\; Cooperative Research Centre for Alertness\, Safety and Productivity\, Melbourne\, Australia)\n*Background and Objecti ves:* The central circadian clock in the hypothalamus controls 24 hour rhy thms in the human body\, from sleep and alertness\, to mood\, metabolism\, and immune response among many others. Knowledge of the phase of the cloc k is central to design of treatments for circadian rhythm disorders\, incl uding shiftwork disorder\, jetlag\, delayed sleep-wake phase disorder\, an d non-24-hour sleep-wake rhythm disorder. Melatonin concentrations in plas ma and saliva\, and the excretion rate of the major urinary melatonin meta bolite\, 6-sulfatoxymelatonin (aMT6s)\, are often used as markers of circa dian phase. The relationship between these markers is complex\, and measur ing melatonin or aMT6s can be impractical\, however\, so quantitative mode ls would prove useful to aid experimental procedures or to design treatmen ts. Here a unified model of arousal and melatonin dynamics is presented th at predicts the rhythms of melatonin and aMT6s in multiple body fluids und er varying light\, sleep\, and circadian misalignment conditions.\n\n*Meth ods:* We used an established model of arousal dynamics in which ordinary d ifferential equations simulate the flip-flop switch between the sleep- and wake-active neuronal populations\, and a dynamic circadian oscillator acc ounts for the effect of light exposure on circadian phase. This model is e xtended to incorporate the circadian-controlled production of melatonin in the pineal gland\, its dynamics in the blood and saliva as well as its co nversion to aMT6s\, and ultimate excretion. Importantly\, the model also i ncludes suppression of melatonin synthesis by light exposure\, which is a key confounding factor in experiments.\n\n*Results:* The model predicts me latonin levels over the sleep-wake/dark-light cycle and enables prediction of widely used melatonin-based circadian phase markers\, such as dim ligh t melatonin onset (DLMO) and aMT6s acrophase under conditions of both norm al sleep and circadian misalignment. The model is tested against data from ten published experimental studies\, including real-world shiftwork studi es\, and is found to quantitatively reproduce the key features of melatoni n and aMT6s dynamics\, including the timing of release\, peak concentratio ns\, and response to controlled lighting.\n\n*Conclusions:* Our model is t he first to quantitatively predict the relationship between light exposure \, circadian phase\, melatonin\, and aMT6s dynamics\, and successfully rep roduces experimental data from a variety of experiments.\n\nhttps://confer ences.maths.unsw.edu.au/event/2/contributions/46/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/46/ END:VEVENT BEGIN:VEVENT SUMMARY:Bond graph modelling of the cardiac action potential DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-430@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michael Pan (University of Melbourne)\nBond graphs a re an energy-based framework for modelling physical systems while adhering to thermodynamic and physical constraints\, and they have recently been e xtended and applied to biochemical and electrophysiological systems. Here we describe a bond graph model of the cardiac action potential and use it to explore the issue of drift in mathematical models of electrophysiology\ , which is a cause of inaccuracy. Previous studies have linked drift to st imulus currents that violate conservation laws\, but those analyses were r estricted to individual models and relied upon the manual identification o f conservation laws. Due to their adherence to conservation principles\, b ond graphs are well-suited for studying conservation laws under a more gen eral framework. Using our bond graph approach\, we found that the conserva tion law derived in previous studies is an example of a ‘conserved moiet y’ within the bond graph modelling and metabolic analysis frameworks. Co nserved moieties explain the occurrence of drift for a general class of mo dels\, demonstrating that bond graphs can provide a systematic approach th at can be used to identify hidden conservation laws and check for the pres ence of drift.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributi ons/430/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/430/ END:VEVENT BEGIN:VEVENT SUMMARY:Oocyte fertilisation\, chemical signalling and waves DTSTART;VALUE=DATE-TIME:20180710T020000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-75@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yvonne Stokes (The University of Adelaide)\nIt has b een known for some decades that fertilisation of some amphibian and fish e ggs is followed by a wave of calcium ions over the surface of the egg\, wh ich is associated with a physical change to the surface. Similar waves are seen at other stages of embryonic development. An unfertilized mammalian egg is surrounded by cumulus cells to form a cumulus-oocyte complex (COC). Just a few years ago\, medical researchers at the University of Adelaide identified\, for the first time\, a wave-like behaviour of the cumulus cel ls in COCs after sperm had been added to the culture medium\, believed to be a response to fertilisation. From the speed of the wave it was inferred that the cells were responding to one or more chemical signals from locat ions on the surface of the egg and that calcium ion concentration was the likely signal. More recently it has been determined that the wave is assoc iated with cumulus-cell death.\n\nI will describe some ongoing modelling a nd experimental work being undertaken to explain the behaviour of the cumu lus cells\, assuming the wave is initiated at the fertilisation site. We w ill examine whether a chemical release by either or both of the oocyte and cumulus cells is qualitatively consistent with experimental observations. \n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/75/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/75/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling of robust genetic switch with a single input\, based on a serine integrase-controlled toggle switch DTSTART;VALUE=DATE-TIME:20180711T054000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-372@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Alexandra Pokhilko (University of Glasgow)\nBinary g enetic switches are widely used in synthetic biology for switching between two expression states\, ON and OFF. In particular\, single input switches \, which alternate between ON and OFF in response to the same input signal s\, are the key elements of counting devices which count the occurrence of a repeated intracellular or extracellular signal. Most existing DNA switc hes require two inputs\, and no single-input switch capable of robust swit ching between two states has been developed so far. Here we use mathematic al modelling to design such a switch by combining two double-input DNA swi tches: a transcriptional toggle switch (TTS) and a DNA inversion switch. T he TTS switches between expression of two transcriptional repressors\, mut ually inhibiting each other. The DNA inversion switch is based on recombin ation by a serine integrase\, inverting a DNA segment located between two attachment sites. Integrase reverses its directionality in the presence of a recombination directionality factor (RDF)\; therefore the alternate ind uction of integrase with or without RDF results in flipping of the DNA seg ment. In the design of our one-input switch the TTS ensures bistability\, while the DNA inversion switch provides a single-input control by flipping the DNA segment with an inducible promoter. The model predicts that the c ombined bistability of the TTS and unidirectionality of DNA recombination ensure nearly 100% efficiency of switching between ON and OFF states in re sponse to repeated pulses of inducer. The switch is predicted to be robust to parameter perturbations and molecular noise\, making it a promising ca ndidate for further use as a basic element of counting devices.\n\nhttps:/ /conferences.maths.unsw.edu.au/event/2/contributions/372/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/372/ END:VEVENT BEGIN:VEVENT SUMMARY:Coadaptation of mitochondrial and nuclear genes\, and the cost of mother's curse DTSTART;VALUE=DATE-TIME:20180711T020000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-114@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tim Connallon (Monash University)\nStrict maternal i nheritance renders the mitochondrial genome susceptible to accumulating mu tations that harm males\, but are otherwise benign or beneficial for femal es. This ‘mother's curse’ effect can degrade male survival and fertili ty if unopposed by counteracting evolutionary processes. Coadaptation betw een nuclear and mitochondrial genomes—with nuclear genes evolving to com pensate for male-harming mitochondrial substitutions—may ultimately reso lve mother's curse. However\, males are still expected to incur a transien t fitness cost during mito-nuclear coevolution\, and it remains unclear ho w severe such costs should be. We present a population genetic analysis of mito-nuclear coadaptation to resolve mother's curse effects\, and show th at the magnitude of the ‘male mitochondrial load’—the negative impac t of mitochondrial substitutions on male fitness components—may be large \, even when genetic variation for compensatory evolution is abundant. We also find that the male load is surprisingly sensitive to population size: male fitness costs of mito-nuclear coevolution are particularly pronounce d in both small and large populations\, and minimized in populations of in termediate size. Our results reveal complex interactions between demograph y and genetic constraints during the resolution of mother's curse\, sugges ting potentially widespread species differences in susceptibility to mothe r's curse effects.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contri butions/114/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/114/ END:VEVENT BEGIN:VEVENT SUMMARY:Population modelling in an applied calculus class using spreadshee ts DTSTART;VALUE=DATE-TIME:20180712T020000Z DTEND;VALUE=DATE-TIME:20180712T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-27@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Anna Mummert (Marshall University)\nIn this talk I w ill describe a series of population modelling computer labs used in an app lied calculus class. The labs showcase different types of population grow th\, including Fibonacci\, exponential\, and logistic. Exponential growth is revisited as a differential equation\, which is approximated by discre te growth\, that is\, approximation via tangent lines\, using different ti me intervals. In some semesters\, students used the world population data to examine the issue of whether the population is growing exponentially o r logistically. Each lab requires the students to use a spreadsheet progr am\, such as Excel\, giving students practice with this essential computer skill.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/27/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/27/ END:VEVENT BEGIN:VEVENT SUMMARY:Bimolecular reactions in the cell membrane exhibit switch-like beh aviour with respect to diffusivity and molecular reach DTSTART;VALUE=DATE-TIME:20180709T053000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-136@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Samuel Isaacson (Boston University)\nMany T cell rec eptors have long\, unstructured cytoplasmic tails that contain tyrosine si tes. These sites can serve as regulators of receptor activation when phosp horylated or dephosphorylated\, while also serving as docking sites for cy tosolic enzymes. We coarse-grain the effective interaction between two tai ls\, and develop a mesoscopic particle-based stochastic reaction-diffusion model to study the combined diffusion of individual receptors within the cell membrane\, and chemical reactions between proteins bound to receptor tails. The model suggests a switch-like behaviour in the dependence of the fraction of activated receptors on both receptor diffusivity\, and on the molecular reach at which two receptor tails can interact. A simplified\, analytically solvable model is developed to approximate the more complicat ed multi-particle system\, and used to illustrate how the switch-like beha viour appears.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributi ons/136/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/136/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling latency using a distribution of life spans among infecte d cells DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T015000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-242@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Josephine Reyes (University of New South Wales)\nUnd erstanding the mechanisms of HIV latency is important in the development o f strategies for managing infection. Time from infection until production of virus has been shown to vary among infected cells\, hence challenging t he dichotomous assumption that cells are either latent or productively inf ected at time of infection. In this paper\, we will explore the implicatio ns of an alternative hypothesis that rates of activation follow a probabil ity distribution\, of which latency is just an extreme of this spectrum. W e show the emerging dynamics from this mathematical model and test its abi lity to explain features or reservoir formation and decay observed in SIV data. Analysis of SIV DNA levels in macaques that start treatment at diffe rent times shows that the decay rates of cells are statistically different in early and late initiation of treatment. Modelling suggests that data c an be explained by a spectrum of reactivation rates of infected cells.\n\n https://conferences.maths.unsw.edu.au/event/2/contributions/242/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/242/ END:VEVENT BEGIN:VEVENT SUMMARY:An anisotropic interaction model for simulating fingerprints DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-15@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Lisa Maria Kreusser (University of Cambridge)\nMotiv ated by the formation of fingerprint patterns we consider a class of inte raction models with anisotropic interaction forces whose orientations depe nd on an underlying tensor field. This class of models can be regarded as a generalization of a gradient flow of a nonlocal interaction potential wh ich has a local repulsion and a long-range attraction structure. In contra st to isotropic interaction models the anisotropic forces in our class of models cannot be derived from a potential. The underlying tensor field int roduces an anisotropy leading to complex patterns which do not occur in i sotropic models. This anisotropy is characterized by one parameter in the model. We study the variation of this parameter\, describing the transitio n between the isotropic and the anisotropic model\, analytically and numer ically. We analyze the steady states and their stability by considering th e particle model and the associated mean-field equations. Besides\, we pro pose a bio-inspired model to simulate fingerprint patterns (and more gener al any desired pattern) as stationary solutions by choosing the underlying tensor field appropriately.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/15/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/15/ END:VEVENT BEGIN:VEVENT SUMMARY:Analysis of high-frequency telemetry data using machine learning e nables differentiation of stages of $\\textit{Plasmodium knowlesi}$ infect ions in non-human primates DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-79@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Zerotti Woods (The University of Georgia)\nHigh-freq uency physiological data poses unique challenges for signal processing and computational analysis. This dataset was obtained from a cohort of *Macac a mulatta* and *Macaca fascicularis* infected with *Plasmodium knowlesi* u sing a customized telemetry system. The data set is comprised of electroca rdiogram signals collected at a sampling rate of 1 kHz\, temperature measu res collected at 1 Hz\, accelerometer data collected at 10 Hz\, and blood pressure readings collected at 500 Hz. The implanted telemetry devices all owed nearly uninterrupted time series data acquisition over the course of an infection experiment. Machine learning algorithms using daily features were used to accurately classify a day of telemetry data between pre-infec tion and liver stage over 90% of the time. The experimental design\, analy sis\, and framework used to address challenges in multi-scale telemetry si gnal processing will be discussed.\n\nhttps://conferences.maths.unsw.edu.a u/event/2/contributions/79/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/79/ END:VEVENT BEGIN:VEVENT SUMMARY:Distinguishing cell shoving mechanisms DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-395@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Barry Hughes (University of Melbourne)\nMotivated by *in vitro* time-lapse images of ovarian cancer spheroids inducing mesothe lial cell clearance\, the traditional agent–based model of cell migratio n\, based on simple volume exclusion\, was extended to include the possibi lity that a cell seeking to move into an occupied location may push the re sident cell\, and any cells neighbouring it\, out of the way to occupy tha t location. In traditional discrete models of motile cells with volume exc lusion such a move would be aborted. We introduce a new shoving mechanism which allows cells to choose the direction to shove cells that expends the least amount of shoving effort (to account for the likely resistance of c ells to being pushed). We call this motility rule ‘smart shoving’. We examine whether agent-based simulations of different shoving mechanisms ca n be distinguished on the basis of single realisations and averages over m any realisations. We emphasise the difficulty in distinguishing cell mecha nisms from cellular automata simulations based on snap-shots of cell distr ibutions\, site-occupancy averages and the evolution of the number of cell s of each species averaged over many realisations. This difficulty suggest s the need for higher resolution cell tracking.\n\nhttps://conferences.mat hs.unsw.edu.au/event/2/contributions/395/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/395/ END:VEVENT BEGIN:VEVENT SUMMARY:Entering a virtuous cycle of niche construction DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-336@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mark Tanaka (University of New South Wales)\nOrganis ms often modify their environments to their advantage through a process of niche construction. Environments that are improved through positive niche construction can be viewed as a public good. If free riders appear that d o not contribute to the shared resource and therefore do not incur any ass ociated costs\, the constructed niche may become degraded resulting in a t ragedy of the commons and the extinction of niche constructors. Niche cons truction can persist if free riders are excluded\, for example if niche co nstructors monopolise the resource they produce to a sufficient degree. We suggest\, however\, that the problem of free riders remains because it is possible that non-niche constructors with an enhanced ability to access t he resource appear and invade a population of constructors. Using mathemat ical models we show that positive niche construction can be maintained if it is inextricably linked to a mechanism that makes free riding costly\, s uch as a trait that confers a benefit to only niche constructors. We disc uss this finding in terms of genetic interactions and illustrate the princ iple with a two locus model. We conclude that positive niche construction can both evolve and be maintained when it has other beneficial effects via pleiotropy. This situation may apply generally to the evolutionary mainte nance of cooperation.\n\nhttps://conferences.maths.unsw.edu.au/event/2/con tributions/336/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/336/ END:VEVENT BEGIN:VEVENT SUMMARY:Coding in the classroom DTSTART;VALUE=DATE-TIME:20180712T010000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-82@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michael Kelly (Transylvania University)\nThere are m any benefits to incorporating coding into mathematics classrooms: students begin to think algorithmically about mathematics\, students learn a trans ferable skill\, and the courses can include more real-world\, data-driven problems. However\, bringing programming into the math curriculum presents challenges. Success and difficulties of integrating programming into the liberal arts mathematics classroom will be presented. In particular\, inco rporating programming in conjunction with the development of an interdisci plinary biomathematics program at a liberal arts college will be discussed .\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/82/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/82/ END:VEVENT BEGIN:VEVENT SUMMARY:On modelling biological network formation DTSTART;VALUE=DATE-TIME:20180711T010000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-126@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Helene Ranetbauer (University of Vienna)\nIn this ta lk we present a mesoscopic model for natural network formation processes\, acting as a bridge between a discrete and continuous network approach pro posed by Hu and Cai. All models describe the pressure field and the dynami cs of the conductance network under pressure force effects.\n\nWe start by presenting the different approaches and analyze their corresponding prope rties. We will focus on special stationary solutions of the mesoscopic mod el including discrete network solutions. \n\nThis involves a proper reinte rpretation of the system in terms of measure valued solutions. To overcome the arising difficulties\, we will also introduce an alternative formulat ion replacing the nonlinear Poisson equation for the pressure field in the original approach by a linear side constraint.\n\nhttps://conferences.mat hs.unsw.edu.au/event/2/contributions/126/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/126/ END:VEVENT BEGIN:VEVENT SUMMARY:Mixing and pumping by pairs of helices in a viscous fluid DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-76@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Amy Buchmann (Tulane University)\nIt is difficult to mix and pump fluid in microfluidics devices because the traditional metho ds of mixing and pumping at large length scales don’t work at small leng th scales. Experimental work has suggested that rotating helical flagella may be used to effectively mix and pump fluid in microfluidics devices. To further explore this idea and to characterize the flow features around ro tating helices\, we study the hydrodynamic interactions between two rigid helices rotating at a constant velocity. Helices are coupled to a viscous fluid using a numerical method based upon a centerline distribution of reg ularized Stokeslets\, and we analyze the effects of spacing and phase shif t on mixing and pumping.\n\nhttps://conferences.maths.unsw.edu.au/event/2/ contributions/76/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/76/ END:VEVENT BEGIN:VEVENT SUMMARY:Flow and movement of organisms through protective layers DTSTART;VALUE=DATE-TIME:20180710T010000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-148@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Christopher Strickland (University of Tennessee\, Kn oxville)\nMicroscale filtering and protective layers appear in a variety o f places throughout the biological world\, with examples including both in ternal physiological examples (extracellular proteins\, microvilli\, cilia ) and external biological structures (trichomes\, swimming legs\, bristled wings). In this talk\, I describe an agent-based framework built for expl oring the biological environment created by these structures and its poten tial effect on small\, lightweight organisms. Using implemented analytical models (e.g. Brinkman) or input from CFD packages to specify the flow fie ld\, the framework can simulate a large variety of behaviours in both 2-D and 3-D time-varying environments as a testing ground for population-level theory. Preliminary numerical results will shown demonstrating some of th e capabilities of the approach as well as future directions.\n\nhttps://co nferences.maths.unsw.edu.au/event/2/contributions/148/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/148/ END:VEVENT BEGIN:VEVENT SUMMARY:Quantitative assessment of the dynamics of soluble form of DNAM-1 (CD226) in human serum explains the mechanism of acute Graft Versus Host D isease (GVHD). DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-394@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yuki Goshima (University of Tsukuba\, Department of school of medicine.)\nAcute graft-versus-host disease (aGVHD) is the major complication of Allogeneic Hematopoietic Stem Cell Transplantation (allo- HSCT). A lot of previous studies showed that the importance of DNAM-1(CD22 6) which is expressed on CD4+ T cells\, CD8+ T cells\, natural killer (NK) cells\, and monocytes Therefore\, DNAM-1 has been considered as essential molecule of developing aGVHD *in vitro* and *vivo* [1]\, [2]. But underst anding the mechanism of aGVHD in human body is not understood well since f ew clinical trials related to the mechanism of aGVHD were performed. Recen tly\, Kanaya *et al*. [3] focused on the soluble form of DNAM-1 (sDNAM-1) and collected the data which were from the subjects who recieved the trans plantation. A form of the data set is time course therefore each subject h as several observations by each time point. Despite of the time course dat a set\, they just focus on the maximum value of the observation i.e. they didn’t assess the dynamics of soluble DNAM-1. Therefore\, they couldn’ t explain the connection between the dynamics of sDNAM-1 and developing aG VHD well. So then\, we analyzed this data set by considering the dynamics of sDNAM-1. In our research\, we made the hypothesis of mechanism of aGVHD and proved it by applying mathematical model and computational simulation to this data set. These results suggest that there exist 3 types of DNAM- 1 after transplantation in the subject’s body. The 1st type of DNAM-1 is released temporally and the 2nd types of DNAM-1 is released constantly. T hose are from donor cells. On the other hand\, 3rd types of DNAM-1 is resi dual one in the recipient body which is released from recipient cells. In addition\, we proved quantitatively that the more 1st type of DNAM-1 exist in the human body after transplantation\, the more the subjects tend to d evelop aGVHD. From the several previous researches and this research\, we conclude that those cells which release DNAM-1 temporarlly can be consider ed as allo reactive T cells. Therefore\, allo reactive T cells which expre sses DNAM-1 can be treatment target for aGVHD.\n\n[1] T. Nabekura *et al*. \, “Critical role of DNAX accessory molecule-1 (DNAM-1) in the developme nt of acute graft-versus-host disease in mice.\,” *Proc. Natl. Acad. Sci . U. S. A.*\, vol. 107\, no. 43\, pp. 18593–8\, Oct. 2010.\n[2] M. Koyam a *et al*.\, “Promoting regulation via the inhibition of DNAM-1 after tr ansplantation.\,” *Blood*\, vol. 121\, no. 17\, pp. 3511–20\, Apr. 201 3.\n[3] M. Kanaya et al.\, “Soluble DNAM-1\, as a predictive biomarker f or acute Graft-Versus-Host disease\,” *PLoS One*\, vol. 11\, no. 6\, pp. 1–12\, 2016.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribut ions/394/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/394/ END:VEVENT BEGIN:VEVENT SUMMARY:Adaptive life-history and eigenfunctions in structured population models DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-424@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ryo Oizumi (National Institute of Population and Soc ial Security Research)\nLife-histories in organisms faced with various sel ection pressures such as heterogeneity\, intra- and inter-specific competi tions\, and variable environment. Ecologists have thought that evolution m aximizes different objects from each pressure. For example\, in the absenc e of the competitions\, conventional Darwinism asserts that the adaptive l ife history maximizes the population growth. On the other hand\, the prese nce of competitions is thought to evolves un-invadable life strategy from any other strategies such as maximizing the carrying capacity that $r/K$-s election theory asserts. Difference of each habitat\, thus\, yields differ ent objective function and diversity of life-histories from precocity to a ltricity. \n\n However\, there is ambiguity involved in necessity for diff erent objective function in each habitat. It is difficult to define the th reshold changing from population growth rate to carrying capacity\, as obj ective function. This difficulty fades $r/K$-selection theory and makes am biguity in categrization of life history evolution. On the other hand\, se veral indices which the fittest species have are suggested (ESS etc.)\, an d these have a common point that the fittest species or genetic group occu py their habitat. If an objective function addresses the common point with out presence and absence of competitions\, and if it evolves all traits th at are precocity\, altricity\, and so on in life history\, evolution of li fe-history can be systematized by maximizing (or minimizing) a unique obje ctive function. \n\nIn this presentation\, I would like to propose that th e adjoint eigenfunction providing reproductive value in a structure popula tion model is a candidate of the unique objective function.\n\nhttps://con ferences.maths.unsw.edu.au/event/2/contributions/424/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/424/ END:VEVENT BEGIN:VEVENT SUMMARY:Shape\, length and location of PAR polarity in asymmetric cell div ision DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-48@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sungrim Seirin-Lee (Hiroshima University)\nAnterior- posterior (AP) polarity formation of cell membrane proteins plays a crucia l role in determining cell asymmetry\, which depends not only on the sever al genetic process but also biochemical and biophysical interactions. In * Caenorhabditis elegans*\, a single fertilized egg cell (P0)\, its daughter cell (P1)\, and the germline precursors (P2 and P3 cells) form two exclus ive domains of PAR proteins on the membrane along the anterior-posterior a xis. Since a mother cell divides into two dissimilar daughter cells with d ifferent properties using this polarity\, the shape and length scale of PA R domains are critical. Furthermore\, the phenomenon of polarity reversal has been observed in which the axis of asymmetric cell division of the P2 and P3 cells is formed in an opposite manner to that of the P0 and P1 cell s. The extracellular signal MES-1/SRC-1 has been shown to induce polarity reversal\, but the detailed mechanism remains elusive. Here\, I explore th e mechanism of symmetry breaking and AP polarity formation using self-recr uitment model of posterior proteins and show how the shape\, length and lo cation of PAR polarity can be form robustly. If time is allowed\, I also i ntroduce a multi-dimensional polarity model including cell's geometrical p roperty and show how the cell geometry can give a critical effect on AP po larity.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/48/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/48/ END:VEVENT BEGIN:VEVENT SUMMARY:Transport phenomena in field effect transistors DTSTART;VALUE=DATE-TIME:20180711T063000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-7@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ryan Evans (Applied and Computational Mathematics Di vision\, National Institute of Standards and Technology)\nTailoring therap ies to individuals for personalized care can be safer and yield superior o utcomes with lower doses for conditions such as diabetes\, Alzheimers dise ase\, or even certain cancers. However\, widespread use of personalized ca re is currently limited by our inability to routinely measure pathology an d detect biomarkers. Moreover\, existing strategies require specialized fa cilities\, can be slow to perform and can be expensive. This has led to th e development of a new portable detection tool known as a field effect tra nsistor (FET). Very well-suited for biomarker measurements due their high charge sensitivity and direct signal transduction\, FETs allow label-free measurements at physiological concentrations. Chemical reactants are inje cted at the top of a solution-well and diffuse through the well to bind wi th another chemical reactant immobilized to a narrow band on the well-floo r. A resulting response curve allows for biomarker measurement and estimat ion of key parameters\, such as binding affinities. A collection of mathe matical models for FET experiments will be presented taking the form of a diffusion coupled to a nonlinear equation that describes the evolution of the reacting species concentration.\n\nhttps://conferences.maths.unsw.edu. au/event/2/contributions/7/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/7/ END:VEVENT BEGIN:VEVENT SUMMARY:Evolution of host defence in response to fluctuating environments: a theoretical and experimental study DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-396@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Charlotte Ferris (University of Sheffield\, UK)\nEnv ironmental fluctuations\, such as those caused by seasonality\, are common \, and climate change is expected to increase the amplitude of environment al oscillations. Therefore it is important to understand how increasing th e amplitude of environmental oscillations will affect evolutionary process es\, and in particular host-parasite evolution\, where the extent of evolu tion is likely to be altered.\n\nHere I present results from a mathematica l study of host defence evolution to parasitism when the host birth rate i s time-dependent. I show how the amplitude and period of seasonality affec t the evolution of the host population\, and how this depends on other lif e-history parameters\, most notably the recovery rate. I also present expe rimental results from a study of the bacteria Pseudomonas fluorescens SBW2 5 and its phage parasite (SBW25Φ2)\, and link these to predictions from t he mathematical model.\n\nhttps://conferences.maths.unsw.edu.au/event/2/co ntributions/396/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/396/ END:VEVENT BEGIN:VEVENT SUMMARY:Heritable tumour cell division rate heterogeneity induces clonal d ominance DTSTART;VALUE=DATE-TIME:20180710T020000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-393@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Margriet M. Palm (Division of Drug Discovery and Saf ety\, Leiden Academic Center for Drug Research\, Leiden University\, The N etherlands)\nTumours consist of a hierarchical population of cells that di ffer in their phenotype and genotype. This hierarchical organization of ce lls means that a few clones (i.e.\, cells and several generations of offsp ring) are abundant while most are rare\, which is called clonal dominance. Such dominance also occurred in published *in vitro* iterated growth and passage experiments with tumour cells in which genetic barcodes were used for lineage tracing. A potential source for such heterogeneity is that dom inant clones derive from cancer stem cells with an unlimited self-renewal capacity. Furthermore\, ongoing evolution and selection within the growing population may also induce clonal dominance. To understand how clonal dom inance developed in the iterated growth and passage experiments\, we built three computational models that simulate these experiments. In the first two models we used the tau-leaping Gillespie algorithm to simulate random growth and passage and we either consider all cells to have an equal proli feration capacity (model 1) or we distinguish between cancer stem cells an d differentiated cells (model 2). In the last model\, we used a dynamic Mo nte Carlo method to simulate the development of a cell population where di vision rates are heritable and vary in between cells due to initial variat ion and mutation (model 3). Only simulations with the model where division rates varied between the cells (model 3) reproduced the clonal dominance that developed in *in vitro* iterated growth and passage experiments. In c ontrast\, the experimental results can neither be reproduced with a model that considers random growth and passage (model 1)\, nor with a model base d on cancer stem cells (model 2). Altogether\, our model suggests that *in vitro* clonal dominance develops due to selection of fast-dividing clones .\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/393/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/393/ END:VEVENT BEGIN:VEVENT SUMMARY:Hybrid agent-based library DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-290@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Rafael Bravo (Integrated Mathematical Oncology Depar tment\, Moffitt Cancer Center)\nThe Hybrid Agent–based Library (HAL) is a Java Library made of simple\, efficient\, generic components which can b e used to model complex spatial systems. HAL's components can broadly be c lassified into: on and off lattice agent containers\, finite difference di ffusion fields\, a GUI building system\, and additional tools and utilitie s for computation and collecting data. These components were designed to o perate independently\, but are standardized to make them easy to interface with one another.\n\nHAL is a useful asset for researchers who wish to bu ild efficient 2D and 3D hybrid models in Java\, while not starting entirel y from scratch. It is available on GitHub at https://github.com/torococo/H AL under the MIT License. HAL requires at least Java 8 or later to run\, a nd the java jdk version 1.8 or later to compile the source code.\n\nThe sp atial components in HAL all use a consistent indexing scheme. Setting valu es in a diffusible field\, for example\, is syntactically similar to setti ng visualization pixel values\, or finding the agents that occupy a positi on. The consistent syntax helps substantially with HAL’s learning curve. It also helps with understanding the source code of models that use compo nents that the reader is not familiar with. \n\nThere are several pre-exis ting general hybrid agent-based modelling frameworks\, the most popular be ing Chaste\, Repast\, Mason\, and Netlogo. Each of these facilitates model ling under a different centralized control structure: In Chaste centralize d control done by a Simulator object\, in Repast this component is called an Engine\, in Mason it is called the Schedule object\, and in Netlogo it is called the Go loop.\n\nHAL shares many characteristics with these frame works\, but primarily differentiates itself with its simplicity and decent ralized design. There is no controller or scheduler\, so the modeler desig ns the logical flow and the scheduling of interactions between components of the model explicitly. This allows the modeller to define the execution of the model using simple programming constructs such as “for loops”\, and sheds the difficulty of learning to manipulate a more complex control architecture.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributi ons/290/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/290/ END:VEVENT BEGIN:VEVENT SUMMARY:Ecological and evolutionary dynamics of multi-strain\, drug-resist ant systems DTSTART;VALUE=DATE-TIME:20180711T054000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-293@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michael Meehan (Australian Institute of Tropical Hea lth and Medicine - James Cook University)\nThe growing threat of antimicro bial drug resistance presents a significant challenge not only to the medi cal community\, but the wider general population. Alarmingly\, resistant s trains of infectious diseases are already endemic in many communities – particularly in developing countries and lower socio-economic settings – with new strains\, which enjoy even more extensive resistance\, continual ly emerging. \n\nTo examine this imminent threat to public health worldwid e we implement a class of coupled\, multi-strain epidemic models designed to simulate the emergence and dissemination of mutant (e.g. drug-resistant ) pathogen strains. In particular\, we investigate the ecological and evol utionary properties of a general class of multi-strain systems to determin e e.g. the necessary and sufficient conditions for strain replacement/inva sion\, the relative contributions from amplification and primary transmiss ion to the overall disease burden and the timescales involved. We also con sider the evolutionary processes of various pathogens and investigate the rates at which both virulence and resistance evolve. This final point in p articular predicates concerns about the ongoing arms race between the evol ution of resistance and the development of novel treatments to treat new e xotic strains – which many fear is being won by the former.\n\nhttps://c onferences.maths.unsw.edu.au/event/2/contributions/293/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/293/ END:VEVENT BEGIN:VEVENT SUMMARY:A dynamical system model of host-pathogen interaction illustrates the role of the immune system in resilience to infection DTSTART;VALUE=DATE-TIME:20180712T005000Z DTEND;VALUE=DATE-TIME:20180712T011000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-274@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Oliver J Maclaren (University of Auckland)\nTraditio nally the study of host response to an infection has focussed on the effec t of the pathogen on host health and the ability of the host immune system to clear the pathogen. In this paradigm the host experiences an initial r eduction in health (assessed by suitable metrics e.g. temperature rise\, w eight loss\, subjective feelings of ill health) as the pathogen load in th e body increases. When the pathogen load is sufficiently high\, the immune response is activated and attempts to clear the pathogen. If the immune s ystem is able to eliminate the pathogen\, the host survives and returns to full or partial health. If not\, the infection results in death of the ho st. This paradigm does not account for the potential deleterious effects o f the immune response on the health of the host. While this concept has be en well studied in autoimmune disorders\, it has not been considered in th e context of diseases caused by pathogens. Here we present a dynamical sys tem model of the interplay between the host\, pathogen and the host immune response. The work utilises an existing two-variable\, nonlinear mathemat ical model of host-pathogen interaction [1] and supplements it with a vari able describing the health of the host. The equation describing the health variable incorporates terms for self repair and interactions with the pat hogen and immune response. The system gives rise to a rich set of behaviou rs that\, in addition to the usual steady states of full host recovery or host death with unbounded pathogen growth\, also includes steady states wi th incomplete pathogen clearance and partial recovery or host death with c omplete pathogen clearance. The trajectories in phase space recapitulate p atterns that have been described empirically [2]. The model was parameteri sed against a published mouse malaria dataset [3] and found to adequately describe the observed trajectories. The model also suggested that the diff erence between host survival and death in the study was governed by the st rength of the health-immune response interaction rather than pathogen medi ated effects.\n\n[1] H. Mayer *et al*.\, *Chaos* 5(1)\, 1995\n[2] D. Schne ider\, *PLoS Biology* 9(9) 2011\n[3] B. Y. Torres *et al*.\, *PLoS Biology *\, 10.1371/journal.pbio.1002436\, 2016\n\nhttps://conferences.maths.unsw. edu.au/event/2/contributions/274/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/274/ END:VEVENT BEGIN:VEVENT SUMMARY:Putting your money where your mouth is: the economics of stomatal development DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-437@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Rachel Denley Bowers (University of Sheffield)\nThe placement of stomata on the leaf surface is regulated by a number of thing s: coordinated asymmetric cellular division\, genetic regulation\, and dis tribution of extracellular signalling molecules. \n\nIt has been noted tha t the number of stomata per non-stomatal epidermal cell can vary between p lants which have the same spatial distribution of stomata\, which suggests that in some circumstances one method of maintaining stomatal placement ( increased cell division\, increased cell expansion\, increased recruitment of cells to the stomatal fate) may be optimal over another. \n\nPerhaps t he reason for this difference in stomatal placement regulation is due to d ifference in the energetic costs to the plant of each of these methods. Us ing a combination of experimental and mathematical biology\, the relations hip between energetic cost and stomatal placement in the model organism *A rabidopsis thaliana* is being investigated.\n\nhttps://conferences.maths.u nsw.edu.au/event/2/contributions/437/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/437/ END:VEVENT BEGIN:VEVENT SUMMARY:A multiscale model to inform the design of nerve repair conduits DTSTART;VALUE=DATE-TIME:20180709T020000Z DTEND;VALUE=DATE-TIME:20180709T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-123@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Simao Laranjeira (UCL Mechanical Engineering\, UCL C entre for Nerve Engineering)\nPeripheral nerve damage afflicts 1 M people p.a. in Europe and the USA [1]. In the most severe cases\, patients experi ence major loss of function. The gold-standard treatment for patients with severe cases is surgery using a graft based on a healthy section of nerve taken from the patient\, however\, only 50% of patients experience functi onal recovery [2].\n\nAfter a nerve is severed\, the distal stump produces chemotactic cues that can stimulate neurite regeneration. At the proximal stump\, neurites start growing and their direction is informed by these c ues. If the gap is short enough\, the neurites are able to respond to thei r environmental cues and grow across the injury site to enter the distal s tump. However\, if the gap is larger than 5 mm\, the regenerative process is unable to establish a supportive environment for neurite growth. \n\nTh e limitations of the current gold-standard therapy to establish functional recovery have motivated the development of engineered replacement tissues and repair conduits to promote regeneration. Several designs have been pr oposed that vary not only in terms of material and therapeutic cell compos ition but also in their spatial distribution. Despite promising results in animal models\, these conduits have not yet progressed to clinical use\, in part because of the expanse of different variables that need to be test ed using experimental models [3].\n\nHere a multiscale mathematical model is proposed to streamline the design of these conduits. The model comprise s of two components. The first is a continuous 3D model of the chemotactic field within the conduit. The release of chemotactic factors from the dis tal stump is captured using a flux boundary condition\, as well as the per meability of the conduit wrap.\n \nWithin this geometry\, at the proximal stump\, a random walk model for individual neurites is initiated. Neurite growth is simulated as a random variable that is biased towards the direct ion of increasing cue\; this cue could either be chemotactic (as described using the continuum model above)\, or durotactic (due to the underlying m aterial distribution). Neurite branching is incorporated into the model\, as this is a fundamental feature during regeneration\, which determines ho w neurites sense the underlying gradient fields. Morphological features of branching are accounted for by implementing the model by Van Pelt *et al. *\, whilst branches can also recede if they encounter a sub-optimal enviro nment\, modelled using a Markov chain process [4\,5].\n\nThe discrete-cont inuum framework is parameterised against *in vitro* and *in vivo* data on neurite progression through engineered conduits\, including neurite counts at the proximal and distal end as well as measurements of neurite lengths . The parameterised framework can be used to explore the optimal arrangeme nt of materials and cells to promote efficient neuronal regeneration follo wing injury.\n\n[1] Chen\, Shan-lin\, *et al.* *Neural regeneration resear ch*\, 10.11 (2015).\n[2] Grinsell\, D.\, and C. P. Keating. *BioMed resea rch international* (2014).\n[3] Angius\, D.\, *et al.* *Biomaterials* 33.3 2 (2012).\n[4] Van Pelt\, J.\, *et al.* *The Journal of Comparative Neurol ogy* 387.3 (1997).\n[5] Britto\, J.M.\, *et al.* *Biophysical Journal* 97. 3 (2009).\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/1 23/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/123/ END:VEVENT BEGIN:VEVENT SUMMARY:Control structures in cancer chemotherapy DTSTART;VALUE=DATE-TIME:20180711T010000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-196@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: James Greene (Rutgers University\, New Brunswick\, N J)\nDrug resistance is a major cause of the failure of chemotherapy. Resi stance manifests through a diverse set of molecular mechanisms\, such as t he upregulation of efflux transporters on the cell membrane\, enhanced DNA damage repair mechanisms\, and/or the presence of cancer stem cells. Cla ssically\, these mechanisms are understood as conferred to the cell by ran dom genetic mutations\, from which clonal expansion occurs via Darwian evo lution. However\, the recent experimental discovery of epigenetics and ph enotype plasticity complicates this hypothesis. It is now believed that c hemotherapy can produce drug-resistant clones. Motivated this by this rec ent experimental evidence\, we introduce a framework of drug-induced resis tance\, which incorporates both random and drug induced effects. We discu ss both structural and practical identifiability issues related to the mod el\, and demonstrate techniques by which the induction rate of an applied chemotherapy may be experimentally determined. This is crucial\, as the d esign of control protocols is heavily influenced by this aforementioned ra te. Specifically\, we seek the treatment protocol which prolongs patient ’s life by maximizing the time of treatment until a critical tumour size is reached. The general control structure is determined as a combination of both bang-bang and singular arcs. We deduce that in the case of purely random mutations\, optimal controls are pure bang-bang\, while singular a rcs exist if treatment causes resistance to emerge. We further characteriz e the precise control structure using a combination of numerical methods a nd higher-order techniques. Thus\, the ability of a drug to induce resista nce generates a completely different control structure from that of the cl assical Darwinian selection paradigm.\n\nhttps://conferences.maths.unsw.ed u.au/event/2/contributions/196/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/196/ END:VEVENT BEGIN:VEVENT SUMMARY:A general stochastic model for evolutionary dynamics of communicab le diseases DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T062000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-296@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Robert Cope (The University of Adelaide)\nInfectious diseases undergo evolutionary changes as they spread and persist in popul ations. Different diseases present substantially different evolutionary dy namics\, with both large-scale changes that create different strains\, or more incremental shifts within a strain. In this talk\, we demonstrate how a general stochastic epidemic model can be used to explain different type s of evolutionary dynamics for infectious diseases. We describe how parame ter choices correspond to evolutionary processes\, and how simple building blocks within the model can be combined into more complex evolutionary be haviours. We compare model outputs to observed phylogenetic data from a va riety of infectious diseases\, including influenza\, dengue\, and Ebola.\n \nhttps://conferences.maths.unsw.edu.au/event/2/contributions/296/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/296/ END:VEVENT BEGIN:VEVENT SUMMARY:Fluid dynamics of nematocyst prey capture DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-103@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Wanda Strychalski (Case Western Reserve University)\ nA nematocyst is a specialized organelle within cells of jellyfish and oth er Cnidarians that sting. Nematocysts are also present in some single cell ed protists. They contain a barbed\, venomous thread that accelerates fast er than almost anything else in the animal kingdom. Here we simulate the f luid-structure interaction of the barbed thread accelerating through water to puncture its prey using the immersed boundary method. For simplicity\, our model describes the discharge of a single barb harpooning a single ce lled organism\, as in the case of dinoflagellates. One aspect of this proj ect that is particularly interesting is that the micron-sized barbed threa d reaches Reynolds numbers above one\, where inertial effects become impor tant. At this scale\, even small changes in speed and shape can have drama tic effects on the local flow field. This suggests that the large variety of sizes and shapes of nematocyst may have important fluid dynamic consequ ences. We find that reaching the inertial regime is critical for hitting p rey over short distances since the large boundary layers surrounding the b arb characteristic of viscous dominated flows effectively push the prey ou t of the way.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributio ns/103/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/103/ END:VEVENT BEGIN:VEVENT SUMMARY:Corrections to predictions of the basic reproduction number DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-125@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Matthew Betti (York University)\nThe basic reproduct ion number\, $R_0$\, derived from ordinary differential equation models is a powerful predictor of the severity of an infection and can help inform prevention and mitigation strategies. Many of the parameters used in ODE m odels are mean values of time-dependent distributions. Here\, we show how we can incorporate properties of these distributions to refine estimates o f $R_0$ for a series of ubiquitous models used in epidemiology. These corr ections are applied to the $R_0$ estimate as opposed to the model itself\, allowing simple models to be used\, and better predictions to be made pos t-hoc as more data becomes available. Moreover\, we address some difficult ies in trying to extend these corrections to more complex models.\n\nhttps ://conferences.maths.unsw.edu.au/event/2/contributions/125/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/125/ END:VEVENT BEGIN:VEVENT SUMMARY:Predicting blood flow and oxygenation in an image-based retinal va scular network DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-89@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Brendan Fry (Metropolitan State University of Denver )\nImpaired oxygen delivery and blood flow have been identified as signifi cant factors that contribute to the loss of retinal ganglion cells in glau coma patients. It is unknown\, however\, whether changes in blood flow to the retina are the cause or effect of retinal ganglion cell death\, and a combined experimental and theoretical approach is needed to analyze the re lationship between blood flow impairment and glaucoma. In this talk\, rece nt data-driven theoretical models will be presented that predict how issue s with blood flow regulation could lead to the impaired oxygenation seen i n experimental glaucoma data. Then\, an updated representation of the reti nal vasculature based on confocal microscopy images will be introduced. Th ese images reveal a complex and heterogeneous geometry of vessels that are distributed non-uniformly into multiple distinct retinal layers at varyin g depths. As a result\, an updated model using a Green's function method i s used to predict oxygen saturation in the retinal arteriolar tree\, in ad dition to predicting blood flow in the entire vascular network. Finally\, a framework will be introduced to incorporate time-dependent blood flow re gulation into the model\, so that vessels in the network can adjust diamet ers in response to changing conditions. The predictions from this mathemat ical model will be used to address the controversy of the cause-and-effect relationship between retinal ganglion cell death and impaired blood flow in glaucoma.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribution s/89/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/89/ END:VEVENT BEGIN:VEVENT SUMMARY:A unified stochastic modelling framework for the spread of nosocom ial infections DTSTART;VALUE=DATE-TIME:20180711T062000Z DTEND;VALUE=DATE-TIME:20180711T064000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-207@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Martin Lopez-Garcia (University of Leeds)\nOver the last years\, a number of stochastic models have been proposed for analysin g the spread of nosocomial infections in hospital settings. These models o ften account for a number of factors governing the spread dynamics: sponta neous patient colonization\, patient-staff contamination/colonization\, en vironmental contamination\, patient cohorting\, or health-care workers (HC Ws) hand-washing compliance levels. For each model\, tailor-designed metho ds are implemented in order to analyse the dynamics of the nosocomial outb reak\, usually by means of studying quantities of interest such as the rep roduction number of each agent in the hospital ward\, which is usually com puted by means of stochastic simulations or deterministic approximations. In this work\, we propose a highly versatile stochastic modelling framewor k that can account for all these factors simultaneously\, and analyse the reproduction number of each agent at the hospital ward during a nosocomial outbreak\, in an exact and analytical way. By means of five representativ e case studies\, we show how this unified modelling framework comprehends\ , as particular cases\, many of the existing models in the literature. We implement various numerical studies via which we: i) highlight the importa nce of maintaining high hand-hygiene compliance levels by HCWs\, ii) suppo rt infection control strategies including to improve environmental cleanin g during an outbreak\, and iii) show the potential of some HCWs to act as super-spreaders during nosocomial outbreaks.\n\nThis work is based on the manuscript López-García M\, Kypraios T (2018) A unified stochastic model ling framework for the spread of nosocomial infections. *Journal of the Ro yal Society Interface*\, under second review.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/207/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/207/ END:VEVENT BEGIN:VEVENT SUMMARY:The coexistence and its sustainability in Batesian mimicry DTSTART;VALUE=DATE-TIME:20180711T064000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-421@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hayato Kato (Hokkaido University)\nBatesian mimicry is a common phenomenon in nature\, and it has been reported in various tax a. In Batesian mimicry\, there are two species that have a similar coloura tion. One species is toxic or unpalatable\, we call it “model-species” . The other is nontoxic or palatable\, we call it “mimic”.\n\nWhile ma ny mathematical models focused on the evolution of mimicry\, only a few ma thematical models focused on community dynamics. Furthermore\, the sustain ability of the coexistence has not been studied. Here\, we addressed the c ommunity dynamics and its sustainability in this study.\n\nA part of the p revious mathematical models has a common framework based on simple and pla usible assumptions such as density-dependent effect and frequency-dependen t predation. However\, even a simple mathematical model based on the frame work has not been analyzed completely. The simple mathematical model is al so important mathematically because it is one of the basic models that hav e both density- and frequency-dependent effects and actually it includes a ratio-dependent predator-prey model.\n\nThe objective of our study is as follows\; first\, to solve a mathematical model based on the common framew ork completely and understand its properties. Secondly\, to examine the im pact of mimicry on community dynamics. Thirdly\, to discuss the sustainabl e coexistence of model-species and mimic.\n\nWe focused on the case that t he intrinsic growth rate of model-species is less than mimic because model -species pay some cost for acquiring toxicity and defined “predation imp act (PI)” as the predation rate divided by the intrinsic growth rate. Th e result is divided into two types using PIs of model-species and mimic sp ecies\; type I is when the predation impact of model-species is small\, ty pe II is when the predation impact of model-species is large. In type I\, model-species and mimic always coexist. In type II\, they can coexist\, bu t not always. In particular\, in type II\, when the ratio of the carrying capacity change and become less than a threshold\, model-species become ex tinct. Thus\, the coexistence of model-species and mimic is unlikely to be maintained in type II under a varying environment. Therefore\, Batesian m imicry in nature is supposed to be maintained in type I.\n\nIn our mathema tical model\, there are only three stable states\; coexistence\, mimic alo ne and both extinction. This result can explain the geographic distributio n of model-species and mimic in more than 10 mimicry systems. For example\ , eastern coral snake is a toxic model and scarlet kingsnake is a nontoxic mimic in North America. In their geographic distribution\, the areas of c oexistence\, mimic alone and both-absence were observed with latitude grad ient. This pattern of the geographic distribution is consistent with the r esult of our mathematical model.\n\nIn addition to the above study\, we co nstruct some models\, taking predator’s learning process into account. W e present the results derived from these models and compare them.\n\nhttps ://conferences.maths.unsw.edu.au/event/2/contributions/421/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/421/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling continuous levels of resistance to multidrug therapy in cancer DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-151@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Heyrim Cho (University of Maryland)\nMultidrug resis tance consists of a series of genetic and epigenetic alternations that inv olve multifactorial and complex processes\, which are a challenge to succe ssful cancer treatments. Accompanied by advances in biotechnology and high dimensional data analysis techniques that are bringing in new opportuniti es in modelling biological systems with continuous phenotypic structured m odels\, we study a cancer cell population model that considers a multi-dim ensional continuous resistance trait to multiple drugs to investigate mult idrug resistance. We compare our continuous resistance trait model with cl assical models that assume a discrete resistance state and classify the ca ses when the continuum and discrete models yield different dynamical patte rns in the emerging heterogeneity in response to drugs. We also compute th e maximal fitness resistance trait for various continuum models and study the effect of epimutations. Finally\, we demonstrate how our approach can be used to study tumour growth regarding the turnover rate and the prolife rating fraction\, and show that a continuous resistance level may result i n a different dynamics when compared with the predictions of other discret e models.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/1 51/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/151/ END:VEVENT BEGIN:VEVENT SUMMARY:Computational insights to high dimensional data from $\\textit{Clo stridium difficile}$ infection DTSTART;VALUE=DATE-TIME:20180710T020000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-8@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Samantha Erwin (NCSU)\nIn recent years\, new technol ogy has allowed us to achieve measurements of hundreds of metabolites and the expression of thousands of genes. With this large scale\, all-encompas sing\, ‘omics’ data comes a critical need to reduce these datasets to the most functional elements so that we can discover key components drivin g disease pathogenesis. Current techniques to analyze omics data are not g eared towards supporting parsimonious mechanistic models of bacterial path ogenesis. Specifically\, networks are common tools for analyzing these dat a\, however\, at times graphical networks can be overwhelming due to the c omplexity of the information. In this work\, we use sparse graphical netwo rks to understand correlations between multiple high dimensional data sets . We apply these method to metabolomics and transcriptomics data from a re cent animal model for *Clostridium difficile* infection in which mice were antibiotic treated with cefoperazone and challenged with *C. difficile* 2 days following treatment. We find significant changes in the *C. difficil e* transcriptome at later time points compared to earlier time points\; wh ile\, most of the amino acid changes occur in the first 24 hours. We find taurine\, proline\, 3-(4-hydroxyphenyl)lactate\, 5-aminovalerate\, 5-oxop roline\, thioproline are the main amino acids contributing to the changes across all time points. Utilizing the key components of the sparse graphic al model we’ve developed and analyzed an ordinary differential equation model to better understand the specific mechanisms leading to *C. difficil e* colonization.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribu tions/8/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/8/ END:VEVENT BEGIN:VEVENT SUMMARY:Bumps in small-world networks DTSTART;VALUE=DATE-TIME:20180711T020000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-91@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Carlo Laing (Massey University)\nWe consider a netwo rk of coupled excitatory and inhibitory theta neurons which is capable of supporting stable spatially-localised “bump” solutions. We randomly ad d long-range and simultaneously remove short-range connections within the network to form a small-world network and investigate the effects of this rewiring on the existence and stability of the bump solution. We consider two limits in which continuum equations can be derived\; bump solutions ar e fixed points of these equations. We can thus use standard numerical bifu rcation analysis to determine the stability of these bumps and to follow t hem as parameters (such as rewiring probabilities) are varied. We find tha t under some rewiring schemes bumps are quite robust\, whereas in other sc hemes they can become unstable via Hopf bifurcation or even be destroyed i n saddle-node bifurcations.\n\nhttps://conferences.maths.unsw.edu.au/event /2/contributions/91/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/91/ END:VEVENT BEGIN:VEVENT SUMMARY:Flagellar swimming in viscoelastic fluids DTSTART;VALUE=DATE-TIME:20180709T010000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-115@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Robert Guy (University of California Davis)\nMany im portant biological functions depend on microorganisms' ability to move in viscoelastic fluids such as mucus and wet soil. The effects of fluid elast icity on motility remain poorly understood partly because the swimmer stro kes depend on the properties of the fluid medium\, which obfuscates the me chanisms responsible for observed behavioural changes. We use experimental data on the gaits of *Chlamydomonas reinhardtii* swimming in Newtonian an d viscoelastic fluids as inputs to numerical simulations that decouple the swimmer gait and fluid type in order to isolate the effect of fluid elast icity on swimming. In viscoelastic fluids\, cells employing the Newtonian gait swim faster but generate larger stresses and use more power\, and as a result the viscoelastic gait is more efficient. Furthermore\, we show that fundamental principles of swimming based on viscous fluid theory miss important flow dynamics: fluid elasticity provides an elastic memory effe ct which increases both the forward and backward speeds\, and (unlike pure ly viscous fluids) larger fluid stress accumulates around flagella moving tangent to the swimming direction\, compared to the normal direction.\n\nh ttps://conferences.maths.unsw.edu.au/event/2/contributions/115/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/115/ END:VEVENT BEGIN:VEVENT SUMMARY:Synchronization of tubular pressure oscillations in coupled nephro ns DTSTART;VALUE=DATE-TIME:20180711T010000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-113@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hwayeon Ryu (University of Hartford)\nThe kidney pla ys an essential role in regulating the blood pressure and a number of its func- tions operate at the functional unit of the kidney\, the nephron. To understand the impacts of internephron coupling on the overall nephrons ’ dynamics\, we develop a mathematical model of a tubuloglomerular feedb ack (TGF) system\, a negative feedback mechanism for nephron’s fluid cap acity. Specifically\, each model nephron represents a rigid thick ascendin g limb only and is assumed to interact with nearby nephrons through vascul ar and hemodynamic coupling along the pre-glomerular vasculature. We condu ct a bifurcation analysis by deriving a characteristic equation obtained v ia a linearization of the model equations. Numerical solutions for the mod el equations are consequently obtained to validate the predictions of the characteristic equation. The model results show that the coupled-TGF syste m with two different coupling effects can produce in-phase as well as anti -phase (out-of-phase) synchronization of tubular pressure oscillations in two coupled nephrons\, as has been observed in experimental studies.\n\nht tps://conferences.maths.unsw.edu.au/event/2/contributions/113/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/113/ END:VEVENT BEGIN:VEVENT SUMMARY:Spatial moment models for collective cell behaviour DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-92@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michael Plank (University of Canterbury)\nMany PDE-b ased models of collective cell behaviour implicitly assume that the popula tion of cells is ‘well mixed’. This is called a spatial mean-field ass umption. In reality\, populations often have a more complex spatial struct ure\, such as clusters and/or spatial segregation of cells. This spatial s tructure is both a cause and an effect of non-local interactions among cel ls and can make a significant difference to model predictions about\, for example\, cell densities and invasion speeds. I will describe an individua l-based model of collective cell behaviour that is based on interactions b etween pairs of cells\, including a novel neighbour-dependent directional bias. I will then show how a continuum approximation to the individual-bas ed model can be derived using spatial moment dynamics. This approximation tracks important features of the population spatial structure and incorpor ates non-local interactions that affect processes such as movement and mor tality. Finally\, I will show how experimental data can be used to estimat e model parameters.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contr ibutions/92/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/92/ END:VEVENT BEGIN:VEVENT SUMMARY:Spatio-temporal canards & bifurcation delay in neural reaction-dif fusion systems DTSTART;VALUE=DATE-TIME:20180710T020000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-158@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Theodore Vo (Florida State University)\nNeural spiki ng and bursting rhythms in space-clamped (i.e.\, ODE) models are typically driven by either canard dynamics or slow passage through Hopf bifurcation s. In both cases\, solutions which are attracted to quasi-stationary state s (QSS) sufficiently before a fold or Hopf bifurcation remain near the QSS for long times after the states have become repelling\, resulting in a si gnificant delay in the loss of stability and hence in the onset of oscilla tions. In this work\, we present the spatio-temporal analogues of these de layed bifurcation phenomena in multi-time-scale reaction-diffusion equatio ns. We show the existence of canard-induced bursting rhythms in a spatiall y extended model of the electrical activity in pituitary cells. We then de rive asymptotic formulas for the space-time boundaries that act as buffers beyond which solutions cannot remain near the repelling QSS (and hence at which the delayed onset of oscillations must occur) for slow passage thro ugh Hopf bifurcations in reaction-diffusion equations.\n\nThis is joint wo rk with Tasso J. Kaper (Boston University).\n\nhttps://conferences.maths.u nsw.edu.au/event/2/contributions/158/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/158/ END:VEVENT BEGIN:VEVENT SUMMARY:How the extracellular matrix promotes the growth of ovarian cancer DTSTART;VALUE=DATE-TIME:20180712T053000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-169@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Pantea Pooladvand (University of Sydney)\nEpithelial Ovarian Cancer (EOC) is one of the deadliest cancers in women. It is the fifth leading cause of cancer-related deaths in the United States. Due to the lack of early detection\, this cancer has an average 5-year survival o f only 27%. We know\, that like other epithelial cancers\, ovarian tumour cells remodel the extracellular matrix (ECM) components in healthy tissue in order to promote a favourable environment for replication and progressi on. However\, the role of ECM in promoting EOC is yet to be explored. In t his presentation\, we aim to highlight some of the key ECM components that play a major role in the progression of tumour cells. We do this by consi dering the ECM as a dynamic system that can support and protect tumour cel ls by adapting its components. Using a system of networked ordinary differ ential equations\, we model the tumour environment and show that\, to unde rstand the role of the ECM in tumour progression\, we must consider the EC M as a collective entity and not just as individual components.\n\nhttps:/ /conferences.maths.unsw.edu.au/event/2/contributions/169/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/169/ END:VEVENT BEGIN:VEVENT SUMMARY:An integrated model linking structural and dynamical properties of cortical microcircuits DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-147@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Pulin Gong (The University of Sydney)\nExperimental studies have begun revealing essential properties of the structural connec tivity and the spatiotemporal activity dynamics of cortical microcircuits. To integrate these properties from anatomy and physiology\, and to elucid ate the mechanistic links between them\, we develop a cortical microcircui t model that captures a range of realistic features of synaptic connectivi ty. We show that the model accounts for the emergence of higher-order conn ectivity structures\, including overrepresented three-neuron motifs and hi ghly connected hub neurons that form an interconnected rich-club. The micr ocircuit model exhibits a rich repertoire of activity states\, ranging fro m asynchronous to localized and global propagating wave states. We find th at around the transition between asynchronous and localized propagating wa ve states\, our model quantitatively reproduces a variety of major empiric al findings regarding neural spatiotemporal dynamics\, which otherwise rem ain disjointed in existing studies. These dynamics include diverse couplin g (correlation) between spiking activity of individual neurons and the pop ulation\, propagating wave patterns with variable speed and precise tempor al structures of neural spikes. We further illustrate how these neural dyn amics are mechanistically linked to the structural connectivity properties by analyzing the contributions of connectivity to neural spiking dynamics and by showing that the rich-club structure is fundamentally related to t he emergence of the diverse population coupling. These findings establish an integrated account of structural connectivity and activity dynamics of cortical microcircuits\, and provide novel experimentally testable predict ions.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/147/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/147/ END:VEVENT BEGIN:VEVENT SUMMARY:A general framework to account for unobserved heterogeneity in epi demiology DTSTART;VALUE=DATE-TIME:20180712T010000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-170@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Gabriela Gomes (Liverpool School of Tropical Medicin e\, UK\, and Centro de Investigação em Biodiversidade e Recursos Genéti cos\, Universidade do Porto\, Portugal)\nUnobserved heterogeneity was intr oduced in 1920 as a modifier of individual hazards. The concept was termed frailty in demography to describe variation in individual longevity [1]\, and has been incorporated in methods for survival analysis. As the fraile st individuals are removed earlier from a heterogeneous group\, mean hazar ds appear to decrease over time – cohort selection – leading to some o f the most elusive effects in population science. Despite the accumulation of documented fallacies induced by cohort selection\, the issue remains l argely overlooked. I will expose the ubiquity of the phenomenon and propos e a general framework to infer and compare trait distributions\, with exam ples of current interest in epidemiology and related disciplines: \n(1) Va ccines appear less effective in high-incidence settings. Are they\, really [2]? \n(2) What is the real effect of *Wolbachia* on mosquito susceptibil ity to dengue viruses [3]? \n(3) As populations of bacteria are exposed to antibiotics\, their mortality rates decline due to selection for noninher ited resistance4. How much does this phenomenon share with what has been d escribed in human demography [1]? \n(4) What does cohort selection add to the debate between neutral and niche theories of biodiversity? \n\n[1] Vau pel JW\, Manton KG\, Stallard E (1979) Impact of heterogeneity in individu al frailty on the dynamics of mortality. *Demography* 16: 439-454.\n[2] Go mes MGM\, Gordon SB\, Lalloo DG (2016) Clinical trials: the mathematics of falling vaccine efficacy with rising disease incidence. *Vaccine* 34: 300 7-3009.\n[3] King JG\, Souto-Maior C\, Sartori L\, Maciel-de-Freitas R\, G omes MGM (2018) Variation in *Wolbachia* effects on *Aedes* mosquitoes is a key determinant of invasiveness and vectorial capacity. *Nat Commun* (in press).\n[4] Balaban NQ\, Merrin J\, Chait R\, Kowalik L\, Leibler S (200 4) Bacterial persistence as a phenotypic switch. *Science* 305: 1622-1625. \n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/170/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/170/ END:VEVENT BEGIN:VEVENT SUMMARY:Gene drive localization and reversal DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-129@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Alun Lloyd (North Carolina State University)\nGene d rives are a powerful technique to reduce the size of a population or to tr ansform it to become less troublesome. Major concerns include accidental e scape of a gene drive\, which might lead to widespread elimination of a sp ecies\, or unintended consequences of released individuals\, which might i nclude evolution of resistance to an effector gene. Both spatial localizat ion of a gene drive and the ability to reverse a gene drive are desirable mechanisms to increase the safety of drives. A number of such approaches h ave been proposed in the literature. Using mathematical modelling\, we wil l explore their likely efficacy and discuss critical weaknesses.\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/129/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/129/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling the argasid tick ($\\textit{Ornithodoros moubata}$) life cycle DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-4@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Holly Gaff (Old Dominion University)\nThe first math ematical models for an argasid tick are developed to explore the dynamics and identify knowledge gaps of these poorly studied ticks. These models fo cus on *Ornithodoros moubata*\, an important tick species throughout Afric a and Europe. *Ornithodoros moubata* is a known vector for African swine f ever (ASF)\, a catastrophically fatal disease for domesticated pigs in Afr ica and Europe. In the absence of any previous models for soft-bodied tick s\, we propose two mathematical models of the life cycle of *O. moubata*. One is a continuous-time differential equation model that represents the t ick life cycle with two stages\, and the second is a discrete-time differe nce equation model that uses four tick stages.Both models use two host typ es: small hosts and large hosts\, and both models find that either host ty pe alone could support the tick population and that the final tick density is a function of host density. While both models predict similar tick equ ilibrium values\, we observe significant differences in the time to equili brium. These models provide the basis for developing future models that in clude disease states to explore infection dynamics and possible management of ASF.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/4/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/4/ END:VEVENT BEGIN:VEVENT SUMMARY:Function central limit theorem for Susceptible-Infected process on configuration model graphs: Further insights into the accuracy of the cor relation equations DTSTART;VALUE=DATE-TIME:20180711T010000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-16@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Wasiur Rahman Khuda Bukhsh (Technische Universität Darmstadt)\nWe study a stochastic compartmental susceptible-infected (SI) epidemic process on a configuration model random graph with a given degree distribution over a finite time interval. We split the population of grap h nodes into two compartments\, namely\, S and I\, denoting susceptible an d infected nodes\, respectively. In addition to the sizes of these two com partments\, we study counts of SI-edges (those connecting a susceptible an d an infected node)\, and SS-edges (those connecting two susceptible nodes ). We describe the dynamical process in terms of these counts and present a functional central limit theorem (FCLT) for them when the number of node s in the random graph grows to infinity. To be precise\, we show that thes e counts\, when appropriately scaled\, converge weakly to a continuous Gau ssian vector semimartingale process in the space of vector-valued càdlàg functions endowed with the Skorohod topology. Based on the results obtain ed\, we further investigate the accuracy of the so-called correlation equa tions from ecology literature. We show that for a certain class of degree distributions\, called Poisson-type (PT) distributions\, the pair approxim ation approach is exact in the sense that it correctly estimates the limit ing first order moments of the various count variables.\n\nhttps://confere nces.maths.unsw.edu.au/event/2/contributions/16/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/16/ END:VEVENT BEGIN:VEVENT SUMMARY:The importance of immigration over niche effects in maintaining is land biodiversity DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T062000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-461@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tak Fung (National University of Singapore)\nIn rece nt times\, unprecedented rates of biodiversity loss have resulted in a pre ssing need for greater understanding of key processes maintaining biodiver sity. These processes are often studied in island communities because they exhibit low complexity relative to their mainland counterparts\, which he lps to simplify experiments\, data analyses and mathematical models. Much previous work on islands has focused on local processes such as competitio n and predation\, but this neglects processes operating at broader\, regio nal scales. In particular\, immigration can carry individuals of new speci es into a local area\, and can therefore play a pivotal role in maintainin g biodiversity. \n\nThe importance of immigration was recognized half a ce ntury ago by the seminal Theory of Island Biogeography\, which postulated that the number of species on an island results from a dynamic balance bet ween immigration and extinction. However\, the theory did not explicitly c onsider the simultaneous effects of local and regional processes on the ab undance dynamics of species populations in island communities\, and hence did not predict which type of process was the dominant driver of island bi odiversity.\n\nIn our work\, we addressed the key knowledge gap identified by quantifying the relative influence of local and regional processes on species richness of islands\, using a suite of dynamic models. Each model represents species populations competing for common resources on an island \, with immigration from a mainland source\; however\, the details of inte rspecific competition differ among models. The models include the classic Lotka–Volterra model and Tilman’s model of resource competition. \n\nW e found that for all models examined\, the equilibrium number of species w as typically low when immigration intensity was low\, regardless of the le vel of competition. In this “niche-structured” phase\, species dynamic s were governed by deterministic competition\, with typically a few specie s coexisting per available niche. However\, as the immigration intensity i ncreased beyond a threshold\, the number of species exhibited a rapid incr ease. In this “immigration-structured” phase\, species dynamics were g overned by stochastic immigration\, which allowed many species to coexist per available niche. These trends in species richness were consistent with data from empirical datasets for 100 archipelagoes worldwide\, covering f ive taxonomic groups and three archipelago types. Our results highlight th e general importance of maintaining immigration to achieve high levels of island biodiversity\, which is directly relevant to conservation and susta inable management.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contri butions/461/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/461/ END:VEVENT BEGIN:VEVENT SUMMARY:Separation of trait-mediated and biomass-mediated indirect effects in a system of a plant and two herbivores DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-118@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Atsushi Yamauchi (Kyoto University)\nTwo consumer sp ecies that share a single resource species can indirectly interact each ot her\, even without direct interactions. A typical indirect interaction is exploitative resource competition that results from a depression of resour ce biomass by consumption\, which can be referred to as “biomass-mediate d indirect effect”. Another type of indirect interaction is called “tr ait-mediated indirect effect”\, which is caused by changes in traits of resource species. For example\, an attack from one herbivore species can e ither reduce biomass or induce defensive traits of the host plant individu al\, which may in turn suppress performance of another herbivore species o n the same host. It is notable that two types of indirect effects are diff icult to detect separately in nature because it is necessary to measure bo th reduction in biomass and changes in traits of plants and observe respec tive effects on herbivore performance. In order to understand the separate and joint influences of two indirect effects\, we analyzed a population d ynamic model of one-plant two-herbivores system\, including an inducible n on-specific defense of plant individuals. Our analysis revealed (1) the in ducible non-specific defense can promote coexistence of three species\, (2 ) the coexistence of three species requires reduction of population densit ies of both herbivores\, (3) in such a case\, one herbivore is controlled by biomass-mediated negative indirect effect\, whereas the other herbivore is controlled by trait-mediated negative indirect effect. This indicates that both types of indirect effects need to co-occur for the coexistence o f consumer species\, suggesting that trait-mediate indirect effect may be as common as biomass-mediated indirect effect.\n\nhttps://conferences.math s.unsw.edu.au/event/2/contributions/118/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/118/ END:VEVENT BEGIN:VEVENT SUMMARY:Stochastic models of epidemic super-spreading events DTSTART;VALUE=DATE-TIME:20180710T010000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-55@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Angela Peace (Texas Tech University)\nThe importance of host transmissibility in disease emergence has been demonstrated in hi storical and recent pandemics that involve infectious individuals\, known as superspreaders\, that are capable of transmitting the infection to a la rge number of susceptible individuals. To investigate the impact of supers preaders on epidemic dynamics\, we formulate deterministic and stochastic models that incorporate differences in superspreaders versus non-superspre aders. In particular\, continuous-time Markov chain models are used to inv estigate epidemic features associated with the presence of superspreaders in a population. We parameterize the models for two case studies\, Middle East respiratory syndrome (MERS) and Ebola. Through mathematical analysis and numerical simulations\, we find that the probability of outbreaks incr eases and time to outbreaks decreases as the prevalence of superspreaders increases in the population. In particular\, as disease outbreaks occur mo re rapidly and more frequently when initiated by superspreaders\, our resu lts emphasize the need for expeditious public health interventions.\n\nhtt ps://conferences.maths.unsw.edu.au/event/2/contributions/55/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/55/ END:VEVENT BEGIN:VEVENT SUMMARY:An accurate and efficient estimation of enzyme kinetics using Baye sian approach DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-17@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Boseung Choi (Korea University Sejong Campus)\nChara cterizing enzyme kinetics is critical to understand cellular systems and t o utilize enzymes in industry. To estimate enzyme kinetics from reaction p rogress curves of substrates\, the Michaelis-Menten equation has been wide ly used for a century. However\, this canonical approach works in a limite d condition such as a large excess of substrate over enzyme. Even when suc h condition is satisfied\, identifiability of parameters is not guaranteed \, and criteria for the identifiability is often not easy to be tested. T o overcome these limits of the canonical approach\, here we propose a Baye sian inference based on an equation derived with the total quasi-steady st ate approximation. Estimates obtained with this approach have a little bia s for any combination of enzyme and substrate concentrations in contrast t o the canonical approach. Furthermore\, with our new approach\, an optimal experiment leading to maximal increase of the identifiability can be easi ly designed by simply analyzing scatter plots of estimates. Indeed\, with this optimal protocol\, kinetics of diverse enzymes with disparate catalyt ic efficiencies such as chymotrypsin\, fumarase and urease can be accurate ly estimated from a minimal number of experimental data. A Bayesian infere nce computational package that performs such accurate and efficient enzyme kinetics is provided in this work.\n\nhttps://conferences.maths.unsw.edu. au/event/2/contributions/17/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/17/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling and genetic analysis of the wave of differe ntiation in the fly brain DTSTART;VALUE=DATE-TIME:20180710T020000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-59@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Makoto Sato (Kanazawa University)\nDuring developmen t of multicellular organisms\, multiple signalling systems play important roles. However\, it is very hard to understand the interplays between many signalling pathways using conventional methods of molecular biology\, bio chemistry and genetics. Mathematical modelling should be combined with the se biological methods to solve biological problem. \n\nThe waves of differ entiation in visual system development are key examples of the complex int erplays between multiple signalling systems. In this study\, we focus on a wave of differentiation called the proneural wave\, which occurs in the d eveloping fly brain and accompanies Notch-mediated lateral inhibition and EGF-mediated neural differentiation. During proneural wave progression\, t he sheet-like neuroepithelial cells (NEs) sequentially differentiate to ne ural stem cells called neuroblasts (NBs). The proneural wave is an ideal m odel system to investigate the roles and dynamics of the interplay between important signalling pathways such as Notch and EGF. \n\nNotch-mediated l ateral inhibition regulates binary cell-fate choice\, resulting in salt-an d-pepper patterns during various developmental processes. The proneural wa ve accompanies Notch activity that is propagated without the formation of a salt-and-pepper pattern. However\, mathematical modelling and genetic an alysis clearly demonstrated that Notch-mediated lateral inhibition is impl emented within the proneural wave. Because partial reduction in EGF signal ling causes the formation of salt-and-pepper pattern\, it is most likely t hat EGF diffusion cancels salt-and-pepper pattern formation *in silico* an d *in vivo*. Moreover\, the combination of Notch-mediated lateral inhibiti on and EGF-mediated reaction diffusion enables a novel function of Notch s ignalling that regulates propagation of the wave of differentiation. \n\nI n our previous results\, Notch signalling is activated only once at the wa ve front. However\, Notch signalling is actually activated again behind th e wave front forming twin peaks *in vivo*. The results of our parameter se arch show that the twin peaks of Notch activity can be reproduced by eleva ting the coefficient of cis-inhibition\, by which Notch activity is autono mously repressed by Delta ligand. Moreover\, the formation of the twin pea ks could be stabilized by introducing strong non-linearity to cis-inhibiti on. The result of our *in vivo* experiment is consistent with the non-line ar behaviour of cis-inhibition. The possible molecular mechanisms of non-l inearity in cis-inhibition will be discussed.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/59/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/59/ END:VEVENT BEGIN:VEVENT SUMMARY:Analysis of effects of vector preference on the transmission of in sect-borne plant diseases DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-235@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sungchan Kim (Pusan National University)\nRecent stu dies have shown that pathogens can alter the behaviour of hosts or vectors to improve their transmission power. This happens not only in animal path osystems but in plant pathosystems. While animal pathogens can alter the b ehaviour of both hosts and vectors in ways that increase frequency of host -host or host-vector encounters\, in plant pathosystems the host does not have mobility\, so the potential for behavioural manipulation is restricte d to just vector mobile component in these systems [1]. \n \nMotivated by [2]\, we investigate how this manipulation affects transmission of specifi c insect-borne plant diseases. To do so\, we use the compartmental model o f vector preference in which the probability of which vectors settle on in dividual host plants. Then we demonstrate that interactions between host a nd vector infection status\, the effect of a vector preference and differe nce of the effect between animal- and plant systems. together with any evo lutionary implications.\n\n[1] Ingwell\, L. L.\, Eigenbrode\, S. D.\, & Bo sque-Pérez\, N. A. (2012). Plant viruses alter insect behavior to enhance their spread. *Scientific Reports*\, 2\, 578.\n[2] Cunniffe\, N. J.\, Kos kella\, B.\, Metcalf\, C. J. E.\, Parnell\, S.\, Gottwald\, T. R.\, & Gill igan\, C. A. (2015). Thirteen challenges in modelling plant diseases. *Epi demics*\, 10\, 6-10.\n\nhttps://conferences.maths.unsw.edu.au/event/2/cont ributions/235/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/235/ END:VEVENT BEGIN:VEVENT SUMMARY:New mathematical models for artemisinin-induced parasite killing a nd growth retardation in blood-stage $\\textit{Plasmodium falciparum}$ DTSTART;VALUE=DATE-TIME:20180711T053000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-24@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: James McCaw (University of Melbourne)\nFalciparum ma laria is a major parasitic disease causing widespread morbidity and mortal ity globally. Artemisinin derivatives – the most effective and widely-us ed antimalarials that have helped reduce the burden of malaria by 60% in s ome areas over the past decade – have recently been found to induce grow th retardation of blood-stage *Plasmodium falciparum* when applied at clin ically relevant concentrations. Furthermore\, novel in vitro experiments i ndicate a complex relationship between drug concentration\, the duration o f exposure\, and the rate of parasite killing.\n\nIn this presentation I w ill discuss how extensions to the pharmacokinetic-pharmacodynamic (PK-PD) modelling paradigm are required to explain in vitro observations and discu ss the implications for our understanding of drug action. Given the stage sensitivity of the parasite to drug and the short half-life of the artemis inin derivates in vivo\, our model-based analyses suggest how drug resista nce may manifest and how alternative dosing strategies\, or alternative an timalarials with altered pharmacokinetic properties\, may aid in maintaini ng clinical efficacy.\n\nhttps://conferences.maths.unsw.edu.au/event/2/con tributions/24/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/24/ END:VEVENT BEGIN:VEVENT SUMMARY:Understanding the impact of climate in seasonal influenza in Austr alia DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T015000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-298@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Robert Cope (The University of Adelaide)\nInfluenza in humans exhibits a strong seasonal cycle in temperate climates\, with a peak of varying intensity appearing each winter. However\, the exact cause of this seasonal cycle remains poorly understood. We develop a climate-ba sed SIR modelling framework to understand influenza seasonality\, with the transmission rate as a function of climate data. By using a variety of cl imate-based functional forms of transmissibility from the literature\, as well as some new forms\, we select the best functional form for climate-de pendent transmissibility via modern Machine Learning model selection metho ds. By analysing a unique dataset comprising ten years of GP-reported infl uenza-like-illness surveillance data from around Australia\, we explore th e relationship between influenza transmission and weather in different cli mate zones.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions /298/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/298/ END:VEVENT BEGIN:VEVENT SUMMARY:The bone ecosystem DTSTART;VALUE=DATE-TIME:20180710T010000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-43@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: David Basanta (H. Lee Moffitt Cancer Center)\nSevera l types of cancer initiate or metastasize to the bone. These include the m ost prevalent and lethal cancers: lung\, breast and prostate. Thus underst anding the bone ecosystem is key if we want to predict what phenotypes wil l successfully metastasize to the bone and the subsequent evolutionary dyn amics that will ensue as the invading tumour cells learn how to co-opt the bone resident cells. This bone ecosystem is very dynamic and responds and maintains homeostasis as micro and macro fractures appear. A variety of h omeostatic processes emerge from the interactions of a myriad of cell type s and signalling factors. Here I will present mathematical models\, biolog ically motivated and tested\, that explain bone repair and homeostasis and allow us to explore how tumours can grow in the bone as well as the impac t of a variety of treatments not only on the tumour cells but also on the bone ecosystem.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribut ions/43/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/43/ END:VEVENT BEGIN:VEVENT SUMMARY:Quantifying the value of monitoring species in multi-species\, mul ti-threat systems DTSTART;VALUE=DATE-TIME:20180712T052000Z DTEND;VALUE=DATE-TIME:20180712T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-343@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Payal Bal (University of Melbourne)\nMaking effectiv e management decisions is challenging in multi-species\, multi-threat syst ems because of uncertainty about the effects of different threats on diffe rent species. To inform management decisions\, we often monitor species to detect spatial or temporal trends that can help us learn about threatenin g processes. However\, which species to monitor and how to monitor to info rm the management of threats can be difficult to determine. Value of infor mation (VOI) analysis is an approach for quantifying the value of monitori ng to inform management decisions. We developed a novel method that applie s VOI analysis to quantify the benefits of different species monitoring st rategies in multi-threat\, multi-species systems. We applied the approach to compare the effectiveness of surveillance monitoring (monitoring specie s without experimentation) to targeted monitoring (monitoring species with experimentation to learn about a specific threat)\, and how prior informa tion drives the benefits of these two different strategies and the species to monitor. We also illustrate the approach by applying it to two contras ting case studies for monitoring and managing declining mammals in Western Australia. Our approach shows that surveillance monitoring generally prov ides far lower benefits than targeted monitoring for managing threats in m ulti-species\, multi-threat systems under economic constraints. Our approa ch also informs the choice of species to monitor and which threats to mana ge experimentally to most improve threat management outcomes. We show that the key parameters driving these choices include: the budget available fo r management\, prior understanding of which threats cause declines in whic h species\, the relative cost of managing these threats\, and the backgrou nd probability of decline. Our new VOI approach allows the evaluation of m onitoring decisions in multi-species\, multi-threat systems in the face of uncertainty\, while explicitly accounting for the improvement in manageme nt outcomes. We recommend that managers need to explicitly consider a rang e of decision parameters when selecting which species to monitor to inform management. Our framework provides an objective way to do this.\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/343/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/343/ END:VEVENT BEGIN:VEVENT SUMMARY:Variance reduction approaches to efficient simulation of biochemic al reaction network models DTSTART;VALUE=DATE-TIME:20180712T052000Z DTEND;VALUE=DATE-TIME:20180712T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-325@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ruth Baker (University of Oxford)\nThe complexity of biochemical reaction networks means that we often rely on stochastic simu lation to investigate their potential behaviours\, generating multiple sam ple paths from the model and using them to estimate summary statistics of interest. However\, for realistic models\, existing Monte Carlo methods ar e often prohibitive when it comes to exploring the range of possible model behaviours\, conducting parameter sensitivity analysis\, or parameter inf erence and model selection. \n\nOne approach that has the potential to mit igate these issues is that of variance reduction. Instead of attempting to reduce the computational cost of generating individual sample paths\, we instead aim to reduce the variability in the summary statistics we are int erested in. Computational savings can then be made because fewer sample pa ths are required to generate estimates to within a specified error. In thi s talk I will describe variance reduction approaches biochemical reaction network models. I will first show how point estimates can be generated sim ply and efficiently\, and then outline how extensions to the basic method allow variance reduction approaches to be applied to a range of problems a nd summary statistics.\n\nhttps://conferences.maths.unsw.edu.au/event/2/co ntributions/325/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/325/ END:VEVENT BEGIN:VEVENT SUMMARY:Mutualistic network maximizing species abundance under exploitativ e competition DTSTART;VALUE=DATE-TIME:20180711T053000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-161@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Deok-Sun Lee (Inha University)\nThe abundance of a p ollinator species can be affected by other pollinators sharing the nutrien ts from the same plants. Such an exploitative competition between the ani mal species may affect the species abundance the network structure of plan t-pollinator mutualistic communities\, which remains to be understood. Her e we study a model of the mutualistic network evolution towards increasing the species abundance with the exploitative competition between pollinato rs and mutualism in the abundance dynamics. We show that hub plants having many pollinators are very rare while a few super-hub pollinators appear w ith the generalized interaction\, contrasted to equally many hubs of both types without the exploitative competition. More interestingly\, it turns out that the abundance of plant species increases slightly with increasing the exploita- tive competition strength. To understand the origin of this pehenomena\, we obtain the inverse of the generalized interaction matrix approximated in the weak-interaction limit. The leading structural factors relevant to the species abundance are identified\, which are shown to be instrumental in optimizing the network structure to increase the mutualist ic benefit and lower the cost of exploitative competition.\n\nhttps://conf erences.maths.unsw.edu.au/event/2/contributions/161/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/161/ END:VEVENT BEGIN:VEVENT SUMMARY:Intermittent preventive treatment and the spread of drug resistant malaria parasites DTSTART;VALUE=DATE-TIME:20180711T063000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-80@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Olivia Prosper (University of Kentucky)\nOver the la st decade\, control measures have significantly reduced malaria morbidity and mortality. However\, the burden of malaria remains high\, with more t han 70% of malaria deaths occurring in children under the age of five. Th e spread of antimalarial resistant parasites challenges the efficacy of cu rrent interventions\, such as Intermittent Preventive Treatment (IPT)\, wh ose aim it is to protect this vulnerable population. Under IPT\, a curati ve dose of antimalarial drugs is administered along with a child’s routi ne vaccinations\, regardless of their infection status\, as both a protect ive measure and to treat subclinical infections. We have developed mathem atical models to study the relative impact of IPT in promoting the spread of drug resistant malaria (compared with treatment of clinically ill indiv iduals)\, and the combined effect of different drug half-lives\, age-struc ture and local transmission intensity on the number of childhood deaths av erted by using IPT in both the short and long-term in malaria endemic sett ings. I will also discuss some consequences of unstable and seasonal tran smission of malaria on the efficacy of IPT.\n\nhttps://conferences.maths.u nsw.edu.au/event/2/contributions/80/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/80/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal control and temperature variations of malaria transmission dynamics DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-110@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Folashade Agusto (University of Kansas)\nIn this se minar\, I will present the results obtained from investigating the optimal control strategies for malaria in the presence of temperature variation u sing a temperature dependent malaria model. A 2015 study by Agusto *et al. * identified the suitable temperature ranges for mosquitoes in four differ ent geographical regions of Sub-Saharan Africa as [22.61$\\rm^o$C - 28.58 $\\rm^o$C] in West African cities\, [16.68$\\rm^o$C - 27.92$\\rm^o$C] in Central African cities\, [19.04$\\rm^o$C - 26.75$\\rm^o$C] in East Africa n cities\, and [16.66$\\rm^o$C - 25.32$\\rm^o$C] in Southern Africa. The optimal control strategies in these temperature ranges suggest on average a high usage of both larviciding and adulticiding followed by a moderate u sage of personal protection such as insecticide-treated bednet. The averag e optimal bednet usage mimics the trajectory of the mosquitoes as the mosq uitoes respond to temperature variations. These results triggered the inve stigation of the impact of insecticide resistance mosquitoes on disease bu rden in the face of temperature variations. The results indicate that opti mal bednet usage on average is higher in the presence of insecticide resis tance mosquitoes. Furthermore\, on average bednet usage increases as tempe rature increases to the optimal temperature suitable for mosquitoes and it decreases thereafter\, a pattern similar to earlier results involving ins ecticide sensitive mosquitoes.\n\nhttps://conferences.maths.unsw.edu.au/ev ent/2/contributions/110/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/110/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling of potential mechanism for the restoration of the T-cell homeostasis along with a sustained decay in viral reservoir upon infusion of CCR5 gene edited T cells in HIV infected subjects DTSTART;VALUE=DATE-TIME:20180710T010000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-137@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Angie Raad (CDM\, York University \, Toronto\, Cana da\,)\nAlthough antiretroviral therapy (ART) suppresses viral replication\ , patients still suffer from both low CD4 T-cell counts and HIV persistenc e\, requiring them to remain on complex ART regimens for life. A naturally occurring 32-base pair deletion in the CCR5 gene\, the major co-receptor for HIV entry\, is associated with infection resistance. \n\nIn the study initiated by Sangamo Therapeutics\, HIV-infected subjects received a singl e infusion of autologous CCR5-modified CD4 T-cells. Following infusion\, w e observed a sustained increase in the CD4 T-cells count (mean ~162 cells/ μL) with a significant decrease in the HIV reservoir (median ~1 log 3yrs post infusion). Long-term persistence of CCR5-modified cells suggested the ir presence within long-lived CD4 populations\, such as T memory stem cell s (TSCM). To investigate the impact of persistence of “HIV-resistant” TSCM on immune homeostasis and the decay of the HIV reservoir\, we develop ed a mathematical model of T-cell dynamics. The model follows a linear tra nsition from the naïve to effector memory (TEM) state and includes thymic input of naïve cells\, proliferation\, death and differentiation rates f or naïve and memory cells. Model fits to patient data pre- and post-injec tion and sensitivity analysis results that increased thymic output\, an in creased TSCM proliferation rate\, a decreased central memory cell death ra te\, and an increased central memory transition rate played an important r ole in increasing the T-cell count and decreasing the HIV reservoir. \n\nF inally\, using a bi-phasic decay model\, we show that purging and replacem ent dynamics of the CD4 T-cells population post infusion account for a sig nificant fraction of the observed decrease in the HIV reservoir. Our resul ts indicate that homeostatic processes can control HIV persistence\, and t hat T-cell restoration post infusion of CCR5-deleted cells leads to the de cay of the HIV reservoir.\n\nhttps://conferences.maths.unsw.edu.au/event/2 /contributions/137/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/137/ END:VEVENT BEGIN:VEVENT SUMMARY:Dynamics of HIV-1 coinfection under different susceptible target c ell populations during cell-free infection in cell culture DTSTART;VALUE=DATE-TIME:20180711T053000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-33@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yusuke Ito (Department of Biology\, Faculty of Scie nces\, Kyushu University\, Fukuoka 819-0395\, Japan)\nHuman Immunodeficien cy Virus typeⅠ (HIV-1) mutations are rapidly accumulated through recombi nation events which are largely caused by HIV-1 coinfection [1]. Therefore \, HIV-1 coinfection has the potential to produce the drug-resistant virus es\, which leads to the high pathologies and disease progression. Recently \, it has been reported that coinfection occurs more frequently than at ra ndom both *in vitro* and *in vivo* [1\,2]\, implying that this viral pheno menon is quite common in HIV-1 infection. Furthermore\, one possible mecha nism of HIV-1 coinfection is driven by the different susceptibility of tar get cells [2\,3]. Thus\, the elucidation of HIV-1 coinfection associated w ith different susceptible target cell populations is required to more accu rately capture the general viral mechanism in HIV-1 infection. In this stu dy\, we constructed ordinary differential equations considering the hetero geneity of target cell populations during cell-free infection in cell cult ure\, and reproduced the cell culture experiment data. Interestingly\, our mathematical analyses demonstrated that 2 different susceptible target ce ll subpopulations could explain coinfection experiments in cell culture us ing the AIC model selection. In addition\, our novel finding is that coinf ected cells are emerged from the most susceptible subpopulation at 98.2% o n average. Taken together\, our mathematical-experimental approach suggest ed that the most susceptible target cell population is the dominant resour ce of HIV-1 infection in cell-free infection.\n\n[1] Q. Dang *et al.*\, 20 04\n[2] J. Chen *et al.*\, 2005\n[3] A. Remion\, *et al.*\, 2016\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/33/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/33/ END:VEVENT BEGIN:VEVENT SUMMARY:Parameter estimation for modelling intermittent androgen suppressi on therapy in prostate cancer patients DTSTART;VALUE=DATE-TIME:20180711T053000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-90@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Rebecca Everett (Haverford College)\nAdvanced prosta te cancer is often treated by androgen suppression therapy\, since prostat e cells depend on androgens for proliferation and survival. To improve the patients' quality of life and possibly delay the development of resistanc e\, intermittent androgen suppression (IAS) therapy can be given rather th an continuous therapy. We consider a mathematical model of IAS therapy inv olving tumour cells\, androgen\, and the biomarker prostate-specific antig en and investigate parameter estimation with clinical data. Specifically\, we implement iterative weighted least squares inverse problems to investi gate the patient-specific parameters that can be confidently estimated.\n\ nhttps://conferences.maths.unsw.edu.au/event/2/contributions/90/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/90/ END:VEVENT BEGIN:VEVENT SUMMARY:Trajectory inference of HIV progression with microbiome data DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-131@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Shinji Nakaoka (PRESTO\, JST\, Japan. Institute of I ndustrial Sciences\, The University of Tokyo\, Japan.)\nInformation analys is of amplicon sequencing of fecal samples from HIV positive individuals s uggested an enrichment of a particular bacterial species in the gut microb iota\, as referred to dysbiosis. Although a sufficient number of samples h as already accumulated for both HIV positive and negative subjects\, time- series datasets are rarely available. Hence difficulty remains in tracing the compositional change of the gut microbiota during HIV infection.\n\nIn this presentation\, we would like to introduce our ongoing research progr ess on the application of trajectory inference methods to construct a pseu do-trajectory that may imitate disease progression of HIV infection. Our c omputational analysis suggested that enrichment of the *enterobacteriaceae * family may occur at the initial phase of HIV infection during which infl ammatory responses would be facilitated in the gut. This finding is consis tent with known observations for the enrichment of the *enterobacteriaceae * family in several inflammatory diseases.\n\nhttps://conferences.maths.un sw.edu.au/event/2/contributions/131/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/131/ END:VEVENT BEGIN:VEVENT SUMMARY:A mathematical analysis of aerobic glycolysis triggered by glucose uptake in cones DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-119@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Erika Camacho (Arizona State University)\nPhotorecep tors are cells in the retina that convert light to chemical signals. To of fset the extreme optical and metabolic demands\, and thereby prevent the t oxic effects of accumulated photo-oxidative products\, photoreceptors unde rgo renewal and periodic shedding of their outer segment (OS) discs. The O S are a substructure that carries the light sensitive molecule\, opsin. Pe ople afflicted with diseases such as Retinitis Pigmentosa (RP) and Age-Rel ated Macular Degeneration (AMD) experience a decline in vision due to phot oreceptor degeneration. When photoreceptors degenerate\, the shedding and renewal is interrupted eventually resulting in the disappearance of the OS and followed by the death of the cells. Currently there is no cure for di seases linked to photoreceptor degeneration. Motivated by photoreceptor de generation\, in particular RP which is typically categorized by a loss of rods (carriers of the faulty gene) followed by the loss of healthy cones\, we focus our efforts on understanding the mechanisms necessary for cone s urvival. In an effort to begin to unravel the key process in photoreceptor functionality and vitality\, this work considers key cone metabolic proce sses in a healthy retina. Recently it was discovered that the protein Rod- derived Cone Viability Factor (RdCVF) preserves the cones by stimulating a erobic glycolysis and accelerating the uptake of glucose needed for OS ren ewal and vitality in cones. Utilizing this understanding we developed a no nlinear system of ordinary differential equations to mathematically model molecular and cellular level interactions. We qualitatively validate the m odel and use uncertainty and sensitivity analysis to identify the processe s and mechanisms that are crucial for cones vitality and functionality. Ou r result indicate that when all processes are functioning properly changes in key parameters at the subcellular level as well as the cellular level can significantly affect the cone population. Our analysis additionally ex amined the role of inefficient glucose use by the cones as well as restric ted availability of RdCVF has on the overall cone populations. These resu lts can lead to important insight into the design of new experiments such as the particular experiments that give the most valuable information\, an d at what time point a particular process (defined by a parameter) should be altered to increase the vitality of the cones.\n\nhttps://conferences.m aths.unsw.edu.au/event/2/contributions/119/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/119/ END:VEVENT BEGIN:VEVENT SUMMARY:A mathematical model of digestion in the colon DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-95@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Arun Moorthy (National Institute of Standards and Te chnology)\nThe relationship between gut microbiota and health has been of keen interest for the past several years. The physical inaccessibility of the colon makes alternative research approaches a valuable addition to the clinical research done in this area. In this seminar\, we discuss the com puGUT - a numerical simulation tool for studying anaerobic digestion and p hysiology in the colon. The underlying mathematical model is a system of p artial differential equations with stiff\, non-linear source terms. Our di scussion will focus on the construction of the model\, with additional dis cussion of the numerical implementation and applications of the software t ool.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/95/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/95/ END:VEVENT BEGIN:VEVENT SUMMARY:A quantitative and systems approach to vertebrate forebrain and he art morphogenesis DTSTART;VALUE=DATE-TIME:20180709T010000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-41@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yoshihiro Morishita (RIKEN Quantitative Biology Cent er)\nUnderstanding how 3D organ morphology is achieved during development is one of the ultimate goals in biology. This is important not only for pu re scientific interests but also for potential medical applications for co ntrolling and designing functional organs. To achieve these goals\, it is essential to clarify the quantitative relationships between microscopic mo lecular/cellular activities and organ-level tissue deformation dynamics. W hile the former has been studied for several decades\, the latter - macros copic geometrical information about physical tissue deformation - has been lacking. One reason for this lack of information is the difficulty in mea surement at high resolution. We recently proposed a Bayesian method to pre cisely reconstruct global deformation patterns for three-dimensional morph ogenesis of curved epithelial sheets using positional data from sparsely-l abeled cells with limited resolution [1]. The applications of the method t o early development of chick forebrain and heart revealed that globally al igned anisotropic deformation (i.e.\, biased tissue stretching)\, rather t han local area growth\, is the predominant morphogenetic mechanism in both cases (specifically\, for optic vesicle formation and C-looping\, respect ively) [2]. Comparing the reconstructed tissue deformation patterns and ce llular behaviours\, we quantitatively revealed the contributions of each c ellular process (e.g.\, division\, size/shape change\, and rearrangement) to the anisotropic tissue deformation. In this talk\, we would also like t o introduce our attempt to build continuum mechanical models to reproduce observed morphologies and deformation patterns.\n\n[1] Morishita *et al.*\ , Nat. Commun.\, 2017\n[2] Kawahira *et al.*\, under review\n\nhttps://con ferences.maths.unsw.edu.au/event/2/contributions/41/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/41/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling transport in the placenta: scaling models to simulate or gan level function DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-96@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Alys Clark (University of Auckland)\nThe placenta is critical for our first nine months of life\, as it provides nutrients fro m mother’s blood and clears waste from the fetal circulation. The main s tructures that make up the placenta are villus trees\, so called because t hey form a complex branching structure\, like the branching of a tree\, to provide a large surface area for exchange. Many pregnancy complications a re associated with alterations in the structure of the villus trees and th e blood vessels that reside within them. This potentially leads to poor ma tching of maternal and fetal blood flow rates at the site of exchange\, an d so impaired placental efficiency. Most computational models ‘smooth ou t’ the structure of the villous trees\, or are limited to functional sub units of the placenta (placentomes) comprising just one of the 60-100 vill ous trees that comprise the placenta. Here I will present computational te chniques to allow simulation of placental exchange at the whole organ scal e\, which include heterogeneity in villous structure. I will present evide nce that the structure of the placenta is such that consideration of isola ted placentomes is not always appropriate in simulation\, and an analysis of how structural perturbations in the placenta (for example cord insertio n at the periphery of the placenta) may impact on its exchange function.\n \nhttps://conferences.maths.unsw.edu.au/event/2/contributions/96/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/96/ END:VEVENT BEGIN:VEVENT SUMMARY:Liver spatial heterogeneities and HBV DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-138@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Shawn Means (University of Auckland)\nThe liver is a spatially complex and heterogeneous network of blood and bile flows coupl ed with metabolic processing and a favoured target for infection by hepat ic viruses. We present here a mathematical model aimed at investigating th ese intrinsic heterogeneities and their impact on the dynamic of the Hepat itis-B variant (HBV). Dramatic spatio-temporal scaling from individual hep atocytes to the entire liver organ invites multi-scale approaches inspirin g assembly of sinusoid-level 'unit models' into a whole organ representati on. Each 'unit-model' sinusoid combines individual hepatocytes communicati ng with blood flow in the sinus in turn connected with other 'unit-model' sinusoids aggregated into a whole liver modelling scheme. This permits inv estigating impacts on the whole organ of precisely distributed spatial het erogeneities such as varying HBV uptake mechanisms (e.g.\, the sodium-taur ochloriate cotransporter or NTCP)\, immune cell responses (e.g.\, cytolyti c or interferon-based) and simple efficiency of HBV replication. We presen t our results showing how heterogeneities of\, in particular\, HBV replica tion efficiencies may be responsible for persistent chronic infections.\n\ nhttps://conferences.maths.unsw.edu.au/event/2/contributions/138/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/138/ END:VEVENT BEGIN:VEVENT SUMMARY:Global shapes of evolutionary trees in trait spaces can be describ ed by the Price equation DTSTART;VALUE=DATE-TIME:20180711T010000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-155@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hiroshi Ito (Department of Evolutionary Studies of B iosystems\, SOKENDAI (The Graduate University for Advanced Studies)\, Haya ma\, Kanagawa 240-0193\, Japan)\nDiversification and extinction are ubiqui tously repeated in the evolutionary histories of biological communities. A minimal mechanism for driving the repeated diversification and extinction is a combination of resource competition in one trait and a weak directio nal selection in another trait\; resource competition induces diversificat ion in the first trait\, but inevitably nonuniform innovations in the seco nd trait among the diversified lineages induce further diversification of the most innovated lineage\, excluding the other outdated ones. In this dy namics\, the evolutionary speed of community average of the second trait c an be partitioned into the contribution by directional evolution of each l ineage consisting the community\, i.e.\, within-lineage evolution\, and t he contribution by changes of those lineages' frequencies\, i.e.\, between -lineage selection. This study generalizes such a partitioning by the Pric e equation for an arbitrary bivariate trait space\, by which the global sh apes of evolutionary trees in the trait spaces can be understood in terms of within-lineage evolution and between-lineage selection.\n\nhttps://conf erences.maths.unsw.edu.au/event/2/contributions/155/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/155/ END:VEVENT BEGIN:VEVENT SUMMARY:Reflected diffusions and (bio)chemical reaction networks DTSTART;VALUE=DATE-TIME:20180712T054000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-388@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ruth Williams (University of California\, San Diego) \nContinuous-time Markov chain models are often used to describe the stoch astic dynamics of networks of reacting chemical species\, especially in th e growing field of systems biology. Discrete-event stochastic simulation o f these models rapidly becomes computationally intensive. Consequently\, m ore tractable diffusion approximations are commonly used in numerical comp utation\, even for modest-sized networks. However\, existing approximation s (e.g.\, linear noise and Langevin)\, do not respect the constraint that chemical concentrations are never negative.\n\nIn this talk\, we propose an approximation for such Markov chains\, via reflected diffusion processe s\, that respects the fact that concentrations of chemical species are non -negative. This fixes a difficulty with Langevin approximations that they are frequently only valid until the boundary of the positive orthant is re ached. Our approximation has the added advantage that it can be written do wn immediately from the chemical reactions. Some numerical examples illust rate the advantages of our approximation over direct simulation of the Mar kov chain or use of the linear noise approximation.\n\nThis talk is based on joint work with Saul Leite\, David Anderson and Des Higham.\n\nhttps:// conferences.maths.unsw.edu.au/event/2/contributions/388/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/388/ END:VEVENT BEGIN:VEVENT SUMMARY:Investigating the effects of childhood vaccination: Rotavirus in C hile DTSTART;VALUE=DATE-TIME:20180712T011000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-345@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Katia Vogt-Geisse (Universidad Adolfo Ibáñez)\nRot avirus is a viral disease - mainly transmitted by the fecal-oral mode - th at is the leading cause of severe acute gastroenteritis among infants and children less than 5 years of age. The symptoms vary from mild to severe d iarrhea with fever and vomiting that may produce rapid dehydration. In mos t of the cases\, severe symptoms require hospitalization and eventually ca n lead to death.\n\nThere exist two licensed rotavirus vaccines that have proven to be safe and effective to prevent rotavirus infections in young c hildren and infants. However\, Chile's national childhood immunization pro gram does not currently include vaccination against rotavirus. The disease is responsible for 47% of the hospitalizations of children less than 3 ye ars of age in Chile\, which represents an important social and economic bu rden for the country. We present an ongoing study that is one of the first steps into making public health recommendations for rotavirus control and prevention in Chile\, using mathematical models. We developed an ordinary differential equations model that describes the disease dynamics of rotav irus and analyzes the effect of vaccination into the country's hospitaliza tion incidence.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribut ions/345/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/345/ END:VEVENT BEGIN:VEVENT SUMMARY:Collective cell migration in an open channel DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-144@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Zoltan Neufeld (University of Queensland)\nThe colle ctive migration of cells during embryogenesis is key to the development of vertebrates\, and improper migration can lead to severe developmental dis eases and deformities. As a simple model for such cell migration we study the particle based Vicsek model in an open channel geometry where cells co ntinuously enter and leave the domain. This results in two distinct types of motion – one corresponds to desired\, well-ordered migration\, while the other corresponds to disordered migration. We characterise the differe nt types of collective behaviour and propose a theoretical description to determine the conditions for coherent collective cell migration.\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/144/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/144/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling brain tumour recurrence patterns following surgical rese ction with ischemia DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-135@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Lee Curtin (School of Mathematical Sciences\, Univer sity of Nottingham)\nGlioblastoma Multiforme (GBM) is the most aggressive primary brain tumour\, with a median life expectancy of only 15 months wit h treatment. Although surgical resection is a standard-of-care procedure\, the migratory nature of the tumour cells limits its efficacy as not all t umour cells can be removed. The tumour will usually re-establish itself al ong the resection cavity wall\, known as a local recurrence\, but it can r ecur elsewhere or become more migratory\, known as a distal recurrence. Cl inical data has shown that patients with ischemia following resection are more likely to have a distally recurring tumour\, with an incidence rate o f 61% for those with ischemia vs 19% for those without. This evidence sugg ests that a lack of nutrients plays a role in the tumour recurrence patter n but does not fully answer the question regarding the difference between tumours that do or do not recur distally under these conditions.\n\nWe pre sent the Proliferation Invasion Hypoxia Necrosis Angiogenesis (PIHNA) mode l that simulates the angiogenic cascade of a GBM as it grows. We have appl ied this mechanistic model to show how an in silico GBM grows following re section and subsequent ischemia\, and to highlight the role of the individ ual tumour kinetics in this behaviour. Our simulations suggest that the di ffusivity of the tumour\, the tumour cell proliferation rate\, and the har diness of the cells all play key roles in the recurrence location of a GBM .\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/135/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/135/ END:VEVENT BEGIN:VEVENT SUMMARY:Multistationarity in biochemical reaction networks’ models DTSTART;VALUE=DATE-TIME:20180711T063000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-11@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Maya Mincheva (Northern Illinois University)\nMultis tationarity is defined as the existence of several positive equilibria of an ordinary differential equations model. Multistationarity is a required property of biological switches- reaction networks that govern important cellular functions\, such as cell differentiation and cell death. This i s the case\, because biological switches are modelled by differential equ ations systems whose solutions can approach different stable equilibria de pending on the initial conditions. Many differential equations models of r eaction networks are known to be multistationary for particular parameter values. However\, reaction networks’ properties are robust in nature. Thus\, for multistationarity to be robust\, a reaction network has to be m ultistationary in some open region of parameter space. We will describe a computational procedure for screening dissipative differential equations models of reaction networks for the existence of multistationary regions . For a model of the double phosphorylation cycle\, we have obtained simpl e parametric inequalities that identify multistationary regions in paramet er space. \n\nThis is a joint work with C. Conradi (HTW-Berlin)\, E. Feliu and C. Wiuf (both from the University of Copenhagen).\n\nhttps://confere nces.maths.unsw.edu.au/event/2/contributions/11/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/11/ END:VEVENT BEGIN:VEVENT SUMMARY:Phenotypic and genotypic competition models on lattice space DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-362@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kazunori Sato (Shizuoka University)\nBarreto *et al* . (2017) studied the rock-paper-scissors games (or cyclic competition game s) by the dynamics of phenotypic and genotypic frequencies corresponding t o three morphs of lizards. In their model they show that both dynamics hav e equal internal equilibrium but the genotypic model has wider parameter r ange for its stability compared to the phenotypic model.\n\nHere\, first o f all\, we investigate phenotypic and genotypic competition models with tw o-species. Then we consider the Barreto *et al*. model with different geno typic correspondence to three phenotypes. Lastly computer simulations for these models are carried out on lattice space and the effects of spatial s tructure are discussed.\n\nhttps://conferences.maths.unsw.edu.au/event/2/c ontributions/362/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/362/ END:VEVENT BEGIN:VEVENT SUMMARY:Memory and time delays in physiological regulation DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-198@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jacques Bélair (Université de Montréal)\nMemory t ranslates into time delays naturally in a number of regulatory processes a t all levels of organisation in the life sciences: transcription and trans lation times in molecular biology\, finite axonal conduction velocities be tween neurons\, maturation times of precursor cells in hematopoiesis and i nfection and temporary immune periods in infectious disease propagation ar e but a few examples of naturally occurring such delays. In many instance s\, mathematical constructions are elaborated to avoid incorporating time delayed arguments in the modelling equations of the system of interest. We present\, by way of examples on two specific physiological and epidemiolo gical systems\, the limitations of this approach and the extent to which t hese approximations may or may not be useful or necessary for a proper und erstanding of the modelled system.\n\nThis talk will serve as an introduct ion to the other presentations of the Minisymposium.\n\nhttps://conference s.maths.unsw.edu.au/event/2/contributions/198/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/198/ END:VEVENT BEGIN:VEVENT SUMMARY:Predicting the regulation of circadian rhythms by RNA methylation DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-171@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Gen Kurosawa (Theoretical Biology Laboratory\, RIKEN \, and CREST\, JST\, Japan)\nEating behaviour is known to influence our sl eep-wake cycle\, and the mechanism remains elusive. We have focused on RNA methylation that possibly connect metabolic and circadian systems. Recent ly\, RNA methylation inhibition was found to elongate circadian period by as-yet-unknown mechanism. Since the regulatory network for circadian rhyth m has been studied well\, modelling can be a powerful tool for predicting the mechanism. Our study aimed at predicting possible mechanisms by which RNA methylation regulates circadian rhythm using a computational model and also a simpler model [1]. To predict the mechanism\, we used information from our experimental collaborators: (1) RNA methylation inhibition stabil izes enzymes\, important for circadian rhythms\, (2) there are many modifi cation processes presumably activated by the enzymes. Based on experimenta l data\, we predicted the most likely process that is activated by the enz ymes and then by RNA methylation inhibition. The prediction was confirmed experimentally by our collaborators.\n\n[1] Kurosawa *et al.* 2017 *PLoS C omp Biol*\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/1 71/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/171/ END:VEVENT BEGIN:VEVENT SUMMARY:Direct parameterisation of an evolutionary game theory model from in vitro experiments DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-134@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jacob Scott (Cleveland Clinic and Case Western Reser ve University School of Medicine)\nEvolutionary game theory has been used to model cancer for more than a decade. Efforts to date have focused on un derstanding the effect of interactions between cancer cells of different t ypes\, and between aspects of the tumour microenvironment and cancer cells . To realise the full potential of these modelling efforts however\, we su bmit that a method for direct parameterisation is required. In this talk\, I will present our novel ‘evolutionary game assay’ designed specifica lly to parameterise a two strategy matrix evolutionary game from *in vitro * experiments comprised of co-culture of cells transfected with different colour fluorescent proteins. I will also show the results of the first gam e we measured\, a game between EML4-ALK translocated non-small cell lung c ancer cells before and after we evolved resistance to Alectinib (a targete d therapy). We find that these cells play either the Leader or Deadlock ga me\, depending on different therapeutic and microenvironmental conditions. This change in game\, as modulated by treatment\, also suggests a novel t herapeutic strategy which we have posited before is possible: treating the game instead of the player.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/134/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/134/ END:VEVENT BEGIN:VEVENT SUMMARY:Most ecological communities are at the limit of structural stabili ty: the evidence DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-111@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Axel G. Rossberg (Queen Mary University of London)\n An ecological community is called *structurally unstable* if it is feasibl e (a positive equilibrium exists) but feasibility is sensitive to changes in parameters\, external pressures\, or species composition. Absent such sensitivities\, a feasible community is called *structurally stable*. \nM athematically one can show that\, due to amplification of perturbations th rough indirect interactions\, structural stability of ecological networks declines with increasing species richness (a negative complexity-stability relation). At some limiting richness structural instability sets in\, th us imposing an inherent limit to sustainable biodiversity. Under sustained invasion pressure this limit is naturally reached\, stabilizing species r ichness despite ongoing temporal turnover in composition. \nWe argue that the combined mathematical\, numerical and empirical evidence strongly sug gests that most natural ecological communities are indeed close to this li mit. This applies to both local and regional scales. At local level\, st ructural instability mechanistically explains\, e.g.\, observed biodiversi ty patterns across trophic levels and body size\; the observed magnitude o f indirect interactions\; the known high parameter sensitivity of food-web models\; and the absence of clear complexity-stability relations in reali sed communities. At regional level\, structural instability mechanistical ly explains\, e.g.\, observed species area relations and range-size distri butions. We urge ecologists to devote more research to the study of ecolo gical network models at the limit of structural instability\, because thes e tend to have particular properties that are commonly found in nature\, b ut not in their structurally stable counterparts.\n\nhttps://conferences.m aths.unsw.edu.au/event/2/contributions/111/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/111/ END:VEVENT BEGIN:VEVENT SUMMARY:Statistical properties of the equilibria of large random ecosystem s DTSTART;VALUE=DATE-TIME:20180712T010000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-139@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Christian Mazza (University of Fribourg)\nThe consen sus that complexity begets stability in ecosystems was challenged in the s eventies\, a result recently extended to ecologically-inspired networks. T he approaches assume the existence of a feasible equilibrium\, i.e. with p ositive abundances. However\, this key assumption has not been tested. We provide analytical results complemented by simulations which show that equ ilibrium feasibility vanishes in species rich systems. This result leaves us in the uncomfortable situation in which the existence of a feasible equ ilibrium assumed in local stability criteria is far from granted. We exten d our analyses by changing interaction structure and intensity\, and find that feasibility and stability is warranted irrespective of species richne ss with weak interactions. Interestingly\, we find that the dynamical beha viour of ecologically inspired architectures is very different and richer than that of unstructured systems. Our results suggest that a general unde rstanding of ecosystem dynamics requires focusing on the interplay between interaction strength and network architecture.\n\nhttps://conferences.mat hs.unsw.edu.au/event/2/contributions/139/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/139/ END:VEVENT BEGIN:VEVENT SUMMARY:A mathematical model for the effect of domestic animals on the bas ic reproduction number of Human African Trypanosomiasis (Sleeping Sickness ) DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-240@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sagi Shaier (Kennesaw State University)\nThe Human A frican Trypanosomiasis (HAT) parasite\, which causes African Sleeping Sick ness\, is transmitted by the tsetse fly as a vector. It has several possib le hosts\, including humans and domestic animals. Because domestic animals can be a host for the parasite\, it has long been assumed that keeping do mestic animals near human populations increases the spread of the disease. However\, several parameters found in the literature\, including the shor ter lifespan of the male vector and the female vector's preference for dom estic animals\, made us question this assumption. \n\nWe have developed a differential equation compartmental model to examine whether increasing th e domestic animal population can be used to deflect the infection from hum ans and reduce its impact. This 9-dimensional system of nonlinear ordinary differential equations includes tsetse flies in their various stages of m aturity\, which is more than most previous models have done. We used the N ext Generation Matrix method to obtain an expression for $R_0$\, the basic reproduction number\, based on the other parameters in the model. \n\nOur study indicates that strategies that were not previously considered\, suc h as vaccinating domestic animals\, may reduce the impact of the disease o n humans even better than vaccinating humans.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/240/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/240/ END:VEVENT BEGIN:VEVENT SUMMARY:Modularity\, criticality and evolvability of a developmental gene regulatory network DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-165@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Berta Verd (University of Cambridge )\nInsects use t wo main modes of segment determination during development: the ancestral s hort-germband mode (eg. *Gryllus bimaculatus*) where new segments are adde d sequentially\, and the more derived long-germband mode (eg. *Drosophila melanogaster*)\, where all segments are determined simultaneously. In dipt eran insects (flies\, midges and mosquitoes)\, which use the long-germband mode of segmentation\, the gap genes are activated by maternal gradients and cross-regulate each other to form the first zygotic layer of regulatio n in the segmentation gene hierarchy. We reverse-engineered a dynamical mo del of the gap genes in *D. melanogaster* from quantitative spatio-tempora l expression data and used it to characterise the dynamics of gap gene pat tern formation along the embryo trunk. We used tools and concepts from dyn amical systems theory\, coupled with a newly developed methodology designe d specifically to address the effect of maternal gradient dynamics in the patterning process. This approach showed that two distinct dynamical regim es govern anterior and posterior trunk patterning. Stationary domain bound aries in the anterior rely on multi-stability. In contrast\, the observed anterior shifts of posterior gap gene domains can be explained as an emerg ent property of an underlying regulatory mechanism implementing a damped o scillator. We have identified a dual-function three-gene motif embedded in the gap gene regulatory network\, which is sufficient to recover both ant erior and posterior dynamical regimes. Which one drives gene expression in a given region depends on the gap genes involved. Interestingly\, this su b-network - known as the AC/DC motif - can also sustain oscillations. Osci llations are not found in the gap gene system but are characteristic of sh ort-germband segmentation\, suggesting that both modes share much more tha n previously thought. Studying the evolution of the gap gene network as an evolving dynamical system will tell us how oscillations could have arisen or ceased\, and this will help us understand how long-germband segmentati on might have repeatedly and independently evolved from the ancestral shor t-germband mode.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribu tions/165/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/165/ END:VEVENT BEGIN:VEVENT SUMMARY:A mathematical model of planar cell polarity DTSTART;VALUE=DATE-TIME:20180710T010000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-108@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Akiyama Masakazu (Research Institute for Electronics Science\, Hokkaido University)\nMany cells within epithelial tissues disp lay polarity along a particular axis. This axis is perpendicular to the ti ssue plane and apico-basal axis (from top to bottom of tissues) of the cel l. This phenomenon is called “planar cell polarity\, PCP”\, and is a c ommon phenomenon found in many multicellular organisms. For example\, hair cells in the inner ear of humans have many hairs on each individual cell\ , and since the hairs are regularly arranged on the cell plane\, we can he ar the sound. Not only hair cells\, but fish scales\, and body hair on mam mals and the wings of birds etc.\, have cell polarity. As a result\, these creatures carry out macroscopic morphogenesis.\nRecently\, since molecula r biological research has developed concerning PCP\, detailed molecular me chanisms have been revealed\, several report is published [1-4]. On the o ther hand\, major problems remain. In particular\, 1. Mechanisms of morpho genesis for macro-level (PCP) and micro-level (molecular) information and 2. in considering PCP\, what are the most important factors?\n\nIn order t o solve these problems\, we construct a simple mathematical model for PCP [5]. This model is based on the molecular mechanisms of PCP. In this talk\ , we will introduce our mathematical model and simulation result. Despite of our model is very simple formulation\, it can reproduce various aspects of the PCP. From the view point of our mathematical model\, let’s think “What is the most important mechanism in PCP”.\n\n[1] Jean-François Le Garrec *et al.*\, Developmental Dynamics 235:235-246. (2006)\n[2] Yoram Burak *et al.*\, PLoS Computational Biology Vol 5(12)\, e1000628. (2009)\ n[3] Benoît Aigouy *et al.*\, Cell\, 142\, 773-786\, September 3. (2010)\ n[4] K. Amonlirdviman *et al.*\, Science Vol 307\, 423-426. (2005)\n[5] Ay ukawa\,T.\, Masakazu\, A. *et al.*\, Cell Reports\, 8(2): p. 610 - 621\, 2 014.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/108/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/108/ END:VEVENT BEGIN:VEVENT SUMMARY:A model of calcium dynamics in anatomically accurate parotid acina r cells DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-260@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Nathan Pages ()\nWe constructed an anatomically-accu rate three-dimensional model of salivary fluid secretion from a cluster of parotid gland acinar cells. \n\nParotid acinar cells are responsible for the secretion of saliva. Olfactory and gustatory stimuli provoke the relea se of agonists that bind to the basal membranes of the acinar cells. This triggers a cascade of events that results in the production of IP3\, which \, in turn\, releases calcium ions from intracellular compartments. Upon r elease of calcium\, chloride channels are activated\, leading to chloride ions flowing out of the cell\, and water following by osmosis.\n\nWe have shown previously that the complex spatial structure of the acinus and the spatial heterogeneities within each acinar cell imposes severe constraints on the possible mechanisms that could explain the saliva secretion proces s.\n\nWe will discuss how could we simplify the models that are able to re plicate the physiological observations under such constraints.\n\nhttps:// conferences.maths.unsw.edu.au/event/2/contributions/260/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/260/ END:VEVENT BEGIN:VEVENT SUMMARY:A prey-predator model with gestation period DTSTART;VALUE=DATE-TIME:20180709T011000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-219@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yoichi Enatsu (Tokyo University of Science)\nIn this talk\, we consider the dynamics of a Lotka-Volterra prey-predator model b y a class of delay differential equations. The number of prey varies due t o a general nonlinear predators' consumption rate with delays. Under the a ssumption that the consumption rate is monotonically increasing with respe ct to the number of prey\, we investigate the effect of the nonlinearity a nd delays on the asymptotic behaviour of the model. For the case where the consumption rate is described not only as Holling type I\,II but also as Holling type III\, some ongoing studies are also introduced. Comparison fo r the assumptions on the incidence rates appearing in prey-predator models with those in epidemiological models\, will be also discussed.\n\nhttps:/ /conferences.maths.unsw.edu.au/event/2/contributions/219/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/219/ END:VEVENT BEGIN:VEVENT SUMMARY:Administration of defective virus via bang-bang control stops deng ue transmission from a calibrated population of infectious patients DTSTART;VALUE=DATE-TIME:20180711T052000Z DTEND;VALUE=DATE-TIME:20180711T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-300@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tarunendu Mapder (ARC CoE for Mathematical and Stati stical Frontiers\, School of Mathematical Sciences\, Queensland University of Technology\, Brisbane\, Australia)\nAs dengue is one of the human dise ases with global concern\, the host-vector shuttle and the bottleneck of d engue transmission is a significant aspect to study. For the four serotype s of dengue virus within host and their transmission to the vectors\, we t ry to capture the variability in blood viremia and antibody levels of pati ents and their infectiousness to mosquitoes. The present model frames the occurrence of defective virus and the virus neutralization by the immune r esponse. In order to calibrate and characterize the intrinsic variability in a dataset\, collected from large number of patients\, the population of models (POMs) is an efficient and reliable technique. We sample the param eters from Latin Hypercube within the biological feasible range to build t he POMs. Once the POM is well-calibrated\, we build a set of control setti ngs simultaneously for every model as a mechanism for preventing transmiss ion in a population. We use a bang-bang type control on the administration of defective virus (transmissible interfering particles\, TIPs) to the sy mptomatic patients in course of their febrile period.\n\nhttps://conferenc es.maths.unsw.edu.au/event/2/contributions/300/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/300/ END:VEVENT BEGIN:VEVENT SUMMARY:When mismatches don't matter: the dynamical consequences of diverg ent ecological and economic scales in coastal fisheries DTSTART;VALUE=DATE-TIME:20180709T060000Z DTEND;VALUE=DATE-TIME:20180709T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-117@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michael Bode (School of Mathematical Sciences\, Quee nsland University of Technology)\nConservation management decisions are of ten implemented at the scale of human communities\, rather than the scale of the most relevant ecological dynamics. Research frequently points out t he loss in efficiency that results from such "scale mismatches". However\, the scale of management is influenced by socio-economic constraints on ma nagement actors - not all people want to cooperate with each other. While it is clear that objectives can be better achieved if management and ecolo gical scales are aligned\, it is not clear whether such benefits justify t he costs of alignment\, or how alignment can be achieved in multi-actor co ntexts. \n\nOn Manus Island in Papua New Guinea\, small customary tenure a reas define the scale of fisheries management decisions\, but their fish s tocks are connected by pelagic larval dispersal. We quantify the extent of this scale mismatch for the serranid *Plectropomus maculatus* by empirica lly estimating larval dispersal distances\, and integrating this data into a bioeconomic model of the multi-actor fishery\, and identifying the coop erative Nash equilibrium. Larval dispersal allows individual communities t o externalise the costs of overharvesting\, and export the benefits of coo perative behaviour\, to non-cooperating groups. Despite these mismatched s cales\, the communities on southern Manus have recently created a tribal n etwork for management and negotiation\, emphasising the importance of soci al capital in avoiding suboptimal outcomes or the need for top-down govern ance.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/117/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/117/ END:VEVENT BEGIN:VEVENT SUMMARY:Homogenisation of a two-phase\, elastic-poroelastic model of a fib re-reinforced hydrogels for tissue engineering of cartilage DTSTART;VALUE=DATE-TIME:20180709T010000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-167@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Helen Byrne (University of Oxford)\nTissue engineeri ng aims to grow artificial tissues to replace those that have been damaged through age\, trauma or disease. A recent approach to engineer artificial cartilage involves seeding cells within a scaffold consisting of an inter connected three dimensional printed lattice of polymer fibres combined wit h a cast or printed hydrogel\, and subjecting the construct (cell-seeded s caffold) to an applied load in a bioreactor. A key question is understandi ng how the applied load is distributed throughout the construct to the mec hanosensitive cells.\n\nTo address this question\, we view the scaffold as a two-phase mixture\, in which the fibres are modelled as a linear elasti c material and the hydrogel as a poroelastic material. We exploit the disp arate length scales (small inter-fibre spacing compared with construct dim ensions) and use homogenisation theory to derive macroscale equations for the effective mechanical properties of the composite material. The resulti ng governing equations reflect the orthotropic nature of the composite. We then validate the model\, by comparing results generated from finite elem ent simulations of the macroscale\, homogenised equations to experimental data describing the unconfined compression of the fibre-reinforced hydroge ls.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/167/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/167/ END:VEVENT BEGIN:VEVENT SUMMARY:Low- and high-waking modes in the corticothalamic system DTSTART;VALUE=DATE-TIME:20180710T010000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-182@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Paula Sanz-Leon (University of Sydney)\nIn this talk presented at the Mathematical Neuroscience Subgroup Minisymposium I will discuss a numerical analysis of the steady-state solutions of a neural fie ld model of the corticothalamic system. The independent synaptic connectio ns of the corticothalamic model define an eight-dimensional parameter spac e\, while specific combinations of these connections parameterize intracor tical\, corticothalamic\, and intrathalamic loops. \n\nThe first part of t he analysis consists of a systematic identification of multistable regions for physiological parameter ranges representing normal arousal waking sta tes in adult humans. Parameter values have been derived from human electro encephalographic recordings (EEG). The key results are the confirmation of the existence of up to five steady-state solutions\, up to three of which are linearly stable. The presence of multiple stable steady-state solutio ns implies that the system has enough degrees of freedom to capture multip le operating points (e.g.\, mutiple global brain states). Indeed\, two out of the three linearly stable steady-state equilibria represent two waking modes for adult human physiology while resting with the eyes closed. Thes e two modes are termed the low- and high- waking modes. \n\nWhile the low- waking mode has been previously identified with normal brain activity duri ng quiet wakefulness\, the high-waking mode has not been fully characteriz ed. The second part of the analysis focus on (i) the spectral features of high-waking mode states\; (ii) the nonlinear attractors between the two wa king modes\; and\, (iii) the switching dynamics between the low- and high- waking modes using small amplitude and bandlimited random perturbations.\n \nWe argue that the high-waking mode may represent hyperarousal waking sta tes. This result opens up the possibility to predict and identify subtypes of primary insomnia in which cortical hyperarousal is the main hallmark f rom human neuroimaging data.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/182/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/182/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical models on tumour-lymphocyte dynamics and checkpoint b lockade therapy DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-185@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Collin Zheng (University of Sydney)\nCytotoxic T-lym phocytes\, commonly called killer T cells\, are among our immune system’ s most potent and well-understood weapons against cancer. However\, checkp oint receptors such as CTLA-4 and PD-1 on the surfaces of T cells inhibit their activation and proliferation. These receptors can be blocked by anti body drugs\, which pave the way for an anti-tumour immune response. We wil l present work-in-progress mathematical models on tumour-lymphocyte dynami cs in the presence of checkpoint blockade therapy\, discuss their clinical implications\, and more broadly discuss the current modelling efforts in this area.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 185/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/185/ END:VEVENT BEGIN:VEVENT SUMMARY:A structured population model with diffusion in structure space DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T005000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-491@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Fabio A. Milner (School of Mathematical and Statisti cal Sciences\, Arizona State University)\nA structured population model is described and analyzed\, in which individual dynamics is stochastic. The model consists of a PDE of advection-diffusion type in the structure varia ble. The population may represent\, for example\, the density of infected individuals structured by pathogen density $x$\, $x\\ge0$. The individuals with density $x=0$ are not infected\, but rather susceptible or recovered . Their dynamics is described by an ODE with a source term that is the exa ct flux from the diffusion and advection as $x\\to0^+$. Infection/reinfect ion is then modelled moving a fraction of these individuals into the infec ted class by distributing them in the structure variable through a probabi lity density function. Existence of a global-in-time solution is proven\, as well as a classical bifurcation result about equilibrium solutions: a n et reproduction number $R_0$ is defined that separates the case of only th e trivial equilibrium existing when $R_01$. Numerical simulation results a re provided to show the stabilization towards the positive equilibrium whe n $R_0>1$ and towards the trivial one when $R_0\n\nhttps://conferences.mat hs.unsw.edu.au/event/2/contributions/491/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/491/ END:VEVENT BEGIN:VEVENT SUMMARY:Effects of interplay between direct and indirect effects on divers ity of ecological communities DTSTART;VALUE=DATE-TIME:20180709T063000Z DTEND;VALUE=DATE-TIME:20180709T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-469@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Toshiyuki Namba (Osaka Prefecture University)\nSpeci es interactions are important to determine structure and stability of ecol ogical communities. In particular\, a variety of indirect effects appear b etween species which do not interact directly. However\, indirect effects do also appear between species that directly interact. For example\, plant species sharing a common herbivore may engage in both interference compet ition directly with other plant species and apparent competition indirectl y through common herbivores. Then\, if a plant species augments herbivores \, then grazing pressure on another plant species increases and decreases in biomass of the latter plant may weaken competitive pressure on the form er plant species. In this way\, there may appear many feedback loops in a complex ecological community where species affect each other through many different paths connecting them. Thus\, we should understand interactive c onsequences of a direct and many indirect effects to understand structure and dynamics of ecological communities. However\, studies on indirect effe cts tend to focus on changes in density of a target species and neglect ch anges in diversity of the whole community.\n\nIn this presentation\, we co nsider a very simple dynamical system model that describes a community com posed of predator\, herbivore and many plant species. In this model\, sinc e predators reduce herbivores and weaken grazing pressure on plants\, ther e appear a positive trophic cascade from the predator to plants. Then\, in creased plant biomass may enhance both direct interference and indirect ap parent competition between plants. Therefore\, it is interesting to invest igate how the presence of predators affects diversity of the plant communi ty. We analytically solve steady state solutions of the model and investig ate effects of predation\, grazing\, and interference competition on the n umber of plant species and total plant biomass. Based on the results\, we discuss the importance of interplay between direct and indirect effects fo r structure of ecological communities.\n\nhttps://conferences.maths.unsw.e du.au/event/2/contributions/469/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/469/ END:VEVENT BEGIN:VEVENT SUMMARY:Chemotaxis Modelling for Sperm Motility DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-97@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: John LaGrone (Tulane University)\nAn important aspec t in the study of reproduction is how sperm are guided toward an egg for f ertilization. One such mechanism is the process of chemotaxis\, in which t he sperm detect changes in concentration (namely of Ca+) in the fluid envi ronment and utilize these changes to alter the waveform of their flagellar beat. This change in beat form results in changes to the swimming path. W e model the swimming sperm using a Kirchhoff elastic rod model coupled wit h the method of regularized Stokeslets for the fluid motion. In order to s imulate the effect of chemical concentrations\, we employ a stochastic dec ision making process.\n\nhttps://conferences.maths.unsw.edu.au/event/2/con tributions/97/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/97/ END:VEVENT BEGIN:VEVENT SUMMARY:Tiny insects clap and fling with flexible wings DTSTART;VALUE=DATE-TIME:20180711T063000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-189@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michael Senter (University of North Carolina)\nVery small insects that are 1 mm in length or less\, such as thrips and fairyfl ies\, often clap their wings together at the end of each upstroke and flin g them apart at the beginning of each downstroke. This 'clap and fling' mo tion augments the lift forces generated during flight\, but very large for ces are required to clap the wings together and to fling the wings apart. As the opposing forces acting normal to each wing nearly cancel during the fling\, these large forces do not have a clear aerodynamic benefit. In th is presentation\, a standard and a elastic version of the 3D immersed boun dary method is used to simulate clap and fling at the low Reynolds numbers characteristic of the smallest insects (Re\n\nhttps://conferences.maths.u nsw.edu.au/event/2/contributions/189/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/189/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematics of wildlife smuggling interdiction DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-338@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Rachel Mclean (The University of Adelaide)\nThe ille gal trade of wildlife is estimated to run into hundreds of millions of dol lars. It is an international problem that exploits both enforcement loopho les and corruption\, and it is a direct threat to the survival of plant an d animal species. Smugglers transport wildlife and their derivatives from sources to destinations across the globe. They are able to choose the rout e they take to move these commodities across international borders. The lo cation where a smuggler enters a country is important as limited biosecuri ty resources are able to be placed at these locations. The locations and a mount of biosecurity resources must be allocated intelligently. Quantitati ve analysis and mathematical methods are required to provide insights into illegal wildlife trade networks. In this talk\, I will discuss a novel t wo player game on a network between smugglers and biosecurity agencies whi ch looks at how best to allocate resources to intercept illegal trade. Thi s framework will then be applied to some networks motivated by data.\n\nht tps://conferences.maths.unsw.edu.au/event/2/contributions/338/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/338/ END:VEVENT BEGIN:VEVENT SUMMARY:Volume transmission and neurotransmitter homeostasis DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-181@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Janet Best (The Ohio State University)\nIn volume tr ansmission\, neurons in one brain nucleus send their axons to a second nuc leus where neurotransmitter is released into the extracellular space. In [ 1] we showed how to calculate the average amount of neurotransmitter at di fferent parts of the extracellular space\, depending on neural properties and the geometry of the projections and extracellular space. We showed how to formulate questions as boundaries value problems for the heat equation with stochastically switching boundary conditions\, and we derived result s in one space dimension. \n\nHere we discuss the two- and three-dimension al problems\, along with mechanistic models of neurotransmitter homeostasi s.\n\n[1] Lawley\, Best\, Reed 2016\n\nhttps://conferences.maths.unsw.edu. au/event/2/contributions/181/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/181/ END:VEVENT BEGIN:VEVENT SUMMARY:Hominid interbirth interval and evolution of paternal care DTSTART;VALUE=DATE-TIME:20180709T054000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-465@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Wataru Nakahashi (Waseda University)\nUnlike any gre at apes\, humans have expanded into a wide variety of habitats during the course of evolution\, beginning with the transition by australopithecines from forest to savanna habitation. Novel environments are likely to have i mposed hominids a demographic challenge due to such factors as higher pred ation risk and scarcer food resources. In fact\, recent studies have found a paucity of older relative to younger adults in hominid fossil remains\, indicating considerably high adult mortality in australopithecines\, earl y *Homo*\, and Neanderthals. It is not clear to date why only human ancest ors among all hominoid species could survive in these harsh environments. In this talk we explore the possibility that hominids had shorter interbir th intervals to enhance fertility than the extant apes. To infer interbirt h intervals in fossil hominids\, we introduce the notion of the critical i nterbirth interval\, or the threshold length of birth spacing above which a population is expected to go to extinction. We develop a new method to o btain the critical interbirth intervals of hominids based on the observed ratios of older adults to all adults in fossil samples. Our analysis shows that the critical interbirth intervals of australopithecines\, early *Hom o*\, and Neanderthals are significantly shorter than the observed interbir th intervals of extant great apes. This result suggests that the child car e burden of hominid mother was reduced by other group members\, including males. In fact\, small canine of early hominids may indicate increasing im portance of male provisioning\, relative to male-male aggression\, for mal es to gain higher reproductive success. To discuss evolutionary causes of these hominid features\, we develop a mathematical model to obtain the con dition for paternal care to evolve.\n\nhttps://conferences.maths.unsw.edu. au/event/2/contributions/465/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/465/ END:VEVENT BEGIN:VEVENT SUMMARY:Coevolution of horizontally transmitted mutualistic systems DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-177@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yu Uchiumi (Meiji Institute for Advanced Study of Ma thematical Sciences\, Meiji University)\nMutualism based on reciprocal exc hange of costly services must avoid exploitation by “free-rides”. Acco rdingly\, hosts discriminate against free-riding symbionts in many mutuali stic relationships. However\, as the selective advantage of discriminators comes from the presence of variability in symbiont quality that they elim inate\, discrimination and thus mutualism have been considered to be maint ained with exogenous supply of free-riders. In this study\, we tried to re solve the “paradoxical” coevolution of discrimination by hosts and coo peration by symbionts\, by comparing two different types of discrimination : “one-shot” discrimination\, where a host does not reacquire new symb ionts after evicting free-riders\, and “resampling” discrimination\, w here a host does from the environment. Our study shows that this apparentl y minor difference in discrimination types leads to qualitatively differen t evolutionary outcomes. First\, although it has been usually considered t hat the benefit of discriminators is derived from the variability of symbi ont quality\, the benefit of a certain type of discriminators (e.g. one-sh ot discrimination) is proportional to the frequency of free-riders\, which is in stark contrast to the case of resampling discrimination. As a resu lt\, one-shot discriminators can invade the free-rider/non-discriminator p opulation\, even if standing variation for symbiont quality is absent. Sec ond\, our one-shot discriminators can also be maintained without exogenous supply of free-riders and hence is free from the paradox of discriminatio n. Therefore\, our result indicates that the paradox is not a common featu re of evolution of discrimination but is a problem of specific types of di scrimination.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributio ns/177/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/177/ END:VEVENT BEGIN:VEVENT SUMMARY:How does diversity relate to feasibility and stability properties of complex ecological networks? DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-190@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yael Artzy-Randrup (University of Amsterdam )\nA cen tral debate when studying ecological communities concerns the relative imp ortance of selective processes relative to stochastic ones. This has signi ficance for understanding the dynamic behaviour of these systems\, for ass essing features such as fragility and resilience\, and ultimately\, for de termining how to correctly approach them. At the core of dealing with this challenge is the need to link ‘observed patterns’ with the ‘underly ing processes’ that created them\; this is a long-standing well known ch allenge in the arenas of ecology and evolution. The application of network s in ecological theory can provide a useful perspective and toolkit for de aling with this challenge. Indeed\, in many cases the selective forces act ing on individual species are frequency dependent and hence need to be pla ced in a community framework in order to understand their ecological role as it depends on the rest of the network\, and how the functioning of the whole network depends on them. \n\nDiversity has played a central role in most studies that address the relationships between structure and function in ecological-network. Here I discuss different views on the concept of d iversity\, both as an indicator of system functioning and as an emergent p roperty of these systems. As a case study I specifically focus on pathogen communities\, where ecological and evolutionary feedbacks act on short ti me scales.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 190/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/190/ END:VEVENT BEGIN:VEVENT SUMMARY:Lattice-free chemical reactions with multiple time scales. DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-160@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mark Flegg (Monash University)\nIn many biological a pplications\, it is useful to model chemical reactions at the level of ind ividual molecules whilst not running costly Brownian dynamics models. Mode lling chemical reactions as interactions at a distance can lead to errors if multiple species and time scales are important to the kinetics (for exa mple\, catalytic reactions). Multiple time scale analysis of equivalent me an-field kinetics can lead to high order reactions which are not just gove rned by the law of mass-action but also nonlinear kinetics such as Michael is-Menten kinetics. In this talk we will discuss some particle-based metho ds which recapitulate these high order kinetics.\n\nhttps://conferences.ma ths.unsw.edu.au/event/2/contributions/160/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/160/ END:VEVENT BEGIN:VEVENT SUMMARY:Disease modelling: how to control and prevent epidemic outbreaks DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T015000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-323@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Elena Aruffo ()\nIn recent years vaccination studies have led to greater understanding and improvements on the development and distribution of vaccines\, especially with respect to certain childhood d iseases. However\, while current vaccination campaigns strive to achieve h erd immunity (a critical threshold of ‘immune’ individuals needed to p rotect an entire population from infection)\, eradication has not been ach ieved and populations continue to be affected by childhood diseases global ly. These outbreaks are usually attributed to the movement of one or more asymptomatic cases from a country affected by the pathogen in question. Ne vertheless\, individuals coming from regions with infection-induced immuni zation can provide protection to the receiving region. Mathematical models are able to describe the dynamics of an infectious diseases in population s\, and they can provide important measurements for public health such as the basic reproductive ratio\, the vaccination threshold needed to achieve herd immunity\, and project the number of cases that could be observed du ring an outbreak. In particular\, metapopulation models can be used to tra ck the movement of individuals through travel or immigration to better und erstand the movement and persistence of infectious diseases\, and border r estriction policies. We propose infectious disease models to study the dis tribution of immunity in a population and how this changes with immigratio n and travel\, by using a Susceptible-Exposed-Infectious-Recovered framewo rk. Our work is in collaboration with Public Health Ontario and has been u sed to better understand the effects of measles immunity in a population. Our results show that the biggest loss in the susceptible population happe ns when the infected individual introduced in the population belongs to th e group of children between 5 and 9 years\, even when vaccination threshol ds recommended by the WHO are achieved.\n\nhttps://conferences.maths.unsw. edu.au/event/2/contributions/323/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/323/ END:VEVENT BEGIN:VEVENT SUMMARY:Assessing the “ID” Part of ID-STEM Learning DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-191@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Lester Caudill (University of Richmond)\nStudent pro gress in “interdisciplinary (ID) thinking” is remarkably resistant to many established means of evaluation. A sophisticated skill\, such thinkin g does not fit well into old instruments\, like timed exams. In contrast t o discipline-specific skill sets\, a student’s ability to view problems from multiple-disciplinary perspectives cannot be evaluated in terms of an objective standard\, and\, therefore\, requires both pre- and post-assess ment. We will discuss issues related to this matter\, and will share poten tial strategies for effective assessment of student gains in ID thinking.\ n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/191/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/191/ END:VEVENT BEGIN:VEVENT SUMMARY:Parallel stochastic simulation of cell-cell communication with spa tially resolved reaction-diffusion kinetics DTSTART;VALUE=DATE-TIME:20180709T020000Z DTEND;VALUE=DATE-TIME:20180709T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-37@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Adrien Coulier (Uppsala University)\nStochastic simu lations are essential to the study of biological cells\, yet there is no c omputational framework allowing for detailed spatial simulations of geneti c regulatory network within large populations of cells.\n\nWe fill this ga p by developing a parallel simulation framework capable of spatially resol ved stochastic simulation of cell-cell signalling in multicellular systems . We use an operator-splitting method to decouple the internal reaction-di ffusion kinetics from the interactions on the cells’ boundaries and allo w for efficient and horizontally scalable simulations of large numbers of interacting cells. Our framework is highly compatible with many existing m ethods and allows for hybrid simulation where both coarse and detailed mod els are considered at the same time. It is also greatly versatile and is d eployable on various high performance computing platforms\, such as cluste rs or clouds.\n\nWe use a small test model to study the convergence of our method as well as larger models to demonstrate weak scalability.\n\nOur m ethod demonstrate the feasibility of detailed stochastic simulations of la rge populations of interacting cells and is the first step toward more com plete simulations including both detailed reaction-diffusion simulations a nd cell mechanics.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contri butions/37/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/37/ END:VEVENT BEGIN:VEVENT SUMMARY:Adaptive defense of a shared pest can enhance efficiency of biolog ical control by two natural enemies DTSTART;VALUE=DATE-TIME:20180709T010000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-116@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yusuke Ikegawa (Ryukyu Sankei Co. Ltd.)\nIt has long been debated whether introduction of two (or more) natural enemies result s in more efficient pest control than that of either one enemy. Intra-guil d predation (IGP) among two natural enemies sharing a single pest has been recognized as an important factor to reduce efficiency of pest control. W hile the classical theoretical model of IGP showed that introduction of tw o natural enemies is less efficient for pest control\, empirical works hav e showed positive\, negative\, and neutral results. However\, the classica l IGP model did not consider any behavioural plasticity of the pest and na tural enemies.\n\nIn this study\, we extended the classical IGP model by c onsidering adaptive defense by the pest and switching predation by the omn ivorous natural enemy (omnivore) and examined separate and joint effects o f them on efficiency of pest control. We assumed that the pest can adaptiv ely allocate efforts toward two kinds of defense respectively against the two natural enemies to increase its own fitness\, with cost of reduction i n its own reproduction. Switching predation by the omnivore is expressed a s the Holling’s type III functional response to the pest and another nat ural enemy (intermediate predator). Equilibrium pest density is used as an index of efficiency of biological pest control.\n\nIf the pest employed t he adaptive defense\, introduction of two natural enemies performed more e fficient pest control than that of either one enemy\, unless the IGP was t oo intensive. This is because the pest allocated more defensive effort aga inst the more threatening enemy\, and thus it was difficult for the pest t o simultaneously prevent predation from the two enemies. On the other hand \, switching predation could not improve biological control by two natural enemies. However\, the type III functional response tempted the pest to a bandon defensive effort against the omnivore\, because the predation press ure was negligible at low pest density and saturated at high density. Sinc e the intermediate predator was suppressed by the undefended omnivore\, de fensive effort against the intermediate predator also diminished. Thus\, s witching predation could offset the effects of defense and the prey densit y could be lowered by two natural enemies even under severe IGP. Consequen tly\, types and combination of behavioural plasticity might cause qualitat ively different outcomes of biological control introducing two natural ene mies.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/116/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/116/ END:VEVENT BEGIN:VEVENT SUMMARY:Mechanisms driving 3D self-organisation of eukaryotic genomes: a s ystems biology approach DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-19@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Karen Lipkow (University of Cambridge and Babraham I nstitute)\nThe three-dimensional structure of eukaryotic genomes is non-ra ndom\, dynamic\, highly regulated\, and can be observed to change accordin g to external signals and differentiation state. Disruptions can lead to d isease\, in which incorrect genomic contacts are responsible for mis-regul ation of gene expression. However\, the underlying mechanisms that organis e the genome are still largely unknown. While most studies focus on the ac tivity of specific proteins which connect two chromatin loci\, we seek to understand how the cells makes use of its entire complexity and of physica l mechanisms. Using stochastic polymer simulations\, which are informed by the analysis of large datasets and verified by quantitative experiments in budding yeast\, we discovered a fundamental mechanism: The mobility of the chromatin fibre is not uniform\, but heterogeneous\, along its length\ , as a result of the unequal distribution of proteins binding along the ge nome. This leads to thermodynamically driven self-organisation\, which we observe experimentally. It achieves spatial clustering of poised genes and mechanistically contributes to the directed relocalisation of active gene s to the nuclear periphery upon heat shock (bioRxiv 106344). I will discus s the implications and present follow-up studies that make use of polymer and particle-based simulations to discover an additional layer of genome o rganisation.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribution s/19/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/19/ END:VEVENT BEGIN:VEVENT SUMMARY:Effects of mechanosensory feedback on swimming behaviour and stabi lity of a flexible body DTSTART;VALUE=DATE-TIME:20180711T053000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-81@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Christina Hamlet (Bucknell University)\nThe lamprey is an eel-like organism used as a model for both neurophysiology and locom otion studies. Like other animals\, the lamprey moves through the use of a neural network called a central pattern generator to generate a rhythmic signals down the body\, inducing muscle contractions. This signal is adjus ted through information using mechanosensors (edge cells) which detect cha nges to the body to improve performance. Here we present a computational s wimming lamprey driven by a central pattern generator (CPG) modelled as a chain of coupled oscillators. The exact functional form of feedback from t he edge cells to the CPG is not known. Using the CPG to drives muscle kine matics in fluid-structure interactions implemented in an immersed boundary framework to produce the emergent swimming mode\, we can examine the effe cts of different proposed functional forms of sensory feedback information . Effects of feedback to the neural activation on swimming performance are estimated and examined.\n\nhttps://conferences.maths.unsw.edu.au/event/2/ contributions/81/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/81/ END:VEVENT BEGIN:VEVENT SUMMARY:Dynamical patterns in brain parenchyma : modelling approach and Is sues DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-355@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Dmitry Postnov (Saratov State University\, Russia)\n Recent advances in understanding of complex interactions between the pro cesses that maintain and control the physiological state of brain parench yma open new possibilities and deliver new challenges for modelling stud ies on topic. Now it is clear that any significant deviation from normal c onditions as well as natural alternations of activity of cortical neurons (say\, during sleep-wake cycle) are accompanied by measurable changes of physiological parameters\, like extracellular ionic concentrations\, astrocytic calcium signalling\, or vascular tone of adjacent blood vessels . The interaction pathways within the so called neural-glial-vascular uni t not only drive the local responses of the cells\, but form the spatia lly extended networks at different functional layers. \n \nBeing normall y on the sidelines\, these physiological mechanisms become dominant dur ing the extreme physiological behaviours of the brain cortex\, such as cor tical spreading depression\, migraine waves\, or spreading depolarizatio n events with stroke or injures. There is a clear room and need for rele vant modelling studies aimed to better understanding of how all this acti vity is orchestrated. However\, this task is very challenging due to the extreme complexity and heterogeneity of system under study. \n\n The presented study addresses the selected aspects of above problem. Being f ocused on dynamical patterns\, we still keep the balance between the p hysiological details and dynamically tractable generalized modelling. Firs t\, we discuss the dynamical consequences of inclusion of extracellular potassium concentration as a state variable in neuron models. Specifical ly\, this additional variable provide both the self -sustained depolariza tion\, and the additional pathway for cell-to-cell signalling which is al so known as "volume connection". Second\, we extend this potassium drive n model to the mathematical model of cortical spreading depression which counts the effects of neurovascular coupling and cerebral blood flow redis tribution. Our most notable finding here is that the combination of vasc ular-mediated spatial coupling with local regulatory mechanisms results in the formation of stationary Turing-like patterns during a course of sprea ding depolarization.\n\nThird\, we describe a way to incorporate in mode l the recently revealed details of astrocyte morphology and functions. T his approach includes the algorithms for the creation and computational tr eatment of spatial patterns resembling the real astrocyte networks.\n\n I n conclusion\, as an outlook\, we discuss how the dynamical redistributi on of extra- and inter-cellular volumes could affect the reported dynam ics\, as well as formulate the issues related to adequate modelling of v ascular-mediated spatial interaction.\n\nhttps://conferences.maths.unsw.ed u.au/event/2/contributions/355/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/355/ END:VEVENT BEGIN:VEVENT SUMMARY:The show-off hypothesis: the evolution of large-game hunting\, and signalling like peacocks DTSTART;VALUE=DATE-TIME:20180709T060000Z DTEND;VALUE=DATE-TIME:20180709T062000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-464@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sara Loo (University of Sydney)\nLarge-game hunting in human hunter-gatherers is a counter-intuitive behaviour. Despite low da ily success rates and large proportions of sharing\, hunter-gatherers inve st in large-game hunting over the less-wasteful strategy of small-game hun ting. Where investment in small-game hunting could provide a more reliable and consistent source of direct benefit to one’s offspring\, large-game hunting is more ecologically and environmentally dependent\, and is a sou rce of benefit to all members of a society\, being shared unbiased to the hunter himself. Hypotheses attempt to explain this as reciprocity or altru ism\, wherein a hunter will share meat obtained as an investment in future returns from receiving beneficiaries of that meat. However\, observations show that there is no correlation between current success rates with futu re obtained goods from others. The Show-Off Hypothesis is an alternate exp lanation of the evolution of large-game hunting\, stating that such huntin g behaviours act as a costly signal of one’s quality as a mate. Better h unters are deemed as better mates\, and hence obtain more paternities in a society. We investigate this\, considering the effect of societal status on the evolution of the strategy of large-game hunting. We develop and pre sent a model that defines measures of hunting success and the survival ben efit of care\, in order to shed light on previously unquantified effects o f status on strategic choice. Within this model\, we demonstrate the effec t of maladaptive competition on male hunting strategic choice\, and provid e measures of the trade-off that drives the behaviour of large-game huntin g.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/464/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/464/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling growth and treatment dynamics in PDGF-driven glioblastom a: how heterogeneity manifests across scales DTSTART;VALUE=DATE-TIME:20180709T060000Z DTEND;VALUE=DATE-TIME:20180709T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-183@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jill Gallaher (H. Lee Moffitt Cancer Center)\nGliobl astoma multiforme (GBM) is a rare brain cancer with a median survival of o nly around 15 months. Intratumoural heterogeneity and extensive infiltrati on into the brain tissue contribute to poor prognosis and probable recurre nce. Predicting the timing of post-treatment recurrence is often limited i f using only MRI imaging measurements\, as a diverse range of treatment ou tcomes can result from similar pre-treatment growth dynamics. To better un derstand the diversity in recurrence\, we analyze multiscale data from an ex vivo rat model during progression to inform an agent-based computationa l model to quantify how heterogeneity in proliferation and invasion affect s both the bulk and individual scale tumour metrics following treatment.\n \nThe rat experiment is a model of platelet-derived growth factor (PDGF) d riven GBM. The production of PDGF by cells allows both autocrine and parac rine stimulated proliferation and migration to drive growth. PDGF in the t issue environment also stimulates and recruits normal progenitor cells. Th roughout this experiment\, bulk tumour size was recorded via MRI\, and sin gle cell tracks were analyzed to quantify proliferation and migration spat ially. Guided by this data\, we built an agent-based model within the gray -white brain tissue context. We fit the model to the growth data alone usi ng a hybrid genetic algorithm approach\, and then fit individual cell prol iferation and migration distributions.\n\nWe find parameter sets that defi ne a suite of fits\, which describe similar bulk scale growth dynamics wit h widely different underlying phenotypes that tend to be more proliferativ e\, more migratory\, or more driven by growth-factor dynamics. A more limi ted set of parameters fits the individual scale dynamics\, with heterogene ity predicted to be both an intrinsic feature and driven by the environmen t. Application of an anti-proliferative treatment on these heterogeneous t umours reduces tumour size\, but leads to recurrence of a less proliferati ve tumour. An anti-migratory treatment is seen to have little effect on gr owth dynamics\, but selects for more proliferative phenotypes. The changes that occur at the imaging scale down to the single cell level lead to a b etter understanding how the evolutionary impact of treatment on GBM can in form treatment regimens.\n\nhttps://conferences.maths.unsw.edu.au/event/2/ contributions/183/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/183/ END:VEVENT BEGIN:VEVENT SUMMARY:Theoretical proofs of evolutionary stabilities in indirect recipro city of private assessment DTSTART;VALUE=DATE-TIME:20180709T062000Z DTEND;VALUE=DATE-TIME:20180709T064000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-463@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Isamu Okada (Soka University)\nPrivate assessment in indirect reciprocity is a natural assumption because individuals can asse ss others privately in this situation. However\, only few studies have con sidered private assessment because of analytical difficulty that it presen t. Here\, we develop an analytical method using solitary observation to so lve private assessment in indirect reciprocity problem without any approxi mation. In this study\, we formulate a model of solitary observation and c alculate the replicator dynamics systems of five leading norms of indirect reciprocity. Our theoretical solution shows that indirect reciprocity in private assessment provides a different result to that in public assessmen t.\n\nAccording to the existence proofs of cooperative evolutionarily stab le (CES) points in the system\, strict norms (stern judging and shunning) have no CES point in private assessment\, while they do in public assessme nt. Image scoring does not change the system regardless of the assessment types because it does not use second-order information. In tolerant norms (simple standing and staying)\, the CES points move to co-existence of nor ms and unconditional cooperators. Surprisingly\, although there is no cent ral coercive assessment system in private assessment\, the average coopera tion rate is greater than that in public assessment. This is because priva te assessment gives unconditional cooperators a role because the unconditi onal cooperators can raise the cooperation level of the society.\n\nOur re sults also show the three advantages of the staying norm in private assess ment: a higher cooperation rate\, easiness of invasion into defectors\, an d robustness to maintain cooperative evolutionarily stable situations. Our results are applicable to general social dilemmas in relation to private information. Under some dilemmas\, norms or assessment rules should be car efully chosen to enable cooperation to evolve.\n\nhttps://conferences.math s.unsw.edu.au/event/2/contributions/463/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/463/ END:VEVENT BEGIN:VEVENT SUMMARY:Multi-scale and multi-compartment modelling provides insight to va ccination dynamics in Tuberculosis DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-244@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Louis Joslyn (Bioinformatics Graduate Program\, Univ ersity of Michigan Medical School)\nTuberculosis (TB) is one of the top 10 causes of death worldwide\, and the WHO’s EndTB strategy requires devel oping an effective vaccine. The H56 vaccine is a candidate currently in ph ase I/IIa trials as a boost to Bacillus Calmette-Guérin (BCG\, the TB vac cine that is currently used in most countries world-wide). We build a mul ti-compartment\, hybrid multi-scale model to 1) improve our understanding of immune response to H56 and 2) predict the role of T cells in preventing TB after vaccination. \n\nFirst\, we develop a two-compartment model of 3 1 non-linear ordinary differential equations (ODEs) that describe T-cell p riming\, proliferation\, and differentiation in lymph nodes and blood. Th ese ODEs allow us to track T cell response following vaccination. We cali brate our ODE model separately to human clinical trial data and non-human primate (NHP) experimental data to display differences in each species res ponse to H56. Next\, we couple our curated agent based model of granuloma formation in the lung\, GranSim\, to our blood and lymph node compartment s to capture the host immune response to infection with *Mycobacterium tub erculosis*. This creation of a multi-scale and multi-compartment model al lows us to represent a pseudo-whole-body response to both vaccination and infection. We use this whole-body model in the form of “virtual clinica l trials” to retrospectively study the human and NHP datasets. In partic ular\, we predict the role of T cells (induced through vaccination) throug hout the course of infection in blood\, lymph node\, and lung granulomas. We use uncertainty and sensitivity analysis to compare and contrast immune response to vaccination and infection in NHPs and humans. We conjecture that vaccine dose may be critically important when evaluating H56 efficacy against *Mycobacterium tuberculosis* infection.\n\nhttps://conferences.ma ths.unsw.edu.au/event/2/contributions/244/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/244/ END:VEVENT BEGIN:VEVENT SUMMARY:The evolution of a geographic cline in flowering time in bamboos DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-72@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yuuya Tachiki (University of Sheffield)\nBamboos are clonal plants that undergo mass flowering followed by simultaneous death after a long-term period of rhizomatous vegetative growth. The time to flo wering after germination depends on species and shows a geographic cline i n which it is short in tropical region and becomes longer as we move to no rthward into temperate region. As another geographic tendency in bamboo\, rhizome systems are different between tropical and temperate region. The s pecies in tropical region have short and thick rhizomes\, called pachymorp h\, resulting in clumped spatial arrangement of ramets. On the other hand\ , species in temperate region have long and slender rhizomes\, called lept omorph. As a result\, individuals are spatially intermingled each other. H ow these types of rhizome emerged in the evolutionary history and how the geographic correlation between flowering interval and rhizome system has b een formed remains elusive. In this talk\, using spatially explicit mathem atical model\, we explore the evolution of rhizome system in heterogeneous environment. We demonstrate that the longer rhizome is adaptive in relati vely homogeneous environment\, and short rhizome can evolve only when spat ial autocorrelation of the quality of environment is high. We also demonst rate that flowering interval affects the evolution of rhizome length\, in which long rhizomes are favoured when flowering interval is long. In addit ion to this\, rhizome system\, in turn\, affects the evolution of flowerin g time.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/72/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/72/ END:VEVENT BEGIN:VEVENT SUMMARY:Understanding pattern formation in interacting cell populations DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-44@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Edward Green (University of Adelaide)\nTissue develo pment requires cells of different types to organise themselves into the ap propriate patterns and structures to produce viable\, functional tissue. S imilar processes occur in tissue repair (e.g. wound healing) or when tissu es are grown in vitro (tissue engineering). Understanding how this organis ation is coordinated is therefore an important basic problem in biology an d medicine.\n\nI will present results from agent-based modelling of intera cting cell populations\, and illustrate how different interactions between the cells affect the patterns of cell organisation observed in tissues. I will explain how these patterns can be quantified using pair-correlation functions\, and discuss the extent to which we can infer cell interactions from observed tissue-scale patterns.\n\nhttps://conferences.maths.unsw.ed u.au/event/2/contributions/44/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/44/ END:VEVENT BEGIN:VEVENT SUMMARY:Fast algorithms for the dense matrices arising from the Method of Regularized Stokeslets DTSTART;VALUE=DATE-TIME:20180709T060000Z DTEND;VALUE=DATE-TIME:20180709T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-40@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Minghao Rostami (Syracuse University)\nThe swimming motion of microorganisms such as sperm and cilia can be modelled by severa l methods\, all of which entail solving equations of fluid-structure inter action. Among them\, the Method of Regularized Stokeslets (MRS) and the Ro tne-Prager-Yamakawa tensor have the advantage of not requiring a 3D Euleri an grid and using the fundamental solutions to the underlying equations in stead. However\, the computations required by both methods entail the use of dense matrices\, and they tend to be large and very costly to work with for practical models in which the number of micro-swimmers is large. \n\n The 'data-sparse' structure of these matrices enables the development of f ast algorithms. To compute the matrix-vector products efficiently\, we ext end the Kernel-Independent Fast Multipole Method (KIFMM) to the kernels as sociated with the MRS. To solve linear systems with the same matrices eff iciently\, we consider both a data-sparser preconditioner and a block-diag onal preconditioner\; to expedite the application of the preconditioners\, we employ a number of techniques such as Krylov subspace recycling. We ap ply the proposed algorithms to study the dynamics of a large group of sper m and the flow field induced by a carpet of cilia.\n\nhttps://conferences. maths.unsw.edu.au/event/2/contributions/40/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/40/ END:VEVENT BEGIN:VEVENT SUMMARY:Campaigning to reduce ivory demand – is it cost effective? DTSTART;VALUE=DATE-TIME:20180709T052000Z DTEND;VALUE=DATE-TIME:20180709T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-327@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Matthew Holden (University of Queensland (UQ))\, Dua n Biggs (Griffith University)\nIllegal exploitation of wildlife is one of the biggest threats to biodiversity\, affecting over 2\,000 species. Tradi tionally\, actions to reduce poaching have focussed on increasing the effi cacy and capacity of law enforcement. However\, recently\, non-governmenta l agencies (NGOs) are heavily investing in alternative interventions to re duce consumer demand for poached wildlife products. But which action is mo re efficient\, policing or demand reduction? Using elephant poaching for i vory as a case study\, and a simple open-access harvest model\, we show th at demand reduction interventions need to reduce ivory price by roughly 29 % to be more cost-effective than investing in the police. We use an analyt ic derivation to show that this threshold is robust to several types of un certainty but sensitive to specific socio-economic factors. The calculatio ns can provide context for stakeholder engagement so that monitoring of iv ory price can better inform decisions for protecting elephants from poachi ng.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/327/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/327/ END:VEVENT BEGIN:VEVENT SUMMARY:A deficiency zero theorem for a class of power law kinetic systems with independent decompositions DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-10@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Angelyn Lao (De La Salle University)\nIn this paper\ , we study power law kinetics on chemical reaction networks with Independe nt decompositions\, i.e. the network is the union of subnetworks whose rea ction sets form a partition of the network's reaction set and the network' s stoichiometric subspace is the direct sum of the stoichiometric subspace s of the subnetworks. Our main result is a Deficiency Zero Theorem when th e subnetworks are weakly reversible and have linear independent reactant c omplexes (we denote the latter property as “zero reactant deficiency”) and have kinetics with linear Independent kinetic order vectors (we denot e this set of kinetics with “PL-RLK”). We elaborate the context of our result by presenting an overview of previous results on network decomposi tion (which we propose to call “Decomposition Theory”) and a discussio n of existing Deficiency Zero Theorems. To our knowledge\, our result is t he first Deficiency Zero Theorem which is valid for a class of kinetics wh ich display non-reactant determined kinetic orders\, i.e. there are reacta nt complexes whose branching reactions have differing kinetic order vector s (we call this set of kinetics “PL-NDK”). In previous work\, we showe d the occurrence of PL-NDK kinetics in numerous models of complex biochemi cal systems. We apply our results to characterize the positive equilibria of a power law approximation of R. Schmitz's model of the earth's carbon c ycle in its pre-industrial state\, which provided the original motivation for our study.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributi ons/10/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/10/ END:VEVENT BEGIN:VEVENT SUMMARY:When Google meets Lotka-Volterra DTSTART;VALUE=DATE-TIME:20180712T053000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-140@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Lewi Stone (RMIT/Tel Aviv University)\nIn his theore tical work of the 70’s\, Robert May introduced a Random Matrix Theory (R MT) approach for studying the stability of large complex biological system s. Unlike the established paradigm\, May demonstrated that complexity lea ds to instability in generic models of biological networks having random i nteraction matrices A. Similar random matrix models have since been applie d in many disciplines. Central to assessing stability is the “circular l aw” since it describes the eigenvalue distribution for an important clas s of random matrices\, $A$. However\, despite widespread adoption\, the “circular law” does not apply for ecological systems in which density- dependence operates (i.e.\, where a species growth is determined by its de nsity). Instead one needs to study the far more complicated eigenvalue dis tribution of the community matrix $S=DA$\, where $D$ is a diagonal matrix of population equilibrium values. Here we obtain this eigenvalue distribut ion. We show that if the random matrix\, $A$\, is locally stable\, the com munity matrix\, $S=DA$\, will also be locally stable\, providing the syste m is feasible (i.e.\, all species have positive equilibria $D>0$). This he lps explain why\, unusually\, nearly all feasible systems studied here are locally stable. Large complex systems may thus be even more fragile than May predicted\, given the difficulty of assembling a feasible system. The degree of stability\, or resilience\, was found to depend on the minimum equilibrium population\, rather than factors such as network topology. Fo r studying competitive and mutualistic systems\, our analysis is only achi evable upon introducing a simplifying “Google-matrix” reduction scheme . In this talk we will explain what happens “when Google meets Lotka-Vo lterra.”\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 140/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/140/ END:VEVENT BEGIN:VEVENT SUMMARY:What drives reproductive synchrony of forest trees? Testing pollen coupling\, veto and correlated environmental variation DTSTART;VALUE=DATE-TIME:20180712T010000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-70@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michał Bogdziewicz (Adam Mickiewicz University)\nTh e highly variable and synchronized production of large seed crops by plant populations\, called masting or mast seeding\, has been reported across a broad group of plant species. While there is consensus on the evolutionar y drivers of masting\, the proximate mechanisms are more controversial. Se veral hypotheses make predictions about the possible drivers of synchrony in masting species\, including density-dependent pollination success (poll en coupling)\, environmental veto\, or correlated environmental variation. The pollen coupling hypothesis predicts that weather and plant resources drive the flowering effort of trees\, which directly translates into the s ize of seed crops through efficient pollination. In contrast\, the veto hy pothesis predicts that weather affects flower to seed transition\, leading to occasional bumper crops. The recently formulated phenology synchrony h ypothesis predicts that veto can arise because of weather effects on flowe ring synchrony\, which\, in turn\, drives pollination efficiency. \n\nI wi ll first present the relationships between weather\, airborne pollen\, and seed production in common European trees\, two oak species (*Quercus petr aea* and *Q. robur*) and beech (*Fagus sylvatica*) with a 19‐yr data set from three sites in Poland. Results show that warm summers preceding flow ering correlated with high pollen abundance and warm springs resulted in s hort pollen seasons (i.e.\, high flowering synchrony) for all three specie s. Pollen abundance was the best predictor for seed crops in beech\, as pr edicted under pollen coupling. In oaks\, short pollen seasons\, rather tha n pollen abundance\, correlated with large seed crops\, providing support for the veto effect and phenology synchrony hypotheses. \n\nNext\, I will show extended the resource budget model of masting with correlated reprodu ctive failure (veto). We parametrized the model for five forest tree speci es (two oaks\, two pines\, and mountain-ash)\, and run the model for 500 y rs. In four out of five species\, among-year variation in resource gain an d correlated reproductive failure were necessary and sufficient to produce masting. In the fifth (*Quercus ilex*) veto and pollen coupling were also required. Mechanisms of masting clearly differ among species\, but enviro nmental variation may drive large-scale synchronization without any other synchronizing mechanisms in a significant pool of species.\n\nhttps://conf erences.maths.unsw.edu.au/event/2/contributions/70/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/70/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling of bacterial growth at different scales: nu merical simulations and laboratory experiments DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-227@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: David Landa Marbán (University of Bergen)\nBiofilms are sessile communities of bacteria housed in a self-produced adhesive ma trix consisting of extracellular polymeric substances (EPS)\, including po lysaccharides\, proteins\, lipids\, and DNA. [1]. Biofilm provokes chronic bacterial infection\, infection on medical devices\, deterioration of wat er quality\, and the contamination of food [2]. On the other hand\, biofil m can be used for wastewater treatment and bioenergy production [3]. In mi crobial enhanced oil recovery (MEOR)\, one of the strategies is selective plugging\, where bacteria are used to form biofilm in the high permeable z ones to diverge the water flow and extract the oil located in the low perm eable zones [4]. Therefore\, it is necessary to build mathematical models that better describe the biofilm mechanisms. One of the motivations to der ive upscaled models is to describe the averaged behaviour of the system in an accurate manner with relatively low computational effort compared to f ully detailed calculations starting at the microscale [5]. In the laborato ry\, biofilm is growth in a T-shape micro-channel. We built a mathematical model including water flux inside the biofilm and different biofilm compo nents (EPS\, water\, active bacteria\, and dead bacteria). Using the best estimate of physical parameters from the existing experiments\, we perform numerical simulations. The stress coefficient is selected to match the ex perimental results. A sensitivity analysis is performed to identify the cr itical model parameters. A reduction of the biofilm coverage area as the w ater flux velocity increases is observed. Homogenization techniques are ap plied in a strip and a tube geometry. Numerical simulations are performed to compare both upscaled mathematical models. In the macro-scale laborator y experiments\, biofilm is growth in cylindrical cores. Permeability chang es over time at different flow rates and nutrient concentrations are studi ed. Numerical simulations are performed to compare with the experimental r esults. \n\n[1] Aggarwal\, S.\, Stewart\, P. S.\, Hozalski\, R. M. (2015). Biofilm Cohesive Strength as a Basis for Biofilm Recalcitrance: Are Bacte rial Biofilms Overdesigned? *Microbiology Insights.* **8s2**\, MBI.S31444. \n[2] Kokare\, C. R.\, Chakraborty\, S.\, Khopade\, A. N.\, Mahadik\, K. R (2009). Biofillm: Importance and applications. *Indian J. Biotechnol.* * *8**\, 159-168.\n[3] Miranda\, A. F. *et al*. (2017). Applications of micr oalgal biofilms for wastewater treatment and bioenergy production. *Biotec hnol. Biofuels.* **10**\, 120.\n[4] Raiders\, R. A.\, Knapp\, R. M.\, McIn erney\, M. J. (1989). Microbial selective plugging and enhanced oil recove ry. *J. Ind. Microbiol.* **4**(3)\, 215-229.\n[5] van Noorden\, T. L.\, P op\, I. S.\, Ebigbo\, A.\, Helmig\, R. (2010). An upscaled model for biofi lm growth in a thin strip. *Water Resour. Res.* **46**\, W06505.\n\nhttps ://conferences.maths.unsw.edu.au/event/2/contributions/227/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/227/ END:VEVENT BEGIN:VEVENT SUMMARY:The metastatic reproduction number DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-22@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Thomas Hillen (University of Alberta)\nThe mathemati cal modelling of metastasis is a challenge. The occurrence of metastasis i s basically random\, hence the use of stochastic modelling seems appropr iate. We introduce a stochastic process called branched random walk with settlement to derive equations for the expected number of particles\, the variance\, the furthest particle and the extinction probability. We are ab le to identify a parameter $R_0$\, such that metastasis spread for $R_0>1$ and they die out for $R_0\n\nhttps://conferences.maths.unsw.edu.au/event/ 2/contributions/22/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/22/ END:VEVENT BEGIN:VEVENT SUMMARY:Exploring the fluid dynamics of collective pulsing behaviour in xe niid corals using the immersed boundary method DTSTART;VALUE=DATE-TIME:20180709T063000Z DTEND;VALUE=DATE-TIME:20180709T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-109@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Julia Samson (University of North Carolina at Chapel Hill)\nXeniid corals\, a family of soft corals (*Alcyonacea*)\, include s pecies displaying a unique pulsing behaviour. Within a colony\, each indiv idual polyp pulses by actively contracting and passively expanding eight t entacles\, increasing the local mixing and enhancing nutrient and gas exch ange. Using the immersed boundary method with finite elements (IBFE)\, we constructed a 3D model of a pulsing polyp. The motion of the polyp tentacl es is based on actual motion data tracked from videos of real polyps. We f ind that individual polyps pull water in radially\, mix it between their t entacles\, and expel the fluid volume in an upward jet. After validating t his 3D IBFE model against experimentally measured flow fields\, we are now using the model to numerically simulate small groups of polyps and to qua ntify the effects of collective pulsing behaviour on the local fluid dynam ics. Here\, we simulate pairs of polyps and vary the pulsing patterns (in- phase and different degrees of out-of-phase) and distance between polyps t o better understand how differences in collective pulsing behaviour affect local flow and mixing.\n\nhttps://conferences.maths.unsw.edu.au/event/2/c ontributions/109/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/109/ END:VEVENT BEGIN:VEVENT SUMMARY:Centralization in self-organized reference networks DTSTART;VALUE=DATE-TIME:20180709T064000Z DTEND;VALUE=DATE-TIME:20180709T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-344@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mariko Ito (SOKENDAI (The Graduate University for Ad vanced Studies))\nWhen one makes his/her decision\, he/she often refers to others’ opinions. We describe this situation by a network model with th e nodes representing individuals and the links representing references bet ween them. Our question is how people’s reference structure self-organiz es\, when each individual tries to provide correct answers by referring to more accurate agents.\n\nTo answer these questions\, we constructed an ad aptive network model. In the model\, in each iteration round\, each agent makes a decision sequentially on a given problem by the majority vote amon g one’s and his/her neighbors’ opinions. Since each agent makes decisi on by the majority vote\, his/her probability to find a correct answer by oneself\, which we call his/her “ability”\, is different from his/her actual probability of finding a correct answer by referring to others\, wh ich we call his/her “performance”. After the correct answer to a given problem is announced\, each agent then rewires his/her links according to the performance of the linked individuals. The rewiring rule is as follow s\; each individual monitors his/her neighbors’ performance and breaks t he link if the neighbor’s performance becomes worth than a preset thresh old. We assume that all agents adopt the same threshold. Therefore the val ue of the preset threshold represents the severity of the society. We also assume that individuals vary in their ability.\n\nIn the self-organized r eference network\, we observed the strong centralization of reference\, in which the number of one’s followers increases more than linearly with h is/her ability. Counter-intuitively\, this tendency was stronger when the rewiring threshold was set lower (when they are more generous to their ref erents). The mean performance of each agent in the self-organized network was higher compared with random networks or the case of independent decisi on-making. However\, the proportion of agents who give correct answers\, w hich we call “group performance”\, fluctuated more in the self-organiz ed network. To sum up\, in the self-organized network\, though the strong centralization of reference towards high ability agents leads to high perf ormance of each agent on average\, it also leads to a heightened risk of a temporal crash in group performance. By analytical calculations\, we have confirmed that the performance-monitoring process assumed in our model yi elds the strong centralization of reference in the self-organized referenc e network.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 344/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/344/ END:VEVENT BEGIN:VEVENT SUMMARY:Elimination dynamics of intra-hepatic malaria parasites by antigen -specific CD8+ T cells DTSTART;VALUE=DATE-TIME:20180712T011000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-316@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Harshana Rajakaruna (University of Tennessee)\nMalar ia is an infectious disease caused by parasites from genus *Plasmodium* th at kills an average of a half a million people around the world annually. *Plasmodium* sporozoites are injected to humans by mosquitoes during their probing for blood. Injected sporozoites migrate to liver and invade hepa tocytes. The liver stage that lasts 7 to 10 days is a target for vaccine development for humans using antigen-specific killer CD8+ T cells. Howeve r\, how CD8+ T cells kill parasites in the liver is not fully understood. Here\, we investigate how the numbers of CD8+ T cells\, clustering around the rodent malaria parasite\, *P. yoelii* (Py)\, in the mouse liver\, is r elated to the likelihood of parasites’ death. We use previously publish ed data on the viability of GFP-expressing Py-sporozoites and the movement patterns of Py-specific T cells\, obtained using intravital microscopy. The data are compared with mathematical models that incorporate different mechanisms of how T cells cluster around Py-infected hepatocytes\, and T c ells kill the parasite\, with the ultimate goal of predicting the optimal number of T cells needed to kill the parasite in a given time period (live r stage lasts 2 days in mice). Preliminary analyses indicate that there is a functional relationship between the states of the vitality indices\, wh ich is measured as the relative intensity of the GFP of the labeled parasi tes\, and the number of T cells near the parasites. We will present the da ta and alternative models that could fit and fail to fit the data to under stand the underlying dynamics of the killing process. We will also outline the limitations of the current data and provide details for future experi mentations with sufficient power to discriminate between alternative model s.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/316/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/316/ END:VEVENT BEGIN:VEVENT SUMMARY:Growth-induced buckling in elastic rods DTSTART;VALUE=DATE-TIME:20180709T064000Z DTEND;VALUE=DATE-TIME:20180709T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-329@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Axel Almet (University of Oxford)\nMechanically-indu ced buckling underlies the shape and function of a number of biological pr ocesses\, such as brain tissue folding\, intestinal crypt fission\, and se ashell formation. Unlike many typical engineering systems in which bucklin g is induced by an external compressive load\, mechanical instability in b iology is driven often by internal growth. In these contexts\, it is just as important to consider how the system evolves beyond the onset of instab ility\, as it is to understand when the instability occurs initially. \n\n In this talk\, we consider a growing\, planar\, elastic rod supported by a n elastic foundation\, as an appropriate starting point a number of possib le biological systems. We analyse the post-buckling behaviour through a co mbination of weakly nonlinear analysis and numerical methods. The effect o f different material parameters on the type of buckling and the buckled sh ape is shown. We then examine how spatial heterogeneity in substrate adhes ion\, elastic rod stiffness\, and growth\, impacts both the instability an d resultant post-buckled shape evolution. These heterogeneities are contra sted with heterogeneity within the foundation shape\, echoing classical re sults by Koiter on imperfection sensitivity and failure [1]. Finally\, we discuss extensions that specialise the model to that of a buckling intesti nal crypt.\n\n[1] Van der Heijden\, Arnold MA\, ed. WT Koiter's elastic st ability of solids and structures. Cambridge: Cambridge University Press\, 2008.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/329/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/329/ END:VEVENT BEGIN:VEVENT SUMMARY:Construction of quasi-potential landscapes using the Sum-of-Square s optimisation DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-422@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Rowan Brackston (Imperial College London)\nThe const ruction of effective and informative landscapes for stochastic dynamical s ystems has proven a long-standing and complex problem\, including for biol ogical systems. Such landscapes may refer to a true energy function for ca ses such as protein folding or to a phenomenological metaphor in the case of Waddington’s epigenetic landscape. In many situations\, constructing a landscape comes down to obtaining the quasi-potential\, a scalar functio n that quantifies the likelihood of reaching each point in the state-space . \n\nIn this work we provide a novel method for constructing such landsca pes using a tool from control theory: the Sum-of-Squares method for genera ting Lyapunov functions. Applicable to any system described by polynomials \, this method provides an analytical polynomial expression for the potent ial landscape\, in which the coefficients of the polynomial are obtained v ia a convex optimisation. The resulting landscapes are based upon a decomp osition of the vector-field of the original system\, such that the inner p roduct of the gradient of the potential and the remaining dynamics is ever ywhere negative. By satisfying this condition\, our derived landscapes pro vide both upper and lower bounds on the true quasi-potential\; these bound s becoming tight if the decomposition is orthogonal. The method is impleme nted in the programming language Julia\, and is demonstrated to correctly compute the quasi-potential for high-dimensional linear systems and also f or a number of nonlinear examples. For a multi-stable stochastic system an alogous to a developing stem cell\, we use the computed potential to evalu ate bounds on the relative likelihood of reaching fixed points equivalent to each of the differentiated phenotypes.\n\nhttps://conferences.maths.uns w.edu.au/event/2/contributions/422/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/422/ END:VEVENT BEGIN:VEVENT SUMMARY:Multiphase modelling of early fibrous cap formation in atheroscler osis DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-153@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michael Watson (University of Sydney)\nAtherosclerot ic plaque growth is characterised by a process of chronic\, non-resolving inflammation that leads to the accumulation of cellular debris and extrace llular fat in the inner artery wall. In advanced plaques\, smooth muscle c ells (SMCs) are recruited from deeper in the artery wall to synthesise a f ibrous tissue cap that sequesters the thrombogenic plaque content from the bloodstream. The fibrous cap therefore provides crucial protection from p laque rupture and the formation of blood clots that occlude vessels and ca use heart attacks and strokes. Despite the important role played by the p laque fibrous cap in preventing the clinical consequences of atheroscleros is\, the mechanisms that underlie cap formation remain poorly understood. In particular\, it is unclear why certain plaques become strong and stable while others become fragile and dangerously vulnerable to rupture.\n\nIn this talk\, we discuss the use of a multiphase approach with non-standard boundary conditions to investigate early fibrous cap formation in the inti mal layer of the artery wall. We model the highly nonlinear process of SMC migration from the media in response to a diffusible chemical signal prod uced at the endothelium. Simulations indicate that the emergence of a stab le fibrous cap requires a critical balance between the relative rates of c ell supply from the media\, chemotactic migration within the intima and ce ll loss by apoptosis (or phenotype change). Moreover\, we identify a numbe r of disease-associated parameters that may be linked to variations in cap stability. This model represents the first detailed *in silico* study of fibrous cap formation in atherosclerosis\, and establishes a framework th at can be extended to investigate other aspects of plaque development.\n\n https://conferences.maths.unsw.edu.au/event/2/contributions/153/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/153/ END:VEVENT BEGIN:VEVENT SUMMARY:Quasi-steady-state approximations in the stochastic models of enzy me kinetics DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-18@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hye-Won Kang (University of Maryland\, Baltimore Cou nty)\nIn this talk I will introduce several quasi steady-state approximati ons (QSSAs) applied to the stochastic enzyme kinetics models. Different as sumptions about chemical species abundance and reaction rates lead to the standard QSSA (sQSSA)\, the total QSSA (tQSSA)\, and the reverse QSSA (rQS SA) approximations. These three QSSAs have been widely studied in the lite rature in deterministic ordinary differential equation (ODE) settings and several sets of conditions for their validity have been proposed. By using multiscaling techniques for stochastic chemical reaction networks\, these conditions for deterministic QSSAs largely agree with the ones for QSSAs in the large volume limits of the underlying stochastic enzyme kinetic net works. I will illustrate how our approach extends to more complex stochast ic networks like\, for instance\, the enzyme-substrate-inhibitor system. T his is joint work with Wasiur Khuda Bukhsh\, Heinz Koeppl\, and Grzegorz R empała.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/18 / LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/18/ END:VEVENT BEGIN:VEVENT SUMMARY:The complex effect of the evolutionary rates on generalized mutual istic communities DTSTART;VALUE=DATE-TIME:20180712T054000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-324@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Shota Shibasaki (Department of General Systems Studi es\, the University of Tokyo)\nMutualism or cooperation between and among species is ubiquitous in nature. The most well-known examples of mutualism are Müllerian mimicry and division of labour. In Müllerian mimicry\, un palatable species have evolved the similar appearances and they are less l ikely to be predated upon because the predators effectively learn that the se species are noxious. In division of labour\, each species specializes i n a special task\, such as producing different nutrients.\n\nConflict can arise in mutualism regarding the roles of each species. In Müllerian mimi cry\, it could be more advantageous to be a model species than a mimic bec ause the life cycles\, the habitats\, and the body plans of model species are innate. In devision of labour\, conflict can arise regarding species t asks\; when producing nutrient\, one type of nutrient might have a greater cost for the organism than another type of nutrient. \n\nThe effect of e volutionary rates on mutualistic symbioses with a degree of conflict has b een conceptualized using the snowdrift game. Bergstrom and Lachmann (2003) [1] have found that in a model of the mutualistic symbiosis between two s pecies\, the slower evolution can be favoured. This effect was named Red K ing effect\, which is converse to Red Queen effect\, where the faster evol ution is favoured mainly in\, but not restricted in\, antagonistic symbios es.\n\nMutualism\, however\, can involve more than two species. In the con text of the mimicry\, such phenomenon is known as the Müllerian mimicry r ing. Mutual symbioses with devision of labour are not always limited in on e-to-one relationship. For example\, green algae can display mutualism wit h several phylogenetically broad fungal species.\n\nIn this study\, the or iginal model in Bergstrom and Lachmann (2003) was expanded by generalizing the number of species $ M $ ($ M \\ge 2 $) in a community. In this model\ , Red Queen effect can shift to Red King effect and vice versa over time. For example\, when $M=3$\, Red Queen effect can remain until one species ( in many cases\, the fastest-evolving species) fixes its strategy\, after w hich Red King effect comes into play and the slowest-evolving species is f avoured. As a result\, the fastest- and slowest-evolving species exploit t he remaining species.\n \nThis result suggests the complexity of the effec t of evolutionary rates on mutualistic coevolution. Even when differences in evolutionary rates of two species are determined\, predicting which spe cies is more likely to exploit the other is challenging\, because a third species with which both species mutually interact could also have an evolu tionary effect on the other two species.\n\n[1] Bergstrom\, C. T.\, and La chmann\, M. (2003). The Red King effect: When the slowest runner wins the coevolutionary race. *PNAS*\, **100**\, 2\, 593-598.\n\nhttps://conference s.maths.unsw.edu.au/event/2/contributions/324/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/324/ END:VEVENT BEGIN:VEVENT SUMMARY:A multiphase model of glioblastoma multiform onset and growth DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-195@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Harsh Jain (Florida State University)\nPatients diag nosed with glioblastoma multiforme (GBM) are expected to survive only 14 m onths and die due to the pressure that the tumour builds in the brain as w ell as the formation of peritumoural edema (PTE). With the view to investi gating the early stages of brain tumour development\, and how it impacts t he healthy brain environment\, we develop a mechanistic model of GBM onset . The model is derived using principles of mass and momentum balances and explicitly includes pressure dynamics within the disease brain and the abi lity/inability of healthy tissue to repair itself in response to these cue s. As a first step we assume an implicit tumour that exerts pressure at a healthy boundary causing the boundary to move into healthy tissue with a v elocity $v$ (thought of as the tumour growth rate). We investigate three v elocity regimes: where $v$ is an order of magnitude slower than the time-s cale of healthy brain tissue renormalization (benign tumour)\; where $v$ i s an order of magnitude higher than the time-scale of healthy brain tissue renormalization (high grade tumour)\; a transition between these where $v $ is the same magnitude as the time-scale of healthy brain tissue renormal ization. Our model shows a correlation between the tumour velocity and the formation of PTE\, which is an indicator of tumour malignancy. The result ing model includes time-varying diffusion on a moving domain\, which prese nts unique numerical challenges. We propose a scheme to solve such equatio ns\, validating our method with a test problem as well as theoretical anal ysis using techniques from asymptotic methods in order to complete this re search aim.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions /195/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/195/ END:VEVENT BEGIN:VEVENT SUMMARY:Cell fate decision in $\\textit{Chlamydia Trachomatis}$ DTSTART;VALUE=DATE-TIME:20180711T021000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-328@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: German Enciso (UC Irvine)\n*Chlamydia trachomatis* i s the most common cause of bacterial sexually transmitted infection. It c an also infect the eyes and is a major cause of blindness in many developi ng countries. During the infection of a mammalian host\, Chlamydia must d ecide when to proliferate and when to convert into a differentiated form\, since the differentiated form is the only form to survive outside the hos t but cannot reproduce. We study the question of Chlamydia cell fate regu lation using experimental data as well as stochastic mathematical modellin g.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/328/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/328/ END:VEVENT BEGIN:VEVENT SUMMARY:Tumour-immune cells interaction shapes tumour morphology: evolutio nary process drives mutations for emerging hallmarks DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-52@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Elena Piretto (Politecnico di Torino)\nThe idea of c ancer as an evolutionary disease is well established. Cancer development i s driven by mutation and selective forces\, including the action of the im mune system\, interspecific competition and therapies. Different tumour ty pes exhibit resistance to the immune system suggesting the investigation o f different aspects of the tumoural microenvironment to better understand cancer.\n\nThe tumoural tissue is composed of different phenotypes\, occur red from genetic and epigenetic mutations and fixed by Darwinian selection . Evolutionary niches\, set up by the competition-coexistence of different cancer clones and by the action of the immune system\, can shape tumour f orm. An analysis of the tumoural morphology can help to classify cancer ty pes\, suggesting a ways to increase the effectiveness of the medical treat ments.\n\nThe aim of this talk is to present a hybrid mathematical model c omprising of an agent based model for the tumour-immune interaction and a system of delay differential equations for the T-cell activation cycle. Di fferent tumour microenvironments are shown to influence the morphological evolution of the tumoural tissue and the genetic instability leading to cr ucial mutations. Shapes are correlated to different evolutionary outcomes that can be altered by therapies. Further\, different treatments induce mo difications to the environment and then to the final outcomes. In particul ar\, immunotherapy cycles and molecular target therapy are studied. Finall y\, a statistical analysis of the model is used to discuss the reliability and the reproducibility of the outcomes.\n\nhttps://conferences.maths.uns w.edu.au/event/2/contributions/52/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/52/ END:VEVENT BEGIN:VEVENT SUMMARY:Dynamic model predicting overweight and obesity in Korean adolesce nts DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-250@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Chunyoung Oh (Chonnam National University)\nObesity is the result of caloric imbalance and is mediated by genetic\, behavioura l\, and environmental factors. Healthy lifestyle habits\, including health y eating and physical activity\, can lower the risk of becoming obese and developing related diseases. The prevalence of obesity among Korean adoles cents aged 13 to 18 years increased from 13.65% in 2007 to 19.3% in 2016 f or boys.\n\nWe analyze trends in adolescents obesity for 6 years and esti mate of adolescents obesity. We adopt the well-known SIR model structure f or infectious diseases. A differential equation system predicted adolescen ts' obesity prevalence trends. The model considers both social environment and obesogenic environment influences on weight gain\, incorporates other known parameters affecting obesity trends.\n\nThe dynamic model predicts that obesity prevalence will plateau independent of current prevention str ategies. The proportion of overweight is lower in middle school than in hi gh school\, but obesity is higher in high school. The adolescents prevalen ce of overweight and obesity for boys will plateau by about 2025 at 6% and 27% respectively.\n\n[1] H. Pontzer\, R. Durazo-Arvizu\, *et al.*\, Const rained Total Energy Expenditure and Metabolic Adaptation to Physical Activ ity in Adult Humans\, *Current Biology*\, 26 (2016)\, 410-417. \n[2] Dian a M. Thomas\, Marion Weedermann\, *et al*.\, Dynamic Model Predicting Ove rweight\, Obesity\, and Extreme Obesity Prevalence Trends\, *Obesity*\, Vo l 22\, Num. 2\, (2014) pp.590-48. www.obesityjournal.org.\n[3] https://yh s.cdc.go.kr/new/pages/pds1.asp\, (2016) (accessed 2017.05.01)\n\nhttps://c onferences.maths.unsw.edu.au/event/2/contributions/250/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/250/ END:VEVENT BEGIN:VEVENT SUMMARY:Three-dimensional excitable wave dynamics depend on the cell geome try in $\\textit{Dictyotelium}$ cells DTSTART;VALUE=DATE-TIME:20180709T020000Z DTEND;VALUE=DATE-TIME:20180709T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-197@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tatsuo Shibata (RIKEN Quantitative Biology Center)\n Phosphatidylinositol (3\,4\,5)-trisphosphate (PtdInsP3) is known to propag ate as waves on the plasma membrane and is related to the membrane protrus ive activities in *Dictyostelium* and mammalian cells. While there have be en a few attempts to study their three dimensional dynamics\, most of thes e studies focused on the dynamics extracted in one dimensional sections al ong the membrane in a single focal plane. However\, the relation between t he dynamics and three-dimensional cell shape remain elusive due to the lac k of signalling information on the remaining non-observed part of the memb rane. Here\, we show that PtdInsP3 wave dynamics are directly regulated by the three-dimensional geometry - size and shape - of the plasma membrane. By introducing an analysis method that extracts the three-dimensional spa tiotemporal activities on the entire cell membrane\, we show that PtdInsP3 waves self-regulate their dynamics within the confined membrane area lead ing to changes in speed\, orientation and pattern evolution following the underlying excitability of the signal transduction system. Our findings em phasize the role of the membrane topology in reaction-diffusion driven bio logical systems and indicate the importance of the plasma membrane topolog y in other mammalian systems.\n\nhttps://conferences.maths.unsw.edu.au/eve nt/2/contributions/197/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/197/ END:VEVENT BEGIN:VEVENT SUMMARY:Strong inference in mathematical modelling: a new twist to an old idea DTSTART;VALUE=DATE-TIME:20180711T052000Z DTEND;VALUE=DATE-TIME:20180711T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-218@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Vitaly Ganusov (University of Tennessee)\nWhile ther e are many opinions on what mathematical modelling in biology is\, in esse nce\, modelling is a mathematical tool which allows consequences to logica lly follow from a set of assumptions. Only when this tool is applied appr opriately\, it may allow to understand importance of specific mechanisms/a ssumptions in biological processes. Mathematical modelling can be less us eful or even misleading if used inappropriately\, for example\, by creatin g a false impression of a good understanding of biological processes. It h as been argued that the best use of mathematical models is not when a mode l is used to confirm a hypothesis but rather when a study shows inconsiste ncy of the model (defined by a specific set of assumptions) and data. Fol lowing the principle of strong inference for experimental sciences propose d by Platt\, I suggest “strong inference in mathematical modelling” as an effective and robust way of using mathematical modelling to understand mechanisms driving dynamics of biological systems. The major steps of str ong inference in mathematical modelling are 1) to develop multiple alterna tive models for the phenomenon in question\; 2) to compare the models with available experimental data and to determine which of the models are not consistent with the data\; 3) to determine reasons why rejected models fai led to explain the data\, and 4) to suggest experiments which would allow to discriminate between remaining alternative models. The use of strong i nference is likely to provide better robustness of predictions of mathemat ical models and it should be strongly encouraged in mathematical modelling -based publications in the 21st century.\n\nhttps://conferences.maths.unsw .edu.au/event/2/contributions/218/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/218/ END:VEVENT BEGIN:VEVENT SUMMARY:Explaining lazy workers in social insect colonies with evolutionar y game theory DTSTART;VALUE=DATE-TIME:20180710T005000Z DTEND;VALUE=DATE-TIME:20180710T011000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-333@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Julian Garcia (Monash University)\nIn social insect colonies we often observe substantial levels of laziness\, i.e.\, workers that do not engage or appear not to engage in any tasks. This is puzzling \, because colonies with lazy individuals seem to be wasteful and may not be using their resources optimally. A common hypothesis is that lazy worke rs are a reserve workforce that can be quickly activated when rapid change s in the environment demand it. \n\nWe present an alternative explanation for laziness based on game theory. We assume that insects play a game in w hich they allocate their energy towards two competing tasks\, foraging and temperature regulation. Both tasks need to be performed successfully for colony survival\, thus the set-up reflects a coordination game.\n\nThe ben efits of regulation are assumed to be concave and maximised at intermediat e levels of task engagement. The benefits of foraging are assumed to be li near in effort. Benefits are shared by the whole colony\, whereas costs ar e borne individually. Individuals learn to play this game by using social learning\, and occasionally experimenting with new strategies. When experi mentation is rare the population is monomorphous most of the time\, and th e learning trajectories of colonies can be modelled by using adaptive dyna mics. Levels of laziness in the long run can be determined by studying the fixed points of the dynamics.\n\nWe find that the level of laziness cruci ally depends on the costs of performing the tasks. In particular\, lazines s can be stable under marginally increasing costs. Constant and marginally decreasing costs result in colonies without lazy individuals. Monte Carl o simulations show that our theoretical prediction is accurate under moder ate levels of noise.\n\nOur model is the first one to link specific ecolog ical features to the puzzle of lazy workers. We discuss potential implicat ions for empirical work and extensions of the model.\n\nhttps://conference s.maths.unsw.edu.au/event/2/contributions/333/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/333/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling saliva secretion DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-258@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Elias Siguenza (University of Auckland)\nWe construc ted a dynamical model of a salivary gland acinar cell with the objective o f investigating the role of two plasma membrane (PM) anion exchangers\, th e Ae2 (Slc4a2) and Ae4 (Slc4a9)\, in primary fluid secretion. Transepithel ial chloride (Cl$^-$) movement drives water transport in salivary gland ac inar cells. Basolateral PM mechanisms accumulate Cl$^-$ to levels well abo ve its electrochemical equilibrium. Following an increase in the intracell ular concentration of calcium (Ca$^{2+}$)\, a Cl$^-$ efflux through apical Ca$^{2+}$-dependent Cl$^-$ channels (TMeM16a) generates a transepithelial osmotic gradient. Water follows this gradient by osmosis. Cl$^-$ uptake v ia basolateral co-transporters (Nkcc1)\, provides the major force for gene rating fluid secretion in acinar cells. Despite this\, Nkcc1 knockout expe riments saw an approximate 70$\\%$ decrease in gland salivary rate. The re sidual secretion is bicarbonate (HCO$_3^-$) dependent and involves two sod ium/proton (Nhe1) paired Cl$^-$/HCO$_3^-$ anion exchangers\, the Ae2 and t he Ae4. Experiments revealed that Ae4 knockout mice displayed a decreased gland fluid secretion ($\\sim$ 30$\\%$ of the control fluid flow rate) whi lst Ae2 knockout mice gland salivation remained intact. The reason behind the results remains a controversial topic. Our model's results reproduce a nd support the experimental observations. More importantly\, they suggest that the Ae4 cotransport of monovalent cations is likely to be important i n establishing the osmotic gradient necessary for optimal transepithelial fluid movement.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribut ions/258/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/258/ END:VEVENT BEGIN:VEVENT SUMMARY:Investigating the role of iron in cancer progression via a multisc ale computational model DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-495@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Reinhard Laubenbacher (UConn Health)\nIt is becoming increasingly clear that tumour cells recruit cells in their surrounding m icroenvironment to aid in their proliferation. Tumour-associated macrophag es and stromal cells are now believed to play a prominent role in tumour g rowth. Some evidence points to the fact that iron is a key player in the c omplex interactions between cancer cells and the microenvironment. This ta lk will present a computational model of tumour growth investigating the r ole of iron and the tumour microenvironment in tumour progression. Further more\, the talk will describe how data gathered from a bioprinter will be used to calibrate the model.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/495/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/495/ END:VEVENT BEGIN:VEVENT SUMMARY:The relationship between blood flow\, oxygen consumption and blood oxygen levels during transient local activation of the cerebral cortex DTSTART;VALUE=DATE-TIME:20180711T020000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-145@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Timothy Secomb (University of Arizona)\nTransient ac tivation of a region of the brain cortex results in an increase in the loc al rate of oxygen consumption\, and stimulates an increase in blood flow t o the stimulated region\, a phenomenon known as neurovascular coupling. Un der normal conditions\, the relative increase in blood flow during activat ion is observed to exceed the relative increase in oxygen consumption\, by a factor $n>1$. As a consequence\, the oxygen content of blood in the sti mulated region increases. The associated change in hemoglobin saturation f orms the basis for the blood oxygen level dependent (BOLD) signal detected during functional magnetic resonance imaging (fMRI) of the brain. Despite the extensive use of this technique\, its physiological basis is incomple tely understood. While MRI techniques allow simultaneous observations of l ocal cerebral blood flow (CBF) and the BOLD signal\, oxygen consumption ra te cannot be measured with similar spatial and temporal resolution. Here\, a Krogh-cylinder-type theoretical model was used to analyze the relations hip between blood flow\, oxygen consumption and hemoglobin saturation duri ng transient activation of rat somatosensory cortex. The equations for tim e-dependent convection and diffusion of oxygen in the blood and tissue wer e solved using the finite-element method. Experimental data [1] on variati on in blood flow and hemoglobin saturation were used to deduce parameters describing the time-dependent variation in oxygen consumption rate. The va lue of $n$ was found to be approximately 3\, consistent with observations in other experimental models. Experimental BOLD signals show a brief initi al dip in hemoglobin saturation at the start of activation\, although this is not consistently observed. In the simulations\, such an initial dip wa s predicted and shown to be sensitive to the timing of the increase in flo w relative to the increase in consumption. This theoretical model provides a method for deducing time-varying oxygen consumption rate from BOLD fMRI observations of the locally stimulated cerebral cortex. Such data can be used to investigate the dynamical characteristics of neurovascular couplin g. \n\n[1] Masamoto *et al.*\, *NeuroImage* 40:442\, 2008\n\nSupported by NIH grant HL133362.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contr ibutions/145/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/145/ END:VEVENT BEGIN:VEVENT SUMMARY:Studying the effect of pre-exposure prophylaxis on the dynamics of different populations susceptible to HIV DTSTART;VALUE=DATE-TIME:20180712T052000Z DTEND;VALUE=DATE-TIME:20180712T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-265@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Renee Dale (Louisiana State University)\nPre-exposur e prophylaxis is a useful method for the preventing the transmission of HI V to susceptible individuals. What target population would provide the big gest impact on HIV dynamics? To answer this question\, we present a differ ential equation model stratified by behavioural risk and sexual activity. Some susceptible individuals have higher rates of risky behaviour that inc rease their chance of contracting the disease. Similarly\, infected indivi duals with risky behaviours are at higher risk of transmitting the disease to a susceptible individual. We further divide the infected population by their diagnosis status. We define model parameters for both the urban cas e\, or high-density sexual network\, and the national case\, or mixture of low- and high-density sexual network. Our results indicate that the undia gnosed high-risk infected group is the largest contributor to the epidemic . Our model suggests that when pre-exposure prophylaxis is applied to the susceptible populations\, its effectiveness extends outside of the group t hat is taking the drug\, providing herd immunity. Our models suggest that a strategy targeting the high-risk susceptible population would have the l argest impact. We also find that such a protocol has similar effects for t he national and the urban case\, despite the smaller sexual network found in rural areas. To further analyze the effect of herd immunity and network density\, we simulate our model using a random walk. The parameters are s ummarized and reduced to include sexual contact rate\, behaviour riskiness \, medication adherence\, and diagnosis rate. These parameters are describ ed using probability distributions\, and the status of an individual at ea ch iteration is determined by random draws from those distributions and a control equation. Susceptible individuals’ adherence to pre-exposure pro phylaxis modifies their transmission risk term. We simulate under both urb an and national network conditions\, as well as low-density or rural sexu al network conditions. The effect of different adherence distributions is also analyzed over varying proportions of susceptible individuals on pre-e xposure prophylaxis medications. We hope this method will better illuminat e the herd immunity effect provided by targeting high-risk susceptible ind ividuals on different sexual networks.\n\nhttps://conferences.maths.unsw.e du.au/event/2/contributions/265/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/265/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal control of MANF to prevent apoptosis in Retinitis Pigmento sa DTSTART;VALUE=DATE-TIME:20180711T063000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-102@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Luis Melara (Shippensburg University)\nProtein misfo lding is one of the major causes of apoptosis in Retinitis Pigmentosa\, wh ere apoptosis is programmed cell death. Mesencephalic-Astrocyte-derived-Ne urotrophic Factor (MANF) is a protein that has been shown to correct prote in misfolding\, thus reducing the death of cells due to “cell suicide” . In this talk\, we formulate an optimal control problem that incorporat es MANF treatment to rescue photoreceptors in the eye. Numerical results are shown and discussed.\n\nhttps://conferences.maths.unsw.edu.au/event/2 /contributions/102/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/102/ END:VEVENT BEGIN:VEVENT SUMMARY:Influence of sex-specific dispersal on local sex ratio\, mating su ccess and spatiotemporal population dynamics DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-101@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Chun-Chia Chou (Research School of Biology\, Austral ian National University)\nSexual dimorphism (SD)\, sexual differences in t raits\, represents one of the most remarkable source of biodiversity in th e world. In most of species\, two sexes play different roles in reproducti on and thus are imposed by selection pressures in different forms and stre ngths. This explains the generality of this phenomenon and the extensive a pplicability of SD theory in nature. In this talk\, I will provide an exam ple demonstrating how sexual differences in the dispersal strategy can inf luence metapopulation dynamics. We developed a sex-structured two-patch mo del and specified that two sexes have different decision-making processes according to the accessibility of reproductive resources\; in brief\, fema les move to the patch with more breeding sites (i.e. carrying capacity min us local population size) whereas males move to the patch with more mating opportunities (i.e. unmated females). Such assumption is valid given that sex-specific dispersal has been commonly recorded in natural systems. Our simulation results illustrated how sex-specific dispersal increased or de creased local population size through changes in local sex ratio and indiv idual reproductive success\; notably\, such results were not able to be ge nerated through conventional\, asexual metapopulation models. We advocate that incorporating the perspective of SD into population dynamic models ar e needed and it can advance our knowledge of population dynamics by disclo sing detailed mechanisms underlying population processes.\n\nhttps://confe rences.maths.unsw.edu.au/event/2/contributions/101/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/101/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical dynamics of clustered ventilation defects in asthmati cs DTSTART;VALUE=DATE-TIME:20180709T080000Z DTEND;VALUE=DATE-TIME:20180709T081500Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-392@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Austin Ibarra (University of Auckland)\nAsthma is a chronic lung disease of reversible airway constriction. Imaging experiment s show that during an asthma attack\, the asthmatic's lung exhibits what i s known as clustered ventilation defects\, which is the hallmark trait of asthma. This phenomenon is when there are some regions of the lung where t he airways are closed\, and some regions where they are open. These cluste rs vary from event to event\, even in the same patient\, and thus it is be lieved that the causes are dynamic rather than structural. We want to unde rstand the dynamic mechanisms behind the physiological implications. Diffe rent mechanisms leading to spatial clustering have been suggested\; we are interested in assessing the physiological viability of some of these mode ls\, particularly with how each model exhibits this spatial clustering. Du ring this talk\, we will go over these models and how they have shown them selves to be different in the dynamics analysis.\n\nhttps://conferences.ma ths.unsw.edu.au/event/2/contributions/392/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/392/ END:VEVENT BEGIN:VEVENT SUMMARY:Quantifying and modelling epithelial morphogenesis DTSTART;VALUE=DATE-TIME:20180709T053000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-6@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kaoru Sugimura (Kyoto University)\nIn the course of animal development\, the shape of macroscopic tissues emerges from collect ive cell dynamics. The challenge faced by researchers in the field is to u nderstand the mechanism by which morphogenetic processes of each individua l cell (i.e.\, when\, where\, and how much individual cells grow\, divide\ , move\, and die) collectively lead to the development of a large tissue w ith its correct shape and size.\n\nAnswering this question requires a coar se-grained description and modelling of cell and tissue dynamics at an app ropriate length scale. In a previous study\, we developed coarse-grained m easurement methods for stress and kinematic fields. These methods are now emerging as powerful tools used for exploring the mechanics of epithelial tissues. Given the advancement of experimental measurement methods\, one c an expect that a theoretical model for kinematics and kinetics in a deform ing tissue\, which can be compared with the experimentally observable fiel ds\, will further advance our understanding of the mechanical control of t issue morphogenesis.\n\nHere\, we present a new continuum model of epithel ial mechanics. This model incorporates stress and deformation tensors\, wh ich can be compared with experimental data. Using this model\, we elucidat ed dynamical behaviour underlying passive relaxation\, active contraction- elongation\, and tissue shear flow. This study provides an integrated sche me for the understanding of the orchestration of morphogenetic processes i n individual cells to achieve epithelial tissue morphogenesis.\n\nhttps:// conferences.maths.unsw.edu.au/event/2/contributions/6/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/6/ END:VEVENT BEGIN:VEVENT SUMMARY:Multiscale modelling accurately predicts $\\textit{in vivo}$ respo nse of combined IL-6 blockade and traditional chemotherapy in stem cell dr iven cancers DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-25@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Trachette Jackson (University of Michigan)\nIt is we ll known that growth and survival of cancer stem cells (CSCs) is highly i nfluenced by tumour microenvironmental factors and molecular signalling\, initiated by cytokines and growth factors. IL-6 is a key regulator of a n umber of cellular processes including proliferation\, survival\, different iation\, migration and invasion and it is also commonly overexpressed in m any cancers. Recent evidence shows that IL-6 is not only secreted by tumou r cells\, but is produced at even higher levels by endothelial cells (ECs) . Research shows that high intratumoural levels of IL-6 enhance the survi val\, self-renewal and tumour initiation potential of cancer stem cells. T hese studies of the impact of IL-6 on CSCs provide strong motivation for t he development of anti-IL-6 therapies for the targeted treatment of stem c ell driven cancers. \n\nIn this talk\, a multi-scale mathematical model t hat operates at the intracellular\, molecular\, and tissue level is develo ped in order to investigate the impacts of endothelial cell-secreted IL-6 signalling on the crosstalk between tumour cells and ECs during tumour gro wth. This endothelial cell-tumour cell (EC-TC) model is used to study the therapeutic impact of Tocilizumab (TCZ)\, a competitive IL-6R inhibitor\, on tumour growth and cancer stem cell (CSC) fraction\, alone and in combin ation with the traditional chemotherapeutic agent\, Cisplatin. The approac h used here is novel in that it includes full receptor occupancy dynamics between endothelial-cell produced IL-6\, IL-6R\, and TCZ. Validation is achieved by directly comparing model predictions to data generated by a se ries of *in vivo* experiments. This multiscale approach provided excellent predictive agreement with the decrease in tumour volumes\, as well as a d ecrease in CSC fraction.\n\nTargeting key regulators of the cancer stem ce ll phenotype to overcome their critical influence on tumour growth is a pr omising new strategy for cancer treatment. This predictive modelling fram ework can serve to rapidly evaluate dosing strategies for IL-6 pathway mod ulation\, as well as providing the basis for proposing combination treatme nts with IL-6 blockade and cytotoxic or other targeted therapies.\n\nhttps ://conferences.maths.unsw.edu.au/event/2/contributions/25/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/25/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal control in a pharmacokinetics/pharmacodynamics model of do ripenum DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-120@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Stephen Wirkus (Arizona State University)\nPharmacok inetics (PK) describes a drug's affect on a medium (such as bacteria or tu mours) while pharmacodynamics (PD) describes how a drug moves throughout a nd is processed by the body (along with changes in drug concentration). Ta ken together\, these models are known as PK/PD models and ordinary differe ntial equations (ODE) are used to describe the system. We consider an exis ting model in the literature of the drug doripenem affect on the bacteria *P. aeruginosa* that considers the count of bacteria and resting bacteria in the central and peripheral compartments of the body. Dosing strategies tend to differ depending on the disease being treated\; however\, a consis tent factor in treatments is an administration of 500mg for one hour\, eve ry eight hours. Treatments of this nature tend to reach concentration leve ls of 50mg/ml\, before tapering off. Exceeding the 500mg dose brings incre ased risk of seizures\, among other dangerous side effects including heada ches\, nausea\, diarrhea\, rashes\, phlebitis\, and anemia. We use control theory to search for an optimal dosing strategy and compare the results t o that of the standard every-eight-hours administration. Our results show that the amount of drug needed in the control case is considerably less c ompared to standard dosing and that we can easily find situations in which the same amount of drug administered in the standard way will not kill th e bacteria but administered in the optimal manner will kill the bacteria. This has potential significance in the case of immune compromised patient s that may not be able to tolerate a standard dosing strategy.\n\nhttps:// conferences.maths.unsw.edu.au/event/2/contributions/120/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/120/ END:VEVENT BEGIN:VEVENT SUMMARY:$R_0$ centrality in metapopulation networks: finding the epidemiol ogical and evolutionary hotspots DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-156@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Akira Sasaki (The Graduate University for Advanced S tudies (SOKENDAI))\nIdentifying the epidemiological key-stone communities in a metapopulation network is primarily important in designing efficient control against an infectious disease. Various network centrality measures commonly utilized for this purpose haven’t directly focused on the most important measure in epidemiology: the basic reproductive number\, $R_0$\ , of epidemiological dynamics on the network\, which determines whether or not the infectious disease spreads over the whole network. We here introd uce a new centrality measure\, $R_0$-centrality\, which quantifies how sen sitive is the control in each local community to the reduction in $R_0$ of the whole network. Our perturbation analysis then reveals that the larges t local population in the network should have extremely large $R_0$ centra lity than the others\, indicating that all the effort in control should be directed to the largest community. For example\, when applied to the comm uter network of the Tokyo metropolitan area\, we found that the impact of control at the largest daytime-population\, that around Shinjuku station\, is more than 1\,000 times stronger than that at the second largest daytim e-population\, that around Tokyo station\, even though the difference betw een population sizes are only 1.5 times between them.\n\nOnce an infectiou s disease has already spread over the network\, we found that the opposite extreme control becomes optimum: indeed\, to reduce the total number host s that have ever exposed to the infectious disease after it has already pe netrated in the network\, the optimal policy is to spreading controls shal lowly and widely over the network. We also discuss the conditions under wh ich “treating-only-the-biggest” control becomes the optimum\, and the key-stone community for the emergence is virulent or resistant pathogens.\ n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/156/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/156/ END:VEVENT BEGIN:VEVENT SUMMARY:Mast seeding: puzzles and mathematical opportunities DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-163@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Dave Kelly (University of Canterbury)\nMast seeding is the intermittent synchronous production of large seed crops by a popula tion of perennial plants. This process is noteworthy in various ways. To t he lay public\, masting is noteworthy because it is very obvious when an o ccasional huge seed crop covers large areas. \n\nIn evolutionary terms it is noteworthy because delayed reproduction imposes inescapable costs on th e plants\, so it cannot occur unless there are compensating advantages (th e search for which has occupied much of the relevant masting literature). \n\nEcologically it is noteworthy because of the need for a mechanism whic h can produce synchrony among plants\, even though the plants cannot commu nicate. Most often this mechanism involves an external cue (usually weathe r)\, combined with some internal mechanisms such as resource sensitivity o f flowering. Ecologically masting is also noteworthy because of the large downstream ecological consequences of pulsed resources.\n\nMathematically masting is noteworthy for four reasons. Firstly\, masting is an emergent ( population-level) phenomenon which reflects the sum of individual plant de cisions. Constructing mechanistic models which have the right population-l evel properties is a challenge.\n\nSecondly there is a competitive tension between model approaches which are driven largely by external cues (such as weather-cue models\, with or without a resource veto)\, versus models l argely driven by internal plant resource dynamics with some modest synchro nizing cue (such as local pollen coupling or occasional flowering failure) . \n\nThirdly some plant flowering time series are mathematically chaotic. Working out ways this complex population-level pattern can be created by simple within-plant mechanisms is interesting. One published example seems to have evolved because of selection on the plants for hard-to-predict ti me series. \n\nFinally one of the proposed underlying mechanisms\, the del ta-T model\, suggests plants are measuring a temperature difference across two summers and using that as the flowering cue. The mechanism by which p lants could measure such a temperature difference is unknown. More interes tingly\, the delta-T model gives a better fit to some synthetic data which were created with a different underlying mechanism (resources plus last y ear’s absolute temperature) than the real underlying mechanism does. Rea sons for this implausibly good predictive ability of the delta-T model are currently unknown.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contr ibutions/163/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/163/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal management strategies to control mammal populations incorp orating behaviourally mediated indirect effect DTSTART;VALUE=DATE-TIME:20180709T020000Z DTEND;VALUE=DATE-TIME:20180709T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-175@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hiroyuki Yokomizo (Natl. Inst. of Environ. Studies)\ nOverpopulated mammal populations cause damage to agricultural crops in Ja pan. We need to keep population sizes at appropriate levels. When we deter mine management plans\, we have to deal with various uncertainties such as population size\, population growth rate\, and agricultural damages cause d by mammals due to lack of sufficient data. It is important to reduce tho se uncertainties and allocate hunting effort under limited budget.\n \nPre y populations change their behaviour due to presence of predators. Predati on risk could cause hehavioural changes of prey such as vigilance at the c ost of time spent grazing\, and population growth rates of prey may decrea se without predation itself (the effect is called as behaviourally mediate d indirect effect). It is possible that population decline in Japan decrea ses negative impacts of human activities on mammal populations. In additio n the agricultural damage could affect human activities. Hence it is impor tant to incorporate the behaviourally mediated indirect effect for effecti ve mammal managements.\n \nWe will introduce a population model incorporat ing a behaviourally mediated indirect effect for a management of wild boar s (*Sus scrofa*) in Chiba prefecture\, Japan. First we estimate population densities and population growth rates using Bayesian model averaging. Sec ond we estimate relationship agricultural damages and population densities in heterogeneous landscapes. Last we derive optimal allocations of huntin g efforts to minimize expected damages to agricultural crops. We discuss h ow incorporating the behaviourally mediated indirect effect is important f or effective wild boar management.\n\nhttps://conferences.maths.unsw.edu.a u/event/2/contributions/175/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/175/ END:VEVENT BEGIN:VEVENT SUMMARY:MGDrivE: a simulation framework for gene drive in spatially-explic it mosquito populations and its application to threshold-dependent systems DTSTART;VALUE=DATE-TIME:20180710T020000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-166@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: John M. Marshall (University of California\, Berkele y)\nThe advent of CRISPR/Cas9-based gene editing and its demonstrated abil ity to streamline the development of gene drive systems has reignited inte rest in its application to the control of mosquitoes and the diseases they transmit. The versatility of this technology has also enabled a wide rang e of gene drive architectures to be realized\, creating a need for their p opulation-level and spatial dynamics to be explored. To this end\, we pres ent MGDrivE (Mosquito Gene Drive Explorer): a simulation framework designe d to investigate the population dynamics of a variety of gene drive archit ectures and their spread through spatially-explicit mosquito populations. MGDrivE is based on a tensor algebraic generalization of the lumped age-cl ass model of mosquito ecology. Treating these population dynamic equations in a variable-dimension tensor form allows them to be left unchanged whil e modifying the dimensionality of the tensor describing inheritance patter ns\, as required by the drive system. Spatial dynamics are accommodated th rough a metapopulation structure in which lumped age-class models run in p arallel and migrants are exchanged between metapopulations at defined rate s. Example MGDrivE simulations are presented for threshold-dependent drive systems: a) reciprocal chromosomal translocations\, and b) toxin-antidote -based underdominant systems. Criteria are described for which these syste ms may be confined to their release community without spreading to neighbo ring communities.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contrib utions/166/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/166/ END:VEVENT BEGIN:VEVENT SUMMARY:Integrative compartmental model of carnitine and its derivatives DTSTART;VALUE=DATE-TIME:20180709T084500Z DTEND;VALUE=DATE-TIME:20180709T090000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-238@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Valentina Fermanelli (Department of Mathematical Sci ences\, Chalmers University of Technology and University of Gothenburg)\nC arnitine is a fundamental compound for humans. Mainly introduced via nutri tion\, but also synthetized in the body\, this metabolite allows the tran sport of long-chain fatty acids in the mitochondria\, where they can under go β -oxidation. Lately\, the attention on carnitine and acyl-carnitine\, carnitine derivatives\, has increased since it has been proposed that ins ulin resistance may be linked to incomplete fatty acid β-oxidation and th e subsequent increase in acyl-carnitine species in different tissues. \n\n Mathematical modelling can give us a quantitative understanding of specifi c rates in the carnitine metabolism\, e.g. synthesis of carnitine derivati ves . Therefore we contribute to the research on carnitine by building a c ompartmental model for carnitine and its derivatives. This model integrate s knowledge about carnitine uptake and synthesis\, carnitine distribution and expulsion\, and carnitine role in the transport of long-chain fatty ac ids\, therefore covering all the carnitine occurrences in the body. Additi onally\, the simultaneous comprehension of carnitine and its derivatives e nables the model to highlight the role of carnitine concentration as a bot tleneck in the transport of the long-chain fatty acids into the mitochondr ia.\n\nOur model utilizes metabolome datasets publically available in the literature for validation.\n\nhttps://conferences.maths.unsw.edu.au/event/ 2/contributions/238/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/238/ END:VEVENT BEGIN:VEVENT SUMMARY:The effect of thermoregulation on honey bee colony health and surv ival DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T015000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-477@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Zeaiter Zeaiter (University of Sydney)\nIn recent ye ars honey bee colonies have been experiencing increased loss of hives. One cause of hive loss is colony collapse disorder (CCD). Colony collapse dis order is characterised by a previously healthy hive having few or no adult bees but with food and brood still present. This occurs over several week s. It is not known if there is an exact cause of CCD but rather it is thou ght to be the accumulation of multiple stressors placed on a hive. One of these stressors is the breakdown of thermoregulation inside the hive. \n\n The bee life cycle begins with eggs that hatch into larvae that in turn pu pate. The eggs\, larvae and pupae together are known as brood. The hive contains combs which are made up of multiple cells\; these cells house th e brood. Pupal cells are capped off by adult bees (and so are known as cap ped brood) and they undergo changes to develop into an adult bee. In order for this capped brood to develop correctly\, the temperature within the h ive must be regulated by the hive bees to ensure optimal development of th e capped brood. Variations in the temperature\, caused by the breakdown of thermoregulation\, lead to suboptimal development in adults that emerge f rom capped brood. In particular\, their brains and flight muscles are comp romised. This later leads to these bees becoming inefficient foragers whic h also have shorter life spans. \n\nWe model the effect of thermoregulatio n on hive health using a system of DDEs which gives insights into how vary ing hive temperatures have an effect on the survival of the colony. We sh ow that thermoregulatory stress has the capacity to drive colony collapse disorder via a saddle-node bifurcation.\n\nhttps://conferences.maths.unsw. edu.au/event/2/contributions/477/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/477/ END:VEVENT BEGIN:VEVENT SUMMARY:Arterial remodelling in atherosclerosis DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-84@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Pak-Wing Fok (University of Delaware)\nThe arterial wall is composed of three distinct layers: the innermost intima\, the medi a\, and the adventitia. Atherosclerosis is an inflammatory disease of the artery characterized mainly by an expansion of the intima. In 1987\, Seymo ur Glagov quantified arterial remodelling as atherosclerosis progressed. H e found that the remodelling occurred in two stages: first a compensatory phase in which the lumen maintained its size\, followed by a negative remo delling phase in which the lumen cross-sectional area decreased. To date\, the exact mechanisms responsible for this behaviour have not been elucida ted.\n\nIn this talk I will discuss a three-layer mechanical model based o n a theory of morphoelastic growth and hyperelasticity. I will present a 1 D axisymmetric model that can explain Glagov Remodelling in humans and int imal thickening in animals\, and a generalization to 2D which is solved us ing finite elements.\n\nhttps://conferences.maths.unsw.edu.au/event/2/cont ributions/84/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/84/ END:VEVENT BEGIN:VEVENT SUMMARY:Temporal dynamics of macrophages plasticity in the bone microenvir onment DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-347@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Etienne Baratchart (Integrated Mathematical Oncology Dept\, H Lee Moffitt Cancer Center)\nTumour associated macrophages have l ong been implicated in the progression of primary solid malignancies inclu ding prostate cancer. Metastatic prostate cancer typically manifests in th e bone where it induces painful osteogenic lesions that are incurable. Bon e is naturally rich in myeloid derived macrophages whose temporal polariza tion into pro- (M1) and anti-inflammatory (M2) phenotypes is critical for regulating the program of bone injury repair mediated by bone resorbing os teoclasts (OCL) and bone building (OBLs). However\, the dynamics of macrop hage polarization in the context of bone metastatic prostate cancer is und erexplored and difficult to address with traditional biological approaches . In order to address it we built a mathematical model describing bone res ident cell population dynamics during bone injury response through a set o f coupled ordinary differential equation (ODE). We informed this model by analyzing macrophage plasticity *in vivo* subsequent to intratibial injury . Bone marrows were isolated at several time points and profiled by flow c ytometry for pro- and anti-inflammatory macrophage content. Contralateral tibias were analyzed for bone volume\, osteoblast and osteoclast numbers. The ODE model was able to predict experimental observations of M1/M2\, OBL \, OCL and bone dynamics. Generation of the ODE model required testing a n umber of assumptions regarding macrophage polarization behaviour. For exam ple\, it is unknown whether M1 resolve at the initial stages of bone injur y repair through death\, or by re-polarizing into M2. For each aspect\, co mpeting mechanistic assumptions were proposed and simulated mathematically by sets of ODEs. The best fitting assumptions for each aspect were integr ated into a comprehensive ODE model to fully describe the dynamics of the bone resident cell populations during bone repair. This experimentally val idated model is now being exploited to address how bone population dynamic s respond to metastatic prostate cancer cells and subsequently identify th e resultant impact on bone formation and cancer growth.\n\nhttps://confere nces.maths.unsw.edu.au/event/2/contributions/347/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/347/ END:VEVENT BEGIN:VEVENT SUMMARY:Mechanical and experimental models of collective cell migration re veals the importance of intercellular interactions DTSTART;VALUE=DATE-TIME:20180709T054000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-382@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Oleksii Matsiaka (Queensland University of Technolog y)\nScratch assays are routinely used to study the collective spreading of cell populations. In general\, the rate at which a population of cells sp reads is driven by the combined effects of cell migration and proliferatio n. To examine the effects of cell migration separately from the effects of cell proliferation\, scratch assays are often performed after treating th e cells with a drug that inhibits proliferation. Mitomycin-C is a drug tha t is commonly used to suppress cell proliferation in this context. However \, in addition to suppressing cell proliferation\, Mitomycin-C also causes cells to change size during the experiment\, as each cell in the populati on approximately doubles in size as a result of treatment. Therefore\, to describe a scratch assay that incorporates the effects of cell-to-cell cro wding\, cell-to-cell adhesion\, and dynamic changes in cell size\, we pres ent a new stochastic model that incorporates these mechanisms. We then emp loy this stochastic model to quantify relative contributions of crowding e ffects and random motility into the collective cell migration in the scrat ch assay experiments containing malignant PC-3 prostate cancer cells.\n\nh ttps://conferences.maths.unsw.edu.au/event/2/contributions/382/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/382/ END:VEVENT BEGIN:VEVENT SUMMARY:Heterogeneity in susceptibility induces unpredictable outbreak DTSTART;VALUE=DATE-TIME:20180710T015000Z DTEND;VALUE=DATE-TIME:20180710T021000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-246@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ryosuke Omori (Hokkaido University)\nReinfection is known to induce complex epidemiological dynamics (e.g. sustained oscillati on) due to the time-series change in susceptibility. The simplest model de scribing reinfection shows three epidemiological dynamics\; disease-free\, epidemic and endemic. These three dynamics can be classified by two repro duction numbers\, basic reproduction number and reproduction number by onl y reinfection. However\, the simplest model takes into account only two va riations of susceptibility\, susceptibility at first infection and second or later infection. To relax this assumption we construct a parsimonious m odel describing three susceptibilities\, i) susceptibility at first infect ion\, ii) partial protection at second or later infection and iii) perfect protection at second or later infection. This model demonstrates an inter esting dynamics\, outbreak occurs after the temporal decrease in the numbe r of infected individuals. We named this dynamics as "delayed outbreak". B asic reproduction number cannot capture outbreak potential of this dynamic s. Our model is too simple to understand rich dynamics induced by heteroge neity in susceptibility\, for example\, endemic situation is not captured in this model. To understand the dynamics with heterogeneity in susceptibi lity\, we expand our model to a model describing the transition of suscept ibility by reinfection. We confirmed that "delayed outbreak" is robust if the heterogeneity in susceptibility against reinfection exists.\n\nhttps:/ /conferences.maths.unsw.edu.au/event/2/contributions/246/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/246/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal control analysis of a mathematical model for breast cancer DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-365@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Segun Oke (University of Zululand\, South Africa)\nI n this paper\, a mathematical model of breast cancer governed by a system of ordinary differential equations in the presence of chemotherapy treatme nt and ketogenic diet is discussed. Several comprehensive mathematical ana lysis was carried out using varieties of analytical methods to study the s tability of the breast cancer model. Also\, sufficient conditions on param eter values to ensure cancer persistence in the absence of anti-cancer dru gs ketogenic diet and cancer emission when anti-cancer drugs\, immune-boos ter\, ketogenic diet are included were established. Furthermore\, optimal control theory is applied to find out the optimal drug adjustment as an in put control of the system therapies to minimize the number of cancerous ce lls by considering different controlled combinations of administering the chemotherapy agent and ketogenic diet using the popular Pontryagin’s Max imum Principle. Numerical simulations are presented to validate our theore tical results.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributi ons/365/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/365/ END:VEVENT BEGIN:VEVENT SUMMARY:Contribution of mass incarceration to HIV and optimal control of S IR model DTSTART;VALUE=DATE-TIME:20180712T054000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-239@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hem Joshi (Xavier University)\nWe develop a Suscepti bles\, Infected and Recovered (SIR) type mathematical model of HIV epide miology to explore a possible mechanism by which mass incarceration can le ad to increased HIV incidence. The results are particularly relevant for t he African American community in the United States that represents only 12 % of the total population but accounts for 45% of HIV diagnoses and 40% o f the incarcerated population. While most explanations of the link betwee n mass incarceration or anything else that leads to a population with a lo w ratio of males to females and higher HIV burden are based on the complic ated idea of sexual concurrency\, we propose a much simpler mechanism base d on the idea of sexual activity compensation. The pool of men will increa se their sexual activity to meet the demands of the female population. Th rough mathematical analysis and numerical simulation\, we demonstrate that these assumptions produce a situation in which mass incarceration lead t o higher HIV incidence.\n\n\nWe also develop an optimal control model of S IR type. In this model\, the control is education or information given t o the public to manage a disease outbreak when effective treatments or va ccines are not readily available or too costly to be widely used. We study stability analysis and use optimal control theory on the system of differ ential equations to achieve the goal of minimizing the infected population . We illustrate our results with some numerical simulations.\n\nhttps://c onferences.maths.unsw.edu.au/event/2/contributions/239/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/239/ END:VEVENT BEGIN:VEVENT SUMMARY:The remarkable simplicity of complex signalling networks DTSTART;VALUE=DATE-TIME:20180709T015000Z DTEND;VALUE=DATE-TIME:20180709T021000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-306@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Robyn Araujo ()\nRobustness\, and the ability to fun ction and thrive amid changing and unfavourable environments\, is a fundam ental requirement for all living systems. Moreover\, it has been a long-s tanding mystery how the extraordinarily complex communication networks ins ide living cells\, comprising thousands of different interacting molecules \, are able to exhibit such remarkable robustness since complexity is gene rally associated with fragility. In this talk I will give an overview of our recent research on robustness in cellular signalling networks\, with a n emphasis on the robust functionality known as Robust Perfect Adaptation (RPA). Our work has now suggested a resolution to the complexity-robustne ss paradox through the discovery that robust adaptive signalling networks must be decomposable into topological basis modules of just two possible t ypes. This newly-discovered modularisation of complex bionetworks has imp ortant implications for evolutionary biology\, embryology and development\ , cancer research and drug development.\n\nhttps://conferences.maths.unsw. edu.au/event/2/contributions/306/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/306/ END:VEVENT BEGIN:VEVENT SUMMARY:Control of the cardiorespiratory system: challenges and opportunit ies DTSTART;VALUE=DATE-TIME:20180709T090000Z DTEND;VALUE=DATE-TIME:20180709T091500Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-443@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Alona Ben-Tal (Massey University)\nMaintaining physi ological levels of oxygen (O$_2$) and carbon dioxide (CO$_2$) in the blood is crucial for survival and is achieved by sophisticated neural control m echanisms affecting both the breathing pattern and heart rate. Neural acti vity\, originated in the brainstem\, drives the respiratory muscles\, prov iding air flow into and out of the lungs where gas exchange takes place an d also affects heart rate and blood flow. Chemoreceptors that sense the le vels of O$_2$ and CO$_2$ in the blood\, mechanical stretch receptors withi n the lungs and blood pressure sensors provide feedback signals to the bra instem networks which then regulate the breathing pattern and heart rate a ppropriately. Understanding how the neural system responds to all the feed back signals it receives is still lacking. I will outline the challenges w e face from a modelling perspective and the different approaches we take i n our attempt to resolve them.\n\nhttps://conferences.maths.unsw.edu.au/ev ent/2/contributions/443/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/443/ END:VEVENT BEGIN:VEVENT SUMMARY:Population epidemiology under toxicant stress: a nested multilevel modelling framework DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T005000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-255@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ross Booton (University of Sheffield )\nPopulations are formed of their constituent interacting individuals\, each with their own respective within-host biological processes. Infection not only spread s within the host organism but also spreads between individuals. We propos e and study a nested multilevel model which links the within-host statuses of immunity and parasite density to population epidemiology under sub-let hal and lethal toxicant exposure. We analyse this nested model in order to better understand how toxicants impact the spread of disease within popul ations. We demonstrate that the outbreak of infection within a population is completely determined by the level of toxicant exposure\, and that it i s maximised by intermediate toxicant dosage. We classify the population ep idemiology into 5 phases of increasing toxicant exposure and calculate the conditions under which disease will spread\, showing that there exists a threshold toxicant level under which epidemics will not occur. In general\ , higher toxicant load results in either extinction of the population or o utbreak of infection. The within-host statuses of the individual host also determine the outcome of the epidemic at the population level. We discuss applications of our model in the context of eco-epidemiology\, particular ly for bee colony losses\, predicting that increased exposure to toxicants could result in more epidemics and therefore greater colony losses. We pr edict that reducing sub-lethal toxicant exposure below our predicted safe threshold could contribute to controlling population level disease and inf ection.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/255 / LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/255/ END:VEVENT BEGIN:VEVENT SUMMARY:Spatial moment description of birth-death-movement processes incor porating the effects of crowding and obstacles DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-379@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Anudeep Surendran (Queensland University of Technolo gy\, Brisbane\, Australia)\nBirth-death-movement processes\, modulated by interactions between individuals\, are fundamental to many biological proc esses such as development\, repair and disease. Similar interactions are a lso relevant in ecology. A key feature of the movement of cells within *in vivo* environments are the interactions between motile cells and stationa ry obstacles\, such as the extracellular matrix and stationary macromolecu les. Here we propose a multi-species individual-based model (IBM) of indiv idual-level motility\, proliferation and death. In particular\, we focus o n examining the case where we consider a population of motile\, proliferat ive agents within an environment that is populated by stationary\, non-pro liferative obstacles. To provide a mathematical foundation for the analysi s of the IBM\, we derive a system of spatial moment equations that approxi mately governs the evolution of the density of agents and the density of p airs of agents. By using a spatial moment approach we avoid making the usu al mean field assumption so that our IBM and continuous model are able to predict the formation of spatial structure\, such as clustering and aggreg ation. We explore several properties of the obstacle field\, such as syste matically varying the obstacle density\, obstacle size\, and the nature an d strength of the interactions between the motile\, proliferative agents a nd the stationary\, non-proliferative obstacles. Overall we find that the spatial moment model provides a reasonably accurate prediction of the dyna mics of the system\, including subtle but important effects\, such as how varying the properties of the obstacles leads to different patterns of clu stering and segregation in the population.\n\nhttps://conferences.maths.un sw.edu.au/event/2/contributions/379/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/379/ END:VEVENT BEGIN:VEVENT SUMMARY:Agent-based modelling of higher order chemical reactions using Smo luchowski kinetics DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-384@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: James Cavallo (Monash University)\nChemical reaction s are traditionally modelled using deterministic methods such as ordinary differential equations. In biology\, we also consider the effect of diffus ion upon a reactive system. For small biological systems\, it is necessary to use stochastic models. In this talk\, we choose to use an agent-based model commonly known as Smoluchowski kinetics.\n\nIn the Smoluchowski mode l\, two molecules diffuse in space\, and react when they are within a crit ical separation distance (Smoluchowski radius). This radius is at a rate p roportional to the reaction rate constant. Over the last 100 years\, the m odel has been extended to incorporate reversible reactions by introducing a second separation distance. \n\nA common problem with Smoluchowski kinet ics is when modelling rapid enzyme reactions\, where the assumptions used to model Smoluchowski kinetics break down. Using differential equations\, these rapid interactions can be easily analysed using a pseudo steady stat e approximation which effectively results in non-linear reactions. Other m odels have utilised multiple timescales to model what is called fast-slow reaction kinetics.\n\nIn this talk\, we theorise that a way to bypass the fast-slow reaction kinetics problem is to extend the Smoluchowski model to reversible trimolecular reactions. We develop these kinetics and apply th em to the canonical Wnt signalling pathway. We model this pathway using tr aditional Smoluchowski kinetics\, and show how the aforementioned issues c ome into effect. We then compare this to our trimolecular model and show h ow the issues disappear.\n\nhttps://conferences.maths.unsw.edu.au/event/2/ contributions/384/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/384/ END:VEVENT BEGIN:VEVENT SUMMARY:An agent-based model for pseudohyphal yeast growth DTSTART;VALUE=DATE-TIME:20180712T052000Z DTEND;VALUE=DATE-TIME:20180712T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-307@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hayden Tronnolone (University of Adelaide)\nBudding yeasts\, such as *Saccharomyces cerevisiae* (baker's yeast)\, that are gro wn on a solid substrate are able to alter their growth pattern to suit the surrounding nutrient level. When nutrient is readily available\, buds sep arate from the mother cell to produce colonies that appear close to circul ar when viewed from above. When nutrient is limited\, the cells reproduce via the pseudohyphal growth pattern\, which is characterised by distal uni polar budding (budding opposite to the birth scar)\, the elongation of cel ls and a persistent connection between mother and daughter cell. This chan ge results in the growth of filaments directed away from the colony\, prod ucing an irregular shape. The precise shape of the colony is dependent on several factors\, such as the nutrient level and strain\, while gene-delet ion mutants may also display different morphologies. As these have an infl uence at the cell level\, there is a need to understand how the behaviour of individual cells influences the overall colony morphology. To address t his\, yeast colony growth is studied using an agent-based mathematical mod el. The model allows for the control of nutrient diffusion and budding mec hanism\, including the change in cell behaviour during the pseudohyphal ph ase. Simulations using this model are found to compare favourably with exp erimental observations and are used to illustrate the relationship between the behaviour of individual cells and the overall colony shape.\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/307/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/307/ END:VEVENT BEGIN:VEVENT SUMMARY:Host- vs diet-derived nutrient balance\, and carbon vs nitrogen li mitation\, determines the effect of dietary intervention on the microbiome . DTSTART;VALUE=DATE-TIME:20180711T052000Z DTEND;VALUE=DATE-TIME:20180711T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-350@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mark Read (University of Sydney)\nThe gut microbiome is implicated in a growing array of diseases\, spanning asthma\, allergie s\, obesity and autoimmunity. The need for interventions that return aberr ant dysbiotic communities to symbiotic partners is clear. Yet\, despite kn own sensitivities to diet\, a conceptual framework through which to design rational interventions remains elusive. \n\nWe adopted an ecological pers pective in building a conceptual model to reason about how diet impacts th e microbiome. Microbes must satisfy their nutritional requirements for lif e. The most readily limiting resources are carbon\, as an energy source\, and nitrogen\, a key element in all amino acids. \n\nMicrobes employ a div ersity of strategies to satisfy these nutritional requirements. Some speci alise on metabolising diet-derived substrates such as fibre. Others can gr ow on mucin\, a host secretion\, alone. We further envisage hybrid strateg ies between these two extremes\, where carbon and nitrogen substrates eith er both originate from the diet or the host\, or one from each. \n\nWe eva luated this ecological conceptualisation's capacity to explain observed mi crobiome responses to diet through the construction of an agent-based mode l. Host mucin secretion and dietary nutrient absorption dynamics have been estimated from literature\, the remaining dietary nutrients being supplie d to a one dimensional simulated gut environment that houses bacteria. Eac h bacteria cell agent internalises nutrients from its local environment\, targeting a 5.2:1 carbon:nitrogen ratio. Nutrient-rich cells exhibit a hig her probability of division\, where nutrient-poor cells likely perish. \n\ nOur modelling work was closely aligned with an *in vivo* murine dietary s tudy. Herein\, 112 mice were administered diets systematically varying in protein:carbohydrate:fat distribution\, and energy density by diluting the se mouse-accessible nutrients with cellulose\, which neither mouse nor its microbiome can metabolise. Their actual intake\, and hence the energy the y derive from each macronutrient\, was recorded. Using generalised additiv e models we interpolated from these 112 samples across a wide dietary inta ke space. As such\, we could ascertain how each microbe responds to a give n diet. We observed two broad patterns of response: microbes that thrive u nder energy-rich or energy-poor diets. The dietary intakes of each of thes e 112 mice were simulated in our model\, which broadly recapitulated these *in vivo* observations. This suggests that the balance of host- versus di et-derived substrates is a critical factor in shaping the microbiome.\n\nO ur model permits a comprehensive exploration of how multiple dietary facto rs\, such as prebiotic administration\, fasting regimes\, macronutrient di stribution and energy density\, interact in impacting the microbiome. The model predicts that interventions such as fasting and prebiotic (fibre) ad ministration do not have uniform effects\, which\, rather\, depend on othe r dietary parameters also. For instance\, prebiotic administration in low- protein diets can have a limited effect\, as under these diets microbes ar e nitrogen-limited\, an the carbon prebiotics supply is of little conseque nce. These results underscore the importance of taking an integrative appr oach to studying diet-host-microbiome interactions\, and tools such as the se offer a promising path to designing personalised dietary interventions to rationally manipulate a person's microbiome.\n\nhttps://conferences.mat hs.unsw.edu.au/event/2/contributions/350/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/350/ END:VEVENT BEGIN:VEVENT SUMMARY:Infection-acquired versus vaccine-acquired immunity in an SIRWS mo del DTSTART;VALUE=DATE-TIME:20180712T005000Z DTEND;VALUE=DATE-TIME:20180712T011000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-263@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tiffany Leung (University of Melbourne)\nWaning immu nity is known to occur for some infectious diseases after natural infectio n and vaccination. We present a susceptible-infectious-recovered-susceptib le (SIRS)-type transmission model that includes the waning and boosting of immunity. We study how the infection prevalence changes with differences in (i) the durations of infection- and vaccine-acquired immunity and (ii) the assumed mechanism through which immune boosting acts to extend protect ion.\n\nOur results show that increasing vaccine uptake always lowers the proportion of primary infections but may lead to an increase in overall tr ansmission. Where the boosting of vaccine-acquired immunity delays a prima ry infection\, the driver of transmission largely remains primary infectio ns. In contrast\, if immune boosting bypasses a primary infection\, second ary infections become the main driver of transmission under sufficiently l ong-lasting vaccine-induced immunity. Our study highlights that for a part icular disease and associated vaccine\, a detailed understanding of how th e duration of protection can influence infection prevalence is important a s we seek to optimise vaccination strategies.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/263/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/263/ END:VEVENT BEGIN:VEVENT SUMMARY:The interplay between feedback and buffering in cellular homeostas is DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-373@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Edward Hancock ()\nNegative feedback and buffering\, the use of reservoirs of molecules to maintain concentrations of key mole cular species\, are the primary known mechanisms for robust homeostatic re gulation. However\, the fundamental principles behind their combined effec t have not been elucidated. Here\, I will present our recent research on t he interplay between buffering and negative feedback in the context of cel lular homeostasis. This research shows that negative feedback counteracts slow-changing disturbances\, whereas buffering counteracts fast-changing d isturbances. Furthermore\, feedback and buffering have limitations that cr eate trade-offs for regulation: instability in the case of feedback and mo lecular noise in the case of buffering. However\, because buffering stabil izes feedback and feedback attenuates noise from slower-acting buffering\, their combined effect on homeostasis can be synergistic. These effects ar e consistent with experimental observations of both ATP homeostasis and pH regulation *in vivo*. The methodology is based on control theory and comp lexity-aware minimal modelling. The discussed principles are crucial for s tudying robustness and homeostasis in biology and biotechnology.\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/373/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/373/ END:VEVENT BEGIN:VEVENT SUMMARY:An approach and tools for research reproducibility across computat ional biology DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-269@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Daniel G Hurley (Systems Biology Laboratory\, Univer sity of Melbourne)\nReproducibility of results is a key part of the scient ific method\; in general\, scientific communication aims to describe a res ult in enough detail that readers and reviewers are able to contextualise the result within their own knowledge\, and to reproduce it themselves giv en the appropriate skills and resources. In the field of computational bi ology\, readers and reviewers face special challenges to contextualise and reproduce results\, because of the size of datasets analysed\, and the in creasing complexity of the computational methods used. To meet these cha llenges\, we present an approach that uses software engineering tools to p roduce complete ‘reference computation environments’\, containing all software and configuration necessary to reproduce a computational result. Existing tools to reproduce results are limited to a single technology o r programming language\; our approach is the first to use a single specifi cation to produce the same environment on a desktop computer\, in a cloud computing service\, or in a managed computing facility. Using these tools \, authors can ensure their published results are easily reproducible by r eaders and reviewers\, and are robust to future changes in software and ha rdware. \n\nThe drive for reproducibility in the computational sciences ha s provoked discussion and effort across a broad range of perspectives: te chnological\, legislative/policy-making\, education\, and publishing. Nat ure Biotechnology has recently implemented standards for reproducibility [ 1] in response to increasing complexity of methods and data requirements i n computational biology. Discussion on these topics is not new [2\,3\, 4]\, but the need to adopt standards for reproducibility of claims made ba sed on computational results is now clear to researchers\, publishers and policymakers. Many technologies exist to support and promote reproductio n of results: this journal and others have discussed containerisation tool s like Docker [5]\, literate programming approaches such as Sweave [6]\, knitr [7]\, iPython [8] or cloud environments like Amazon Web Services [9] . But these technologies are tied to specific programming languages (e .g. Sweave/knitr to R\; iPython to Python) or to platforms (e.g. Docker fo r 64-bit Linux environments only). No single approach to date is able to span the broad range of technologies and platforms represented in computat ional biology and biotechnology. \n\nTo enable reproducibility across co mputational biology\, we demonstrate for the first time an approach and a set of tools that is suitable for all computational work\, and not tied to a particular programming language or platform. Our approach extends ou r previous work in this area [10] to produce ‘reference environments’ for reproducing results that can be deployed across platforms and can use any and all of the replication tools described above. We achieve this by adopting innovative open-source tools from software engineering [13\,14]\ , and we are now involved in the community contributing to the development of these tools\, and acting as advocates for scientific computing within that community. We present published examples from a series of papers a cross research groups in different areas of computational and systems biol ogy\, spanning the major languages and technologies in the field (Python/R /MATLAB/Fortran/C/Java). We also include examples reproducing studies in network analysis by Feizi *et al*. [11] and Barzel *et al*. [12]\, results which have been recently commented upon in this journal [1]. We also pr esent results from another study demonstrating that different output value s can be produced from the same data and code given different versions of the MATLAB software used by the Feizi and Barabasi codebases. Since very few reviewers and readers will run the same code using multiple software v ersions\, this could be interpreted as inability to reproduce the publishe d work\, underlining the need for a reference environment as produced by o ur approach. Our approach produces a transparent and flexible process f or replication and recomputation of results\, but ultimately its most valu able aspect is the decoupling of methods in computational biology from the ir implementation. Separating the ‘how’ (method) of a publication fr om the ‘where’ (implementation) promotes genuinely open science and be nefits the scientific community as a whole. \n\n[1] Editorial. *Nat Biote ch*. Nature Publishing Group\, a division of Macmillan Publishers Limited. All Rights Reserved.\; 2015\;33: 319. \n[2] Barnes N. *Nature*. 2010\;467 : 753. doi:10.1038/467753a\n[3] Merali Z. *Nature*. Nature Publishing Grou p\; 2010\;467: 775–777. \n[4] Ball P. *Nature*. 2003\; \n[5] Docker. [ci ted 8 May 2015]. Available: https://www.docker.com/\n[6] Leisch F. Hardle W\, Ronz B\, editors. Compstat 2002: Proceedings in Computational Statisti cs. Heidelberg: Physica-Verlag Gmbh & Co\; 2002. \n[7] Xie Y. Implementing Reproducible Research. Chapman and Hall/CRC\; 2014. doi:doi:10.1201/b1686 8-3\n[8] Pérez F *et al*. *Comput Sci Eng*. 2007\;9: 21–29. doi:10.1109 /MCSE.2007.53\n[9] “Amazon Web Services.” [cited 8 May 2015]. Availabl e: http://aws.amazon.com/\n[10] Hurley DG *et al*. *Brief Bioinform*. Oxfo rd University Press\; 2014\; bbu043. doi:10.1093/bib/bbu043\n[11] Feizi S *et al*. *Nat Biotechnol*. 2013\;31: 726–33. doi:10.1038/nbt.2635\n[12] Barzel B *et al*. *Nat Biotechnol*. NATURE PUBLISHING GROUP\, 75 VARICK ST \, 9TH FLR\, NEW YORK\, NY 10013-1917 USA\; 2013\;31: 720–5. doi:10.1038 /nbt.2601\n[13] Vagrant. [cited 8 May 2015]. Available: https://www.vagran tup.com/\n[14] Packer. [cited 11 Mar 2015]. Available: packer.io/\n\nhttps ://conferences.maths.unsw.edu.au/event/2/contributions/269/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/269/ END:VEVENT BEGIN:VEVENT SUMMARY:Identifying differences in the rules of interaction between indivi duals in moving animal groups DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T015000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-331@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Timothy Schaerf (School of Science and Technology\, University of New England)\nThe spectacular patterns of collective animal movement have been\, and remain\, a long standing and major interest in ma ny branches of science\, including biology\, mathematics\, physics and com putational science. It is thought that the emergent patterns of coordinate d motion are the consequence of individuals applying simple rules to adjus t their velocity based on the relative locations and movements of nearby g roup members.\n \nFrom the early 1980s onwards\, the dominant methods for examining hypotheses about simple rules of interaction leading to coordina ted\, and sometimes complex\, group motion have been discrete time self-pr opelled particle models. Common to many of these models are interaction ru les chosen such that individuals will adjust their velocity to: avoid coll isions with nearby neighbours\, align their direction of motion with group members located at intermediate relative distances\, and move towards oth er group members that are at relatively greater distances.\n \nIn the last decade advances in automated visual and GPS tracking methods have led to the exciting development of techniques for estimating the local rules of i nteraction used by real animals to coordinate collective motion directly f rom observational data. Analysis of tracking data\, particularly of birds or fish in motion\, suggests that the form of interaction rules chosen in self-propelled particle models is indeed plausible\, with real animals adj usting their velocities consistent with collision avoidance at short range \, matching directions of motion\, and attraction to distant group mates. However\, the mechanics of real interactions differ in detail to those ado pted in models\, even if the broad principles appear the same.\n \nIn this talk I will discuss an averaging technique for estimating how individual ’s adjust their velocity as a function of the relative coordinates of th eir partners\, and potentially other independent variables\, directly from tracking data. Such techniques were first developed in concurrent studies by Katz *et al*. [1] and Herbert-Read *et al*. [2]\, and have since been further refined (see for example\, [3]). I will then present some results that illustrate some of the commonalities and differences seen in the rule s of interaction of different species of shoaling fish. I will discuss how randomisation methods can be used to identify when there are statistical differences in observed interaction rules of individuals belonging to diff erent categories (for example hungry animals versus those that have recent ly fed to satiation). Finally\, I will use these methods to examine differ ences in interaction rules between pairs of fish where one fish dominates leadership positions\, and the other follows.\n\n[1] Katz *et al*. *PNAS*\ , 108:18720-18725\, (2011)\n[2] Herbert-Read *et al*. *PNAS*\, 108:18726-1 8731\, (2011)\n[3] Schaerf *et al*.\, *Science Advances*\, 3:e1603201\, (2 017)\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/331/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/331/ END:VEVENT BEGIN:VEVENT SUMMARY:Unravelling the within-host dynamics of Group A Streptococcus infe ction from population-level observations of strain diversity and infection prevalence DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T015000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-264@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Rebecca Chisholm (University of Melbourne)\nGroup A *Streptococcus* (GAS) is a ubiquitous human pathogen composed of over 230 different molecular sequence types. GAS is responsible for a broad spect rum of diseases - from superficial infections of the skin and throat to li fe-threatening invasive infections and post-infection sequelae. Even thoug h most GAS infections are mild and easily treated\, GAS-related disease re mains a major cause of death and disability globally. This burden is great est in settings of poverty\, including developing countries and in Indigen ous populations of many developed countries. Safe and effective vaccines a gainst GAS are urgently needed to reduce this overall burden\, and reduce health inequalities. \n \nDevelopment of vaccines and other disease reduc ing strategies is currently hampered by our incomplete understanding of th e within and between-host dynamics of GAS infection\, immunity and transmi ssion. Studies provide limited information on the progression of GAS disea se without treatment (the natural history of disease)\, on the relative co mpetitiveness of GAS strains within and between hosts\, and on the immune response to GAS skin infection (the predominant infection type in many hos t settings where GAS disease is hyper-endemic). Assessments of these key v ariables are all confounded by the considerable diversity of GAS. Epidemi ological studies provide relevant data on the total population prevalence of GAS infections and associated disease\, in relation to the diversity of GAS strains circulating in different host populations. Meta-analyses of these studies demonstrate that the level of GAS transmission and GAS-relat ed disease in a particular host population is positively associated with t he total number of strains circulating at any one time. Specifically\, stu dies conducted in settings where GAS disease is hyper-endemic report dozen s of different circulating strains\, while those conducted in low prevalen ce settings report circulation of only a handful of distinct strain types. \n \nIn this work\, we use an individual-based model of GAS transmissio n to explore hypotheses about the within-host dynamics of GAS infection an d immunity. Specifically\, we examine the conditions that must hold with r espect to within-host dynamics to generate observed population-level assoc iations between infection prevalence and strain diversity. Our results rev eal how a positive association between these two population-level measures can emerge for multi-strain pathogens that elicit strong strain-specific immunity following infection with low to intermediate levels of cross-stra in immunity protecting against re-infection. The same association between prevalence and diversity can also emerge for pathogens that elicit weak s train-specific immunity following infection\, but only if they can co-infe ct hosts with multiple strains. Given that a strong strain-specific immun e response following GAS skin infection is unlikely\, we propose that co-i nfection is a key enabler of high levels of strain diversity in host setti ngs where GAS disease is hyper-endemic. Our findings also suggest that de velopment of vaccines capable of eliciting strong cross-immunity over mult iple strain types will be needed to impact on the burden of GAS disease.\n \nhttps://conferences.maths.unsw.edu.au/event/2/contributions/264/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/264/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling Carpageddon - the deliberate release of CyHV-3 DTSTART;VALUE=DATE-TIME:20180711T005000Z DTEND;VALUE=DATE-TIME:20180711T011000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-266@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Stephen Davis (RMIT University)\nThe deliberate rele ase of Cyprinid herpes virus 3 (CyHV-3) to control invasive common carp (C yprinus carpio) in the Murray-Darling Basin of south-eastern Australia has been dubbed `Carpageddon' and is highly controversial. Common carp now re present up to 90% of the biomass in invaded waterways and mortality rates of 70-80% have been observed during outbreaks of CyHV-3 in the northern he misphere. Hence\, the release of CyHV-3 carries the risk that decompositio n following mass-mortality of carp may lead to severe oxygen depletion and subsequent anoxic events. I will present mathematical modelling that is t he basis for (i) developing a low-risk release strategy\, and (ii) advice to the Australian government on the long-term benefits of releasing the vi rus. The model couples a stage based demographic model with an SEIR-type m odel\; recruitment of young carp is determined by available spawning habit at and the river system hydrology. We show that the long-term virus impact and the dynamics predicted by the model depend largely on the presence of a latent class that allows for virus reactivation and onward infection. T he impact of CyHV-3 is also sensitive to where density-dependence occurs i n the life cycle of carp because of the potential for virus mortality to e ither replace\, or be in addition to\, density-dependent mortality.\n\nhtt ps://conferences.maths.unsw.edu.au/event/2/contributions/266/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/266/ END:VEVENT BEGIN:VEVENT SUMMARY:Predicting the response of breast cancer to neoadjuvant chemothera py with an imaging-driven\, mechanics-coupled\, reaction-diffusion model a ccounting for patient-specific therapeutic regimens DTSTART;VALUE=DATE-TIME:20180709T054000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-210@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Angela M. Jarrett (University of Texas at Austin)\nC linical methods for assessing tumour response to neoadjuvant therapy large ly rely on monitoring the temporal changes in tumour size. Our goal is to predict tumour response to neoadjuvant therapy in breast cancer using a ma thematical model that utilizes non-invasive imaging data obtained from ind ividual patients. Previously\, a mechanically-coupled\, reaction-diffusion model with logistic growth for breast cancer was shown to outperform clin ically used measures for predicting tumour response to therapy when initia lized with patient specific magnetic resonance imaging (MRI) data. This mo del has since been extended to include patients’ therapy using correspon ding dynamic contrast-enhanced (DCE-) MRI data to determine areas for drug delivery\, improving the concordance correlation coefficient of the predi cted tumour cellularity compared to the calculated cellularity from 0.85 t o 0.99 (p\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/2 10/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/210/ END:VEVENT BEGIN:VEVENT SUMMARY:Epidemiological consequences of different vaccination strategies a gainst infectious diseases in domestic livestock DTSTART;VALUE=DATE-TIME:20180711T011000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-278@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Vasiliki Bitsouni (The Roslin Institute\, University of Edinburgh)\nA vaccine is a biological preparation\, providing long-ter m protection of the host to a disease by miming the interactions between t he pathogen and the immune response. For decades vaccines have been the mo st effective means to fight and eradicate infectious diseases\, from human diseases to animals diseases\, including poultry and porcine viruses. One of the most significant endemic swine disease causing major animal and ec onomic losses all over the world is porcine reproductive and respiratory s yndrome (PRRS). Although different types of vaccines are on the market and various vaccination strategies have been trialled to control the disease\ , PRRS continues to persist\, sometimes at high prevalence. The failure of some vaccination strategies to combat the disease leaves open questions r egarding the major effect that the vaccine should have\, as well as the mo st efficient vaccination strategy. We present an SIR model of a non-vacci nated population and extend it to a model where vaccination is applied. We use numerical simulations to evaluate vaccine efficacy for different type s of vaccines and vaccination strategies to predict determinants for disea se prevention. The study provides important guidelines for vaccine develop ment and application in livestock populations.\n\nhttps://conferences.math s.unsw.edu.au/event/2/contributions/278/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/278/ END:VEVENT BEGIN:VEVENT SUMMARY:An optimal impulse control problem in anti-cancer therapeutic stra tegies DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-352@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Naïma El Farouq ()\nWe present an optimal impulse c ontrol problem related to anti-cancer therapeutics. Our model takes into a ccount both the instantaneous toxicities of the treatments and the adverse effects of targeted and non-targeted antineoplastic therapies.\n\nhttps:/ /conferences.maths.unsw.edu.au/event/2/contributions/352/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/352/ END:VEVENT BEGIN:VEVENT SUMMARY:Evolutionary cancer therapy DTSTART;VALUE=DATE-TIME:20180711T052000Z DTEND;VALUE=DATE-TIME:20180711T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-445@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Alexander Anderson (Moffitt Cancer Center)\nHeteroge neity in cancer is increasingly being recognized as a key determinant of t umour progression and response to therapy. However\, much of our current u nderstanding of this heterogeneity has been driven by our ability to measu re it\, and therefore has largely focused on the genomic scale. Ultimately such heterogeneity is realized through the generation of distinct phenoty pes. In recent years there has been a deeper appreciation for how phenotyp ic variation is modulated by a range of biological mechanisms over differe nt spatial scales - specifically epigenetic\, metabolic and microenvironme ntal. Within a growing tumour\, multiple cellular phenotypes and a spatiot emporally-varying microenvironment form a complex ecosystem that exhibits unintuitive\, nonlinear behaviour. \n\nTreatment of advanced cancers has b enefited from new agents that supplement or bypass conventional therapies. However\, even effective therapies fail as a heterogeneous tumour cell po pulation deploys a wide range of resistance strategies. We propose that ev olutionary dynamics ultimately determine survival and proliferation of res istant cells\, therefore evolutionary treatment strategies should be used with conventional therapies to delay or prevent resistance. Using an agent -based framework to model spatial competition among sensitive and resistan t populations\, we apply anti-proliferative drug treatments to varying rat ios of sensitive and resistant cells. We compare a continuous maximum tole rated dose schedule with an adaptive schedule aimed at tumour control thro ugh competition between sensitive and resistant cells. We find that contin uous treatment cures mostly sensitive tumours\, but with any resistant cel ls\, recurrence is inevitable. We identify two adaptive strategies that co ntrol heterogeneous tumours: dose modulation controls most tumours with le ss drug\, while a more vacation-oriented schedule can control more invasiv e tumours.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 445/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/445/ END:VEVENT BEGIN:VEVENT SUMMARY:Data-driven prediction and origin identification of epidemics in p opulation networks DTSTART;VALUE=DATE-TIME:20180710T011000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-308@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Karen Larson (Brown University)\nWhile there exist a number of mathematical approaches to modelling the spread of disease on a network\, analyzing such systems in the presence of uncertainty introduce s significant complexity. In scenarios where system parameters must be inf erred from limited observations\, general approaches to uncertainty quanti fication can generate approximate distributions of the unknown parameters\ , but these methods often become computationally expensive if the underlyi ng disease model is complex. In this talk\, I will apply transitional Mark ov chain Monte Carlo (TMCMC) using a massively parallelizable Bayesian unc ertainty quantification framework to a model of disease spreading on a net work of communities\, showing that the method accurately and tractably rec overs system parameters and selects optimal models in this setting.\n\nhtt ps://conferences.maths.unsw.edu.au/event/2/contributions/308/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/308/ END:VEVENT BEGIN:VEVENT SUMMARY:Error-correcting DNA barcodes for high-throughput sequencing DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-389@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: John Hawkins (Institute for Computational Engineerin g and Science\, Department of Molecular Biosciences\, and Institute for Ce llular and Molecular Biology\, The University of Texas at Austin\, Austin\ , TX 78712\, USA)\nMany large-scale high-throughput experiments use DNA ba rcodes—short DNA sequences prepended to DNA libraries—for identificati on of individuals in pooled biomolecule populations. However\, DNA synthes is and sequencing errors confound the correct interpretation of observed b arcodes and can lead to significant data loss or spurious results. Widely- used error-correcting codes borrowed from computer science (e.g.\, Hamming and Levenshtein codes) do not properly account for insertions and deletio ns in DNA barcodes\, even though deletions are the most common type of syn thesis error. We present and experimentally validate FREE (Filled/truncate d Right End Edit) barcodes\, which correct substitution\, insertion\, and deletion errors\, even when these errors alter the barcode length. FREE ba rcodes are designed with experimental considerations in mind\, including b alanced GC content\, minimal homopolymer runs\, and reduced internal hairp in propensity. We generate lists of barcodes with different lengths and er ror-correction levels that may be useful in diverse high-throughput applic ations\, including $>10^6$ single-error correcting 16-mers that strike a b alance between decoding accuracy\, barcode length\, and library size. More over\, concatenating two or more FREE codes into a single barcode increase s the available barcode space combinatorially\, generating lists with $>10 ^{15}$ error-correcting barcodes. Our software for creating barcode librar ies and decoding sequenced barcodes is efficient and designed to be user-f riendly for the general biology community.\n\nhttps://conferences.maths.un sw.edu.au/event/2/contributions/389/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/389/ END:VEVENT BEGIN:VEVENT SUMMARY:Looking beyond the wavelength: exploring the impacts of electrophy siological variability on rotor-driven re-entries using emulation DTSTART;VALUE=DATE-TIME:20180711T015000Z DTEND;VALUE=DATE-TIME:20180711T021000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-341@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Brode Lawson (ARC Centre of Excellence in Mathematic al and Statistical Frontiers (ACEMS) - Queensland University of Technology )\nVariability in electrophysiological properties\, between different cell s in a given heart and between the hearts of different members in a popula tion\, has a profound impact on deciding both the susceptibility to danger ous arrhythmias and the success or failure of anti-arrhythmic treatments. This variability also complicates the interpretation of both experimental and clinical data\, and the predictions of *in silico* models. A key bioma rker in the understanding of arrhythmias is the wavelength of excitation f ronts\, a measure of how much tissue remains refractory in the wake of an excitation impulse. However\, this tissue-level biomarker is found to be u nable to predict the susceptibility to wavebreaks that trigger fibrillatio n. It is therefore important to consider variability in underlying cell-le vel properties more directly. Using a novel combination of supervised lear ning and emulation\, we are able to greatly reduce the computational costs involved with exploring variability in large numbers of parameters\, henc e identifying how differences in these properties impact on some key aspec ts of rotor-driven re-entries\, including risk factors for the devolution into fibrillation.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contri butions/341/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/341/ END:VEVENT BEGIN:VEVENT SUMMARY:Fixation probabilities of mixed-strategies for bimatrix games in f inite populations DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-272@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Takuya Sekiguchi (RIKEN Center for Advanced Intellig ence Project)\nStochastic evolutionary game dynamics in finite populations has recently been examined not only for symmetric games [1] but also for bimatrix games [2]. While in these studies the fixation probabilities of p ure strategies are investigated\, this study examines the evolutionary dyn amics of two-player 2 by 2 bimatrix games with mixed-strategies in finite populations under weak selection. The game has two populations for row and column players. In the population consisting of row (column) players\, tw o types of players\, i.e.\, mutant and wild-type players\, have different mixed-strategies which assign different weight to the two row (column) str ategies. Each player’s fecundity is determined by the average payoff obt ained by interactions with all players in the opposite population. The pro cess of death and birth of players is modelled by the frequency-dependent Moran process.\n\nFor this game\, I derived the fixation probabilities tha t a pair of mixed-strategies by mutants in the row and column populations takes over the entire populations from a given initial state. Moreover\, b ased on the probabilities\, I discuss the stochastic stability of the pair of mixed-strategies played by wild-type players.\n\nIn addition\, the fix ation probabilities of mixed-strategies of mutant players when the selecti on is weak because of mixed-strategies played by mutant and wild-type play ers being very close in terms of a probability distribution over the set o f possible strategies\, which are the counterparts of Wild and Traulsen [3 ] in bimatrix games\, are also discussed.\n\n[1] Nowak\, M. A.\, Sasaki\, A.\, Taylor\, C.\, & Fudenberg\, D. (2004). Emergence of cooperation and e volutionary stability in finite populations. *Nature*\, 428(6983)\, 646.\n [2] Sekiguchi\, T.\, & Ohtsuki\, H. (2017). Fixation probabilities of stra tegies for bimatrix games in finite populations. *Dynamic Games and Applic ations*\, 7(1)\, 93-111.\n[3] Wild\, G.\, & Traulsen\, A. (2007). The diff erent limits of weak selection and the evolutionary dynamics of finite pop ulations. *Journal of Theoretical Biology*\, 247(2)\, 382-390.\n\nhttps:// conferences.maths.unsw.edu.au/event/2/contributions/272/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/272/ END:VEVENT BEGIN:VEVENT SUMMARY:Evidence for history-dependence of influenza pandemic emergence DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T005000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-206@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Edward Hill (University of Warwick)\nInfluenza A vir uses have caused a number of global pandemics\, the most recent being the H1N1 pandemic in 2009\, resulting in considerable human mortality. Despite influenza pandemics being rare events\, with it currently being nearly im possible to predict the next influenza emergence event\, it may be the cas e that the virus itself provides us with outbreak signals that should prom pt us to be more prepared. Specifically\, knowing whether or not influenza pandemic occurrences are uniformly random in time can inform the interven tion strategies that would be best suited to reduce the risk of further pa ndemic events. \n\nTo determine whether the emergence of new pandemic stra ins is a memoryless or history-dependent process\, we analyse the time per iods between influenza pandemics since 1700 statistically under different modelling assumptions. Using Bayesian model selection between exponential and gamma distributions for these time periods\, we demonstrate from these small but informative datasets support for the hypothesis of history depe ndence under eight out of nine sets of modelling assumptions. Using the fi tted parameters to make predictions shows a high level of variability in t he modelled number of pandemics from 2010–2110. \n\nThough the approach we take relies on limited data\, so is uncertain\, it provides cheap\, saf e and direct evidence relating to pandemic emergence\, a field where indir ect measurements are often made at great risk and cost. Our findings suppo rting the presence of history dependence enhances the motivation for imple mentation of active surveillance at the human-animal interface\, in partic ular to elucidate the biological processes behind the observed spacing bet ween pandemics.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribut ions/206/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/206/ END:VEVENT BEGIN:VEVENT SUMMARY:Calcium dynamics within the nuclei of cardiac muscle DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T015000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-309@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hilary Hunt ()\nCardiovascular disease is the leadin g cause of death in Australia\; responsible for 30% of deaths. Diseases th at affect the heart are commonly accompanied by a condition known as hyper trophy — heart enlargement through cell growth. This condition leads to uneven heart beats and\, eventually\, heart failure. \n\nHypertrophy is re gulated by the flow of calcium ions within the cell. Calcium dynamics cont rol the activation of the proteins required for hypertrophic gene expressi on and their localisation to the cell nucleus. However\, there has been li ttle research done on calcium flow within the nuclei of normal heart cells let alone those of diseased hearts.\n\nWe focus specifically on modelling the mechanics of calcium flow within the nucleus and distinguishing the s ignal for heart cell growth in the nucleus where gene expression takes pla ce over the background signal for the heartbeat. Using a finite element mo del\, we describe the spatiotemporal properties of these background calciu m oscillations as they propagate into the nucleus. We verify this model wi th existing data to produce a clearer picture of the calcium dynamics invo lved in initiating hypertrophy.\n\nhttps://conferences.maths.unsw.edu.au/e vent/2/contributions/309/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/309/ END:VEVENT BEGIN:VEVENT SUMMARY:Topological analysis of the three dimensional structure of antibod y DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-398@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Haru Negami (The University of Tokyo)\n*In silico* p rediction of the relationships between the protein structure and its physi ological activity is an important research topic for drug design. Broad pi cture of my research is to construct a topological model to clarify the an tibody-antigen recognition system\, since immunotherapy is applied to wide range of severe diseases such as cancer [1].\n \nTo achieve the goal\, we focus on a topological method called “Fatgraph models of proteins” [2 ]. Fatgraph models of proteins are topological two-manifold with boundary components (surface) which have one to one correspondence with three-dimen sional protein structures listed on Protein Data Bank (PDB) [3] with only a few exceptions. The traits of each surface for each protein are describe d by the following invariants\; Euler characteristics\, number of boundary components\, and genus. Fatgraph is also called ribbon graph and has alre ady proven their utility in theoretical physics including string theory [4 ].\n\nIn this research\, we constructed fatgraph models of antibodies and investigated the traits of antigen-binding fragments (Fab). Then\, we topo logically examined the transformations of the fatgraphs of the proteins du e to the changes of protein sequences or existence of ligands.\n\n[1] Pate l\, Shetal A. et al. (2018) Combination Cancer Therapy with Immune Checkpo int Blockade: Mechanisms and Strategies\, *Immunity*\, Volume 48\, Issue 3 \, 417 - 433\n\n[2] R. C. Penner\, *et al*.\, (2010) Fatgraph models of pr oteins\, *Communications on Pure and Applied Mathematics*. Volume 63 \, Is sue 10 \, 1249 - 1297.\n\n[3] H.M. Berman\, *et al*. (2000) The Protein Da ta Bank\, *Nucleic Acids Research*\, 28: 235 - 242. http://www.rcsb.org/\n \n[4] R. C. Penner\, (2016) Moduli spaces and macromolecules. *Bull. Amer. Math. Soc.* 53\, 217 - 268.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/398/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/398/ END:VEVENT BEGIN:VEVENT SUMMARY:Model of adipocytes size distribution DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T005000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-205@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hedi Soula (Sorbonne University\, PARIS)\nAdipose ti ssue and adipocytes play a central role in the pathogenesis of metabolic d iseases related to obesity. Size of fat cells depends on the balance of sy nthesis and mobilization of lipids and can undergo important variations th roughout the life of the organism. These variations usually occur when sto ring and releasing lipids according to energy demand. This energy is store d as lipid droplets in their cytoplasm therefore adipocytes can adapt thei r size according to the lipid amount to be stored. Adipocyte size variatio n can reach one order of magnitude inside the same organism which is uniqu e among cells. A striking feature in adipocytes size distribution is the l ack of characteristic size since typical size distribution are bimodal. Si nce energy can be stored and retrieved and adipocytes are responsible for these lipid fluxes\, we proposed a model of size-dependent lipid fluxes th at exhibits bimodal equilibria with generic conditions. This model is a no n-linear transport equation structured by the size of adipocytes and we pr ovide a dedicated a stable numerical scheme solver able to capture the sin gular behaviour of solutions as concentration to Dirac masses. Using this solver\, we are able to infer parameters related to lipid fluxes from siz e distribution. Performing recurrent surgical biopsies on rats\, we measur ed the evolution of adipose cell size distribution for the same individual throughout the duration of feeding/refeeding experiments and use this dat a to assess fluxes parameters variations throughout the experiment.\n\nhtt ps://conferences.maths.unsw.edu.au/event/2/contributions/205/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/205/ END:VEVENT BEGIN:VEVENT SUMMARY:Investigating the dynamics of coupled epidemiological transmission models with application to Group A Streptococcus and Scabies DTSTART;VALUE=DATE-TIME:20180710T021000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-209@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Michael Lydeamore (The University of Melbourne)\nInf ections with Group A Streptoccocus (GAS) are highly prevalent in remote co mmunities in\nthe Northern Territory\, Australia. One of the primary drive rs of GAS infection is scabies\, a small mite which causes a break in the skin layer\, potentially allowing GAS to take hold. This biological connec tion is reaffirmed by the observation that mass treatment for scabies in t hese remote communities sees a reduction in the prevalence of GAS infectio n\, despite GAS not being directly targeted. In the most extreme case\, it has been hypothesised that the eradication of scabies in remote communiti es may lead to an eradication of GAS related infection.\n\nWe start by pro posing a model of GAS transmission that assumes that scabies dynamics are at equilibrium. We assume that GAS follows a Susceptible – Infectious – Susceptible (SIS) structure\, but individuals who are infected with sc abies experience an increased force of infection compared to those who are not infected with scabies. In consequence\, we are able to calculate the required prevalence of scabies required to ensure that GAS is eradicated\, as a function of $R_0$ and the coupling strength between the two infectio ns.\n\nIn order to more accurately model the impact of mass treatment for scabies\, we extend this model to include the dynamics of scabies infectio ns. We consider two different scabies models: one which includes the full dynamics of the scabies mites\, and one which collapses these dynamics dow n to a far simpler phenomenological model. We investigate the difference i n the scabies rebound dynamics after mass treatment for these two models\, and consider the impact of this difference on the dynamics of GAS. We sho w that despite the two scabies models having different mean field dynamics \, parameter uncertainty and the small population size mean that this diff erence is severely muted when considering the post-scabies treatment on GA S. Finally\, we compute a value for the increased force of infection exper ienced by those infected with scabies\, below which eradication for GAS wo uld be achieved if scabies were eradicated.\n\nhttps://conferences.maths.u nsw.edu.au/event/2/contributions/209/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/209/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling of cancer cell morphological and phenotypic plasticity in response to the extracellular matrix DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-261@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Vlada Rozova (Macquarie University)\nThe occurrence of distant metastases greatly reduces or even removes the possibilities of curative treatment for cancer patients. The development of tools for pred icting and diagnosing the onset of secondary tumours has long been a signi ficant subject of cancer research effort. Moreover\, it is widely known th at while in some tissues cancer cells exhibit higher proliferation\, in ot hers they are more invasive so the best treatment strategy should be chose n accordingly.\n\nA novel tissue engineering approach was created in our g roup in order to gain insight into the processes of cell growth\, motility and invasion. Organ-specific scaffolds were seeded with highly invasive t riple negative breast cancer cells. These tissue engineering constructs (T ECs) were then cultured in vitro for 4 weeks and the resulting patterns of cell colonisation of extracellular matrix (ECM) were analysed.\n\nOne of the most noteworthy results of this experiment is the emergence of two alt ernative strategies of matrix colonisation depending on the origin and str ucture of the underlying ECM. In particular\, we observed significant diff erences in cellular attachment efficiency\, morphology\, density and invas ion of the breast cancer cells.\n\nTo gain a better understanding of cellu lar behaviours and validate the hypothesis that colonisation pattern stron gly depends on the properties of ECM\, we developed a corresponding mathem atical model of tumour growth in TECs. For these purposes\, we used a latt ice-based stochastic approach based on the energy formalism\, where the co ncept of cell adhesion is considered the key mechanism of cell-cell and ce ll-ECM interactions. Our model reproduces the early stage of the experimen t (the stage characterised by rapid colonisation of surface and subsurface matrix layers) showing a clear distinction in cell morphology and spatial distribution when varying the density of adhesion molecules expressed on the matrix. \n\nFurther\, to expand the computational model and attribute the role of the underlying ECM to cell invasion and clustering inside the tissue\, we ran a set of single-factor experiments\, each designed to reve al the effect of a specific physical property of the matrix. Statistical a nalysis of the experimental data provides estimations of model parameters and complements the picture of cell-matrix interactions. \n\nWe believe th at this data-driven approach will allow predicting phenotypical and morpho logical changes of cancer cells and the subsequent preferred mode of tissu e colonisation\, which is essential for the choice of appropriate treatmen t.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/261/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/261/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling of a moving net observed in a plant endoplasmic reticulu m DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-284@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Akiko Nakamasu (Kumamoto University)\nAn endoplasmic reticulum (ER) is a tubular organelle observed in cells of eukaryote incl uding the plants and animals. Interacting with flow of actin cytoskeleton\ , the net-like pattern organized by ER in plant cells is continuously movi ng.\n\n For the understanding of this system\, we constructed a mathematic al model based on a partial differential equation (PDE). By combining two spatially distributed structures\, an arbitral periodic pattern by PDE and an actin mesh dependent perturbation\, we successfully obtained the dynam ics of the system. \n\nIn this model\, it was found that the filamentous a ctin distribution was not necessarily needed and static perturbations were sufficient to move the pattern. Then the pattern periodicities were distu rbed when the dynamics of system could be observed. Therefore\, we inferre d that\, though it might seem paradoxical\, the capacity to maintain the o rder and the symmetry of pattern generate the dynamics.\n\nThis theory is considered to explain one of the basic elements to generate a dynamic patt ern\, therefore\, further discussions are needed to define the minimal con ditions for giving the motility. We will comparative investigate the follo wing points (1) pattern property effected by the perturbations and (2) dis tribution manners and types of perturbation. Then the periodicity and the motilities of pattern will be analyzed quantitatively.\n\nhttps://conferen ces.maths.unsw.edu.au/event/2/contributions/284/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/284/ END:VEVENT BEGIN:VEVENT SUMMARY:Comparative physiological energetics of three commercial tuna spec ies DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-475@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Marko Jusup (Tokyo Institute of Technology)\nIntersp ecies comparisons of physiological energetics are possible only through th e prism of a formal metabolic approach such as the Dynamic Energy Budget ( DEB) theory which uniformly describes how individuals of different species acquire and utilise energy. We used the DEB theory to infer the energy bu dgets of three commercial tuna species (skipjack\, Pacific bluefin\, and A tlantic bluefin) throughout all stages of ontogenetic development---from a n egg to an adult individual and its eggs. Energy budgets were inferred fr om scarce and disjointed data sets fed into a DEB-based mathematical model tailored for tuna fish until reaching a high goodness of fit and thus the reliable estimates of the model parameters.\n\nThe results show that life histories of all three species are strongly influenced by morphological a nd physiological adaptations which accelerate ontogeny during the larval s tage\, although the effect is more pronounced in bluefin than skipjack tun a. We identify that in energetic terms the accelerated ontogeny is a simul taneous improvement of energy acquisition (higher intake) and utilisation (higher expenditure) without changing the capacity of fish to build energy reserve as intake and expenditure increase in unison. High energy expendi ture\, an even higher intake by necessity\, and a limited capacity to buil d energy reserve\, make all three tuna species vulnerable to starvation\, thereby theoretically underpinning the description of tuna fish as “ener gy speculators”. We furthermore find that energy allocation to reproduct ion maximises fecundity of all three tuna species\, thus suggesting that t he evolution of tuna favoured higher fecundity at the expense of growth.\n \nThinking beyond just physiological energetics (e.g.\, wild stock project ions)\, we discuss why DEB-based models are a natural foundation for physi ologically structured population dynamics wherein the environment influenc es the population growth rate via metabolism. We suggest several concrete modelling techniques which allow progress in this direction.\n\nhttps://co nferences.maths.unsw.edu.au/event/2/contributions/475/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/475/ END:VEVENT BEGIN:VEVENT SUMMARY:A multiscale PDE model of hepatitis C virus infection formulated t o ODE model DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-406@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kitagawa Kosaku (Graduate School of Systems Life Sci ences\, Kyushu University\, Japan.)\nDirect-Acting antivirals (DAAs) targe t intracellular viral replication and have realized high effectiveness for hepatitis C virus (HCV) patients. Now\, many kinds of DAA drugs have disc overed and the HCV treatment is improving day by day. A popular strategy o f HCV treatment is combination of double or triple DAA drugs with differen t action mechanisms. Mathematical model is used to analyze the dynamics o f virus infection and effectiveness of antiviral drugs. For DAA treatment\ , multiscale model formulated by partial differential equations (PDE) desc ribing both intercellular virus infection and intracellular virus RNA repl ication is used. However\, in general\, numerical computation of PDE often converge poorly and is time consuming. So it is somewhat hard to estimate parameters\, and we should transform the PDE to easier form in advance of analyzing the model. In our study\, we transformed the PDE model to ODE f orm without any assumption. Thus our ODE model and the previous PDE model are mathematically identical. By this transformation\, the time required f or numerical simulation is reduced greatly and we can apply some basic ana lysis methods for dynamical systems of ODEs to the multiscale model.\n\nht tps://conferences.maths.unsw.edu.au/event/2/contributions/406/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/406/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling the spread of antimicrobial resistance in hospital DTSTART;VALUE=DATE-TIME:20180711T064000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-310@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mochamad Apri (Dept. of Mathematics\, Institut Tekno logi Bandung\, Indonesia)\nAntibiotic resistance has become one of the maj or health issues in the world. It kills around 700\,000 people each year w orldwide\, and will become even worse if no new antibiotics are developed (Nature\, 2017). Therefore\, serious efforts are required to prevent more severe conditions in the future. One important effort in this case is unde rstanding the dynamics of the problem so that effective policies can be pr epared. To understand the dynamics of the problem\, we propose a mathemati cal model that describes the interaction between sensitive and resistant b acteria with human population. Here\, we focus on the spread of antimicrob ial resistance in the hospital environment. We assume that bacteria popula tion can be grouped into two compartments\; resistant and sensitive popula tions\, whereas patients population can be distinguished as uncolonized pa tient\, sensitive-colonized patient\, or resistant-colonized patient. Thus \, the model that we develop is a two-level population model. A sensitive bacterium can be resistant due to\, e.g.\, interactions with resistant bac teria\, gene mutation\, etc. An uncolonized patient or sensitive-colonized patient can be contaminated by resistant bacteria when he/she gets contac t with unsterilized medical equipment\, contaminated environment\, etc. We consider the cases when patients are treated and not treated with antibio tics. In the first case\, even if we consider that all patients that are a dministered to the hospital are uncolonized\, eventually all of them will become colonized by resistant bacteria from the environment after a certai n time interval. Therefore\, apart from applying different strategies on t he use of antibiotic\, hygiene of environment is also playing crucial role in controlling the spread of the resistance. We show this via stability o f the disease-free and endemic equilibrium of the model. Some numerical si mulations will also be presented.\n\nhttps://conferences.maths.unsw.edu.au /event/2/contributions/310/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/310/ END:VEVENT BEGIN:VEVENT SUMMARY:Influence of receptor recharge on the statistics of captured parti cles DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-245@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Gregory Handy (University of Utah)\nWe consider a se tup in which $n$ particles are initially released into a domain and diffus e freely. Part of the boundary consists of absorbing "escape" regions\, wh ere the particles can escape the domain\, and reflecting regions. The rest of boundary consists of "capture" regions (receptors)\, that can switch b etween being reflecting and absorbing. Specifically\, after capturing a pa rticle\, the capture region becomes reflecting for an exponentially distri buted amount of time (recharge time). We are interested in the distributio n of the number of particles that are captured before they escape.\n\nOur mathematical results are derived from considering our system in several wa ys: as a full spatial diffusion process with recharging traps on the bound ary\; as a continuous-time Markov process approximating the original syste m\; and lastly as a system of ODEs in a mean-field approximation. \n\nCons idering the full spatial diffusion process\, we prove that the total expec ted number of the captured particles has an upper-bound of the order of (l og $n$). We then consider a few examples investigating the implications o f this result\, including a neural system in which recharge reduces the nu mber of neurotransmitter bindings by several orders of magnitude.\n\nSeeki ng additional understanding of this process over a wide range of parameter values\, we then present a well-defined algorithm to approximate the full spatial diffusion process with a continuous-time Markov process in order to eliminate computationally expensive simulations. We highlight the condi tions required for the approximation to yield similar quantitative results as the full spatial process. We then apply the approximation\, and the as sociated mean-field model\, to investigate time courses for the expected n umber and higher ordered statistics of captured particles. Specifically\, we find that the number of expected captures as a function of time appears to grow linearly\, before leveling off\, and find an analytical expressio n for the duration of the linear growth. This result may be particularly h elpful for understanding applications where multiple puffs of particles ar e inserted in the domain over a period of time (e.g. neuronal synapses)\, and can provide a bound on the time between puff events such that particle s in different puffs no longer interact. We also find that the amount of v ariation observed in the total number of captured particles varies non-mon otonically with the mean recharge time. Lastly\, we combine these results together to predict stochastic properties of intracellular signals resulti ng from receptor activation.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/245/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/245/ END:VEVENT BEGIN:VEVENT SUMMARY:Stopping waves: geometric analysis of coupled bursters in an asymm etric excitation field DTSTART;VALUE=DATE-TIME:20180709T054000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-311@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Iulia Martina Bulai (University of Padova\,Italy)\nB ursting is a type of electrical activity seen in many neurons and endocrin e cells where episodes of action potential firing are interspersed by sile nt phases. Pancreatic $\\beta$-cells show so-called square-wave bursting w hen stimulated by glucose\, which causes ${\\text Ca^{2+}}$ oscillations a nd pulsatile insulin secretion. $\\beta$-cells are electrically coupled wi thin pancreatic islets\, and excitation waves are observed to propagate th rough the $\\beta$-cell population. When the islet is exposed to a glucos e gradient\, so that some cells would be active also when uncoupled while others would be below the activity threshold and thus silent\, ${\\text Ca ^{2+}}$ waves propagate only partly through the islet and stop approximate ly where the glucose concentration is at the threshold for cellular activi ty. Simulations of existing mathematical models of coupled $\\beta$-cells produce waves that propagate too far into the region of "silent" cells\, c ompared to experiments\, unless unrealistic model assumptions are imposed. Here\, we investigate why $\\beta$-cell models fail to reproduce the expe rimentally observed wave properties and tend to synchronize the $\\beta$-c ell population too easily\, by using a prototypical polynomial bursting mo del and slow/fast bifurcation analysis. Our analyses indicate how to modif y the model so that the excitation waves stop at the border between "activ e" and "silent" cells. We verify this property by simulations using such a modified model for a chain\, and for a cubic cluster\, of coupled $\\bet a$-cells. Furthermore\, we show how our one- and two-parameter bifurcation analyses allow us to predict where the simulated waves stop\, for both th e original model and the modified version. Our results indicate the geomet rical structure that biophysical $\\beta$-cell models should have to posse ss biologically realistic wave and synchronization properties.\n\nhttps:// conferences.maths.unsw.edu.au/event/2/contributions/311/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/311/ END:VEVENT BEGIN:VEVENT SUMMARY:Unravelling molecular basis of masting from transcriptome analysis and mathematical modelling DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-71@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Akiko Satake (Department of Biology\, Fuculty of Sci ence\, Kyushu University\, Japan)\nThe intermittent and synchronized produ ction of a large amount of flowers and seeds is called masting or mast see ding. A family of resource budget models have been effective to evaluate p roximate causes of masting. Applying recent advances in molecular and gene tic studies about flowering time control to masting species is increasingl y useful to unravel the underlying mechanism of masting. To uncover the mo lecular basis of masting\, we performed global gene expression analyses in a typical masitng species\, *Fagus crenata Blume*. Using nonlinear time-s eries analyses\, we examined causal relationships between gene expression\ , physiological status\, and external environmental conditions. Our analys es unraveled the non-intuitive relationship between seasonal environment a nd expression profiles of genes involved in photoperiod and circadian cloc k pathways. The most striking result was the causal interaction between ni trogen transporter activity and expression of floral pathway integrator\, *FLOWERING LOCUS T*. This result supports our previous finding that nitrog en is the key regulator of flowering in *F. crenata*. Our results highligh t the importance of linking plant reproductive dynamics and nutrient cycli ng at ecosystem levels.\n\nhttps://conferences.maths.unsw.edu.au/event/2/c ontributions/71/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/71/ END:VEVENT BEGIN:VEVENT SUMMARY:Multi-cellular modelling of cellular mechanisms gives insights on the maintenance of epidermal tissue structure DTSTART;VALUE=DATE-TIME:20180709T060000Z DTEND;VALUE=DATE-TIME:20180709T062000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-330@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Claire Miller (The University of Melbourne)\nThe int er-follicular epidermis (IFE) forms the outer-most layer of the skin. Many individual components fundamental to healthy IFE structure are known: pro liferation occurs only in a basal layer\; above this layer cells different iate into keratinocytes forming further distinct layers before they are sh ed from the surface. However\, a definitive understanding of how the balan ce between proliferation\, differentiation\, and cell shedding is maintain ed in IFE tissue during homeostasis does not yet exist.\n \nWe have develo ped an agent-based multi-cellular computational model to simulate tissue h omeostasis in the skin. Epidermal cells are represented as overlapping sph eres\, and cell divisions are represented as stochastic time-driven events . Cell movement is determined by adhesive attractive forces and repulsive forces between other cells and the basal membrane. The magnitude of these forces depends upon the types of the interacting bodies\, and can vary dep ending on factors such as cell age and location.\n \nUsing this model we h ave analysed the impact of different cell mechanisms and behaviours on the tissue in order to investigate alternate hypotheses around maintenance of tissue structure. Results of this study provide insights into the critica l mechanisms and behaviours\, and will guide the future integration of det ailed biochemical regulation processes.\n\nhttps://conferences.maths.unsw. edu.au/event/2/contributions/330/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/330/ END:VEVENT BEGIN:VEVENT SUMMARY:Discriminating response across treatments using the patient-specif ic model-derived days gained metric DTSTART;VALUE=DATE-TIME:20180711T054000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-403@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kyle Singleton (Precision Neurotherapeutics Innovati on Program\, Department of Neurological Surgery\, Mayo Clinic\, Phoenix\, AZ)\nAccurate clinical assessment of a patient's response to treatment is a critical task in the era of precision medicine. Glioblastoma (GBM)\, a p rimary brain tumour with dismal median survival times of 12-16 months\, ha s a highly heterogeneous\, invasive profile\, causing tumour dynamics and therapeutic response to vary widely from patient to patient. Currently\, t wo sets of standard assessment criteria are used\, RANO and iRANO (for sta ndard radiation and chemotherapy versus immunotherapy\, respectively)\, fo r evaluating changes in tumour size following treatment to determine whet her a patient responded to that treatment. In addition\, when complex imag ing transformations\, such as pseudo-progression\, occur in response to th erapy these metrics require long follow-up times of 3-6 months. Therefore\ , it has been difficult for physicians to use existing metrics to define o ptimal treatment schedules\, including when to maintain or switch therapie s.\n\nUsing the Proliferation-Invasion (PI) model\, the unique kinetics of individual patients’ tumours can be simulated using derived rates of ce ll proliferation (ρ) and invasion (D) from serial magnetic resonance imag ing (MRI). These models serve as untreated virtual controls of tumour grow th\, enabling comparisons against post-treatment imaging to generate a pat ient-specific “Days Gained” (DG) response metric. DG values were evalu ated across a variety of primary and secondary therapies for thresholds di scriminating long and short-term survivors.\n\nSignificant DG thresholds w ere found using follow-up imaging 1-2 months post therapy in patients rece iving cytotoxic\, radiation\, and immunotherapeutic treatments. High DG th resholds were associated with better survival in standard radiation and ch emotherapy treatments. In contrast\, low DG values were discriminative of longer survival for immunotherapy due to the well known pseudo-progression effect of image-detectable inflammation response. The DG metric therefore demonstrated utility as a single\, patient-specific method for judging re sponse across multiple therapies with different response profiles that cur rently require distinct evaluation criteria (RANO and iRANO respectively). In addition\, Days Gained was assessable in a similar or shorter time win dow than the existing metrics. Taken together\, these data support the uti lity of the model-derived response metric\, Days Gained\, in a diversity o f clinical settings to quantitatively connect response with patient surviv al.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/403/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/403/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling and characterizing the folding patterns of the human bra in DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-447@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Monica Hurdal (Florida State University\, Department of Mathematics)\nThe human brain consists of folds (gyri) and valleys (su lci) that vary dramatically in their size\, extent\, and shape across indi viduals. There is considerable debate among biologists as to how the foldi ng patterns develop and if the folding patterns can be used to diagnose di sease. In this presentation\, I will discuss some of the mathematical and modelling approaches my research group is developing to study coritical fo ld formation\, Turing patterns\, topology\, conformal mapping\, and confor mal invariants are some of the methods we are using to model and character ize the folding patterns of the brain in development\, health\, and diseas e. By altering various model parameters\, including domain size and scalin g\, results from our model can be correlated with cortical folding disease s such as lissencephaly and microcephaly.\n\nhttps://conferences.maths.uns w.edu.au/event/2/contributions/447/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/447/ END:VEVENT BEGIN:VEVENT SUMMARY:Multiscale adaptive analysis of circadian rhythms in the study of acute insomnia DTSTART;VALUE=DATE-TIME:20180711T011000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-452@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Maia Angelova (Deakin University)\nCircadian analysi s is becoming increasingly important as a diagnostic tool to quantify devi ations from regularity in circadian cycles. Circadian rhythms become less dominant and less regular with ageing and disease. It has been hypothesize d that insomnia might be related to alterations\, albeit small\, in circad ian and ultradian rhythms\, but this topic remains an open problem. In thi s work\, we propose a novel data-adaptive technique\, singular spectrum an alysis (SSA)\, to investigate in a model-free way quasiperiodic components and noise fluctuations in time series data. SSA was applied to one-week c ontinuous actigraphy data in young adults with acute insomnia and healthy age-matched controls [1]. The findings suggest a small but significant del ay in circadian components in the subjects with acute insomnia. The ultrad ian components follow a fractal $1/f$ power law for controls\, however for individuals with acute insomnia this power law breaks down due to an incr eased variability at the 90min time scale. This is reminiscent of Kleitma n's basic rest-activity (BRAC) cycles. It indicates that for healthy slee pers attention and activity can be sustained at time scale required by cir cumstances\, while for individuals with acute insomnia this capacity may b e impaired and they need to rest or switch activities in order to stay foc used. Traditional methods of circadian rhythm analysis are unable to detec t the more subtle effects of day-to-day variability and ultradian rhythm f ragmentation at the specific 90min time scale.\n\n[1] R Fossion\, AL River a\, JC Toledo-Roy\, J Ellis and M Angelova. Multiscale adaptive analysis o f circadian rhythms and intradaily variability: Application to actigraphy time series in acute insomnia subjects. *PLOS One*\, 12(7): e0181762 (2017 ).\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/452/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/452/ END:VEVENT BEGIN:VEVENT SUMMARY:How feedback mechanisms shape calcium oscillations in Hepatocytes DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-314@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ielyaas Cloete (University of Auckland)\nVariation o f calcium concentration in hepatocytes (liver cells) is known to modulate diverse cellular functions\, including bile secretion\, glucose and energy metabolism and vesicular trafficking. A major question in the study of ca lcium signalling in hepatocytes is how these distinct cellular processes a re controlled and organised via coordinated spatial and temporal calcium s ignals.\n\nDownstream cellular responses are controlled via intracellular calcium oscillations but the underlying mechanisms which shape these oscil lations have yet to be elucidated. We are interested in determining the ef fects of various types of calcium feedback mechanisms such as calcium feed back on Phospholipase C (PLC) and the calcium-mediated protein kinase C (P KC) feedback on the hormone receptor have on the whole-cell calcium signal s. Recent experimental data suggests that hormone-induced calcium oscillat ions require positive calcium feedback on PLC to generate inositol trispho sphate oscillations\, yielding cross-coupling between calcium and inositol trisphosphate. Furthermore\, it appears that there is also a negative fee dback pathway\, cross-coupling PLC activation to PKC\, which serves to ter minate calcium spikes.\n\nThis talk will discuss recent progress in constr uction and analysis of a model of calcium oscillations that incorporates t he new experimental results about likely feedback mechanisms in hepatocyte s.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/314/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/314/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling for pacemaker-neuron-dependent molecular rh ythm alteration by Drosophila clock mutant DTSTART;VALUE=DATE-TIME:20180711T013000Z DTEND;VALUE=DATE-TIME:20180711T015000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-429@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Euimin Jeong (KAIST)\nIn Drosophila\, circadian (~24 h) behaviour is regulated by about 150 pacemaker neurons. To generate and maintain 24h rhythm\, circadian gene expression in each pacemaker neurons is driven by transcriptional-translational feedback loop (TTFL). In TTFL o f Drosophila\, dCLOCK-CYCLE (dCLK-CYC) binds to the E-box (CACGTG) and act ivates the expression of period (per) and timeless (tim). Translated PER a nd TIM proteins repress their own transcription by removing dCLK-CYC dimer from the E-box. Interestingly\, dCLK-Δ\, which is a mutant of dCLK delet ed amino acids (AA) 657-707 region and has impaired binding with PER\, ind uces different effect on molecular rhythms depending on pacemaker neurons. For oscillation of PER\, amplitude is largely reduced in ventral lateral neurons (LNvs)\, but not in dorsal neurons (DNs). However\, how dCLK-Δ/CY C controlled TTFL operates differently in pacemaker neurons is unclear. To investigate this unexpected phenomenon\, we established the mathematical model for the TTFL in Drosophila and predicted that pacemaker-neuron-depen dent alteration of the molecular clockwork is caused by the difference of molecular composites between LNvs and DNs. This is confirmed by the follow up experiment. This work shows that clockworks at the molecular level hav e a critical role for specific functions of each pacemaker neurons.\n\nhtt ps://conferences.maths.unsw.edu.au/event/2/contributions/429/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/429/ END:VEVENT BEGIN:VEVENT SUMMARY:The response of net primary production to future climate change an d CO2 under RCP4.5 in China DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-226@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Guodong Sun ()\nIn this study\, the maximal extent o f future NPP uncertainties are explored by employing the conditional nonli near optimal perturbation related to parameters (CNOP-P) approach and the Lund-Potsdam-Jena (LPJ) model based on future climate change assessments\, which are provided by 10 general circulation models (GCMs) of the Coupled Model Intercomparison Project 5 (CMIP5) under the Representative Concentr ation Pathway (RCP) 4.5 scenario at the North-South Transect of Eastern Ch ina (NSTEC). We find that the future NPP will increase due to climate chan ge and CO2\; however\, there is a difference in the extent of the variatio n resulting from the 10 GCMs and the CNOP-P approach. Future NPPs are esti mated from 3.89 Gt C (MRI-CGCM3 model) to 4.51 Gt C (bcc-csm1-1 model) usi ng the LPJ model driven by the outputs of 10 GCMs. The estimates of NPP wi th two types of CNOP-P-type climate change scenarios are 4.74 Gt C and 5.3 1 Gt C and are larger than other estimates of NPP. The above results imply that the terrestrial ecosystem supplies possible conditions for future ca rbon sinks for all climate change scenarios\, especially for the CNOP-P-ty pe climate change scenarios\, although the estimates remain uncertain. Sti mulative photosynthesis due to high precipitation and restrained autotroph ic respiration due to low temperatures may play important roles in the car bon sink due to the CNOP-P-type climate change and CO2 in all climate chan ge scenarios. In addition\, it is found that the combination of climate ch ange and CO2 is also a key factor in the increase of NPP.\n\nhttps://confe rences.maths.unsw.edu.au/event/2/contributions/226/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/226/ END:VEVENT BEGIN:VEVENT SUMMARY:Mass depending maze exploration strategy for true slime mold DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-286@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kentaro Ito (Department of Frontier Bioscience\, Hos ei University)\nTrue slime mold *Physarum polycepharum* is a large uni-cel lular amoeba-like organism and it can sense environmental information and change its behaviours. Large true slime mold extends its frontal parts for foraging. To study its exploration strategy\, we observed how *physarum* spreads in a *binary-tree-shaped* maze. We found that slime mold changes i ts searching strategies when its total mass changes. To explain this resul t\, we made a new mathematical model which consists of cylinders filled wi th liquid\, periodic contracting active springs\, tubes connecting between cylinders and the elastic sheet. In our model\, the pressure has an impor tant role to transmit information among frontal parts. Our model reproduce s fundamental characteristics of the front expanding and the searching beh aviours of slime mold.\n\nhttps://conferences.maths.unsw.edu.au/event/2/co ntributions/286/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/286/ END:VEVENT BEGIN:VEVENT SUMMARY:Reconstruction of the complex trajectories of cell developments ba sed on single-cell RNAseq data DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-369@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Lin Wan ()\nThe unprecedented accumulation of high-t hroughput single-cell RNAseq data provides an essential opportunity for re searchers to study the dynamics of biological systems. At the same time\, it raises new questions and grand challenges in view of the key characteri stics of these data that include high-dimensionality and heterogeneity. In response\, we develop a data-driven computational framework to map and re construct of dynamical trajectories of cell based on the high-dimensional molecular profiles from snapshot single-cell data. By integrating tools fr om topological data analysis (level-set method) and the nonparametric stat istics\, we first perform nonlinear dimension reduction on the data to con struct the cell developmental landscape\, and then reconstruct the complex trajectories by finding the cell state transition path on the landscape. We apply this method in the analysis of cell developmental processes and p rovide novel insights into the field of mathematical and computational bio logy.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/369/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/369/ END:VEVENT BEGIN:VEVENT SUMMARY:Numerical study of airway smooth muscle and airway wall coupled dy namics. DTSTART;VALUE=DATE-TIME:20180711T021000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-446@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Anand Rampadarath (The University of Auckland)\nAsth ma is fundamentally a disease of airway constriction. Due to a variety of experimental challenges\, the dynamics of airways are poorly understood. O f specific interest is the narrowing of the airway due to forces produced by the airway smooth muscle (ASM) wrapped around each airway. The interact ion between the muscle and the airway wall is crucial for the airway const riction which occurs during an asthma attack. While crossbridge theory is a well-studied representation of complex smooth muscle dynamics\, and thes e dynamics can be coupled to the airway wall\, this comes at significant c omputational cost\, even for isolated airways. Because many phenomena of i nterest in pulmonary physiology cannot be adequately understood by studyin g isolated airways\, this presents a significant limitation. We present re sults associated with the development of an approximated method (distribut ion moment approximation) which provides orders of magnitude reduction in computational complexity whilst retaining rich ASM dynamics. This method i s then used to model physiological processes such as airway contraction\, bronchodilatory effect of a deep inspiration and preliminary results assoc iated with heterogeneity of branched airways.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/446/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/446/ END:VEVENT BEGIN:VEVENT SUMMARY:A common theory for proportion regulation in animals DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-252@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mayuko Iwamoto (Shimane University)\nOne of the fund amental problems in biology would be the method by which organisms can reg ulate a distribution in response to global information. For example\, a cl uster of organisms can regulate the proportion of individuals that perform various roles or modes as if each individual is aware of the overall situ ation without a leader. Slow or rapid self-organized pattern formations wi th time evolution on animal skins might also be one of the processes of ra tio regulation of pigment cells. Thus\, in various species\, a specific ra tio exists at multiple levels\, from the process of cell differentiation i n multicellular organisms to the situation of social dilemma in a group of human beings. In this study\, we consider individual that means a particl e who has a certain size and internal mode\, then propose a common basis f or regulating collective behaviour that is realized by a series of local c ontacts between individuals. The most essential behaviour of individuals i s to change their internal mode by sharing information when in contact wit h others. Our numerical simulations and analysis for regulating the propor tion in two kinds of modes show that asymmetric properties in local contac ts are essential for adaptive regulation in response to global information . In this poster\, some actual examples of proportion regulation are descr ibed and applicability of our theory would be verified. We will discuss th at this simple mechanism of this theory could indicate that well-organized groups in nature can be regulated through local contacts only.\n\nM. Iwam oto & D. Ueyama\, “Basis of self-organized proportion regulation resulti ng from local contacts”\, *Journal of Theoretical Biology*\, 440 (2018) 112–120.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 252/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/252/ END:VEVENT BEGIN:VEVENT SUMMARY:Stability analysis of a mathematical model with distributed delay DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-232@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Zenab Alrikaby ()\nGene expression and genetic regul atory networks (GRNs) have become important areas of study because they pl ay an important role in solving issues related to human health such as can cer diseases. Cancers can be hard to recognise and the best way to improve their defected is to understand the underlying mechanisms of genetic reg ulatory dynamics. This means introducing and improving mathematical model s of GRNs to reflect oscillatory phenomena. In this work\, we propose a l ac operon model with time delay and nonlinear degradation rate for mRNA an d investigate the nonlinear dynamical behaviour arising from the model\, such as stability and Hopf bifurcation of the equilibrium\, by taking the average delay as the bifurcation parameter. From the dynamical behaviour o f this system: the equilibrium is stable in the absence of delay or when t he delay is small\; as time delay increases gradually then the stability c hanges and Hopf bifurcation happens. Then reverse a Hopf bifurcation to translate the equilibrium of the system from unstable to stable steady st ate.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/232/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/232/ END:VEVENT BEGIN:VEVENT SUMMARY:Quantifying convergence of the Kingman coalescent via the ancestra l process per generation DTSTART;VALUE=DATE-TIME:20180709T095900Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-501@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Paul Slade ()\nError threshold being the forefront o f the issue for computationally-intensive methodologies and statistical mo dels based on Kingman’s coalescent\, six main points arise: (i) discrepa ncy between the exact and linearized non-coalescence probability\; (ii) va lidity of the linearized coalescence probability\; (iii) conditional proba bilities of single-pair and multi-coalescences given at least one coalesce nce\; (iv) parity of reduced ancestral processes that suppress multi-coale scences\, when compared to the exact ancestral process\; (v) genealogical topology\; and (vi) subsequent inter-arrival times. Regions of adherence and detraction from the Wright-Fisher ancestral process were identified\, in terms of transition probabilities and expected inter-arrival times\, du e to the linearization of Kingman’s coalescent that neglects multi-coale scence events. Empirically\, expected genealogical parity of the single-p air restricted Wright-Fisher haploid model exceeds 99% where $n\\leq \\fra c{1}{2} \\sqrt[3] N$\; similarly\, per expected interval where $n\\le {1\\ over 2} \\sqrt{N\\over 6}$. Quantitative parametric analysis on the varie ties of multi-coalescence events in restricted Wright-Fisher models\, rath er than stochastic realization\, avoids elaboration of the genealogical sa mple space under multi-coalescence. Mutational activity\, such as site f requency spectra\, will not be accurately measured with the Kingman coales cent when sample sizes exceed these criteria.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/501/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/501/ END:VEVENT BEGIN:VEVENT SUMMARY:The analysis of the effect of cell dynamics on Delta-Notch interac tion during retina vasculature development DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-287@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Toshiki Oguma (Kyushu University)\nPattern formation by Delta-Notch interaction has been well studied experimentally and theor etically. The Delta-Notch system is observed in various pattern formation process such as somitogenesis\, neuroendocrine cell differentiation in lun g\, T cell differentiation and blood vessel development. Recent studies ha ve shown endothelial cell proliferation and movement happen during this pr ocess. However\, to our knowledge\, there is little theoretical research a bout the effect of cell dynamics on Delta-Notch interaction.\n\nIn the pre sent study\, we examined the effect of cell dynamics on Delta-Notch patter n formation during retina vasculature development. We incorporated cell mo vement and proliferation to the model for Delta-Notch interaction. Using t he model\, we analytically derived the instability condition and numerical ly generated the patterns which have the similarity with the three pattern s observed in vivo. It is difficult to capture the dynamics of cell moveme nt and proliferation with standard linear stability analysis of fastest gr owing wavenumber component. Therefore\, to consider all wavenumber compone nts\, we introduced the instability index\, $\\Psi(t)$\, as the mean of sq uare of Delta expression values. Based on Parseval's theorem regarding dis crete Fourier analysis\, we can derive that $\\Psi(t)$ is equivalent to th e average of power spectrum. Therefore\, by considering the values of powe r spectra\, we can evaluate the instability of the system.\n\n$$\\displays tyle\n{D}_x =\\sum_{m=0}^{n-1} \\delta_k \\mathrm{e}^{ \\lambda_k t + i k x} \\\\\n\\displaystyle \\Psi(t) := \\frac{1}{n} \\sum_{x=1}^n {D_x}^2 = \ \frac{1}{n} \\sum_{m=0}^{n-1} |\\delta_{\\frac{2\\pi m}{n}}|^2\n$$ \n\n$D_ x$ is the expression values of Delta\, $\\delta_k$ is the discrete Fourier transform of $D_x$\, $n$ is the number of the cells\, $k=\\frac{2\\pi m}{ n}$.\n\nThese analyses and numerical calculations suggest that the vascula ture which express homogeneous pattern shows high motility and proliferati on rate of their endothelial cells. Based on these theoretical results\, w e experimentally observed cell dynamics during retina vasculature developm ent by organ culture and immunohistochemistry. The results showed random e ndothelial cell movements and proliferations happened more frequently in v ein than in artery\, which are consistent with analytical and numerical re sults. These results suggest that cell dynamics affect artery-vein differe ntiation via Delta-Notch interaction.\n\nhttps://conferences.maths.unsw.ed u.au/event/2/contributions/287/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/287/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling cell proliferation times DTSTART;VALUE=DATE-TIME:20180711T062000Z DTEND;VALUE=DATE-TIME:20180711T064000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-426@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Catherine Penington (Macquarie University)\nTypicall y\, discrete stochastic models of cell proliferation use a rate to determi ne whether or not a cell proliferates at a particular time\, producing an exponential distribution for the time between proliferation events. Actual experiments\, however\, suggest that cells actually have a Gaussian distr ibution in their time to proliferate\, with a relatively small standard de viation. This talk will discuss the similarities and differences in the gr oup behaviour depending on the proliferation model: both the surprising ma tch after a single time step\, and the large differences as simulations pr ogress.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/426 / LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/426/ END:VEVENT BEGIN:VEVENT SUMMARY:Parameterizing continuum models of heat transfer in heterogeneous living skin using experimental data DTSTART;VALUE=DATE-TIME:20180711T005000Z DTEND;VALUE=DATE-TIME:20180711T011000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-425@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sean McInerney (Queensland University of Technology) \nIn this presentation we consider a recent experimental dataset describin g heat conduction in living porcine tissues. This novel dataset is import ant because porcine skin is similar to human skin\, and improving our unde rstanding of heat conduction in human skin is directly relevant to underst anding burn injuries\, which are common\, painful and can require expensiv e treatments. A key feature of skin is that it is layered\, with differen t thermal properties in different layers. Since the experimental dataset involves heat conduction in living tissues of anesthetized animals\, an im portant experimental restriction is that the temperature within the skin i s only measured at one location within the layered skin. Our aim is to de termine whether this data is sufficient to infer the heat conduction param eters in layered skin\, and we use a simplified two-layer model of heat co nduction to mimic the experimental dataset. Using synthetic data at one l ocation in the two-layer model\, we explore whether it is possible to infe r values of the thermal diffusivity in both layers. After this initial ex ploration\, we then examine how our ability to infer the thermal diffusivi ties changes when we vary the location at which the experimental data is r ecorded\, and in the hypothetical situation where we monitor two locations . Overall\, we find that our ability to parameterize a model of heterogene ous heat conduction with limited experimental data is extremely sensitive to the location where data is collected\, and our modelling results can be used to provide guidance about future experimental designs.\n\nhttps://co nferences.maths.unsw.edu.au/event/2/contributions/425/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/425/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling for cancer recurrence caused by premalignan t lesions formed before the first treatment DTSTART;VALUE=DATE-TIME:20180711T060000Z DTEND;VALUE=DATE-TIME:20180711T062000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-400@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mitsuaki Takaki (Kyushu University)\nResidual premal ignant lesions after the first treatment such as surgery and chemotherapy are considered to be a cause of cancer recurrence. A previous study showed that the presence of premalignant lesions surrounding the primary tumour drives the high rate of local cancer recurrence. If cancerization requires m specific mutations in one cell\, cells which have less than m mutations are still not cancer cells but have higher risk of cancerization than nor mal cells. In this study\, we constructed a mathematical model of cancer r ecurrence caused by premalignant lesions (m=2 in this model). There are th ree populations in the model: (i) normal cells with no mutation\, (ii) pre malignant cells with one mutation\, and (iii) cancer cells with two mutati ons. The total number of a healthy tissue is kept constant and there is a rare chance of mutation every time cell divides. Once a cancer cell with t wo mutations arises\, the population proliferates exponentially\, ignoring the number restriction. Under this assumption\, we investigated the dynam ics of accumulating mutations by combining Moran process and branching pro cess. As a result\, we derived analytical solutions for the probability di stribution of the number of cancer cells over time and confirmed the accur acy by comparing them to the results from stochastic simulations. Finally\ , we found that premalignant lesions have a greater effect on time to recu rrence when patients are older or growth rate of cancer cells is lower.\n\ nhttps://conferences.maths.unsw.edu.au/event/2/contributions/400/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/400/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling tuberculosis granulomas – chronic immune lesions in th e lung DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-85@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Denise Kirschner (University of Michigan Medical SC hool)\nTuberculosis (TB) is the number one cause of death world-wide due t o infection. 2 billion are infected and 10 million die each year. Understa nding the immune response to TB is crucial to developing vaccines and impr oving treatment strategies. The immune response to infection with *Mycobac terium tuberculosis* (Mtb)\, the bacteria that causes TB\, results in the formation of granulomas\, spherical lesions\, physically containing while immunologically restraining the bacteria. These lesions are a collection o f immune cells\, bacteria\, dead tissue and other products including lipid s\, which serve as a food source and oxygen products. Two key adaptations of Mtb are a non-replicating phenotype and accumulation of lipid inclusion s in response to hypoxic conditions. To explore how these adaptations infl uence granuloma-scale outcomes in vivo\, we present a multiscale in silico model of granuloma formation in tuberculosis. We build on an Agent-based model\, GranSim\, that we have been curating continuously since 2004 and i nclude a flux balance model (FBM) describing the metabolism of Mtb within GranSim creating a multi-scale model. The model comprises host immunity\, Mtb metabolism\, Mtb growth adaptation to hypoxia\, and nutrient diffusion . We calibrated our model to in vivo data from nonhuman primates and rabbi ts and apply the model to predict Mtb population dynamics and heterogeneit y within granulomas. We found that bacterial populations are highly dynami c throughout infection in response to changing oxygen levels and host immu nity pressures. Our results indicate that a non-replicating phenotype\, bu t not lipid inclusion formation\, is important for long-term Mtb survival in granulomas.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributi ons/85/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/85/ END:VEVENT BEGIN:VEVENT SUMMARY:Efficient adaptive uniformisation for the analysis of biochemical reaction networks DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-326@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Casper Beentjes (University of Oxford)\nA common mod elling technique to include stochastic effects in biochemical reaction net works is the use of discrete-state continuous time Markov chains. Analytic results for the resulting systems are rare and one often has to rely on s tochastic simulation approaches to quantitatively probe their dynamics. Ma ny conventional simulation methods\, however\, become prohibitively slow i f the system is characterised by multiple different time scales\, i.e. for stiff systems.\n\nIn this contribution we consider the application of ada ptive uniformisation techniques which can significantly reduce the number of simulation trajectories needed to estimate summary statistics of the re action network. By making the uniformisation rate adaptive\, rather than f ixed\, this method can efficiently deal with multiple scales in the dynam ics of reaction networks.\n\nhttps://conferences.maths.unsw.edu.au/event/2 /contributions/326/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/326/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal cancer screening regimes in gastrointestinal evolution usi ng mathematical modelling DTSTART;VALUE=DATE-TIME:20180709T010000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-124@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kit Curtius (Barts Cancer Institute)\nMathematical m odelling of the stochastic evolutionary process of carcinogenesis can be u sed to derive and to optimize the timing of clinical screens so that the p robability is maximal that an individual is screened within a certain "win dow of opportunity" for intervention when early cancer development may be observed. By using data from epidemiological studies with long-term patien t follow-up\, empirical approaches aid in screening design and may inform cost-effectiveness analyses to compare proposed screening and intervention strategies. However\, mechanistic modelling that incorporates a greater l evel of biological understanding and detail for how and when normal tissue s progress to cancer can be used for a more refined screening design than typically implemented in population screening studies. With examples in i nflammation-driven premalignant disease of the gastrointestinal tract\, I will introduce calibrated multistage clonal expansion models of carcinogen esis\, derive probability equations used for optimal screening times and r isk estimation\, and present results for screening strategies using inferr ed parameters from US cancer incidence data. These results 1) provide a ro bust statistical framework for quantifying when it is optimal to screen an d begin surveillance for premalignant changes\, and 2) are shown to be cos t-effective in Barrett’s esophagus patients\, particularly with increasi ngly sensitive and minimally invasive sampling procedures used in clinical practice.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 124/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/124/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling the force-dependent morphogenesis of fish vertebra with topology optimization DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-346@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Misaki Sakashita (Osaka University)\nWolff’s law s tates that bone morphology evolves according to their external mechanical loading. Following this law\, researchers have tried to simulate bone shap e formation\, especially for trabecular bone\, using topology optimization [1]. Less attention has been given to the bone outer shape\, composed of cortical bone. However\, trabecular bone and cortical bone are both mainly formed by osteoblasts and osteoclasts. Therefore\, we hypothesize that th e bone outer shape also adapts to the external forces. The aim of this res earch is to understand the mechanism that generates the bone outer shape b y reproducing the latter using topology optimization. \n\nThe fish vertebr a can be divided into two parts: an inner hourglass-like structure and an outer lateral structure. Based on our observations\, it turns out that num erous species present a similar hourglass-like structure but that the late ral structure strongly depends on the fish species. Lateral structures can be classified into two types. The first type exhibits a ridge structure w ith one or more thick plate-like bones and the second type exhibits a netl ike structure in which thin plate-like bones are randomly oriented. These differences seem related to the fish motion\, i.e. the swimming type of th e fish\, and therefore\, it is assumed that lateral structures also evolve based on external loading conditions.\n\nIn standard topology optimizatio n\, the density at each material point is only constrained by the total vo lume of material. However\, the activity of osteoblast and osteoclast is m ore a local phenomenon. Hence\, the standard topology optimization problem is supplemented with a local density penalization to mimic this local phe nomenon. To solve the optimization problem\, a method based on a time depe ndent reaction-diffusion equation is employed [2]. The equation is driven by the sensitivity $S$\, in which the Lagrangian multiplier $\\lambda$ is introduced. Solving this optimization problem gives an optimized structure with respect to the imposed boundary and loading conditions. The penaliza tion term enables to control locally the feature size. \n\nUsing this equa tion\, we developed a 3-D mathematical model to generate fish vertebra. Wi thout local density penalization\, thick beams appear similarly to the rid ge structure. Penalizing locally the density\, thinner beams are promoted and they tend to form a netlike structure. Numerical results show that the proposed model can produce both types of lateral structures\, i.e. ridge structure and netlike structure\, which are similar to the actual fish bon e. In the future\, it would be interesting to be able to produce various f orms of fish vertebra by only adjusting a few parameters of the penalizati on law.\n\n[1] Jang *et al.*\, 2009\n[2] Kawamoto *et al.*\, 2013\n\nhttps ://conferences.maths.unsw.edu.au/event/2/contributions/346/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/346/ END:VEVENT BEGIN:VEVENT SUMMARY:Model-based morphometrics for plant phenotyping DTSTART;VALUE=DATE-TIME:20180709T052000Z DTEND;VALUE=DATE-TIME:20180709T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-428@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Koji Noshita (JST PRESTO\, The University of Tokyo)\ nCurrently\, high-resolution point cloud data can be acquired easily and c ost-effectively. For example\, a pipeline using Structure from Motion (SfM ) and Multi-View Stereo (MVS)\, which is a promising technique to reconstr uct a 3D surface as point cloud data from a series of 2D images taken from different angles\, has been implemented in several libraries and software products. In this study\, we developed a workflow for measuring and quant ifying the canopy growth of soybean cultivars to compare growth speed base d on point cloud data acquired from the SfM and MVS pipeline. First\, we t ook multi-view 2D images of soybean plants growing in a field with a digit al camera (EOS 60D\, Canon\, Tokyo). The images of plants in a single plot were taken from ca. 40 different directions. From these multi-veiw 2D ima ges\, point cloud data of soybean canopies were reconstructed by using the SfM and MVS pipeline. Second\, we segmented the point cloud of plants and their leaves for each plot from the reconstructed data. Finally\, we fitt ed several models to the point cloud data for estimating phenotypic values of plant organs constituting canopy architecture (e.g. leaf area\, leaf s hape\, curvature). For example\, we reconstructed 3D surfaces of leaves fr om the point cloud data with the penalized B-spline surface fitting by reg arding a leaf as a 2D closed surface embedded in the Euclidean space ℝ$^ 3$. When field conditions were not desirable (e.g. wind\, change in light conditions) for acquiring corresponding points among multi-view images\, h owever\, incomplete point cloud data were reconstructed.\n\nhttps://confer ences.maths.unsw.edu.au/event/2/contributions/428/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/428/ END:VEVENT BEGIN:VEVENT SUMMARY:Role of household size and community structure on the spread of tu berculosis DTSTART;VALUE=DATE-TIME:20180712T021000Z DTEND;VALUE=DATE-TIME:20180712T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-339@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Julien Arino (University of Manitoba\, Winnipeg\, Ma nitoba (Canada))\nSome northern communities in Canada see inordinately hig h tuberculosis incidence compared to the rest of the country. Most of the affected locations are isolated First Nations communities and while this m eans that the usual argument of tuberculosis as an indicator disease of po verty is applicable\, it does not explain the specifics of the situation. To try to understand the role of the various factors at play\, we focus on two specific aspects: household size and community structure. We investig ate this using a simple discrete-time model for households\, which we stud y analytically and with numerical simulations. \nThis is joint work with R yan Sherbo.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions /339/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/339/ END:VEVENT BEGIN:VEVENT SUMMARY:A multiphase spatial model for HDL-assisted stabilisation of early atherosclerotic plaques DTSTART;VALUE=DATE-TIME:20180712T010000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-86@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ishraq Uddin (University of Sydney)\nAtherosclerosis is among the leading causes of death worldwide due to its implication in heart attacks and strokes. The disease is characterised by the localised t hickening of artery walls due to the buildup of fatty cholesterol-filled s treaks. A key factor in determining whether an atherosclerotic plaque beco mes problematic is the interplay between low density lipoprotein (LDL) and high low density lipoprotein (HDL)\, which are responsible for transporti ng cholesterol around the body. LDL is pro-atherogenic and its buildup in the artery wall will trigger an immune response whereby the recruited immu ne cells become engorged on lipid and remain in the artery wall. HDL in co ntrast has the atheroprotective properties of enabling lipid export and th e egress of immune cells from the plaque. Plaque dynamics consist of many nonlinear interactions between various cellular and biochemical species in cluding the interactions between immune cells and lipoproteins.\n \nIn thi s talk\, we present a multiphase PDE model for an early stage atherosclero tic plaque. The model accounts for interactions between macrophages\, apop totic cells\, and lipids. We model the plaque on a 1D domain with a moving boundary. Our model is based on a multiphase framework\, and incorporates the effects of cell crowding by having the domain expand or contract acco rding to the total amount of material in the plaque. We discuss how this m odel gives insight into how early plaque growth and regression depends on the levels of LDL and HDL in the bloodstream\, and the roles of foam cell egress and HDL-enabled reverse cholesterol transport in slowing plaque gro wth and preventing the accumulation of potentially problematic levels of a poptotic material.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contri butions/86/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/86/ END:VEVENT BEGIN:VEVENT SUMMARY:Using the classic Raup shell growth model as a morphometric tool t o investigate genetic variation DTSTART;VALUE=DATE-TIME:20180709T054000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-334@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jenny Larsson (University of Sheffield)\nTwo ecotype s of the marine snail species *Littorina saxatilis* have\, as a result of strong natural selection\, maintained different shell shapes in distinct\, adjacent environments. Being able to quantify and compare the underlying growth structure for the two ecotypes should provide a better insight into the reasons behind the variability of shell shapes\, and connect this to the genetics and selective pressures in their respective habitats.\n\nBuil ding on the ideas of Raup\, we can construct models of snail shells using logarithmic curves containing a set of biologically descriptive growth par ameters. This way of modelling illustrates the construction process of the shells\, and the growth parameters are therefore expected to relate close ly with the underlying genetics. \n\nPrevious biological shape research ha s mainly analysed the shells using variation of a set of landmarks after P rocrustes alignment. This method can quantify the shape differences\, but does not give an explicit explanation of how or why they occur. Because of the substantial amount of landmark coordinate data available for *L. saxa tilis*\, we have developed a geometric method for inferring the growth par ameters from these points.\n\nApplying this new analysis to snails collect ed across contact zones between ecotypes gives the result that growth para meters differ between them and that snails from the hybrid zone show inter mediate values\, which is consistent with the previous morphometric analys is. However\, since the growth parameters are biologically meaningful they should be more informative from a developmental and genetic point of view \, and we are going to investigate the performance of both shape character izations in explaining the genetic variation.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/334/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/334/ END:VEVENT BEGIN:VEVENT SUMMARY:The mathematics of wound healing DTSTART;VALUE=DATE-TIME:20180712T033000Z DTEND;VALUE=DATE-TIME:20180712T043000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-200@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jennifer Flegg (University of Melbourne)\nThe proces s by which a skin wound heals is complicated and requires the concerted ac tion of a large number of cell types\, chemicals and fibres. There have be en many attempts to mathematically describe the wound healing process usin g a variety of different mathematical approaches. In this talk\, I will re view some of the earlier mathematical models developed for wound healing a nd the biological impact they have made. My own research into the mathema tical modelling of wound healing is aimed at informing clinical treatment of non-healing wounds by devising governing equations which capture the es sential behaviour of the complex system. In this talk I will discuss seve ral of these mathematical models\, the clinical insight gained by numerica l and analytical investigation of them and the future challenges that I se e in this research area.\n\nhttps://conferences.maths.unsw.edu.au/event/2/ contributions/200/ LOCATION:University of Sydney -/--Eastern Avenue Auditorium URL:https://conferences.maths.unsw.edu.au/event/2/contributions/200/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling of tissue growth in a spatially-varying per meability tissue engineering scaffold DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-448@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Daniel Fong (United States Merchant Marine Academy)\ nTissue engineering is a rapidly growing field\, attracting a huge concent ration of research effort. An important subfield of tissue engineering foc uses on the use of bioreactors\, devices that attempt to simulate a physio logical environment in order to promote the growth of functional cell or t issue *in vivo*. In this talk we present a mathematical model to simulate both nutrient transport and cell proliferation within a spatially-varying permeability scaffold inside a perfusion bioreactor\, and compare results from this model with experimental results from the literature.\n\nhttps:// conferences.maths.unsw.edu.au/event/2/contributions/448/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/448/ END:VEVENT BEGIN:VEVENT SUMMARY:Coagulation-fragmentation dynamics in macrophage populations DTSTART;VALUE=DATE-TIME:20180712T020000Z DTEND;VALUE=DATE-TIME:20180712T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-173@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hugh Ford (University of Oxford\, University of Sydn ey)\nInflamed tissues are densely populated with macrophages that influenc e the balance between inflammation amplification and resolution. Macrophag es that accumulate immunogenic substances such as cholesterol (in atherosc lerosis) and uric acid (in gout) become pro-inflammatory and drive inflamm atory responses that never resolve.\n\nI use *in vitro* experiments to sho w that substances dynamically accumulate within macrophage populations via a coagulation-fragmentation process. This informs a coagulation-fragmenta tion equation that models macrophage accumulation of substances *in vitro* . This model generalises to a non-local PDE model of macrophage population s during tissue homeostasis and inflammation. Model analysis shows that im munogenic substances coalesce to extraordinarily large quantities inside m acrophages during tissue inflammation but not homeostasis. \n\nAtheroscler osis is considered as a specific example. The model is used to understand the dynamics of lipid accumulation inside macrophages that populate the in flamed artery wall. Our model can simply explain several complex hallmarks of atherosclerosis disease progression such as the formation of lipid-lo aded macrophage foam cells and extracellular pools of necrotic debris.\n\n https://conferences.maths.unsw.edu.au/event/2/contributions/173/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/173/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical and experimental models for wound closure in two dime nsional “sticker” assays DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-301@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Scott McCue (Queensland University of Technology)\nI n order to explore the role of initial geometry in wound closure\, we deve loped a new two-dimensional wound healing assay which we refer to as a sti cker assay. Stickers are produced and attached to a tissue culture plate before cells are seeded into the centre of a dish. The stickers are then removed to leave a wound in the dish\, which is an area with no cells. We performed a number of sticker assays using NIH 3T3 fibroblast cells and v arious initial wound shapes\, including circles\, squares\, triangles and rectangles. By applying an edge detection method in ImageJ\, we tracked th e wound interface (and area) at discrete times up to 96h and found that di fferent shaped wound closed at different rates. To explore these experimen tal results further\, we applied two mathematical models\, the first being a lattice-based random walk algorithm in two dimensions with nearest-neig hbour exclusion\, the second being a continuum-limit description based on the Fisher-Kolmogorov equation. By calibrating our models to the experime ntal data\, we find that the parameter estimates for each initial wound sh ape are similar\, suggesting that\, while the closure rate is different fo r each initial wound shape\, the underlying mechanisms that drive wound cl osure are the same. Finally\, we revisit our continuum model by allowing f or nonlinear degenerate diffusion of the type that occurs in the porous me dium equation (charaterised by an index $n$). We explore the hypothesis t hat circular wound closure is self-similar and circular wound boundaries a re unstable for an increasing number of $k$-fold symmetric perturbations a s the index $n$ decreases. In particular\, we highlight the consequences for wound closure with an initially rectangular wound\, where both numeric al and experimental results suggest that the wound becomes very long and t hin in the limit that it closes.\n\nhttps://conferences.maths.unsw.edu.au/ event/2/contributions/301/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/301/ END:VEVENT BEGIN:VEVENT SUMMARY:Immune selection of malaria quasi-species DTSTART;VALUE=DATE-TIME:20180711T021000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-251@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: David Gurarie (Case Western Reserve University\, Cle veland\, OH 44122)\nMultiple selective pressures drive evolution of malari a parasite\, and determine its phenotypic traits\, like virulence\, transm issibility\, drug resistance\, as well as its population structure in host communities. Immune regulation plays an important part in this process\, both within-host and on population level. The key to parasite survival wit hin host is its antigenic variation\, whereby parasite can avoid immune cl earing by switching on and off multiple antigenic variants. In *P. falcipa rum* species\, this process is controlled by a multigene var family\, expr essed on infected erythrocytes.\nTo study within-host parasite- immune int eractions and the resulting selection processes we develop an agent based approach\, that accommodates most salient features of malaria infection - RBC depletion\, immune stimulation and clearing\, antigenic variation. \nI n out setup\, each parasite strain has a specific genetic makeup (collecti on of var genes)\, drawn from a large pool. Multiple strains of such quasi -species\, compete within-host via cross-reactive immunity. Furthermore\, mixed stains can recombine in mosquito agent to produce new types. Parasit e diversity in host population can change in response to external factors\ , intensity of transmission and host immune status.\nWe apply our model to examine individual and population level outcomes\, and quantify the relat ionship between environmental inputs (intensity of transmission\, immune c ompetence)\, and the evolution of parasite population structure.\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/251/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/251/ END:VEVENT BEGIN:VEVENT SUMMARY:Coupled social and ecological dynamics for ecosystem management DTSTART;VALUE=DATE-TIME:20180710T230000Z DTEND;VALUE=DATE-TIME:20180711T000000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-201@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yoh Iwasa (Kwansei-Gakuin University)\nFor successfu l ecosystem management and biodiversity conservation\, in addition to ecol ogical and evolutionary processes\, we need to consider social and economi c influences on the management target. Here\, we introduce four models tha t address economic and social aspects of human society in the context of e cosystem management. \n\n 1. Lake water pollution. Players choose between cooperative (but costly) option and economical option. Their decision is a ffected by the fraction of cooperators in the community and by the importa nce of water pollution problem. This social dynamics is coupled with the d ynamics of lake water pollution. Oscillation of large amplitude is generat ed if social change occurs faster than ecosystem responses.\nIf phosphorus is removed more effectively either from the inflow or from the lake water \, the pollution level may increase (rather than decrease) due to the decl ine in people's willingness to cooperate (paradox of nutrient removal). \ n 2. Herders in a southern Mongolian rangeland. Herders choose foraging si tes for their animals in the dry season. If grazing pressure is very stron g\, the grass biomass becomes depleted and more herders choose to move the ir animals to an alternative rangeland. They may return to the focal range land when the quantity and quality of the grass improves. The system may e xhibit bistability with a strong dependence on the initial condition or pe rpetual large-amplitude fluctuation. Implications for rangeland management are discussed.\n 3. Profit-sharing of plantation management. Illegal logg ing is a very serious threat to tropical forests. The owner chooses the ag e of trees to cut\, and the workers choose their monitoring effort to prev ent illegal logging. After the trees were removed\, the owner hires worker s to replant young trees. Under the presence of illegal logging pressure\, the owner may find it profitable to share the income by selling logs with the workers to solicit their monitoring efforts. \n 4. Graduated sanctio n for common pool resource management. From field studies\, E. Ostrom disc overed the severity of punishment to rule deviators need to increase with the amount of harm caused by the selfish action. We conclude that graduate d punishment is the most efficient way to ensure cooperation when evaluati on errors are unavoidable and when the social group is heterogeneous with respect to the sensitivity of its members to utility difference.\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/201/ LOCATION:University of Sydney -/--Eastern Avenue Auditorium URL:https://conferences.maths.unsw.edu.au/event/2/contributions/201/ END:VEVENT BEGIN:VEVENT SUMMARY:Complex Role of NK cells in regulation of OV-Bortezomib therapy DTSTART;VALUE=DATE-TIME:20180712T010000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-21@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yangjin Kim (Konkuk University)\nOncolytic viruses s uch as herpes simplex virus-1 (oHSV) are genetically modified to target an d kill cancer cells while not harming healthy normal cells and are current ly under multiple clinical trials for safety and efficacy [1]. Bortezomib is a peptide-based proteasome inhibitor and is an FDA-approved drug for my eloma and mantle cell lymphoma. Yoo *et al.* [2] have previously demonstra ted that bortezomibinduced unfolded protein response (UPR) in many tumour cell lines (glioma\, ovarian\, and head and neck) up-regulated expression of heat shock protein 90 (HSP90)\, which then enhanced viral replication t hrough promotion of nuclear localization of the viral polymerase in vitro. This led to synergistic tumour cell killing in vitro\, and a combination treatment of mice with oHSV and bortezomib showed improved anti-tumour eff icacy *in vivo* [2]. This combination therapy also increased the surface e xpression levels of NK cell activating markers and enhanced pro-inflammato ry cytokine secretion. These findings demonstrated that the synergistic in teraction between oHSV and bortezomib\, a clinically relevant proteasome i nhibitor\, augments the cancer cell killing and promotes overall therapeut ic efficacy. Therefore\, there is a sound ground for combining these agent s in a clinical trial. In the present paper we investigated the role of NK cells in combination therapy with oncolytic virus (OV) and bortezomib. NK cells display rapid and potent immunity to metastasis and hematological c ancers\, and they overcome immunosuppressive effects of tumour microenviro nment. We developed a mathematical model\, a system of PDEs\, in order to address the question of how the density of NK cells affects the growth of the tumour. We found that the anti-tumour efficacy increases when the endo genous NKs are depleted\, and also when exogenous NK cells are injected in to the tumour. These predictions were validated by our in vivo and in vitr o experiments. \n\n[1] Kanai R\, Wakimoto H\, Cheema T\, Rabkin SD (2010) Oncolytic herpes simplex virus vectors and chemotherapy: are combinatorial strategies more effective for cancer? *Future Oncology* 6(4):619–634.\n [2] Yoo J\, *et al.* (2014) Bortezomib-induced unfolded protein response increases oncolytic hsv-1 replication resulting in synergistic antitumor e ffect\, *Clin. Cancer Res.*\, 20(14)\, 3787-3798.\n\nhttps://conferences.m aths.unsw.edu.au/event/2/contributions/21/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/21/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling of the immune response to cancer: an indivi dual based approach DTSTART;VALUE=DATE-TIME:20180709T052000Z DTEND;VALUE=DATE-TIME:20180709T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-348@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Fiona Macfarlane (University of St Andrews)\nThe adv ances in cell imaging technology has allowed for deeper understanding of t he movement mechanisms of immune cells. Experimental evidence suggests tha t cytotoxic T lymphocytes and dendritic cells undergo and unrestricted sea rch motion until they switch to a more restricted motion induced by activa tion by tumour antigens. This change in movement is not often considered i n the existing mathematical models of the interactions between immune cell s and cancer cells. We present a spatially structured individual-based mod el of tumour-immune competition that takes explicitly into account the dif ference in movement between inactive and activated immune cells\, using L évy walks and Brownian motion to capture this motion\, respectively. The effects of activation of immune cells\, the proliferation of cancer cells and the immune destruction of cancer cells are also included in the model. We illustrate the ability of our model to reproduce qualitatively the spa tial trajectories of immune cells observed in experimental data of single cell tracking. Computational simulations of our model further clarify the conditions for the onset of a successful immune action against cancer cell s and suggest possible targets to improve the efficacy of cancer immunothe rapy. Overall\, our theoretical work highlights the importance of taking i nto account spatial interactions when modelling the immune response to can cer cells.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 348/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/348/ END:VEVENT BEGIN:VEVENT SUMMARY:Insights from including the microtubule cytoskeleton in modelling mRNA localization DTSTART;VALUE=DATE-TIME:20180709T052000Z DTEND;VALUE=DATE-TIME:20180709T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-303@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Veronica Ciocanel (Mathematical Biosciences Institut e at The Ohio State University)\nThe cellular cytoskeleton ensures the dyn amic transport\, localization and anchoring of various proteins and vesicl es. In the development of egg cells into embryos\, messenger RNA (mRNA) is transported along microtubule filaments and must accumulate at the cortex of the egg cell on a certain time and spatial scale. We present two equiv alent methods of deriving the effective transport properties of mRNA at la rge time: using analysis of partial differential equations\, and using ren ewal rewards processes in a stochastic model formulation. The dynamical sy stems model approach can be extended to include the geometry of the microt ubule filaments. This allows us to better predict the spread of the partic les\, and to investigate the contribution of an anchoring mechanism to the timescale of localization. Our numerical studies using model microtubule structures predict that anchoring of mRNA-molecular motor complexes may be most effective in keeping mRNA localized near the cortex and therefore in healthy development of oocytes into embryos.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/303/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/303/ END:VEVENT BEGIN:VEVENT SUMMARY:Bayesian modelling on the expected extinction time of species. DTSTART;VALUE=DATE-TIME:20180709T021000Z DTEND;VALUE=DATE-TIME:20180709T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-342@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Saritha Kodikara (Discipline of Mathematical Science s\, School of Science\, RMIT University\, Melbourne\, Australia)\nIn this study\, we propose a new Bayesian approach to calculate the expected extin ction time of a species based on historical sighting record data. Unlike o ther work\, our model allows comprehensively for uncertainties\, provides the expected extinction time and the probability of extinction. It is ex tremely difficult to determine whether a species is extinct based on histo rical sighting records because knowing whether the last surviving individu al of a species has finally died\, or is just unobserved\, remains proble matical. Moreover\, an incorrect classification of a species as extinct c an lead to failure in conserving a threatened species. On the other hand\, it is also undesirable to classify a species as extant when it is actuall y extinct as it can lead to misallocation of funds. Sightings with uncerta in validity (uncertain sightings) play an important role in the inferences made and need to be taken into account better than they have been. Recen t studies have considered uncertain sightings while making inferences abou t extinction\; however\, the difficulty of the problem requires making a n umber of limiting assumptions that significantly reduce realism. We have a ttempted to derive a more general model by incorporating sighting validity into a new Bayesian model development. We employ the underlying idea of t he beta-geometric/beta-binomial (BG/BB) model to build our Bayesian approa ch for the analysis of extinction. Using the likelihood for the sighting d ata\, along with the prior distributions of sighting probability and extin ction probability\, we calculate the expected extinction time using a Mark ov Chain Monte Carlo (MCMC) method which we simulate with JAGS. We apply t his new approach to the sighting records of Caribbean monk seal (CMS)\, Do do and Ivory-Billed Woodpecker species. Unlike other approaches that consi der uncertainties in the sightings\, our model gives Bayesian confidence i ntervals for the expected extinction time of a species.\n\nhttps://confere nces.maths.unsw.edu.au/event/2/contributions/342/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/342/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling of the healing of venous leg ulcers DTSTART;VALUE=DATE-TIME:20180709T052000Z DTEND;VALUE=DATE-TIME:20180709T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-449@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Sontosh Kumar Sahani (The University of Melbourne)\n A leg wound which does not heal because of problems with the veins in the leg is called a venous leg ulcer (VLU). Chronic VLUs are the most common c hronic wounds in western countries and their treatment is both costly and time consuming. In this work\, we present a mathematical model of the heal ing of a VLU which incorporates the key biological features of this wound type. We have modelled the role of oxygen\, fibroblasts and extra-cellular matrix (ECM) within the wound site. The model consists of a system of non linear partial differential equations describing their interactions in spa ce and time coupled with a moving wound outer boundary. The blood vessels that surround the wound supply the oxygen that is needed to support the pr ocesses of fibroblasts and ECM to repair the wound tissue. We consider a w ound in a simplified one-dimensional geometry and the model equations are discretised in space using the finite difference method and then solved in MATLAB. Numerical results are presented for the oxygen\, fibroblasts and ECM distribution within the wound space using parameter values sourced fro m literature\, where possible. This model can be used as a predictive tool in a clinical setting to compare treatments of VLUs including compression bandages.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 449/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/449/ END:VEVENT BEGIN:VEVENT SUMMARY:Vector feeding preference annihilates backward bifurcation and red uces endemicity DTSTART;VALUE=DATE-TIME:20180712T020000Z DTEND;VALUE=DATE-TIME:20180712T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-187@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Rocio Marilyn Caja Rivera (University of Notre Dame) \nWe propose and analyze a mathematical model of a vector-borne disease th at includes vector feeding preference for carrier hosts and intrinsic incu bation in hosts. Analysis of the model reveals the following novel results . We show theoretically and numerically that vector feeding preference for carrier hosts plays an important role for the existence of both the endem ic equilibria and backward bifurcation when the basic reproduction number $R_0$ is less than one. Moreover\, by increasing the vector feeding prefer ence value\, backward bifurcation is eliminated and endemic equilibria for hosts and vectors are diminished.\n\nTherefore\, the vector protects itse lf and this benefits the host. As an example of these phenomena\, we prese nt a case of Andean Cutaneous Leishmaniasis (ACL) in Peru. We use paramete r values from previous studies\, primarily from Peru to introduce bifurcat ion diagrams and compute global sensitivity of $R_0$ in order to quantify and understand the effects of the important parameters of our model. Globa l sensitivity analysis via partial rank correlation coefficient (PRCC) sho ws that $R_0$ is highly sensitive to both sandflies feeding preference and mortality rate of sandflies.\n\nhttps://conferences.maths.unsw.edu.au/eve nt/2/contributions/187/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/187/ END:VEVENT BEGIN:VEVENT SUMMARY:Uncertainty quantification of HIV dynamics using hierarchical mode ls DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-358@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yunjeong Lee (Yonsei University\, Republic of Korea) \nIt is an interesting topic to predict how dynamics change in disease pro gression. Our goal is to predict dynamics of the vital cells in the human immune system using the hierarchical HIV models. We assumed that the param eters are random variables with intra-level noise and inter-level noise. I ndividual-level parameters of HIV model are estimated by generalized least squares method based on the field data. At the population-level\, it is n ot desirable to estimate joint distribution of all the parameters because of computational cost and overfitting. Thus\, we build a model by estimati ng the distribution of only a few selected by the parameter reduction usin g the sensitivity matrices. Then\, we estimate the joint probability distr ibution of remaining parameters employing algorithms for population parame ter estimation. Finally\, we solve ordinary differential equations with ra ndom coefficients to predict the dynamics of target cells.\n\nhttps://conf erences.maths.unsw.edu.au/event/2/contributions/358/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/358/ END:VEVENT BEGIN:VEVENT SUMMARY:Use of data assimilation to infer the effects of sink strength on plant carbon balance processes DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-490@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kashif Mahmud (Western Sydney University)\nPredictin g the carbon balance of terrestrial plants\, and its vulnerability to envi ronmental change\, is a fundamental problem common to agriculture\, ecolog y and ecosystem science. Plant productivity is fuelled by the carbon taken up during photosynthesis\, but other limitations to growth may restrict t he ability of plants to utilise this carbon in production\, a phenomenon k nown as sink limitation. Understanding how sink limitation affects the car bon balance of plants is one of the key challenges to developing better pr edictions of productivity. Here\, we applied data assimilation (DA) to an experiment in which sink limitation was induced by restriction of the root ing volume of *Eucalyptus tereticornis* seedlings\, in order to infer how carbon balance processes were affected. The ultimate goal of our study was to examine how carbon balance models should be modified to represent sink limitation of growth\, whilst maintaining mass balance. \n\nOur results d emonstrate that several process representations need to be modified\, incl uding a clear need to incorporate a temporary storage pool of carbon as no n-structural carbohydrate (NSC)\, with a dynamic utilization rate for grow th. We were able to infer that\, in addition to a reduction in photosynthe tic rates\, sink limitation reduced the NSC utilization rate\, increased g rowth respiration\, modified the carbon allocation pattern and accelerated senescence. The attribution analysis indicated that all of these process responses contributed significantly to the overall reduction in biomass ob served under low rooting volume. Our DA-model analysis of this root volume restriction experiment provided significant new insights in the response of key carbon balance processes to sink limitation. Applying this approach more broadly would potentially allow us to identify general patterns in t hese responses that could then be formulated for inclusion into models. Ov erall\, this approach provides important insights into the relationship be tween carbon uptake and plant growth\, and could significantly advance our models of vegetation responses to global change.\n\nhttps://conferences.m aths.unsw.edu.au/event/2/contributions/490/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/490/ END:VEVENT BEGIN:VEVENT SUMMARY:Reproducing reproduction: understanding and modelling masting in E uropean tree species DTSTART;VALUE=DATE-TIME:20180712T053000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-127@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Giorgio Vacchiano (Università di Milano)\nMasting i s the highly variable and synchronous production of seeds by plants. Masti ng can have cascading effects on plant population dynamics and forest prop erties such as tree growth\, carbon stocks\, regeneration\, nutrient cycli ng\, or future species composition. However\, the spatio-temporal patterns and drivers of masting at the continental scale remain unknown. As a cons equence\, masting has often been missing from forest simulation models. \n \nHere we detail the ongoing efforts to build a comprehensive dataset of s eed production for the main European tree species. This dataset has been u sed\, for example\, to demonstrate that climate-masting relationships acro ss the entire geographical range of European beech are (a) temporally and spatially consistent in the last century at the continental scale\, and (b ) are driven by low frequency modes of climate teleconnections (the Northe rn Atlantic Oscillation).\n\nOur large research collaboration has also rev iewed more than 200 published papers on mechanistic formulations of mastin g\, to summarize how the main processes involved in masting and their rela ted patterns (variability\, synchrony\, and frequency) can be incorporated into forest models with different degrees of complexity.\n\nFuture work w ill involve building empirical and mechanistic models to explore the trade offs between climate\, resources\, masting\, and resource allocation\, and using long-term\, large-scale masting data to explore the effects of clim ate change on masting frequency\, variability and synchrony at the populat ion and continental scale.\n\nhttps://conferences.maths.unsw.edu.au/event/ 2/contributions/127/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/127/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling immunity: a multi-scale problem DTSTART;VALUE=DATE-TIME:20180709T230000Z DTEND;VALUE=DATE-TIME:20180710T000000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-500@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jane Heffernan (York University\, Toronto\, Canada)\ nInfectious diseases affect individuals (immunology) and populations (epid emiology). While these two scales of infection are intimately linked\, the vast majority of studies of infectious diseases ignore or greatly simplif y the effects of the other scale. As a result\, public health programs can be ill-informed. Mathematical models that link the in-host and population scales of infection can better inform public health programs. However\, t hese models can become very complex very quickly\, even in their most simp lified forms. We focus our mathematical modelling studies on the effects o f immunity\, the key outcome of infection at the in-host level (developmen t of immune memory)\, and the key indicator of pathogen spread at the popu lation level (through susceptibility and transmissibility). Immuno-epidemi ological models that are well-informed by our in-host and population level studies are then developed. In this talk I will discuss our immunological \, epidemiological\, and immuno-epidemiolgical modelling studies of influe nza\, HIV\, measles and pertussis. The effects of vaccination and waning i mmunity will be highlighted.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/500/ LOCATION:University of Sydney -/--Eastern Avenue Auditorium URL:https://conferences.maths.unsw.edu.au/event/2/contributions/500/ END:VEVENT BEGIN:VEVENT SUMMARY:Feedback control of epidemic models using Hamilton-Jacobi-Bellman equation DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-357@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yoon-gu Hwang (Yonsei University)\nIn this research\ , we study feedback control problem in the context of deterministic epidem ic models. Feedback control is obtained by solving Hamilton-Jacobi-Bellman (HJB) equation\, which is employed to overcome limitations of previous wor k. There are three key factors in the implementation of this methodology\, decoupling value function and control variables\, truncation of unbounded domain\, and numerical solver for 1st order hyperbolic PDE. While this ap proach seems complicated\, it has an obvious advantage in generalization t o stochastic optimal control problem. With proper treatments for technical challenges\, we provide a tool that can be widely applied.\n\nhttps://con ferences.maths.unsw.edu.au/event/2/contributions/357/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/357/ END:VEVENT BEGIN:VEVENT SUMMARY:Dynamical models of tuberculosis transmission and optimal treatmen t strategies in the Republic of Korea and Philippines DTSTART;VALUE=DATE-TIME:20180712T015000Z DTEND;VALUE=DATE-TIME:20180712T021000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-268@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Eunok Jung (Konkuk University)\nIn this talk\, we wi ll present several mathematical models of tuberculosis (TB) based on the r eported data in the Republic of Korea and Philippines\, and also propose t he optimal treatment strategies depending on the various scenarios in each country. Korea has ranked the highest TB incidence among members of the O rganization for Economic Cooperation and Development (OECD). TB is the six th leading cause of morbidity and mortality in the Philippines. The least- square curve fitting have been used for best fitting the parameters in our models to the observed data. To determine the optimal intervention strate gy which is reducing the number of exposed and infectious individuals and the cost of control measures\, optimal control theory was used [1]. Import ant issues has been addressed from our research: implementing the smoking controls\, not with TB controls\, can derive significant reduction of the incidence of TB transmission [3]. We suggested the rearrangement of the Ko rean government TB budget based on optimal treatment strategies from model ling [2]. Finally\, in the Philippines enhancing active finding control is a significant control factor to curtail the spread of TB [4]. \n\n[1] Sunhwa Choi\, Eunok Jung\, Sungim Whang\, A dynamic model for tuberculosis transmission and optimal treatment strategies in South Korea\, *JTB* 279 (2011) 120-131\n[2] Sunhwa Choi\, Eunok Jung\, Optimal Tuberculosis Preven tion and Control Strategy from a Mathematical Model Based on Real Data\, * BMB* (2014) 76:1566-1589\n[3] Sunhwa Choi\, Eunok Jung\, Seok-Min Lee\, Op timal intervention strategy for prevention tuberculosis using a smoking-tu berculosis model\, *JTB* 380 (2015) 256-270\n[4] Soyoung Kim\, Aurelio A. de los Reyes V\, Eunok Jung\, Mathematical Model and Intervention Strategi es for Mitigating Tuberculosis in the Philippines\, *JTB* 443 (2017) 100-1 12\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/268/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/268/ END:VEVENT BEGIN:VEVENT SUMMARY:Beyond the knock-out: float through the cytosol\, sting like p53 DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-356@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Elizabeth Fedak (University of Utah)\np53\, a cellul ar damage response regulator\, is mutated in 50% of all cancers. We have c onstructed a mathematical model showing how different p53 dynamics after U V radiation and $\\gamma$-irradiation exposure allows cells to respond pro perly to both slowly and quickly detected damage. We extend this model wit h an apoptosis module accounting for the transcription-dependent and -inde pendent activities of p53\, which is then used to analyze and classify con trasting apoptosis evasion strategies in commonly used tumour cell lines. In particular\, we predict that lower levels of basal p53 contribute to th e radiosensitivity observed in many cancers\, and that self-overregulation of p53 is only one of many ways in which gain-of-function p53 mutations c an be advantageous to tumour cell survival. Moreover\, the downregulation of p53 by its canonical antagonist\, Mdm2\, has been well-studied in the n ucleus\, but this same interaction in the cytosol may be responsible for w eakening the transcription-independent p53 pathway in humans. These models provide a unified framework for studying the broad and surprising array o f effects of p53\, far beyond the loss-of-function mutations well-known ac ross cancers.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributio ns/356/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/356/ END:VEVENT BEGIN:VEVENT SUMMARY:Male mating strategies and primate monogamy DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-479@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Danya Rose (University of Sydney)\nPrimates exhibit an array of mating behaviours and arrangements\, from monogamy to promiscu ity\, or mate-guarding to multiple-mating. We have previously explored the role of adult sex ratio in determining the likelihood of males choosing e ither promiscuity or monogamy\, but many questions remain open. In particu lar\, do (and\, if so\, *how* do) longevity and life history contribute to the choice of male strategy? And how can we characterise the effectivenes s of guarding for those males who employ that strategy? We examine some of the trade offs that arise\, and how they can influence the choice of male strategy.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 479/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/479/ END:VEVENT BEGIN:VEVENT SUMMARY:Local and systemic consequences of radiation DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-88@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Heiko Enderling (Moffitt Cancer Center)\nTo date we have no understanding of why two patients with similar clinical stage and molecular profile would have different radiotherapy outcomes. Reliable bio markers are direly needed to predict which patients will be cured\, with t he hope to de-escalate dose when possible or increase where necessary. It is increasingly appreciated that radiation can induce a robust antitumour immune response that provides a second wave of cell kill and tumour regres sion. We develop a variety of mathematical models to study the local and s ystemic cytotoxic and immunological consequences of radiation therapy and discuss their clinical implications.\n\nhttps://conferences.maths.unsw.edu .au/event/2/contributions/88/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/88/ END:VEVENT BEGIN:VEVENT SUMMARY:Stochastic models of cell invasion with fluorescent cell cycle ind icators DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-368@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Matthew Simpson (Queensland University of Technology )\nFluorescent cell cycle labelling in cell biology experiments provides r eal time information about the location of individual cells\, as well as t he phase of the cell cycle of individual cells. We develop a stochastic\, lattice-based random walk model of a two-dimensional scratch assay where t he total population is composed of three distinct subpopulations which we visualise as red\, yellow and green subpopulations. Our model mimics FUCC I technology in which cells in the G1 phase of the cell cycle fluoresce re d\, cells in the early S phase fluoresce yellow\, and cells in the S/G2/M phase fluoresce green. The model is an exclusion process so that any pote ntial motility or proliferation event that would place an agent on an occu pied site is aborted. Using experimental images and measurements we expla in how to parameterise the stochastic model\, and we apply the stochastic model to simulate a scratch assay performed with a human melanoma cell lin e. We obtain additional mathematical insight by deriving an approximate pa rtial differential equation (PDE) description of the stochastic model\, wh ich leads to a novel system of three coupled nonlinear reaction diffusion equations. Comparing averaged simulation data with the solution of the co ntinuum limit description shows that the PDE description is accurate for b iologically-relevant parameter combinations.\n\nhttps://conferences.maths. unsw.edu.au/event/2/contributions/368/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/368/ END:VEVENT BEGIN:VEVENT SUMMARY:Influencers in ant colonies revealed by temporal network analysis DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-276@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Masato Abe (Riken AIP)\nInformation transfer is thou ght to play a key role in adaptive complex systems such as social insects\ , brain and human society\, while epidemic spreading through interactions can impact on survival in the individuals and society. Social insects suc h as ants and bees are one of the most sophisticated complex systems exhib iting collective decision making\, providing us the opportunity of studyin g how the information transfer and disease spreading occur through the int eractions. Recent advances in tracking systems enable us to collect quanti tative and massive data of each individual and interactions in a colony.  A recent empirical study [1] used an automatic tracking method based on im age analysis\, and revealed rapid spreading dynamics in honey bee colonies . However\, the attributes of each individual including age\, caste\, and activity were not considered\, although such heterogeneity of individuals may be crucial for the adaptability of the colony. Thus\, the relationship between the heterogeneity in the colony and the spreading dynamics is les s understood. In the present study\, we used an image-based tracking syste m (Bugtag\; Robiotec Inc.) to detect the movements and interactions of ant s (*Diacamma sp.*). To reveal the relationship between the spreading dynam ics and the heterogeneity in individual attributes\, we investigated how i nteractions spread the information or diseases by using temporal networks  which are promising tools for understanding spread dynamics\, and then q uantified heterogeneity in individual attributes such as age. The results show that the spreading was more rapid than randomized data conserving deg ree sequence\, and younger individuals tended to be influencers which prom oted the rapid spreading. We will discuss the adaptive significance of th e relationship between rapid spreading dynamics and differences in individ ual attributes.\n\n[1] Gernat\, Tim\, *et al*. "Automated monitoring of be havior reveals bursty interaction patterns and rapid spreading dynamics in honeybee social networks." *Proceedings of the National Academy of Scienc es* 115.7 (2018): 1433-1438.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/276/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/276/ END:VEVENT BEGIN:VEVENT SUMMARY:The role of cytoplasmic proteins on cell polarity formation of asy mmetric cell division DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-224@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tomohiro Nakahara (Hiroshima University)\nAsymmetric cell division is one of the widespread mechanisms for generating cell div ersity\, for which a mother cell creates a polarity in both membrane and c ytosol. In both experiment and theoretical approaches\, PAR polarity of *C . elegans* embryo has been extensively well-studied and it was found that Anterior-Posterior (AP) polarity of cell membrane proteins plays a crucial role in determining cell asymmetry. However\, most of previous studies ha ve not considered the role of cytoplasmic proteins on AP polarity formatio n\, although AP polarity is occurred with a tight regulation of both membr ane and cytoplasmic proteins such as MEX-5/6 and PAR- 5. Here\, we develop a multi-dimensional polarity model including cell’s geometrical propert y and show how the cytoplasmic protein plays an important role in creating a robust AP polarity. We also show that the cell geometry can give a crit ical effect on AP polarity\, and the temporal and spatial regulation for t he robust AP polarity is based on the harmony of biochemical\, mechanical\ , and cell geometric properties.\n\nhttps://conferences.maths.unsw.edu.au/ event/2/contributions/224/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/224/ END:VEVENT BEGIN:VEVENT SUMMARY:Evolution and maintenance of mutualism between tubeworms and sulfu r-oxidizing bacteria DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-466@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Masato Sato (SOKENDAI)\nTubeworms and sulfur-oxidizi ng bacteria mutualism\, an essential part of the chemosynthetic ecosystem in the deep-sea\, has several puzzling features. After acquiring sulfur-ox idizing bacteria from the environment\, tubeworms becomes fully dependent on their symbiont bacteria for nutrient intake. Once ingested by the tubew orm larva\, no additional symbionts join from the environment\, and no sym bionts are released until the host tapeworm dies. Despite this very narrow window for symbionts\, some tubeworm species can live for >200 years. Suc h a restricted release of symbionts could lead to a shortage of symbiont b acteria in the environment without which tubeworms could not survive. In o ur study\, we examine the conditions under which this mutualism can persis t\, and whether the host mortality evolves toward a low value\, using a ma thematical model for the tubeworm-symbiont bacteria system.　Our model re veals that mutualism can persist only when host mortality is within an int ermediate range. Moreover\, with weak competition among symbionts and thei r slow growth within a host\, host mortality evolves toward a low value\, without driving either host or symbiont to extinction. We also found the p arameter conditions that lead to the unlimited evolutionary escalation of host mortality toward extinction of both tubeworms and symbionts populatio ns (evolutionary suicide).\n\nhttps://conferences.maths.unsw.edu.au/event/ 2/contributions/466/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/466/ END:VEVENT BEGIN:VEVENT SUMMARY:A conceptual model for the network of potential routes of exposure of pollinators to pesticides DTSTART;VALUE=DATE-TIME:20180710T015000Z DTEND;VALUE=DATE-TIME:20180710T021000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-502@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: John Purdy (Abacus Consulting Services Ltd.)\nA conc eptual model was constructed to define the network of potential routes of exposure of pollinators to pesticides in greater detail than has previousl y been done. This model provides a basis for biologically and ecologically realistic basis for mathematical estimation of exposure versus time both individually and at the colony level. It also shows the distinction betwee n primary exposure routes\, such as contact during foraging with vegetatio n and soil\, contamination of drinking water\, and secondary routes of exp osure in the hive including consumption of pollen\, and nectar that are co llected by foragers or the honey and bee bread produced in the hive. Secon dary exposure from contact with nest construction materials such as wax ar e included. These secondary routes of exposure can affect both adults and immature life stages of social pollinators in the hive or nest. The concep tual model allows detailed consideration of the overall pattern of potenti al exposure\, including the dynamics of exposure to various castes and lif e stages of social bees. This conceptual model also aids in assessing the completeness of the risk assessment and identifying exposure pathways that require further investigation.\n\nhttps://conferences.maths.unsw.edu.au/e vent/2/contributions/502/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/502/ END:VEVENT BEGIN:VEVENT SUMMARY:Age structure as key to delayed logistic proliferation in scratch assays DTSTART;VALUE=DATE-TIME:20180709T060000Z DTEND;VALUE=DATE-TIME:20180709T062000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-374@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ana Victoria Ponce Bobadilla (Heidelberg University) \nScratch assays are standard *in vitro* experimental methods for studying cell migration. In these experiments\, a scratch is made on a cell monola yer and imaging of the recolonisation of the scratched region is performed to quantify cell migration rates. Typically\, scratch assays are modelled by continuum reaction diffusion equations depicting cell migration by dif fusion and carrying capacity-limited proliferation by a logistic source te rm. In a recent work [1]\, the authors observed that on a short time\, the re is a disturbance phase where proliferation is not logistic\, and this i s followed by a growth phase where proliferation appears to be logistic.\n \nIn this talk\, I will introduce an age-structured population model that aims to explain the two phases of proliferation in scratch assays. The cel l population is modelled by a McKendrick-von Foerster partial differential equation. The conditions under which the model captures this two-phase be haviour are presented.\n\n[1] Jin\, W. *et al*. *Bull Math Biol* (2017)\n\ nhttps://conferences.maths.unsw.edu.au/event/2/contributions/374/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/374/ END:VEVENT BEGIN:VEVENT SUMMARY:Parameter estimation of an S-system model using hybrid genetic alg orithm with the aid of sensitivity analysis DTSTART;VALUE=DATE-TIME:20180709T005000Z DTEND;VALUE=DATE-TIME:20180709T011000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-312@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Renier Mendoza (Institute of Mathematics University of the Philippines Diliman)\nA biochemical system is a biological system c onsisting of a collection of chemical compounds interacting with each othe r. One way to model and analyze a biochemical system is by using S-systems \, which are coupled ordinary differential equations based on power-law fo rmalism. In this work\, we do a parameter estimation on an S-system model called HS96. This model\, proposed by Hlavacek and Savageau in 1996\, desc ribes a simple genetic network consisting of five dependent variables $X_i \,$ $i=1\,2\,...\,5$. As a preliminary method\, sensitivity analysis of HS 96 is conducted to investigate the change in model outputs with respect to the changes in model parameters. Usual model outputs are $X_i$ and $\\dot {X}_i\,$ $i=1\,2\,...\,5$. From the results of sensitivity analysis\, mode l outputs are selected which are then used to estimate the parameters of t he HS96 model. A hybrid of genetic algorithm with the interior point metho d is used in the parameter estimation.\n\nhttps://conferences.maths.unsw.e du.au/event/2/contributions/312/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/312/ END:VEVENT BEGIN:VEVENT SUMMARY:Bifurcation analysis of an epizootiological model of avian malaria DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-391@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kyle Dahlin (Purdue University)\nAvian malaria is a mosquito-borne parasitic disease of birds caused by protists of the genera Plasmodium\, most notably *Plasmodium relictum*. This disease has been id entified as a primary cause of the drastic decline and extinctions of ende mic birds on Pacific Islands. In this work\, we formulate an epizootiologi cal model of the transmission dynamics of avian malaria between a generic bird species and mosquito using a system of ODEs. We derive the basic repr oduction number as well as criteria for the existence and stability of dis ease-free and enzootic equilibria. We discuss strategies for minimizing th e impact of avian malaria in two scenarios: disease-free populations which may be invaded by avian malaria and populations where this disease is enz ootic but where bird species have not developed resistance.\n\nhttps://con ferences.maths.unsw.edu.au/event/2/contributions/391/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/391/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal flow patterns in branching lymphatic vessels DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-31@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Anne Talkington (University of North Carolina at Cha pel Hill)\nUnderstanding lymphatic development is clinically relevant in a pplications from the viability of embryos\, to chronic inflammation\, to c ancer metastasis. I specifically quantify the branching structure of devel oping lymphatic vessels and numerically solve for the flow through these v essels. Branching in arterial development is understood to consistently fo llow Murray’s Law\, which states that the cube of the radius of a parent vessel is equal to the sum of the cubes of the radii of the daughter vess els\, thus minimizing the cost and maintenance of fluid transport. I have found that an optimization law for lymphatic vessels is less straightforw ard. The derivation of Murray’s Law includes several assumptions\, such as vessels of constant diameter filled with a Newtonian fluid\, fully dev eloped and unidirectional flow\, and long segments between junctions. Sev eral of these necessary assumptions do not hold for lymphatic capillaries. The relationship between the parent and daughter vessels is upheld throu gh a strictly additive rule\, and the daughter vessels are smaller than wo uld be predicted by the hypothesized radius-cubed law. The variability in vessel diameter and potential for bidirectional flow suggest a different o ptimization strategy based on the geometry and function of the system. In this presentation\, the immersed boundary method is used to numerically s olve the equations of fluid flow through branching vessels. The results ar e then used to test the assumptions of Murray’s Law as well as several h ypotheses regarding branching geometry.\n\nhttps://conferences.maths.unsw. edu.au/event/2/contributions/31/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/31/ END:VEVENT BEGIN:VEVENT SUMMARY:Transport network designed by current-reinforcement rule DTSTART;VALUE=DATE-TIME:20180709T033000Z DTEND;VALUE=DATE-TIME:20180709T043000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-211@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Toshiyuki Nakagaki (Hokkaido University)\nNetwork of transport is found in a wide range of living system. The typical examples are vascular network in vertebrates and tracheal network in vascular plan ts\, and mycelial network in fungi. Such a network structure is found in s elf-organized colony of unicellular bacteria: a biofilm that is a sheet-li ke aggregate of many bacteria and sticky polysaccharides secreted from the bacteria. Comparative study of various kinds of bio-network of transport along phylogenetic tree is probably interesting since an insight into evol utionarily sophisticated designing of adaptive network is obtained in a wi der perspective. \n \nAt the interface between unicellular and multicellu lar branches\, there is an unique organism with highly flexible body shape with network structure\, true slime mould Myxomycete (or Mycetozoa). *Ph ysarum polycephalum* Schw. is a well-studied species of true slime mould i n cell biology and biophysics last seventy years although several hundreds of species are known. By using this organism\, comparative study of bio-n etwork rises for the last one or two decade(s).\n \nA kind of huge amoeboi d organism named *Physarum* plasmodium constructs a intricate network of veins for circulating nutrients and signals over the entire body. The netw ork shape (topology of connectivity\, and sequence of branching in vein ne twork\, for instance) is drastically re-organized within hours in response to external conditions. The past studies showed that the network shape wa s optimized to maximize possibility of survival\, in some senses. So we ma y extract an algorithm for optimal design of functional network from the p rimitive organism. The key thing is adaptive dynamics of current-reinforce ment rule: each vein of network becomes thicker when current is large enou gh through the vein itself\, while it becomes thinner and dies out otherwi se. \n\nWe propose the equations of motion for this simple rule\, and func tions and formation of transport network is analyzed. We will show that th e rule is applicable to the other bio-systems: (1) social dynamics of publ ic transportation\, (2) formation of network structure in porous tissues b one (bone remodelling in other words). A tractable perspective to think s imilarly of a variety of bio-network is given from the viewpoint of curren t-reinforcement rule.\n\nhttps://conferences.maths.unsw.edu.au/event/2/con tributions/211/ LOCATION:University of Sydney -/--Eastern Avenue Auditorium URL:https://conferences.maths.unsw.edu.au/event/2/contributions/211/ END:VEVENT BEGIN:VEVENT SUMMARY:Stochastic-Spatio-temporal lattice (SSTL) Models of tree infestati on DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-289@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: John Holden (Newcastle University\, University of Le eds)\nUsing a simple lattice model describing infectious tree disease dyna mics on a homogeneous landscape we can observe an Epiphytotic phase transi tion from local confinement of the pathogen to a global epidemic through t he forest. The phase transition can be understood in terms of the forest t ree density and the pathogen virulence. One interesting application of the model involves capturing the pathogen spread-velocity and applying simple statics to pre-empt the phase transition into the Epiphytotic regime. The oretically this yields an early warning system. The early warning phase tr ansition could potentially be utilised to inform control strategies and ne gate system wide devastation of plant species.\n\nhttps://conferences.math s.unsw.edu.au/event/2/contributions/289/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/289/ END:VEVENT BEGIN:VEVENT SUMMARY:Patterning in development and the role of short and long range sig nalling DTSTART;VALUE=DATE-TIME:20180709T011000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-364@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Adriana Dawes (Ohio State University)\nMany biologic al systems rely on both long range and short range signals in order to pro duce proper cell patterns during development. These patterns\, such as alt ernating cell fates\, are defined by different gene and protein expression levels. However\, the relative contribution of these two signalling modes in establishing proper patterns is not well understood. Using vulval deve lopment of two nematode worm species\, *C. elegans* and *C. briggsae*\, as motivation\, we derive an asymptotic PDE based on a simplified signalling network consisting of EGF\, Notch and Wnt. We demonstrate that additional long range signals can provide a framework for understanding species-spec ific differences and that variations in short range signalling can amplify long range signals. These results suggest that long and short range signa ls have critical roles to play in proper cell patterning in development. T his work is joint with Helen Chamberlin and Carly Williamson.\n\nhttps://c onferences.maths.unsw.edu.au/event/2/contributions/364/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/364/ END:VEVENT BEGIN:VEVENT SUMMARY:The coevolution of transitive inference and memory capacity in the hawk-dove game DTSTART;VALUE=DATE-TIME:20180711T015000Z DTEND;VALUE=DATE-TIME:20180711T021000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-420@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kazuto Doi (Department of Innovation Science\, Tokyo Institute of Technology)\nTransitive inference (TI) that uses known relat ionships to deduce unknown ones (using A > B and B > C to infer A > C give n no direct interactions between A and C) to assess the opponent’s stren gth\, or resource-holding potential (RHP)\, is widely reported in animals living in a group. This sounds counter-intuitive because the mechanism of TI seems to require social cognition and large memory capacity\; individua ls\, in the TI mechanism\, need abilities to identify others\, observe con tests among others and keep the results in memory. We examine the coevolut ion of memory and transitive inference by the evolutionary simulations\, u sing the asymmetric hawk-dove game when a cost for losers is higher than a reward for winners. We found that the immediate inference strategy (II)\, which estimates the opponent's strength based on the past history of the direct fights\, evolves with the large memory capacity\, while the TI stra tegy\, which estimates the unknown opponent's strength by transitive infer ence\, evolves with the limited memory capacity. When a cost for losers is slightly higher than a reward for winners\, the II strategy with the larg e memory capacity has an evolutionary advantage over the TI strategy with the limited memory capacity. It is because the direct fights are not so co stly that more information about the fights leads to more accurate estimat ion of the opponent's strength and results in the accurate rank of the RHP s. When a cost for losers is much higher than a reward for winners\, the T I strategy with the limited memory capacity has an evolutionary advantage. It is because a good way to avoid the costly fights is the prompt formati on of the dominance hierarchy which does not necessarily reflect the actua l rank of the RHPs\; the TI strategy builds the dominance hierarchy much f aster than the II strategy regardless of memory capacity\, and the large a mounts of information are not required for the TI strategy to form the dom inance hierarchy promptly. Our study suggests that even smaller memory cap acity is evolutionarily favoured in TI. The TI strategy tends to reinforce the hierarchy once it is built\, regardless of whether it is consistent w ith RHP or not\, because results of direct fights are always counted. Smal ler memory capacity allows players to adjust the hierarchy well if it does not represent RHP. These results prove that TI can evolve in animals\, wh ich do not have the large memory capacity.\n\nhttps://conferences.maths.un sw.edu.au/event/2/contributions/420/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/420/ END:VEVENT BEGIN:VEVENT SUMMARY:Transport of intermediate filaments in cells DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-385@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Stéphanie Portet (University of Manitoba\, Winnipeg \, Manitoba (Canada))\nRecently\, it has been shown that intracellular tra nsport of assembled intermediate filament proteins is one major determinan t of their organization in cells. Based on experimental data\, mathematica l models of the spatio-temporal distribution of intermediate filaments in cells are developed to investigate the contributions of different types of transport such as retrograde flow of actin and motor proteins. Furthermor e\, models for the motion of single filaments driven by motor proteins are also proposed.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribut ions/385/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/385/ END:VEVENT BEGIN:VEVENT SUMMARY:On mathematical standard structure of a binary digit of memory in a cell and its application to biological or life science phenomena DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-253@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Isamu Ohnishi (Hiroshima University)\nA mathematical standard structure of a binary digit of memory in a cell is presented. Th is is based on a kind of frequency model with scale effect. This model has ability of "on-off" switching property\, and moreover\, this is affected by scale effect to make the memorable ability be reinforced. This property is derived from multiple covalent modification cites inducing important e nzyme reaction\, which is represented by the Michaelis-Menten type nonline arity. \n\nSome examples of application is also presented. One example is Cyanobacterial allosteric circadian rhythm of *Synechococcus*. Another is about Biological Nitrogen Fixation ability of *Nostochineae* cyanobacteria . I will explain briefly that scale effect affects the phenomena effective ly to make the system be robust.\n\nhttps://conferences.maths.unsw.edu.au/ event/2/contributions/253/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/253/ END:VEVENT BEGIN:VEVENT SUMMARY:A model of vascular refilling with inflammation DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-434@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Victoria May Paguio (Institute of Mathematics\, Univ ersity of the Philippines)\nMonitoring the fluid status of end-stage renal disease (ESRD) patients remains an important aspect in hemodialysis. Rec ently\, de los Reyes *et al*. developed a two-compartment model describing vascular refilling with ultrafiltration during short-term hemodialysis in ESRD patients. Ultrafiltration is taking out fluid from the vascular spa ce\; and vascular refilling occurs through the capillaries and by lymph fl ow\, driven by pressure and concentration gradients in the plasma and inte rstitial spaces. A feature common in ESRD patients on hemodialysis is inf lammation. Inflammation is believed to greatly contribute to the progress ion of cardiovascular disease\, the most common cause of mortality among h emodialysis patients. Increased vascular permeability associated with infl ammation is likely to influence the capillary wall properties that may cau se perturbations affecting capillary refilling. We propose a way to quant ify inflammation by considering the concentration of the inflammatory biom arker C-reactive protein (CRP). A model that incorporates inflammation to the vascular refilling model is presented. Simulations and parameter est imation related to CRP and capillary wall properties are also presented.\n \nhttps://conferences.maths.unsw.edu.au/event/2/contributions/434/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/434/ END:VEVENT BEGIN:VEVENT SUMMARY:Ecotoxicological dynamics subject to stoichiometric constraints DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-467@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Md Nazmul Hassan (Texas Tech University)\nThe develo pment of ecotoxicological models over the last couple decades has signific antly contributed to interpreting how contaminants impact organisms and cy cle through food webs. However\, there is increasing evidence that organi sms experience interactive effects of contaminant stressors and food condi tions\, such as resource stoichiometry and nutrient availability. *Stoichi ometric Ecotoxicology* modelling efforts shed light on nutrient and chemic al contaminant cycling and ultimately can help improve toxicological risk assessment protocols. We are formulating a series of empirically testable and robust models of algae-*Daphnia* population dynamics subject to concur rent nutritional and contaminant stressors. In parallel to developing the models\, we are conducting laboratory experiments manipulating the nutrit ional content of algae fed to *Daphnia* exposed to Cadmium\, Arsenic\, and Copper. Here\, we present modelling and empirical results and discuss th e synthesis of the two approaches.\n\nhttps://conferences.maths.unsw.edu.a u/event/2/contributions/467/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/467/ END:VEVENT BEGIN:VEVENT SUMMARY:The effect of environmental variability and periodic fluctuations on disease outbreaks in stochastic epidemic models DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-399@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kaniz Fatema Nipa (Texas Tech University)\nSeasonali ty and contact patterns due to environmental fluctuations and social behav iour affect the dynamics of disease outbreaks. Recent studies applied to d eterministic epidemic models with periodic environments have shown that th e average basic reproduction number is not sufficient to predict an outbre ak. We extend these studies to stochastic epidemic models with periodic e nvironments to investigate the combined effect of periodicity and variabil ity on disease outbreaks. The deterministic models are extended to continu ous-time Markov chain and stochastic differential equations. A numerical s tudy of the dynamics of several stochastic SIR and vector-host models with environmental variability and periodicity are investigated in terms of pr obability of an outbreak.\n\nhttps://conferences.maths.unsw.edu.au/event/2 /contributions/399/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/399/ END:VEVENT BEGIN:VEVENT SUMMARY:Crosstalk in transition: Akt translocation as a damped harmonic os cillator DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T005000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-315@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Catheryn Gray (University of New South Wales)\nAkt/P KB (Protein Kinase B) is a major crosstalk node in the mammalian cell. Loc ated as the juncture of several key signalling pathways\, it is involved i n many cellular processes\, such as glucose metabolism\, cell growth and t he suppression of apotosis. Dysregulated Akt signalling is implicated in a range of human disorders\, from diabetes to cancer.\n\nInitially\, Akt is synthesised in the unactivated state on the endoplasmic reticulum. Howeve r\, the activation (phosphorylation) of Akt in response to insulin stimula tion only occurs at the plasma membrane\, necessitating the translocation of Akt from the interior to the periphery of the cell. At the moment\, the understanding of this translocation process is still in its infancy\, but there are some indications that it is a staged process. \n\nWe have devel oped a deterministic\, three-compartment\, ordinary differential equation (ODE) model of Akt translocation. Given a conservation relation implicit i n the model\, it can be shown that this system is equivalent to the damped harmonic oscillator equation\; a classic\, well-studied ODE. With this fr amework\, we investigate the different modes of downstream signalling that can be produced by the model and the conditions for their manifestation.\ n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/315/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/315/ END:VEVENT BEGIN:VEVENT SUMMARY:Exploring differential regulation of blood clot degradation DTSTART;VALUE=DATE-TIME:20180712T052000Z DTEND;VALUE=DATE-TIME:20180712T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-492@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Brittany Bannish (University of Central Oklahoma)\nB lood clots are physiologically degraded via a biochemical cascade initiate d by tissue plasminogen activator (tPA). tPA\, which is also used clinical ly to treat stroke\, creates plasmin\, the main protein involved in degrad ation. We explore the effects of tPA unbinding and diffusion on clot degra dation. We propose that plasmin can “force” tPA to unbind from the clo t\, which has significant implications for the resulting clot degradation. Using a 3-dimensional stochastic multiscale model\, four different regula tory mechanisms are explored when tPA is forced to unbind: 1) tPA is immed iately able to rebind to fibrin\; 2) tPA is immediately removed from the s ystem\; 3) tPA is bound to a fibrin degradation product (FDP) that is smal l enough to diffuse through the clot\, and after some time determined by t he kinetic unbinding rate\, the tPA unbinds from the FDP and is available for rebinding\; 4) tPA is bound to an FDP that can only diffuse along or a way from the clot (due to its size)\, and after some time determined by th e kinetic unbinding rate\, the tPA unbinds from the FDP and is available f or rebinding. We discuss the contributions of each mechanism in clot degra dation\, the surprising role of plasmin\, and the implications for stroke treatment.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 492/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/492/ END:VEVENT BEGIN:VEVENT SUMMARY:Uncertainty analysis applied to model peristalsis to understand ev olution DTSTART;VALUE=DATE-TIME:20180712T020000Z DTEND;VALUE=DATE-TIME:20180712T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-179@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Laura Miller (Univ. of North Carolina at Chapel Hill )\nBiologists are interested in functional performance based on complicate d mechanical systems to understand how structures may have evolved. Since direct manipulation of these systems in an organism are not always possibl e\, many functional systems are modelled using computational methods\, suc h computational fluid dynamics. These functional systems and their simplif ied models involve many parameters which may or may not affect the perform ance output of the system in strong ways\, in other words\, the functional output often has varying sensitivity to each input parameter in the syste m. Therefore variation\, both a natural consequence of development and the raw material on which natural selection operates\, is difficult to quanti fy with typical methods on computational models\, such as single parameter sweeps of simulations while other parameters are held constant. In this w ork\, we apply existing uncertainty quantification methods on CFD models o f a functional system to answer the question: how does variation in the in put parameter space affect model output in a way similar to what natural s election would act upon? Through the use of generalized polynomial chaos a nd calculation of Sobol indices\, we quantify the uncertainty on a model o f circulatory flow using two methods of driving peristaltic motion (two op posing sine waves and a traveling pinch). Sensitivities of three input par ameters are discussed: Womersley number\, compression ratio (the percent o cclusion of the tube during a compression)\, and compression frequency. Sp ecific predictions about natural diversity are made based on sensitivities \; those parameters that are very sensitive should be highly constrained v ersus those that are insensitive should exhibit high levels of diversifica tion.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/179/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/179/ END:VEVENT BEGIN:VEVENT SUMMARY:Inverse and recursive approaches to discover and predict emergent behaviour in complex biosystems comprising human tissues DTSTART;VALUE=DATE-TIME:20180711T230000Z DTEND;VALUE=DATE-TIME:20180712T000000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-499@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Melissa Knothe Tate (Paul Trainor Chair of Biomedica l Engineering\, University of New South Wales Sydney)\nThrough combination of novel microscopy protocols for imaging live cells and tissues as well as experimental mechanics methods\, we have begun to elucidate mechanisms underpinning emergent properties of hierarchical materials such as tissues [1\,2]. We refer to the process as Microscopy Aided Design And Manufactur e (MADAMe). We apply this paired imaging and computational technology appr oach to engineer advanced materials that emulate the smart mechanical prop erties of tissues. These materials have applications in diverse arenas\, f rom medical implants to the transport and sports industries. Our “bottom up” approach to emulating mechanically responsive natural materials int egrates the fields of multiscale biomechanics and mechanobiology in novel ways and underscores the role of mechanics in life. It also elucidates how “brainless” cells adapt to dynamic mechanical environments by constan tly weaving and thereby adapting their own niche [3]. In addition\, our co nnectomics approach to understanding cell networks *in situ*\, in tissues as diverse as brain and bone\, provides a basis for a new approach to diag nostics\, predicting emergent disease states using an epidemiological appr oach in cell populations within individual patients [3\,5\,6]. Challenges to the connectomics approach include acquisition\, handling and archiving of massive data sets\, discrepancies in technical capacities (e.g. resolut ion) of imaging methods\, and hard and software approaches\, as well as br idging and upskilling of research teams to apply a transdisciplinary appro ach using innovative conceptual\, experimental\, and translational approac hes. This talk integrates our understanding of cells\, expert tissue proto typers\, and their networks\, to emulating cellular approaches to engineer and manufacture materials and medical devices of the future.\n\n[1] Knoth e Tate ML (2017) *Science/AAAS\, A New Age in Scanning Electron Microscopy : Applications in the Life Sciences*\, pp. 19-23.\n[2] Ng J *et al.* Sci R eports (2017) 7\, 40396.\n[3] Knothe Tate ML *et al. Adv Healthcare Mat* ( 2016) 5\, 1581.\n[4] Knothe Tate ML *et al. BioArchitecture* (2016) 6\, 85 .\n[5] Eberle A-L *et al. J Microscopy* (2015) 259\, 114.\n[6] Pereira A * et al. PLoS Comp Biol* (2016) 12\, e1005217.\n\nhttps://conferences.maths. unsw.edu.au/event/2/contributions/499/ LOCATION:University of Sydney -/--Eastern Avenue Auditorium URL:https://conferences.maths.unsw.edu.au/event/2/contributions/499/ END:VEVENT BEGIN:VEVENT SUMMARY:SMB Education Subgroup Business Meeting Lunch and Panel on Assessm ent of Interdisciplinary Thinking DTSTART;VALUE=DATE-TIME:20180712T023000Z DTEND;VALUE=DATE-TIME:20180712T030000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-203@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Carrie Diaz Eaton (Bates College\, USA)\, Robert May es (Georgia Southern University)\n**Carrie Diaz Eaton**\, *Moderator and E ducation Subgroup Chair\, Bates College\, USA*\nAs higher education moves towards evidence-based curriculum reform\, assessing interdisciplinary thi nking becomes a challenge for those in multidisciplinary frontiers. We wil l discuss how to best support SMB Education subgroup members. We will also introduce some resources for assessing interdisciplinary thinking in your courses.\n\n**Robert Mayes**\, *Georgia Southern University\, USA*\nThe Q M BUGS assessment measures students' proficiency in quantitative modelling (QM - ability to develop a model). The assessment is intended to be given in undergraduate biology courses where quantitative skills are preparing students or actively engaging students in quantitative modelling within bi ological contexts. Assessment consists of 30 questions: 19 multiple choice questions (5 options) addressing quantitative modelling understanding and 11 Lickert questions (1 NA\, 2 Strong Disagree to 5 Strongly Agree) addre ssing student confidence about modelling in biology.\n\n**Lou Gross**\, *U niversity of Tennessee\, USA*\nThe underlying goal of this project is to d evelop and evaluate an interdisciplinary instrument--a Biology Calculus Co ncept Inventory (BCCI)--which will allow assessment of calculus concept le arning goals in the context of concrete\, real-world life science data exa mples and models.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contrib utions/203/ LOCATION:University of Sydney New Law School/--Foyer URL:https://conferences.maths.unsw.edu.au/event/2/contributions/203/ END:VEVENT BEGIN:VEVENT SUMMARY:Calcium signalling in the sperm head DTSTART;VALUE=DATE-TIME:20180709T052000Z DTEND;VALUE=DATE-TIME:20180709T054000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-376@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Julie Simons (California State University Maritime A cademy)\nCalcium signalling is a ubiquitous mechanism that many cell types use to control a plethora of biological processes. In particular\, calciu m plays a large role in fertility both for egg and sperm cells. In this pr esentation\, we will focus on the acrosome reaction\, which is a calcium-m odulated vesicle release that must occur for sperm to successfully fertili ze the egg. We will discuss the important biological components in this re action and develop a mathematical model that highlights how multiple pathw ays interact to drive this unique calcium-driven event.\n\nhttps://confere nces.maths.unsw.edu.au/event/2/contributions/376/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/376/ END:VEVENT BEGIN:VEVENT SUMMARY:Quantifying the influence of nanoparticle polydispersity on cellul ar delivered dose DTSTART;VALUE=DATE-TIME:20180709T062000Z DTEND;VALUE=DATE-TIME:20180709T064000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-304@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Stuart Johnston (University of Melbourne)\nNanoparti cles provide a promising approach for the targeted delivery of therapeutic \, diagnostic and imaging agents in the body. However\, it is not yet full y understood how the physicochemical properties of the nanoparticles influ ence cellular association and uptake. Cellular association experiments are routinely performed in an effort to determine how nanoparticle properties impact the rate of nanoparticle-cell association. To compare experiments in a meaningful manner\, the association data must be normalised by the am ount of nanoparticles that arrive at the cells\, a measure referred to as the delivered dose. The delivered dose is calculated from a model of nanop article transport through fluid. A standard assumption is that all nanopar ticles within the population are monodisperse\, namely\, the nanoparticles have the same physicochemical properties. We present a semi-analytic solu tion to a modified model of nanoparticle transport that allows for the nan oparticle population to be polydisperse. This solution allows us to effici ently analyse the influence of polydispersity on the delivered dose. Combi ning characterisation data obtained from a range of commonly-used nanopart icles and our model\, we find that the delivered dose changes by more than a factor of two if realistic amounts of polydispersity are considered.\n\ nhttps://conferences.maths.unsw.edu.au/event/2/contributions/304/ LOCATION:University of Sydney New Law School/--107 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/304/ END:VEVENT BEGIN:VEVENT SUMMARY:The influence of molecular reach and diffusivity on the effectiven ess of membrane-confined reactions DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-229@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ying Zhang (Boston University)\nTethered enzymatic r eactions are a key component in signalling transduction pathways. It is fo und that many surface receptors rely on the tethering of cytoplasmic kinas e to initiate and integrate signalling. A key factor to such reaction is t he molecular reach\; however\, the role of it is incompletely understood. To date\, a large number of compartment-based ODE and stochastic models ha ve been developed to study this problem. In recent years\, spatial-stochas tic models have emerged as a more realistic representation for such proces ses\, among which lattice-based stochastic reaction-diffusion models are a popular approach for studying complex spatio-temporal processes inside ce lls. To understand the role of molecular reach in tethered signalling\, we employed an accurate and convergent lattice-based stochastic reaction-dif fusion model (CRDME). We find that the molecular reach can increase or dec rease biochemical reactions depending on the diffusion coefficient in 2D m embrane but not in 3D cytosol.\n\nhttps://conferences.maths.unsw.edu.au/ev ent/2/contributions/229/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/229/ END:VEVENT BEGIN:VEVENT SUMMARY:How do the dynamics of carbon and nitrogen allocation impact plant growth? DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-438@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Bethany Holland (University of Sheffield)\nImproving crop yield is essential to meet increasing global food demands. Crop yiel ds depend on the coordinated acquisition of carbon and nitrogen by the lea ves and roots respectively and the use of these nutrients within each part of the plant. Changes in environmental conditions cause fluctuations in c arbon and nitrogen availability. This leads to crosstalk between the signa lling pathways for carbon and nitrogen. Carbon- and nitrogen-derived signa ls have been observed in plant growth\, but how these signals cooperate to gether with changes in nutrient availability is still unknown. Here\, we d iscuss the implementation of such feedback mechanisms using a carbon and n itrogen transport model for plant growth.\n\nhttps://conferences.maths.uns w.edu.au/event/2/contributions/438/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/438/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling of cytosolic liquid-liquid phase separation DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-377@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Kelsey Gasior (University of North Carolina)\nIntrac ellular phase transitions are an emerging mechanism for cell organization. These membrane-less compartments are formed via liquid-liquid demixing an d subsequent concentration of cellular components in a specific region. B y undergoing these localized phase separations\, cells are able to create dynamic compartments that help maintain the regulation of biomolecular int eractions and localize factors such as RNAs and proteins. The utility of l iquid-liquid phase transitions and the assembly of cytosolic compartments is especially critical in large\, multinucleate cells. These types of cell s are common in the biosphere and include skeletal muscle tissue\, the pla centa\, many filamentous fungi\, and certain types of cancer. A powerful m odel organism for studying liquid-liquid phase separations (LLPS) is the b ranching\, multinucleate fungus *Ashbya gossypii*. In *Ashbya*\, Whi3\, a polyQ tract-containing RNA binding protein\, binds to and localizes multip le different mRNAs by forming liquid-like droplets in the cell. Under norm al physiological conditions\, Whi3 alone cannot form liquid droplets\, *in vitro*\, as this is a phenomenon that only occurs once it is able to bind with RNA. However\, how Whi3 and RNA combine to form complexes and how th ese complex influence droplet properties remains elusive. This issue is fu rther complicated due to the many possible subcomplexes of RNA and protein that can exist. Specifically\, the target RNAs have multiple binding site s for the Whi3 protein and the Whi3 protein has two possible RNA binding s ites and likely interacts with itself using the polyQ tract. This means th at there are many possible types of interactions between components. Addit ionally\, while preliminary work within the Gladfelter Lab has shown that there is a fairly consistent average ratio of Whi3 to RNA in each droplet of a population\, it is unclear what distribution of the different protein -RNA combinations gives rise to this average ratio. To understand the role that the different combinations of Whi3 and RNA play in the initial phase separation and the properties of the droplet population\, such as size\, shape and spatial distribution of droplets\, we have created a mathematica l model that employs the use of the phase field method. With phase variabl es to represent the volume fractions of Whi3\, RNA\, and the complexes the y form\, we propose a model that employs the use of mass action kinetics a nd a modified double-well free energy to represent the complex dynamics pr esent in the cytosol. We report modelling and experimental progress on the se cytosolic liquid-liquid phase separations in *Ashbya* as they help guid e our understanding of the mechanisms behind droplet formation in the cyto sol\, as well as how these droplets function in cellular regulation.\n\nht tps://conferences.maths.unsw.edu.au/event/2/contributions/377/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/377/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling of intracellular calcium responses in the presence of dy namic stimuli DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-273@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Agne Tilunaite (Systems Biology Laboratory\, School of Mathematics and Statistics\, University of Melbourne\, Parkville\, AU\; Centre for Mathematical Medicine and Biology\, School of Mathematical Sci ences\, University of Nottingham\, Nottingham\, UK)\nCalcium is a universa l messenger that participates in a great variety of physiological function s including muscle contraction\, neuronal plasticity and immune responses. There is now compelling evidence that transient changes in the intracellu lar calcium concentration are key for achieving such versatility. \n\nTo d ate\, most of these findings have been obtained from constant stimulation or step change protocols. However\, under physiological conditions\, cells often experience time dependent stimuli such as transient changes in neur otransmitter or oscillations in hormone concentrations. How cells transduc e such dynamic stimuli into an appropriate response is an open question. W e exposed HEK293 cells and astrocytes to dynamically varying time courses of carbachol and ATP\, respectively\, and investigated the corresponding c ellular calcium activity. While single cells generally fail to follow the applied stimulation due to their intrinsic stochasticity and heterogeneity \, faithful signal reconstruction is observed at the population level. We provide a number of transfer functions that translate the extracellular st imuli into the ensemble calcium spike rates. By computing the mean root sq uare error between the predicted responses (based on the transfer function s) and the actual responses\, we identify a simple leaky integrator model as a a powerful approach. For this\, we show how to invert the transfer fu nction to estimate the stimulus that should be applied in order to achieve a specific response. Throughout the analysis we pay particular attention to the non-stationarity of both the applied stimuli and the calcium respo nses.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/273/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/273/ END:VEVENT BEGIN:VEVENT SUMMARY:Teaching mathematical modelling in ecology: experiences from a new interdisciplinary course DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-26@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jennifer Prairie (University of San Diego)\nAlthough many of the most important academic problems lie at the interface of trad itional disciplines\, undergraduate students are rarely exposed to true in terdisciplinary learning in their courses. Indeed\, despite the necessity for mathematical and computational skills in modern biological and environ mental research\, most life science students lack any experience with high er-level mathematics or how to apply it. Here\, I present experiences from a newly developed interdisciplinary Mathematical Modelling in Ecology cou rse taught by myself (in the Department of Environmental and Ocean Science s) and a colleague (Dr. Amanda Ruiz in the Department of Mathematics) at t he University of San Diego (USD). In this course\, both Environmental and Ocean Sciences majors and Mathematics majors and minors learned about how mathematical concepts can be applied to address ecological questions. This course used a novel "linked" design in which the two groups of students w ere enrolled in separate classes but that were offered at the same time\; this allowed the two student groups to learn at different paces\, but to s ometimes be combined to facilitate peer learning and collaborative problem solving. In addition\, each week there was a joint 3-hour lab\, in which students from both classes worked together in groups on complex interdisci plinary assignments to address ecological questions using both mathematica l and computational techniques. I will discuss both the successes and chal lenges from our first time teaching this course\, both from a faculty pers pective\, and from end-of-the-semester student surveys. Lastly\, I present potential future directions for this course and similar courses at other universities with the aim of further developing interdisciplinary curricul um at the interface of mathematics and biology.\n\nhttps://conferences.mat hs.unsw.edu.au/event/2/contributions/26/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/26/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling drug action on parasites during blood stage Plasmodium i nfection. DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T005000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-295@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Rosemary Aogo (Kirby Institute\, UNSW\, Sydney)\nThe artemisinins are our most effective class of antimalarials\, and are the internationally recommended drugs for treating malaria. This class of anti malarials has been an important factor in reducing mortality due to malari a globally. However\, the emergence of resistance to this most effective a nd widely used class of antimalarials threatens this progress. Despite the ir high efficacy the artemisinins are known to have high treatment failure when used without a longer acting partner drug. It has been proposed that this may be due to a persisting population of parasites that goes dormant and emerge after drug pressure has waned. Further\, artemisinin resistant parasites have been studied and it has been found that they have an alter ed development pathway\, which protects parasites during treatment. More r ecently\, we have observed that a non-drug based stress can cause parasite s to mature more slowly\, highlighting the possibility that altering the d evelopmental cycle is a general survival strategy of the parasite. Hence\, we are interested in studying the development of parasites through their life cycle with and without treatment and to quantify how drugs perturb no rmal development. Here\, we used a novel experimental system to track the development of malaria parasites after being exposed to different antimala rials in mice. We do this by measuring the RNA and DNA content of parasite s over time. Using a Gaussian mixture model (GMM) and partial differential equations we attempt to determine what fraction of parasites had their li fe-cycle perturbed and whether perturbed parasites matured more slowly or not at all.\nBy fitting the GMM to data and simulating the PDE model\, our preliminary results suggest that in the case of antimalarial drug treatme nt\, we have two distinct parasite populations. We observed a population w ith arrested maturation and a second population with slower maturation com pared to the untreated parasites. This work is ongoing\, but preliminary r esults indicate that antimalarial drugs completely arrest a proportion of the exposed parasites\, and alter the maturation of the surviving populati on.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/295/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/295/ END:VEVENT BEGIN:VEVENT SUMMARY:Analysis and simulation of a mathematical model for rabies transmi ssion in the Philippines DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-228@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: May Anne Mata (University of the Philippines Mindana o)\nRabies is a fatal zoonotic disease and remains to be a priority health concern in the Philippines. Dogs remain to be the principal carrier of ra bies and despite the fatality of rabies\, it is a vaccine-preventable dise ase. Currently\, the Philippine health officials have been conducting mass dog vaccination campaigns with the goal of having a rabies-free Philippin es by the year 2020. However\, statistical information about the disease p oses a challenge and gives rise to doubts on whether the goal is achievabl e. In line with this goal\, our aim for this study was to see whether elim inating dog rabies in the country is possible. Here\, we developed a simpl e mathematical model\, following the SEIR framework\, that describes the d ynamics of rabies infection among dogs in the presence of mass vaccination wherein some model parameters were calibrated from actual data sets. We u sed the model to predict the long-term rabies incidence and to analyticall y find an expression for the basic reproduction number in terms of vaccina tion rate\, dog reproduction rate\, transmission rate\, and rate of vaccin ation immunity loss. By numerical simulations\, we were able to determine the parameter combinations or scenarios for zero rabies infection. We asse ssed the validity and feasibility of these scenarios via data analysis. Ou r preliminary findings pointed to mathematical modelling as an important t ool to make realistic projections about the rabies disease.\n\nhttps://con ferences.maths.unsw.edu.au/event/2/contributions/228/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/228/ END:VEVENT BEGIN:VEVENT SUMMARY:Bifurcation analysis of cervical cancer mathematical modelling DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-363@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tri Sri Noor Asih (Universitas Negeri Semarang)\nIn Noor Asih *et al*. (2016) already given mathematical modelling as the dyna mic of HPV infection on cervical cancer. Also given five scenarios for the existence of equilibrium points and their local stability. From the anal ysis of the system it is found the basic reproduction number is depends on the infection rate\, the number of new virion that produce by infected ce lls\, the death rate of virus\, the growth rate of infected cells and prog ression rate. The existence and the local stability of equilibrium points are depend on basic reproduction number\, the growth rate of pre-cancer ce lls and invasion rate. So we predict that there are some bifurcation param eters on that model. While we do some simulation by continuing those param eters we found some bifurcation such as fold bifurcation\, cusp bifurcatio n and zero Hopf bifurcation. Further we analyze domain of each bifurcation parameter.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions /363/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/363/ END:VEVENT BEGIN:VEVENT SUMMARY:Ranking dose-normalized antiviral effect of drug combination treat ments against hepatitis C virus DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-230@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yukino Ikoma (Kyushu University)\nSince many kinds o f Direct Acting Antivirals (DAA) have become the main treatment instead of interferon-α (IFN-α) against hepatitis C virus (HCV)\, combinations of these DAA are now standard treatment strategies. These treatments are very effective\, however\, at the same time\, this provokes the problems which drug combination is more or most effective for each patient. Therefore\, we established a viral replicon system for HCV to quantify the efficacy of each drug or drug combination easily. In this study\, we used 15 differen t kinds of DAA (telaprevir\, danoprevir\, asunaprevir\, simeprevir\, sofos buvir\, VX-222\, dasabuvir\, nesbuvir\, tegobuvir\, daclatasvir\, ledipasv ir\, IFN-α\, IFN-λ\, cyclosporin A\, and SCY-635) and quantified the eff icacy of (single and) multiple drug combinations using the replicon system . Then\, we calculated instantaneous inhibitory potential (IIP) which capt ures the effectiveness of each drug combination as a function of the drug concentration. Furthermore\, we defined and calculated the critical concen tration index (RCI) that achieves 95% reduction in HCV replication is show n for each drug combination. The RCI intrinsically varies among the drug c ombinations. As an example\, we found SMV&IFN-α yielded the lowest RCI va lues among the tested double-combinations. We would like to further discus s how our framework could enable drug usage optimization by quantifying th e antiviral activity in preclinical settings\, and presenting basic eviden ces for cost-effective drug selection.\n\nhttps://conferences.maths.unsw.e du.au/event/2/contributions/230/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/230/ END:VEVENT BEGIN:VEVENT SUMMARY:Identification of regulatory enhancer regions DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-275@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Dominic Maderazo (The University of Melbourne)\nIn g enetics\, enhancer regions are short non-coding strands of DNA belonging t o a class of elements known as cis-regulatory. These regions\, typically i n intergenic regions\, encompass binding sites for proteins (transcription factors) that regulate gene expression. Changes to the DNA sequence in th ese enhancer regions are thought to provide a mechanism to explain changes of gene expression even though the genes across species may display some sequence conservation. \n\nThe challenge in the identification of these en hancers is that\, unlike protein-coding genes\, they do not follow a clear genetic code. Sequence conservation across species is often used as a pro xy to identify regulatory regions with the rationale that functional eleme nts are under some evolutionary pressure to maintain biological function a nd\, hence\, less subject to mutations. However\, there is emerging eviden ce that functional non-coding sequences that show conservation of biologic al function in the combination of transcription factor binding sites but s how little to no conservation at a sequence level using traditional alignm ent tools. Hence\, our ultimate goal is the identification of conserved no n-coding sequences by alternative methods to “traditional” sequence al ignments.\n\nIn this work\, we obtain an alignment between the DNA assembl ies of human (hg38) and mouse (mm9) around the gene tbx5 and perform a cur sory statistical analysis to identify and classify non-coding functional r egions. The model is developed in a Bayesian framework and we obtain a seg mentation using the segmentation classification algorithm\, changept. The algorithm samples segmentations using a Markov chain Monte Carlo method th at generalises the Gibbs sampler. We aim to incorporate a diverse set of d ata types into the model to increase accuracy and applicability.\n\nhttps: //conferences.maths.unsw.edu.au/event/2/contributions/275/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/275/ END:VEVENT BEGIN:VEVENT SUMMARY:Predator-prey interactions in wastewater treatment plants DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-441@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Mark Nelson (University of Wollongong)\nThe activat ed sludge process (ASP) is the most widely used process for the biological treatment of both domestic and industrial wastewaters. Wastewater treatme nt plants (WWTPs) based on the ASP are in widespread use in both developed and developing countries.\n\nThe ASP uses microorganisms which grow by co nsuming organic pollutants that are present in the wastewater. This produc es new organisms whilst simultaneously cleaning the wastewater. The microo rganisms flocculate to form settleable solids\, the `activated sludge'.\n\ n Central to the success of the ASP is the activated sludge. However\, a significant drawback of the ASP is the production of excess `sludge'. The expense for treating this can account for 50--60% of the total operating costs in a WWTP. Traditional methods for disposing of excess sludge are be coming increasingly unattractive due to a combination of increasing land c osts and environmental concerns about the presence of toxic elements. Thus there is a growing interest in methods that reduce the volume of excess s ludge produced by the ASP.\n\nA promising method to reduce sludge formatio n is to introduce a higher order organism\, such as protozoa or metazoa\, into the system which predate upon the microorganisms. This is potentiall y very attractive\, since once the predators have been released into the r eactor there are no `running' costs.\n\nWhy does predation reduce sludge? The ASP can be considered to be a food-chain\, in which the biomass extrac ts mass and energy from the substrate. The introduction of a predator intr oduces a new layer into the food-chain: mass and energy are now transferre d from the microorganisms to the predator. At each step in the food chain not all of the available energy and material are transferred to the next l evel: some energy\, a significant proportion of the energy\, is used for m aintenance processes\, respiration and reproduction. Thus predation on mic roorganisms may lead to a lower total biomass\, i.e. sludge reduction.\n\n Predation has been shown to be an effective technique in lab-scale experim ents and pilot-scale systems. Although a variety of predators could be use d\, much attention has focused on the use of worms. Worm growth is clearly a prerequisite for sludge reduction through predation. Relatively little is known about the growth and development of worms during sludge predation . However\, it has been shown that the wrong choice of aeration rate\, tem perature and predator (worm) density can adversely effect worm growth and consequently sludge reduction.\n\nOne of the main barriers to the adoption of predation as a cost-effective mechanism to reduce sludge formation is the phenomenon of uncontrollable growth of predators. Predator density in full scale plants can often reach very high densities. Associated with th is is the well-known phenomenon of worm blooms\, in which predator populat ion densities[ display peaks followed by a sudden disappearance of the pop ulation. The development of methods to control worm proliferation is a cha llenging problem that needs to be overcome.\n\nIn this presentation a simp lified model for a wastewater treatment plant is extended to include pred ators. Mechanisms which lead to the unsuccessful introduction of predators are identified.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribu tions/441/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/441/ END:VEVENT BEGIN:VEVENT SUMMARY:Agent-based modelling demonstrates the impact of localised tumour cell proliferation and death on macrophage infiltration DTSTART;VALUE=DATE-TIME:20180711T020000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-410@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Joshua Bull (University of Oxford)\nGrowing tumours are infiltrated by a variety of immune cells\, including macrophages\, a t ype of immune cell which can adopt a range of pro- or anti-tumour phenotyp es depending on microenvironmental cues. The spatial distribution of macro phages within a tumour varies from patient to patient and between differen t tumour types\, and is related to patient outcome. There is considerable interest in understanding the mechanisms regulating the spatial localisati on of macrophages within solid tumours and in exploiting tumour associated macrophages to deliver treatment to cancer cells [1\, 4].\n\nAs a first s tep to understanding patterns of macrophage localisation within solid tumo urs\, we consider the roles played by tumour cell proliferation and death in driving cell movement from proliferative tumour regions to hypoxic regi ons. This movement\, induced by oxygen gradients within a tumour\, must be taken into consideration when characterising patterns of macrophage infil tration. To understand the impact that this background movement has on mac rophage infiltration\, we first consider the infiltration of inert polysty rene microbeads into a tumour spheroid using data from [2]. We use the CHA STE modelling framework [3] to develop an agent-based model of microbead i nfiltration into a spheroid\, and show how varying the rates of tumour cel l proliferation and death influences the patterns of bead infiltration int o the tumours.\n\nWe then extend our model to include macrophages and CSF- 1\, a macrophage chemoattractant produced by hypoxic tumour cells. By comp aring the infiltration patterns of the macrophages in this model with thos e of the microbeads\, we identify components of macrophage infiltration du e to active (chemotactic) movement and passive components associated with tumour cell proliferation and death. Identifying which variations in macro phage distribution are due to active or passive processes may help determi ne which patients are most likely to respond to treatment with CSF-1 inhib itors [4]. \n\n[1] Bronte\, V.\, & Murray\, P. J. (2015). Understanding Lo cal Macrophage Phenotypes In Disease: Modulating macrophage function to tr eat cancer. *Nature Medicine*\, 21(2)\, 117–119. http://doi.org/10.1038/ nm.3794 \n\n[2] Dorie\, M. J.\, Kallman\, R. F.\, Rapacchietta\, D. F.\, V an Antwerp\, D.\, & Huang\, Y. R. (1982). Migration and internalization of cells and polystyrene microspheres in tumor cell spheroids. *Experimental Cell Research*\, 141(1)\, 201–209. http://doi.org/10.1016/0014-4827(82) 90082-9\n\n[3] Mirams\, G. R.\, Arthurs\, C. J.\, Bernabeu\, M. O.\, Borda s\, R.\, Cooper\, J.\, Corrias\, A.\, … Gavaghan\, D. J. (2013). Chaste: An Open Source C++ Library for Computational Physiology and Biology. *PLo S Computational Biology*\, 9(3). http://doi.org/10.1371/journal.pcbi.10029 70 \n\n[4] Pradel\, L. P.\, Ooi\, C.-H.\, Romagnoli\, S.\, Cannarile\, M. A.\, Ries\, C. H.\, Sade\, H.\, & Dominik\, R. (2016). Macrophage suscepti bility to emactuzumab (RG7155) treatment. *Molecular Cancer Therapeutics*\ , 15(12)\, 3077–3086. http://doi.org/10.1158/1535-7163.MCT-16-0157\n\nht tps://conferences.maths.unsw.edu.au/event/2/contributions/410/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/410/ END:VEVENT BEGIN:VEVENT SUMMARY:An experimental-computational approach for predicting the spatial- temporal response of tumour and vasculature to radiation therapy DTSTART;VALUE=DATE-TIME:20180711T062000Z DTEND;VALUE=DATE-TIME:20180711T064000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-414@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: David A. Hormuth II (The University of Texas at Aust in)\n*Introduction.* Radiation therapy is a critical portion of the standa rd-of-care for patients with brain tumours\, as it targets residual diseas e and non-operable tumours. However\, one of the shortcomings of radiation therapy is the heterogeneity of response observed in the patient populati on which may be due to fundamental limitations in the way radiation therap y plans are currently selected. To this end\, we are developing a coupled system of biophysical models of tumour growth and angiogenesis to predict the spatial-temporal response to radiation therapy within a tumour that is initialized and calibrated on an individual basis from non-invasive magne tic resonance imaging (MRI) data.\n\n*Methods.* To evaluate this model sys tem\, we use subject-specific diffusion-weighted MRI (DW-MRI) and dynamic contrast enhanced MRI (DCE-MRI) acquired at seven time points (collected e very 48 hrs) in rats (n = 7) with C6 gliomas. Three imaging time points (t 1-t3) were acquired before the rats received a single fraction of either 2 0 Gy (n = 4) or 40 Gy (n = 3) dose of x-ray radiation delivered over the w hole brain\, while the remaining time points (t4 - t7) were collected post -treatment. DCE-MRI data was used to identify tumour regions of interest a nd estimate the blood volume fraction (vb) on a voxel basis. Tumour cell n umber (Ntc) was estimated using DW-MRI data. The spatial-temporal evoluti on of Ntc and vb in 3D was described by two coupled\, partial differential equations describing the motility\, proliferation\, and death of tumour c ells and blood vessels. Model parameters were calibrated from data on t1- t4\, which were then used in a forward evaluation of the model from t5-t7. Error was assessed by calculating the percent error in the predicted a nd observed tumour volume. Agreement between the spatial distributions of Ntc and vb was assessed be calculating the concordance correlation coeffic ient (CCC) between the measured and observed quantities. \n\n*Results.* Fo r the rats that received 20 Gy of radiation\, the error between the predic ted and observed tumour volume ranged from 6% to 13% from t5 to t7. Addit ionally\, the CCC between the predicted and observed Ntc ranged from 0.65 to 0.73 for all rats\, while the CCC for vb ranged from 0.47 to 0.85. Hig her error was observed for the rats who received 40 Gy of radiation\, wher e the error between the predicted and observed tumour volume ranged from 1 0% to 18% on days t5-t7. A high level of agreement CCC greater than 0.70 was observed on t5 for both the vb and Ntc\, while CCCs less than 0.5 were observed on t6 and t7. \n\n*Conclusion and Discussion.* The results of t his study indicate the potential to accurately model the spatial-temporal evolution of tumour and blood volume fractions from clinically relevant im aging data following radiation therapy. Further development of subject-spe cific mathematical models\, such as the one presented here\, will facilita te individualized radiation therapy plans to address the heterogeneity of response to treatment. \n\n*Acknowledgments.* We gratefully acknowledge th e support of NCI U01 CA174706 and CPRIT RR160005.\n\nhttps://conferences.m aths.unsw.edu.au/event/2/contributions/414/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/414/ END:VEVENT BEGIN:VEVENT SUMMARY:To remain in the natal stream or migrate to the ocean-density-depe ndent growth of juvenile salmonids could lead to fluctuating populations a nd evolutionary bistability DTSTART;VALUE=DATE-TIME:20180711T062000Z DTEND;VALUE=DATE-TIME:20180711T064000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-473@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Junnosuke Horita (Kyushu university)\nMale juveniles of several species of salmonids spawning in fresh water streams migrate t o the ocean and return to their natal stream when they mature (migratory t actic)\; others stay and mature in the stream (resident tactic). Large ind ividuals become residents and small ones become migrants. This is an evolu tionary outcome according to the status-dependent strategy model\, which a ssumes that the juveniles exhibit the optimal tactic based on their status . In this study\, we consider the case in which the density of adult resid ents suppresses juvenile growth\, and explore the dynamics of alternative tactics and the evolution of threshold size. We show that a fraction of th e migratory tactic that might converge into a stable state or continue to fluctuate wildly\, and that the evolutionary outcome may be evolutionarily bistable\, resulting in a clearly different threshold size. In the case o f evolutionary bistability\, two threshold sizes differ in ecological dyna mics: a stable fraction of migratory tactic in one and two-year periodic f luctuation in the other.\n\nhttps://conferences.maths.unsw.edu.au/event/2/ contributions/473/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/473/ END:VEVENT BEGIN:VEVENT SUMMARY:Identifiability analysis in enzyme kinetics using profile likeliho od DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-241@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Rejo Anto Britto (University of Auckland)\nThe aim o f this research was to explore the potential of profile likelihoods for i dentifiability analysis in the context of real enzyme kinetics data\, col lected ourselves.\n\nParameter identifiability concerns the question of wh ether the type of experimental data we have collected properly determines the parameters of our mathematical models. Identifiability issues arise be cause not all biological variables involved in the system can be measured\ , and even those that can be measured can be structurally decoupled from s ome of the parameters of interest. Although structural non-identifiability is in principle an all-or-nothing concept\, in practice parameters may al so be only weakly identified or may be practically non-identifiable given finite data. Profile likelihood has proven to be one of the few promising general methods of identifiability analysis that is applicable to multi-pa rameter\, nonlinear problems\, but it has not yet been widely adopted in t he mathematical/computational biology community. Thus we sought to further explore its usefulness for typical models in this area\, and using real e xperimental (as opposed to synthetic) data.\n\nIn this study\, we collecte d data on the activity of the enzyme tissue plasminogen activator (tPA) un der variety of scenarios\, including different initial substrate and pH le vels. We developed a series of simple reaction kinetics models\, including both Michaelis-Menten velocity-concentration models and full time-depende nt ODE models\, and generated profile likelihoods under the various experi mental conditions. For the simple Michaelis-Menten model we found that par ameters were generally identifiable/weakly identifiable but tended to beco me less identifiable (approaching practical non-identifiability) at lower pH levels. On the other hand\, individual parameters of the full ODE mode l of enzyme kinetics showed full structural non-identifiability. This led us to consider the identifiability of targeted ‘interest’ parameters\ , motivated by the parameters in the simpler system. Using this approach w e found that certain combinations of rate parameters\, corresponding to th ose in the simpler Michaelis-Menten model\, were better identified in the full model.\n\nOverall we found profile likelihood to be a promising tech nique for identifiability analysis of enzyme kinetics models. For complex models\, however\, choosing targeted interest parameters appears to be es sential to avoid structural non-identifiability. Further work is needed on systematically motivating these interest parameters based on\, for exampl e\, simpler models and/or model reduction procedures. In the context of tP A kinetics\, more complex reactions involving the inhibitor neuroserpin an d interactions of H+ ions with the enzyme should be considered.\n\nhttps:/ /conferences.maths.unsw.edu.au/event/2/contributions/241/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/241/ END:VEVENT BEGIN:VEVENT SUMMARY:Dispersal heterogeniety and the spreading speeds of marine invasio ns. DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-470@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: James Watmough (University of New Brunswick)\nWe pro pose a structured integro-difference equation model for an invasive marine species with a pelagic larval stage and examine the role of dispersal het erogeniety on the spreading speed. The spread of the green crab up the n orthwest coast of the Atlantic is used as a case study. We find that the relationship between spreading speed and demographic and dispersal paramet ers is similar to the relationship found in Fisher's equation. We also fi nd that temporal variation in dispersal results in a faster spread rate th an predicted by a time-averaged dispersal kernel. This is joint work wi th Lin Wang\, Myriam Barbeau and Ali Gharouni.\n\nhttps://conferences.math s.unsw.edu.au/event/2/contributions/470/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/470/ END:VEVENT BEGIN:VEVENT SUMMARY:Division of labour in social insects: ecologies can drive modes of specialisation DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T005000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-472@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Bernd Meyer (Monash University)\nAll social insects live in elaborately organised societies. Their social structures enable th em to continuously manage a large set of simultaneous tasks\; from scoutin g and foraging to colony defence\, nest building\, thermoregulation\, and brood care. To ensure colony survival and reproduction it is vital that th e colony workforce is adequately allocated to these different tasks. Socia l insect colonies are able to perform such task allocation with an amazing degree of flexibility\, continuously adjusting to changes in environmenta l conditions. The resulting division of labor (DOL) is a cornerstone of al l social insect societies and commonly credited as a key factor for their enormous ecological success.\n\nThe vast majority of DOL modelling has eit her focussed on physiological factors or on individual-based behavioural m echanisms. Comparatively little attention has been given to how social int eractions regulate task allocation. None of the existing frameworks provid es a direct link to integrate environmental conditions as an integral part of the modelling process (beyond task-related stimulus levels). Entomolo gists are now investigating specifically these factors as the keys to a be tter and more comprehensive understanding of workforce allocation.\n\nWe p ropose a new mathematical modelling framework for task allocation in socia l insects that directly incorporates social interactions and environmental conditions as first class elements. We use evolutionary game theory to i nvestigate how task preferences develop during the lifetime of a colony an d how DOL emerges and morphs as a result. We model the task preferences of individuals as continuous strategy choices in a simple game\, in which i ndividuals choose how to divide their efforts between different tasks. Tas k execution results in rewards that may be shared between colony members or go directly to the individual. The amount of reward is modulated by the collective level of investment into the task as well as by environmental factors.\n\nBased on this framework we show that ecological conditions are a crucial determinant for the emergence of different forms of specialisat ion. We also find strong interactions between the prevailing learning mech anisms and colony specialisation. \n\nContrary to intuition we find that s trong specialisation does not always relate to improved colony efficiency. Particularly\, social learning appears to lead  to high colony performan ce only in a limited range of environment types and can drive a colony int o “over-specialisation” in other conditions. This suggests that social learning should only have evolved in a limited range of environments and for certain tasks. Our theoretical results thus point towards promising ne w directions for empirical work that can bring us a step closer to underst anding how social insects achieve their outstanding ecological success.\n\ nhttps://conferences.maths.unsw.edu.au/event/2/contributions/472/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/472/ END:VEVENT BEGIN:VEVENT SUMMARY:Data analysis of single-HSC transplantation DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-283@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Shoya Iwanami (Kyushu University)\nHematopoietic sys tem is maintained by hematopoietic stem cells (HSCs) with dual abilities o f long-term self-renewal and differentiation to all types of blood cells. Recently\, using a single-cell transplantation system and mice expressing a fluorescent protein\, myeloid-restricted progenitors with long-term repo pulating activity (MyRPs) were found. Moreover\, by using paired daughter cell assay\, MyRPs were directly differentiated from HSCs.\n\nIn this stud y\, we investigated hematopoietic system incorporating the novel insight t hat there existed a cell type that exclusively differentiated to myeloid l ineages. There were four types of populations in the model: (i) HSCs\, (ii ) MyRPs\, (iii) progenitors\, and (iv) differentiated cells. Differentiate d cells includes B cell and T cell which are lymphoid cells and platelet\, erythrocyte and neutrophil/monocyte as myeloid cells. Myeloid progenitors were produced via two ways\, from HSCs directly and via MyRP (myeloid byp ass)\, after transplantation of a single HSC\, while lymphoid progenitors were produced from only HSCs directly. This is the first study of investig ating hematopoiesis with MyRPs.\n\nWe estimated some parameters which were growth rate\, production rate and death rate using full data set of singl e-cell transplantation. From the result of data analysis\, we will discuss the role of myeloid bypass after transplantation and the change of hetero geneity of HSC population with age.\n\nhttps://conferences.maths.unsw.edu. au/event/2/contributions/283/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/283/ END:VEVENT BEGIN:VEVENT SUMMARY:Quantitative modelling by biology undergraduate students DTSTART;VALUE=DATE-TIME:20180711T050000Z DTEND;VALUE=DATE-TIME:20180711T052000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-222@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Robert Mayes (Georgia Southern University)\nQuantita tive Undergraduate Biology Education and Synthesis (QUBES) is an NSF funde d project with the mission to improve learning opportunities for all stude nts enrolled in undergraduate biology courses by reflecting the centrality of quantitative approaches in modern biology. We will provide an overview of the QUBES project\, then discuss the Quantitative Modelling assessment QM BUGS. The diagnostic assessment and associated RTOP observation protoc ol have been administered in biology classes at two universities. The asse ssment consists of 30 questions on quantitative modelling ability and stud ent confidence about modelling. We will report the findings from a pilot a dministration in Fall 2017 and discuss revision of the assessment informed by Rasch Analysis.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contr ibutions/222/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/222/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling the Endothelial Glycocalyx layer in the microcirculation using homogenisation DTSTART;VALUE=DATE-TIME:20180712T054000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-450@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tet Chuan Lee (University of Auckland)\nThe Endothel ial Glycocalyx Layer (EGL) is a porous macromolecular layer that lines the insides of blood vessels. It is located on the important interface betwee n the endothelium and flowing blood and as such is believed to play a numb er of important roles including transducing mechanical signals from flowin g blood and regulating vessel permeability. Previous work modelling the EG L at the continuum level has typically assumed that it is a homogenous iso tropic porous media and that if deformable\; it does so as a linear-elasti c block. In this work\, we use homogenisation theory to derive a more soph isticated model of the EGL that takes into account what is known about the underlying periodic microstructure of the EGL.\n\nHomogenisation theory i s a method of multiple scales that allows us to exploit the periodicity in the problem as well as the much smaller length scale (compared to the mac roscopic scale) over which this periodicity exists. This allows us to deri ve an overall continuum level model of the EGL that takes into account thi s microstructure while still retaining a lower level model for the flow ar ound the microstructure. In deriving this model\, we find that it differs from other fluid flow models typically obtained from homogenisation theory as the EGL is only periodic tangentially to the vessel surface and not no rmally.\n\nThis more sophisticated model allows us to investigate the effe cts of anisotropy in the model at the continuum level as endowed by the ge ometry of its microstructure. In addition\, the underlying microstructural model allows us to obtain measures such as the solid shear stress experie nced by the endothelium and the torque induced by flow over the EGL that c annot be directly obtained from previous continuum level models and is an important measure for functions such as mechanotransduction.\n\nhttps://co nferences.maths.unsw.edu.au/event/2/contributions/450/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/450/ END:VEVENT BEGIN:VEVENT SUMMARY:The role of neutrophils in $\\textit{Mycobacterium tuberculosis}$ infection DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-248@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Caitlin Hult (Microbiology and Immunology\, Universi ty of Michigan Medical School)\nTuberculosis remains a widespread and dead ly disease\, infecting approximately two billion people worldwide. Gainin g a better understanding of the immune response to *Mycobacterium tubercul osis* is crucial\, and the increased prevalence of multi-drug resistant st rains\, the current complexity and length of treatment\, and the inherent difficulties of experimental work each highlight the need for new approach es. Computational modelling of the complex immune response which results in the formation of lung granulomas can enable analysis of what is current ly a relatively black box for scientists. In particular\, the role of neu trophils in the granuloma response to *M. tuberculosis* infection remains largely unknown\, as neutrophils are easily activated and short-lived\, an d thus pose unique experimental challenges to wet lab study. Through the incorporation of a neutrophil cell type into our existing hybrid agent-bas ed computational model\, we investigate the spatiotemporal dynamic formati on of lung granulomas in response to *M. tuberculosis* infection. We are interested in determining how neutrophil presence induces both global and localized features of granulomas\, the dynamics of neutrophil interactions with other cells and *M. tuberculosis*\, whether the neutrophil response to *M. tuberculosis* is beneficial or detrimental to the host\, and how th at response can be harnessed to aid in therapies. Our goal is to not only identify the sufficient biological assumptions necessary to reproduce exp erimental datasets from our collaborators\, but to shed insights on the me chanistic basis for neutrophil-directed immunopathogenesis in *M. tubercul osis* that are beyond current experimental capabilities.\n\nhttps://confer ences.maths.unsw.edu.au/event/2/contributions/248/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/248/ END:VEVENT BEGIN:VEVENT SUMMARY:Programming human sleep/wake patterns in the real-world: emergent patterns from simple rules DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-164@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Andrew Phillips (Monash University)\nMaintaining reg ular and sufficient sleep is important to many aspects of human health. Ma thematical models of human sleep/wake patterns have typically been trained against highly regular\, prescribed schedules in healthy individuals unde r laboratory conditions or idealized versions of real-world work schedules . Consequently\, most models are deterministic and do not capture measured inter-individual variability or intra-individual variability in sleep/wak e timing and duration. We extended a mathematical model of human sleep/wak e patterns to incorporate aspects of real-world schedules. The model was b ased on the neurophysiological circuits in the brainstem and hypothalamus that regulate sleep/wake patterns\, including the circadian clock and its response to light. Three simple additions to the base model were made: (i) Constraints on sleep times\, representing weekly work and social constrai nts\; (ii) Self-selection of light patterns\, including exposure to natura l light sources if awake during daytime and artificial light sources if aw ake during nighttime\; (iii) Day-to-day variability in sleep onset tendenc y\, reflecting tendency to persist with engaging behaviours (or to ruminat e in insomnia) close to bedtime. From these simple rules emerged key quant itative properties of real-world sleep patterns\, including: (i) Social je t-lag (i.e.\, mismatch between weekday and weekend sleep times)\; (ii) Int er-individual and intra-individual variability in sleep timing and duratio n\, including pathological cases such as insomnia\; and (iii) Challenges a dapting to certain phases of rotating shift-work schedules. These findings indicate that\, although human behaviour is highly complex\, individual-l evel and population-level sleep/wake patterns can be largely recapitulated by simple rules applied to physiologically based models.\n\nhttps://confe rences.maths.unsw.edu.au/event/2/contributions/164/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/164/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling with data in an introductory numerical methods course DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-83@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Celestine Woodruff (James Madison University)\nModel ling with real data in the classroom not only gives students a sense of wh y the mathematics matters\, but it also gives them perspective on how mess y the real world is and how we adapt our models to suit non-perfect data. We present a class activity and project for an introductory numerical meth ods course in which Calculus 1 and 2 are prerequisites. In the classroom w e introduce curvature and a method for calculating curvature using discret e points. We then explore how we could use curvature to identify sinkholes given data from high resolution digital elevation models (DEMs). Outside of class\, groups of students create codes in Matlab to calculate the curv ature at each boundary point of some given depression. Each group then dec ides how to use these individual curvatures to determine whether a depress ion is a sinkhole. Once all projects are complete the students present the ir methods in class and test their codes on actual geological data. Althou gh this project is geological in nature\, it could be used with any applic ation in which identification is based on roundness.\n\nhttps://conference s.maths.unsw.edu.au/event/2/contributions/83/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/83/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling for pharmacological manipulation of primate ’s circadian rhythm and precision medicine for advanced sleep phase diso rder DTSTART;VALUE=DATE-TIME:20180712T020000Z DTEND;VALUE=DATE-TIME:20180712T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-133@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Daewook Kim (Korea Advanced Institute of Science and Technology)\nCircadian (~ 24 h) rhythms can be synchronized to the earth ’s 24 h periodic environment through external cues such as light - dark (LD) cycle. The misalignment of circadian timings with the external enviro nment can lead to crucial physiological problems\, such as jet lag\, bipol ar disorders and cancer. To treat the misalignment problem\, we investigat e the pharmacological manipulation of circadian phase of primates\, Cynomo lgus monkeys using the casein kinase1 δ/ε inhibitor\, PF-670462. Surpris ingly\, we observed that the PF-670462-induced phase shift of primates (di urnal species) is less than that of mice (nocturnal species) under LD whil e that of primates is larger than that of mice under DD. To understand thi s unexpected phenomenon\, we used mathematical modelling and found that th e light sensitivity of primate’s circadian rhythm depending on circadian phase is different to that of mouse’s circadian rhythm. Furthermore\, t he PF-670462-induced phase shift is dramatically different depending on do sing amount and timing\, light condition and chronotype. Thus\, it is chal lenging to identify the dosing amount and timing to induce a desired phase shift. Here\, we found a simple strategy to identify personalized dosing amounts and timing regardless of season and chronotype to treat advanced s leep phase disorder using mathematical modelling.\n\n[1] Jae Kyoung Kim *e t. al.*\, Modeling and Validating Chronic Pharmacological Manipulation of Circadian Rhythms\, CPT: *Pharmacometrics & Systems Pharmacology* (2013)\n [2] Jeffrey Sprouse *et. al.*\, Inhibition of casein kinase1ε/δ\, produc es phase shifts in the circadian rhythms of Cynomolgus monkeys\, *Psychoph armacology*\, pp. 735-742 (2009)\n[3] Caroline H.Ko *et. al.*\, Molecular components of the mammalian circadian clock\, *Human Molecular Genetics*\, Vol. 15\, pp. 271-277 (2013)\n[4] Jae Kyoung Kim *et. al.*\, A mechanism for robust circadian timekeeping via stoichiometric balance\, *Molecular S ystems Biology* (2010)\n[5] Florian Geier *et. al.*\, Entrainment in a Mod el of the Mammalian Circadian Oscillator\, *Journal of Biological Rhythms* (2005)\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/133 / LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/133/ END:VEVENT BEGIN:VEVENT SUMMARY:Tracking the dynamics of multiple granulomas during infection with $\\textit{Mycobacterium Tuberculosis}$ DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-280@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Timothy Wessler (University of Michigan)\nInfection with the bacteria *Mycobacterium tuberculosis* (Mtb) causes a dynamic immu ne response that spans multiple organs across multiple time scales. The i nfection may start with just a few Mtb infecting a few macrophages within the lungs\, but sites of infection quickly experience local immune respons es\, and soon after draining lymph nodes become involved to mount an even greater defense. Different mathematical tools are required to simulate thi s complicated immune response\, from the recruitment of the cells from the lymph nodes and their transport through the blood to the sites of infecti on\, to the formation of granulomas\, which are the hallmark of Mtb infect ion and are comprised of immune cells\, bacteria\, and other molecules. Ag ent-based modelling has been an effective multiscale approach to simulate the immune response during infection that forms a single granuloma. Howeve r\, the computational cost of running these simulations begs for a quicker \, coarser approach in order to study an infection across multiple granulo mas within a single host lung. We propose a novel hybrid agent-based model that uses ordinary differential equations to evolve populations of cells\ , Mtb\, and other molecules within each individual granuloma\, that is the n simulated as an agent within a whole-lung in silico infection model. The lung compartment can be connected to lymph nodes with granuloma agents sp reading between compartments. This will allow for a higher-scale host resp onse simulation to allow us to better address questions at the whole host scale and also be able to calibrate to datasets of whole human hosts.\n\nh ttps://conferences.maths.unsw.edu.au/event/2/contributions/280/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/280/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling the renal disease epidemic among HIV-infected individual s DTSTART;VALUE=DATE-TIME:20180709T010000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-112@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Elissa Schwartz (Washington State University)\nThe n umber of HIV+ individuals who develop end stage renal disease (ESRD) and r equire life-long dialysis treatment has been continually rising in some re gions around the world. A differential equation-based mathematical model was developed to assess the impact of antiretroviral therapy on the progre ssion to disease and to project the future prevalence of HIV+ ESRD. The go als of this study are to parameterize the model with new data on the popul ations of individuals with HIV/AIDS and those with HIV+ ESRD\, and to exte nd the model to take into account greater complexity in the population dyn amics. We also expand the model’s analysis to predict treatment recommen dations for the population of HIV+ individuals at risk for developing rena l disease. Further studies will use the model to estimate how much the dev elopment of renal disease and treatment levels have changed over time\, an d to predict the treatment levels needed to slow the increase of this epid emic.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/112/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/112/ END:VEVENT BEGIN:VEVENT SUMMARY:A hyperbolic curvature flow for biological tissue growth and its a pplication to determine cell behaviour during the infilling of irregular p ores DTSTART;VALUE=DATE-TIME:20180712T054000Z DTEND;VALUE=DATE-TIME:20180712T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-432@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Pascal Buenzli (Queensland University of Technology) \nThe growth of several biological tissues is known to be controlled by lo cal geometrical cues\, such as the curvature of the tissue interface. Geom etry modulates cells collectively through the evolving space available to the population of cells\, but it may also modulate the individual behaviou rs of cells. In this contribution\, I will first present how the influence of curvature on the collective crowding or spreading of cells growing new tissue leads to a new type of hyperbolic curvature flow (with curvature-d ependent normal acceleration) for the evolution of the tissue interface. D epending on the strength of diffusive damping\, the model exhibits complex growth patterns such as undulating motion\, efficient smoothing of irregu larities\, and the generation of cusps. Insights into these growth pattern s are provided by analysing the shock structure in the zero-diffusion and infinite-diffusion limits. In a second part\, I will present how this mode l can be used with experimental data on the infilling of irregular bone po res to single out the collective influence of geometry\, and gain access t o the geometric regulation of individual cell behaviours.\n\nhttps://confe rences.maths.unsw.edu.au/event/2/contributions/432/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/432/ END:VEVENT BEGIN:VEVENT SUMMARY:A mathematical light on initiation of colorectal and intestinal ca ncer DTSTART;VALUE=DATE-TIME:20180711T064000Z DTEND;VALUE=DATE-TIME:20180711T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-460@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ali Mahdipour-Shirayeh (Princess Margaret Cancer Cen tre)\nRapidly dividing tissues\, like intestinal crypts\, are frequently c hosen to investigate the process of tumour initiation\, because of their h igh rate of mutations. To study the interplay between normal and mutant as well as immortal cells in the human colon or intestinal crypt\, we develo ped a 4-compartmental stochastic model for cell dynamics based on current discoveries. Recent studies of the intestinal crypt have revealed the exis tence of two stem cell groups. Therefore\, our model incorporates two stem cell groups (central stem cells (CeSCs) and border stem cells (BSCs))\, p lus one compartment for transit amplifying (TA) cells and one compartment of fully differentiated (FD) cells. However\, it can be easily modified to have only one stem cell group. We find that the main deficiency occurs wh en CeSCs are mutated\, or an immortal cell arises in the TA or FD compartm ents. The probability of a single advantageous mutant CeSC being able to t ransform all cells into mutants is more than 0.2\, and one immortal cell a lways causes all FD cells to become immortals. Moreover\, when CeSCs are e ither mutants or wild-type individuals\, their progeny will take over the entire crypt in less than 100 days if there is no immortal cell. Unexpecte dly\, if the CeSCs are wild-type\, then non-immortal mutants with a higher fitness are washed out faster than those with a lower fitness (net reprod uction rate). Therefore\, we suggest one potential treatment for colon can cer might be replacing or altering the CeSCs with the normal stem cells.\n \nhttps://conferences.maths.unsw.edu.au/event/2/contributions/460/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/460/ END:VEVENT BEGIN:VEVENT SUMMARY:Understanding the influence of tick co-aggregation on R0 for tick- borne pathogens DTSTART;VALUE=DATE-TIME:20180709T081500Z DTEND;VALUE=DATE-TIME:20180709T083000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-444@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Simon Johnstone-Robertson (RMIT)\nTick-borne pathoge ns are transmitted when ticks take blood meals from vertebrate hosts. Tick s need to take blood meals to progress through immature life-stages and re ach adulthood. For the most important zoonotic pathogens\, including *Borr elia burgdorferi* (the causative agent of Lyme disease)\, two immature lif e-stages of the tick vector\, termed larvae and nymphs\, maintain the path ogens. Key features of tick feeding behaviour\, and therefore of tick-host contact patterns\, include the aggregation of ticks on hosts (whereby mos t ticks of a given life-stage feed on only a small minority of the hosts) and the co-aggregation of larval and nymphal ticks on the same minority of hosts.\n\nA mechanistic network model is presented for tick-borne pathoge n transmission that explicitly accounts for larval and nymphal tick co-agg regation and coincident coaggregation\, also known as co-feeding. Co-feedi ng of nymphs and larvae allows transmission from an infected nymph to susc eptible larvae feeding in close proximity and at the same time\, but witho ut the involvement of a systemic infection in the vertebrate host. By rela ting the next generation matrix epidemic threshold parameter $R_{0}$ to th e in- and out-degrees of vertebrate host nodes in the mechanistic network model\, a simple analytic expression for $R_{0}$ that accounts for the co- aggregation and coincident coaggregation of ticks is derived. Simulations of Lyme disease transmission on finite realizations of tick-mouse contact networks are used to visualize the relationship between $R_{0}$ and the ex tent of tick co-aggregation.\n\nThe derived analytic equation explicitly d escribes the relationship between $R_{0}$ and the strength of dependence b etween counts of larvae and counts of nymphs on vertebrate hosts. Tick co- aggregation always leads to greater values for $R_{0}$\, whereas higher le vels of tick aggregation only increases the value of $R_{0}$ when larvae a nd nymphs also co-aggregate. Aggregation and co-aggregation have a synergi stic effect on $R_{0}$ such that their combined effect is greater than t he sum of their individual effects. Co-aggregation has the greatest effec t on $R_{0}$ when the mean larval burden of hosts is high and also has a l arger relative effect on the magnitude of $R_{0}$ for pathogens sustained by co-feeding transmission (e.g. TBE virus in Europe) compared with those predominantly spread by systemic infection of the vertebrate host (e.g. L yme disease).\n\nCo-aggregation increases $R_{0}$\, particularly in geogra phic regions and seasons where larval burden is high and for pathogens tha t are mainly transmitted during co-feeding. For all tick-borne pathogens t hough\, the effect of co-aggregation can be to lift $R_{0}$ above the thr eshold value of 1 and so lead to persistence.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/444/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/444/ END:VEVENT BEGIN:VEVENT SUMMARY:Imaging of CD8+ T cells in the malaria infected liver reveals key processes for effective protection DTSTART;VALUE=DATE-TIME:20180709T020000Z DTEND;VALUE=DATE-TIME:20180709T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-180@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ian Cockburn (Australian National University)\nCD8+ T cells can kill *Plasmodium* parasites in the liver of the mammalian host \; a protective effect that can be harnessed for malaria vaccination. We h ave previously used intra-vital imaging to measure the interaction of CD8+ T cells in the liver and *Plasmodium* infected hepatocytes. We have previ ously observed that CD8+ T cells in the liver undertake LFA-1 dependent cr awling motility in the allowing them to scan the liver and find infected h epatocytes. Subsequently we have observed that clusters of CD8+ T cells fo rm around the infected hepatocyte\, which may potentiate parasite killing. Key questions are how do these clusters form? And how are the parasites k illed? Mathematical modelling suggested that clusters could form by at lea st two different processes. In the first process clusters form as a result of a positive feedback loop in which cells in the cluster recruit further effectors. Another model posits that clusters may form because it becomes harder for cells to leave the vicinity of an infected hepatocyte as clust ers increase in size. To distinguish these possibilities we have imaged th e behaviour of T cells in the liver to determine if they show evidence of directed migration towards infected hepatocytes. Moreover using Pertussis toxin mediated inhibition of chemokine receptors\, chemokine receptor knoc kout mice and mice lacking key effector molecules we aim to understand the molecular processes underlying T cell clustering and parasite killing.\n\ nhttps://conferences.maths.unsw.edu.au/event/2/contributions/180/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/180/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal monitoring and decision support for the end of an eradicat ion campaign DTSTART;VALUE=DATE-TIME:20180709T015000Z DTEND;VALUE=DATE-TIME:20180709T021000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-305@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Christopher Baker (The University of Queensland)\nIn troduced species are a critical threat to Australian ecosystems and specie s. Particularly noxious examples include the European carp\, feral cats\, and a variety of weeds. A central aspect of introduced species management is eradication – if they can be completely removed from a region\, the i mpact can be nullified. A central problem population eradications is knowi ng whether the species has been successfully removed or not. We develop a framework to model populations through time\, explicitly accounting for im perfect detection and unknown detection probability. We use changing detec tion rates throughout a removal project to calibrate the model\, which pro vides a quantitative method to trigger the end of a project. While invasiv e species are often the focus of removal efforts\, they can also occur to prevent disease spread in an endangered species. I will describe how we ap plied this method to a Tasmanian devil depopulation\, which enabled the es tablishment of a Tasmanian devil facial tumour disease population on Fores tier Peninsular\, Tasmania.\n\nhttps://conferences.maths.unsw.edu.au/event /2/contributions/305/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/305/ END:VEVENT BEGIN:VEVENT SUMMARY:Individual based modelling of the effects of cannibalism on geneti c resistance to Bt in the fall armyworm DTSTART;VALUE=DATE-TIME:20180709T005000Z DTEND;VALUE=DATE-TIME:20180709T011000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-340@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: William Jamieson (University of Nebraska-Lincoln)\nT he fall armyworm (*Spodoptera frugiperda*) is a pest insect which has the propensity to destroy a wide variety of common crops. It ranges over Easte rn and Central North America and\, since 2016\, has been invasive in Afric a resulting in significant economic damage. The fall armyworm is susceptib le to Bt derived insecticides\, making Bt modified crops a viable method f or controlling this species. However\, there is evidence to suggest that t here is a small subpopulation of the fall armyworm which is resistant to B t. This population remains relatively small in the wild due to the cost of resistance\, which is partially mediated by the aggressive cannibalism ex hibited by the larvae\, since resistant larvae grow at a slower rate. Thus it may be possible to control the rise of resistance to Bt in a fall army worm population via the creation of refuges for the nonresistant larvae wh o will in turn cannibalize the resistant larvae.\n\nHere we use an individ ual base modelling (IBM) approach to model an infestation of fall armyworm s\, which models every individual’s entire life cycle including cannibal istic encounters and the effects of its Bt resistance genotype. First\, we explore the best underlying mathematical models to describe the individua l insects in the IBM. Then we examine the problem of controlling the accum ulation of resistance to Bt via adjustments to the size and spacial layout of the refuge while limiting the damage to the effected crops.\n\nhttps:/ /conferences.maths.unsw.edu.au/event/2/contributions/340/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/340/ END:VEVENT BEGIN:VEVENT SUMMARY:Genomic and immune features of anti-PD-1 response in diverse solid tumours DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-442@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Ping Ye ()\nImmunotherapy using checkpoint inhibitor s has demonstrated clinical efficacy for cancers ranging from melanoma to non-small-cell lung cancer and other types. Despite some success\, many pa tients do not respond to the therapy\, and a subset of patients develops “hyper-progressive” disease. Biomarkers that predict response or toxic ity to checkpoint inhibitors will help to select patients who are most lik ely to benefit from these novel immune agents. Clinical-grade next generat ion sequencing is becoming more prevalent\, providing information about ge nomic alternations\, which could serve as potential new biomarkers to immu notherapy agents.\n\nIn this retrospective study\, we included 43 patients treated in a community cancer center who had diverse solid organ malignan cies\, completed sequencing of tumour DNA before the initiation of immunot herapy\, and received at least one cycle of a PD-1 or PD-L1 inhibitor. Hal f of the patients had breast and gynecologic cancers\, which have been les s investigated for checkpoint blockade.\n\nWe found that response to check point inhibitors was associated with i) fewer previous treatment lines\, i i) longer duration of immunotherapy\, iii) higher frequencies of periphera l blood monocytes and lymphocytes after treatment\, and iv) higher tumour mutational burden (TMB). In addition\, base substitutions and indels in PR KDC and LRP1B and amplification of BCL6 occurred more frequently in respon ders. PRKDC and LRP1B mutations showed significant association with higher levels of TMB\, which was confirmed by large-scale cancer genomics data.\ n\nResults from this study may be used to inform patients who will have a better response to PD-1/PD-L1-based immunotherapy\, possibly indicating a first-line therapy in their treatment.\n\nhttps://conferences.maths.unsw.e du.au/event/2/contributions/442/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/442/ END:VEVENT BEGIN:VEVENT SUMMARY:Unravelling the role of IL-10 in the development and function of t he TB Granuloma DTSTART;VALUE=DATE-TIME:20180711T011000Z DTEND;VALUE=DATE-TIME:20180711T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-297@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Stephanie Evans (University of Michigan)\nTuberculos is (TB)\, a deadly infectious disease caused by the bacterium Mycobacteriu m tuberculosis (Mtb). The disease is characterized by the development of g ranulomas consisting of immune cells that form a cluster around the bacter ia to limit bacterial growth and disease outcomes. Control of the TB epide mic is limited by a complicated drug regimen\, development of antibiotic r esistance\, and the lack of an effective vaccine against infection and dis ease. \n\nThere are a range of pro- and anti-inflammatory molecules associ ated with Mtb infection and it has been shown that depletion of a specific anti-inflammatory molecule\, namely IL-10\, is associated with improved v accine efficacy in mice. However\, there are conflicting results in both m ice and monkeys as to the effects of IL-10 depletion on disease\, with som e studies showing that the depletion of anti-inflammatory factors improves disease outcome and others demonstrating that this depletion causes more severe disease. In previously published modelling studies\, we suggest tha t depleting IL-10 can increase the probability that a granuloma is cleared in non-human primates (NHPs).\n\nUsing GranSim\, our previously published hybrid\, multiscale\, agent-based model of granuloma formation following Mtb infection\, we explore the role of IL-10\, on granuloma development an d function. In this exploratory study\, we simulate the depletion of IL-10 from two discrete time points. The first time point coincides with the in fection time of Mtb\, and allows us to examine the role of IL-10 in granul oma formation. Elucidating the mechanisms by which IL-10 affects granuloma formation allows us explore whether the improvement in vaccine efficacy t hat has been identified in mice can also be observed in our model. The sec ond time point is at 200 days post infection when a stable granuloma is al ready established to allow us to identify the mechanisms by which IL-10 is acting upon granuloma function and maintenance. Understanding the effect of IL-10 depletion on established TB granulomas is important to identify n ew therapeutic pathways for this disease.\n\nhttps://conferences.maths.uns w.edu.au/event/2/contributions/297/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/297/ END:VEVENT BEGIN:VEVENT SUMMARY:Dead zone formation by negative feedback loops in the circadian cl ocks DTSTART;VALUE=DATE-TIME:20180712T010000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-30@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Koichiro Uriu (Kanazawa University)\nCircadian clock s of many organisms consist of cell autonomous rhythms of gene expression in a pacemaker tissue. Negative feedback loops in clock gene regulation ar e responsible for the generation of the expression rhythms. One of the cha racteristics of the circadian clock is its phase responses to light input signals. A light signal changes the rates of biochemical reactions in the negative feedback loops and causes a phase shift depending on the state of the clock. The phase response curve (PRC) for short light stimulations in various organisms revealed the following features. A light pulse at morni ng advances the phase of the clocks\, while a light pulse at evening delay s the phase. Remarkably\, light input signals cause only slight phase shif ts during the day. Such time window where the phase of the circadian clock is insensitive to a light signal is referred to as dead zone. Several pre vious theoretical studies revealed that the presence of a dead zone in the PRC increased the robustness of the circadian clock. However\, it remains unclear how a dead zone arises in the negative feedback loop underlying r hythmic gene expression. Here we reveal mechanisms that can produce the de ad zone in the PRC using phase sensitivity analysis for Goodwin-type model s. When light signals enhance degradation of repressor proteins such as TI MELESS in *Drosophila*\, the cancelation of subsequent changes in transcri ption is critical for the dead zone formation. The influence of light sign als can be nullified during the day\, if the levels of repressor proteins are close to zero and transcription rate is already saturated. In contrast \, when light signals induce transcription of clock genes like *Periods* i n mammals\, the saturation of translation of repressor protein can create a dead zone by removing the influence of excess amount of mRNA induced by the light signals. Taken together\, our results suggest that the saturatio n of biochemical reactions in the negative feedback loops would be an unde rlying principle for a dead zone formation\, regardless of the differences in how light signals modulate biochemical reactions in the clocks for dif ferent organisms.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contrib utions/30/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/30/ END:VEVENT BEGIN:VEVENT SUMMARY:Inequality in resource allocation among individuals and population dynamics models DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T015000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-427@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Masahiro Anazawa (Tohoku Institute of Technology)\nT he Hassell equation is a classic discrete-time population model which has been widely used to model population dynamics of species with seasonal rep roduction. This equation is a generalization of the Beverton-Holt equatio n with an additional exponent\, and can describe various types of reproduc tion curves exhibiting from exact-compensation (contest competition) to ov er-compensation (scramble competition) depending on the value of the expon ent. The value of the exponent and the resulting density dependence is th ought to be related to the degree of inequality in resource allocation amo ng individuals\; contest curves result from unequal resource allocation\, and scramble curves\, from equal allocation. However\, as the model is a phenomenological one at the population level\, this relation between the e xponent and the inequality in resource allocation has mostly been discusse d only phenomenologically. Although some authors have actually derived th e Hassell equation from first-principles by considering specific competiti on models among individuals\, the exponent of the derived models does not match the naive expectation above. This study explores whether it is poss ible to derive from first-principles such a Hassell model that its exponen t is related to the inequality in resource allocation by considering resou rce competition among individuals. I demonstrate that such a Hassell mode l can indeed be derived by assuming that each individual obtains a constan t amount of resources (a resource unit) at a time\, and that the competiti on for such a discrete resource unit among individuals is repeated many ti mes. Different sizes of the resource unit generate different degrees of i nequality\, and the exponent of the derived model turns out to depend on t hat size\, thus being related to the degree of the inequality. The derive d model reduces to the Beverton-Holt model when the inequality is highest\ , and to the Ricker model when the inequality is lowest. Finally\, I disc uss how replacing an assumption on fecundity with more realistic one chang es the functional form of the derived model\, and the extension to two-spe cies competition models as well.\n\nhttps://conferences.maths.unsw.edu.au/ event/2/contributions/427/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/427/ END:VEVENT BEGIN:VEVENT SUMMARY:Grab Your Glasses! Modelling Cancer Immunology in 3D DTSTART;VALUE=DATE-TIME:20180712T020000Z DTEND;VALUE=DATE-TIME:20180712T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-77@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Paul Macklin (Indiana University)\nImmune responses to cancer-including innate responses and immunotherapy-involve complex bio chemical and biomechanical interactions between tumour cells and many type s of immune cells. To date\, most modelling has not focused on the spatial and mechanical effects of these interactions. In this talk\, we will adap t PhysiCell (an open source platform for 3-D multicellular systems biology [1]) to simulate individual immune cells as they respond to tumour-secret ed immunostimulatory signals\, adhere to cells\, test immunogenicity\, and induce apoptosis before repeating their search for new immunogenic target s. We will examine the key roles played by random motility and spatial geo metry in the success or failure of an immune response. We will show ongoin g work to bridge molecular and multicellular systems biology in 3-D multis cale simulations (e.g.\, [2]). Lastly\, we will discuss and demonstrate th e potential for high-throughput multicellular systems biology\, where larg e parameter investigations can be run on supercomputers to efficiently exp lore 3-D multicellular dynamics under many sets of hypotheses [3]\, with e xamples in cancer immunology. With HPC-deployed versions of PhysiCell\, we can complete a year's worth of mechanistic computational investigations i n a little over a day. In the future\, we believe that high-throughput mat hematical model investigations will help drive biological discovery and ev en engineering of the immune system and other complex multicellular system s. \n\n[1] Ghaffarizadeh *et al.*\, "PhysiCell: An open source physics-bas ed cell simulator for 3-D multicellular systems\," PLoS Comput Biol (2018) \, http://dx.plos.org/10.1371/journal.pcbi.1005991 \n[2] Letort *et al.*\, "PhysiBoSS: a multi-scale agent based modelling framework integrating phy sical dimension and cell signalling\," bioRxiv 267070 (2018)\, https://doi .org/10.1101/267070 \n[3] Ozik *et al.*\, "High-throughput cancer hypothes is testing with an integrated PhysiCell-EMEWS workflow"\, bioRxiv 196709 ( 2017)\, https://doi.org/10.1101/196709\n\nhttps://conferences.maths.unsw.e du.au/event/2/contributions/77/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/77/ END:VEVENT BEGIN:VEVENT SUMMARY:Validating a mathematical model of brain tumour growth with the ap parent diffusion coefficient DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-405@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Pamela R. Jackson (Precision Neurotherapeutics Innov ation Program\, Department of Neurosurgery\, Mayo Clinic)\nThe Proliferati on-Invasion (PI) mathematical model of patient specific glioblastoma (GBM) growth utilizes T1 and T2-weighted/fluid attenuated inversion recovery (F LAIR) magnetic resonance (MR) images to estimate net proliferation (`ρ`) and net invasion (D) rates. We have previously developed methods to parame trize this model from these routine MRIs such that higher D/`ρ` tumours a re considered more invasive than lower D/`ρ` tumours. More advanced MR im aging methods such as diffusion-weighted imaging (DWI) allow for the calcu lation of quantitative measurements. The apparent diffusion coefficient (A DC)\, which is calculated from DWI\, is believed to be predictive of tumou r cellularity and microstructure. Our objective is to validate that the PI model’s measure of invasiveness D/`ρ` derived from routine MRIs is con sistent with quantitative MRI measurements. We hypothesize that D/`ρ` wil l be correlated with the distributions of ADC values within the tumour. Fu rther\, we expect that the proportion of high ADC values values (low cellu larity) will predominate for low D/`ρ` (highly invasive) tumours. T1Gd a nd FLAIR images were segmented and regions of interest (ROIs) created for patients with contrast-enhancing GBMs. A FLAIR penumbra ROI was created by excluding the T1Gd ROI from the corresponding FLAIR ROI. ROI’s were the n used to mask the co-registered ADC maps and the ADC values from within t he ROI were plotted as a histogram. The ADC histogram from the FLAIR ROI w as fit using a bimodal Gaussian model. ADC histogram peak boundaries were calculated as being +/- one averaged standard deviation from the averaged peak location (FLAIR ROI histograms). The averaged boundaries were then ap plied to each histogram. We calculated the percent of ADC voxels classifie d as being below each peak\, within the lower or upper peak\, within both peaks\, or above the peaks. The percentage of voxels within each region we re then plotted against D/`ρ`. Understanding the relationship between D/` ρ` and ADC allows us to connect observations on multiparametric imaging a nd elucidate the tumour biology. These results support the practical appli cability of the PI mathematical model in quantifying patient-specific inva sion characteristics by cross-correlating those findings with that seen on other imaging techniques and parameters\, in this case ADC.\n\nhttps://co nferences.maths.unsw.edu.au/event/2/contributions/405/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/405/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimal control with multiple human papillomavirus vaccines DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-42@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tufail Malik (Merck & Co.\, Inc.\, USA)\nMany human papillomavirus (HPV) vaccination programs currently administer three vacci nes - a bivalent\, a quadrivalent and a nonavalent vaccine - for a two-dos e course. In this talk a model will be presented to explore optimal vaccin ation strategies using the three vaccines\, which differ in protection bre adth\, cross-protection\, and type-specific efficacy. Assuming the HPV inf ection prevalence in the population under the constant vaccination regime\ , optimal control theory will be used to discuss optimal vaccination strat egies for the associated non-autonomous model when the vaccination rates a re functions of time. The impact of these strategies on the number of infe cted individuals and the accumulated cost will be assessed and compared wi th the constant control case. Switch times from one vaccine combination to a different combination including the nonavalent vaccine will be assessed during an optimally designed HPV immunization program.\n\nhttps://confere nces.maths.unsw.edu.au/event/2/contributions/42/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/42/ END:VEVENT BEGIN:VEVENT SUMMARY:Multiscale image based modelling in biology DTSTART;VALUE=DATE-TIME:20180708T230000Z DTEND;VALUE=DATE-TIME:20180709T000000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-498@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Tiina Roose (University of Southampton)\nIn this tal k I will describe the application of state of the art image based modellin g to several seemingly different areas of biology. I show examples from bi omedical (lymphatic\, vascular and lung system) and agricultural problems of plant soil interaction. I will describe the workflow from imaging (X-ra y CT\, XRF\, SEM-EDX\, histology)\, image reconstruction\, image segmentat ion\, computation and how to utilize this work stream to synthesise new sc ientific knowledge. In particular I will also outline several challenges a nd bottle necks in this process to hopefully encourage more mathematicians to get involved in the full pipeline.\n\nhttps://conferences.maths.unsw.e du.au/event/2/contributions/498/ LOCATION:University of Sydney -/--Eastern Avenue Auditorium URL:https://conferences.maths.unsw.edu.au/event/2/contributions/498/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematics of climate change and malaria transmission dynamics DTSTART;VALUE=DATE-TIME:20180709T010000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-66@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Abba Gumel (Arizona State University)\nClimate chang e is known to significantly affect the dynamics of vector-borne diseases\, such as malaria. In particular\, the species involved in the transmissio n dynamics of malaria are affected by various abiotic conditions\, such as temperature\, precipitation\, humidity and vapor pressure . A number of m odels\, typically statistical (using data and statistical approaches to co rrelate some climate variables with malaria incidence) or mechanistic (acc ounting for the detailed dynamic nonlinear processes involved in disease t ransmission)\, have been employed to assess the likely impact of anthropog enic climate change on malaria transmission dynamics and control. These m odels have (generally) reached divergent conclusions\, with some predictin g a large expansion in the continental land area suitable for transmission and in the number of people at risk of malaria\, while others predict onl y modest poleward (and altitudinal) shifts in the burden of disease\, with little net effect\, and the issue remains unresolved thus far. I will di scuss some of our recent results on modelling the effect of climate variab les (notably temperature) on the dynamics of malaria vector and disease.\n \nhttps://conferences.maths.unsw.edu.au/event/2/contributions/66/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/66/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematics of a sex-structured model for Syphilis transmission dy namics DTSTART;VALUE=DATE-TIME:20180709T020000Z DTEND;VALUE=DATE-TIME:20180709T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-68@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Oluwaseun Sharomi (Khalifa University of Science and Technology)\nSyphilis\, a major sexually-transmitted disease\, continues to pose major public health burden in both under-developed and developed n ations of the world. This study presents a new two-group sex-structured mo del for assessing the community-level impact of treatment and condom use o n the transmission dynamics and control of syphilis. Rigorous analysis of the model shows that it undergoes the phenomenon of backward bifurcation. In the absence of this phenomenon (which is shown to arise due to the re-i nfection of recovered individuals)\, the disease-free equilibrium of the m odel is shown to be globally-asymptotically stable (GAS) when the associat ed reproduction number is less than unity. Furthermore\, the model can hav e multiple endemic equilibria when the reproduction threshold exceeds unit y. Numerical simulations of the model\, using data relevant to the transmi ssion dynamics of the disease in Nigeria\, show that\, with the assumed 80 % condom efficacy\, the disease will continue to persist (i.e.\, remain en demic) in the population regardless of the level of compliance in condom u sage by males. Furthermore\, detailed optimal control analysis (using Pont raygin's Maximum Principle) reveals that for situations where the cost of implementing the controls (treatment and condom-use) considered in this st udy is low\, channeling resources to a treatment-only strategy is more eff ective than channeling them to a condom-use only strategy. Furthermore\, a s expected\, the combined condom-treatment strategy provides a higher popu lation-level impact than the treatment-only strategy or the condom-use onl y strategy. When the cost of implementing the controls is high\, the three strategies are essentially equally as ineffective.\n\nhttps://conferences .maths.unsw.edu.au/event/2/contributions/68/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/68/ END:VEVENT BEGIN:VEVENT SUMMARY:Glioblastoma invasiveness may predict response to therapies with h igh or low blood brain barrier penetrability DTSTART;VALUE=DATE-TIME:20180709T063000Z DTEND;VALUE=DATE-TIME:20180709T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-65@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Susan Christine Massey (Precision Neurotherapeutics Innovation Program\, Department of Neurosurgery\, Mayo Clinic)\n*Introduct ion:* Glioblastoma (GBM) is a very aggressive primary brain cancer\, noted for its diffuse infiltration into surrounding normal–appearing brain. T his particular nature makes GBM notoriously difficult to treat\, as these diffusely invading cells cannot be resected surgically\, are difficult to target with radiation therapy\, and thus must be targeted with chemotherap y. However\, this too presents a challenge\, as these invading GBM cells r eside beyond the dense tumour regions where angiogenesis causes disruption of the blood brain barrier (BBB) and allows drugs to more readily enter t he central portion of the tumour. Thus\, it is critical to determine predi ctors of drug distribution in individual patients’ tumours and surroundi ng brain tissue to ensure the invading GBM cells are exposed to the therap y.\n\n*Objective:* Determine predictors of drug distribution and effect fr om non-invasive imaging using minimal mathematical approaches. \n\n*Method s:* Following experiments treating murine orthotopic patient-derived xenog rafts (PDXs) of GBM with various anti-tumour therapies\, we compiled data from both the xenografts and the original patients from which the PDX line s were derived. This data included bioluminescence imaging (BLI)\, lamin –stained histological sections\, and magnetic resonance imaging (MRI) fr om the PDXs\, as well as patient MRIs and clinical data. Using the time se ries BLI data from PDXs\, we developed and parameterized minimal different ial equation models of PDX tumour growth for individual PDX lines\, adjust ed for lead time bias using a nonlinear mixed effects approach. This gave us an overall growth rate for each of the PDX lines across multiple subjec ts. Next\, we compared these growth and invasion characteristics with ther apeutic response in patients and PDX subjects to agents with different CSF to plasma ratios\, indicating the degree of blood brain barrier penetrabi lity of these drugs. \n\n*Results:* Individual PDX lines have different gr owth kinetics\, and recapitulate the kinetics observed in the original pat ients from which the lines are derived. Further\, these growth kinetics ap pear to be correlated with differential drug response\, with more diffusel y infiltrating tumours responding better to drugs with higher CSF to plasm a ratios. \n\n*Conclusion:* While further work is needed to verify our res ults across more PDX lines\, our results suggest that noninvasive imaging- based characterization of tumour invasiveness may be able to aid in matchi ng patients to the best therapy for their individual tumours.\n\nhttps://c onferences.maths.unsw.edu.au/event/2/contributions/65/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/65/ END:VEVENT BEGIN:VEVENT SUMMARY:Predation or frequency dependence\, which of them controls dimorph ism oscillations in prey predator system? DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T005000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-468@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Satoshi Takahashi (Nara Women's University)\nOscilla tion of lateral asymmetry diorphism is first found in scale eating cichlid \, Perrisodus microlepis. Fraction of their lefty morph oscillates around 0.5 in about 5 year period. Other fish or aquatic invertebrates also rev eal lateral asymmetry dimorphism and oscillation of morph fractions. One of key factors of oscillation is cross predation dominance: lefty predator eats more righty prey than lefty prey\, and vice versa. When lefty is ma jor in predator\, righty prey decrease\, then larger fraction of lefty pre y increases righty predator\, and so on. This cycle appears to lead to th e laterality oscillation. However the story is not such simple. A simple ODE model of prey predator system with cross predation dominance has no l imit cycles\, its coexisting equilibrium is stable\, though almost neutral . Introduction of time delays due to growth periods destabilizes the coex isting equilibrium and leads to a limit cycle of oscillating dimorphism fr action. However\, this laterality dimorphism oscillation due to time dela ys of growth periods and predation cycle can not explains that observed in fields. Amplitude and period of fraction oscillation are almost 1.0 and 50 ~ 250 years in the model\, while they are 0.1 ~ 0.3 and 3 ~ 6 years in fields. Another factor of oscillation in morph fraction is frequency dep endence. When lefty scale eaters are more common\, righties eat more scal es and have higher reproductive success. We introduce frequency dependent predation success into the model: rarer predator eats more prey. This fr equency dependence\, however\, ends up with the vanish of oscillation by e ither stabilization of coexisting equilibrium\, or fixation one laterality morph. Another frequency dependence\, that of prey selection\, i.e. pred ator eats more common prey morph\, stabilizes coexisting equilibrium. The model with both of frequency dependence finally shows oscillations with r ealistic amplitudes and periods. We conclude that oscillation of lateral asymmetry morphs is caused not by predation cycle\, but by frequency depen dence in both of prey and predator\, i.e. rarer predator or prey morph is advantageous and become common after a few years.\n\nhttps://conferences.m aths.unsw.edu.au/event/2/contributions/468/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/468/ END:VEVENT BEGIN:VEVENT SUMMARY:Regression of tumour cells in breast cancer administrating chemoth erapy using MTD and metronomic techniques DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-361@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Fatemeh Ansarizadeh ()\nTo gain deep insights into t he interactions among major types of cells\, such as healthy\, tumour\, an d immune cells\, in a tumour-bearing host\, we propose a mathematical mode l consisting of four delay differential equations by considering the inher ent delay in the tumour cells’ life cycle. When choosing model parameter s\, sensitivity analysis justified previous assumptions had been considere d.\n\nSince the impact of immune system is decisive on the regression of t umour cells\, stability analysis is performed for two different levels of immune system surveillance\, that is\, healthy and compromised tumour-bear ing host. \n\nTheoretically\, it has been showed that in a healthy host th e immune system is able to eradicate the tumour cells completely whereas i n presence of weak immune system tumour cells have the opportunity to keep proliferating.\n\nThe latter case\, necessitates an efficient treatment\, and more precisely a combination of different treatments\, for being able to fight and demise tumour cells.\n\nNowadays\, Chemotherapy is the most common treatment which is administrated in various protocols. Among them\, MTD (Maximum Tolerated Dosage) and Metronomic are of great significance i n clinical observations. Our model suggests that Metronomic technique surp asses MTD after introducing this treatment. The last but not the least\, s ince the results of mathematical experiments illustrate the administrated Chemotherapy protocols are not able to eradicate the tumour cells\, the pr oposed model unveils the demand for an adjunct treatment.\n\nhttps://confe rences.maths.unsw.edu.au/event/2/contributions/361/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/361/ END:VEVENT BEGIN:VEVENT SUMMARY:The geometry of leukemic proliferation DTSTART;VALUE=DATE-TIME:20180712T010000Z DTEND;VALUE=DATE-TIME:20180712T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-78@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Reginald McGee (Mathematical Biosciences Institute)\ nComplex protein interaction networks complicate the understanding of what most promotes the rate of cancer progression. High dimensional data provi des new insights into possible mechanisms for the proliferative nature of aggressive cancers\, but these datasets often require fresh techniques and ideas for exploration and analysis. In this talk\, we consider expression levels of tens of proteins that were recorded in individual cells from ac ute myeloid leukemia (AML) patients via mass cytometry. After identifying immune cell subpopulations in this data using an established clustering me thod\, we use topological data analysis to search for subpopulations that are most actively proliferating. To conduct the search within these subpop ulations\, we build on the differential geometric perspective that led to our recent statistic for testing aggregate differences in protein correlat ions between patients with different subtypes of AML.\n\nhttps://conferenc es.maths.unsw.edu.au/event/2/contributions/78/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/78/ END:VEVENT BEGIN:VEVENT SUMMARY:Same-same but different: how heterogeneity within tumours can dera il immunotherapy! DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-162@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Adrianne Jenner (University of Sydney)\nCancer prese nts one of the largest problems in our modern society. Understanding even the smallest aspect of this disease is immensely challenging due to its he terogeneous nature\, a characteristic we term the 'same-same but different ' nature of cancer. Heterogeneity can exist across tumour types depending on what stage the tumour is at or what organ the tumour exists in. There a re many contributing factors that can be affected by differences between c ancers\, e.g.: tumour growth rate\, tumour cell S-phase length\, vasculari sation and many more. The effects of these differences on the outcome of c ancer therapies are still not fully understood and present a hurdle to mod ern cancer therapies. To add to the complexity of this problem\, within tu mours themselves\, there is an array of 'same-same but different' characte ristics that tumours can have\, such as structure\, pressure and anti-vira l immune responses. Using mathematical modelling\, we investigate the effe ct of tumour heterogeneity on the outcome of virotherapy and immunotherapy . Using distributed delay models and agent-based modelling we unravel the layers of tumour heterogeneity and answer two key questions "why does hete rogeneity within a tumour derail immunotherapy?" and "how can we overcome this obstacle?" Optimisation of current experimental data helps us tie dow n parameter values and suggest with some level of confidence how treatment s\, such as immunotherapy\, can be improved to overcome the challenges pre sented by dissimilarities within and across tumour types.\n\nhttps://confe rences.maths.unsw.edu.au/event/2/contributions/162/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/162/ END:VEVENT BEGIN:VEVENT SUMMARY:Flu ACHOO! Modelling the immune response to influenza-bacterial co infection DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-192@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Amber Smith (University of Tennessee Health Science Center)\nInfluenza A virus (IAV) infections are often complicated by bacte rial pathogens like *Streptococcus pneumoniae* (SP\, pneumococcus)\, which have accounted for 40-95% of IAV-associated mortality. IAV-SP coinfection is characterized by rapid\, uncontrolled bacterial growth\, a rebound in viral titers\, and a robust inflammatory response. Several factors contrib ute to influenza-pneumococcal pathogenicity\, including aberrant immune re sponses\, tissue destruction\, and pathogen strain and dose. To determine the contribution\, regulation\, and time-scales of different mechanisms\, we analyze infection kinetics with mathematical models then experimentally validate our model predictions. Through this model-experiment exchange\, we have identified how virus induced alveolar macrophage (AM) depletion di ctates bacterial establishment and initial growth kinetics\, and that bact eria enhance virus replication efficiency by blocking interferon (IFN) sig nalling. Because additional mechanisms may contribute to the development o f pneumonia in coinfected animal\, we infected mice with IAV then SP at di fferent times post-influenza and simultaneously measured numerous variable s. Modelling these data suggests that new infections contribute to the vir al rebound\, that suppressed T cell responses and exacerbated IFN response s have little impact\, that the increased AM depletion is bacterial mediat ed. Collectively\, our models and data provide insight into the mechanisms of IAV-SP coinfection\, demonstrate the accuracy and predictive power of theoretical models\, and highlight the importance of validating model pred ictions.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/19 2/ LOCATION:University of Sydney New Law School/--028 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/192/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical models to predict clinically relevant events in cance r patients DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-433@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jeremy Mason (University of Southern California)\nCa ncer is one of the leading causes of morbidity and mortality worldwide. Ma ny of the disease related events\, such as metastatic progression\, treatm ent resistance\, and overall survival\, generate much uncertainty and are oftentimes viewed as random. Applying current modelling techniques and met hodologies to existing data can produce a forecasting framework that can b e leveraged to predict these significant events that impact clinical decis ion making. We used a retrospective\, longitudinal dataset of 3\,505 patie nts with primary bladder cancer to build forecasting models that could be used prospectively in newly diagnosed patients. We built Markov models fro m individual patient progression pathways and used these models to simulat e and predict future locations of metastatic spread. Additionally\, we use d machine learning techniques to temporally predict disease progression an d overall survival. Analyzing the results of these models revealed that pa tterns of metastatic spread emerged in distinct subgroups of patients when stratified by gender and also by pathologic stage. Additionally\, analysi s of patient variables showed higher associations with both recurrence and survival for pathologic staging (post-operative) as compared to clinical staging (pre-operative). Incorporating additional longitudinal data such a s treatment information and genomic data could lend to the predictions of therapy resistance and side effect development.\n\nhttps://conferences.mat hs.unsw.edu.au/event/2/contributions/433/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/433/ END:VEVENT BEGIN:VEVENT SUMMARY:Temperature sensitivity of PO/AH neurons DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-174@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Martin Wechselberger (University of Sydney)\nThermor egulatory responses are partially controlled by the preoptic area and ante rior hypothalamus (PO/AH)\, which contains a mixed population of temperatu re-sensitive and insensitive neurons. In [1] based on physiological data\, a Hodgkin-Huxley-like conductance based model was constructed. This model suggests that most PO/AH neurons have the same types of ionic channels\, but different levels of channel expression can explain the inherent proper ties of the various types of temperature-sensitive and insensitive neurons which is encoded in their frequency sensitivity relative to temperature.\ n\nHere we present a detailed bifurcation analysis of this model to confir m these observations. We focus on three main physiological bifurcation par ameters\, the temperature T and the maximum conductances of two specific b ackground potassium leak channels\, $g_{task}$ and $g_{trek}$\, that are k nown to be expressed in these PO/AH neurons. These three bifurcation param eters are sufficient to explain the dynamics of PO/AH neurons observed in experiments. \n\nIf time permits\, we also discuss the multiple timescales inherent in this model and explain the creation of action potentials base d on a geometric singular perturbation analysis.\n\n[1] Wechselberger *et al.*\, 2006\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions /174/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/174/ END:VEVENT BEGIN:VEVENT SUMMARY:How mathematics can be used in nature conservation DTSTART;VALUE=DATE-TIME:20180711T033000Z DTEND;VALUE=DATE-TIME:20180711T043000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-497@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hugh Possingham (The Nature Conservancy)\nThere are now over 50 conservation science journals and the field is booming. The w orld’s top journals\, Science and Nature\, routinely cover conservation science issues\, but the field has been dominated by ecologists. Solving conservation problems is as much about maths and economics\, as it is abou t ecology. Our group at the University of Queensland\, and our national A RC Centre of Excellence or Environmental Decisions (CEED) has been using m odels and tools from operations research to formulate and solve pressing c onservation problems. In this talk I will provide an array of examples of how operations research and ecological modelling has delivered outcomes f or nature conservation – from locating places for national parks to savi ng threatened species.\n\nhttps://conferences.maths.unsw.edu.au/event/2/co ntributions/497/ LOCATION:University of Sydney -/--Eastern Avenue Auditorium URL:https://conferences.maths.unsw.edu.au/event/2/contributions/497/ END:VEVENT BEGIN:VEVENT SUMMARY:Lifelong CMV infection minimises age-related decline in the divers ity of T cells recruited into the immune response to another infection DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T005000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-299@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Vanessa Venturi (Kirby Institute\, UNSW Sydney)\nThe elderly population is particularly susceptible to infectious diseases\, s uch as influenza\, as evidenced by increased occurrence and severity of in fection\, and reduced vaccine efficacy. Studies suggest an association bet ween persistent cytomegalovirus (CMV) infection and deficiencies of the ag ed immune system. CMV is a common herpes virus that infects up to 85% of t he population aged 40 years or over. Healthy individuals rarely experience symptoms after the initial CMV infection. However\, the virus remains in the body in an inactive state and constant surveillance by the immune syst em is required to detect and suppress reactivation of the virus. It is unc lear whether this lifelong burden on the immune system to control persiste nt CMV infection plays a causal role in age-related compromise of the immu ne system to fight infections and respond to vaccines.\n \nThe effect of a ge on the immune system is multifactorial. One factor is a decline in the diversity of CD8+ “killer” T cells recruited by the immune system to f ight a particular infection. In this study we investigated whether the pre sence of lifelong CMV infection impacts the diversity of T cells respondin g to another infection in aged mice. The diversity of T cells responding t o infection was assessed using single-cell Sanger sequencing and bioinform atics analysis of the T cell receptors\, which are expressed on the surfac e of individual T cells to enable the detection of virus. Various features of the T cell receptors\, including diversity\, gene usage\, sequence len gth\, and conserved patterns of amino acid usage were quantitatively compa red between three groups of mice: young adult and old adult mice with no C MV infection and old mice with lifelong CMV infection. T cell diversity wa s quantified using ecological measures of diversity and rarefaction to sta ndardize for differences in sample sizes. Our results demonstrate that\, i n the absence of persistent CMV infection\, T cell responses in old mice w ere significantly less diverse than in young adult mice. In contrast\, T c ell diversity was maintained in the old mice with CMV infection and we did not observe the age-related narrowing of the T cell population that occur red in the absence of persistent CMV infection. Next-generation sequencing of the broader T cell populations that have not previously encountered in fection showed similar T cell diversity in all three groups of mice\, incl uding the presence of T cell receptors that were recruited into the immune response in CMV-infected old mice but not in old mice without CMV infecti on.\n\nThese results suggest that lifelong CMV infection may actually impr ove T cell immunity in later life by broadening the diversity of T cells t hat can be effectively recruited and/or maintained in immune responses to other infections. Furthermore\, these results challenge the paradigm that CMV has a negative impact on the ageing immune system.\n\nhttps://conferen ces.maths.unsw.edu.au/event/2/contributions/299/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/299/ END:VEVENT BEGIN:VEVENT SUMMARY:Stationary fronts in competition-diffusion models in randomly fluc tuating environments DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-482@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Merlin Christopher Köhnke (Osnabrück University)\n The spatio-temporal intra- and interspecific competition of two diffusing similar populations is considered. The growth of both populations is eithe r logistic or shows an Allee effect. Conditions of spatial segregation wit hout mixing are investigated. Furthermore\, the impact of density-dependen t environmental noise on the occurring stationary fronts is studied. A spe cial focus is set on the development of functions describing the density-d ependent noise intensity. The obtained results are associated with a biolo gical case study related to the competition of two invasive weeds.\n\nhttp s://conferences.maths.unsw.edu.au/event/2/contributions/482/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/482/ END:VEVENT BEGIN:VEVENT SUMMARY:Relating explicit spatial structure in population connectivity wit h biodiversity DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-481@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yuka Suzuki (Okinawa Institute of Science and Techno logy Graduate University)\nOne of the challenging questions in Ecology is how spatial structure influences the formation of biodiversity patterns. H ere\, we explore networks that represent population connectivity including cases where dispersal is symmetric and asymmetric\, looking for the relat ionship between population connectivity network structure and biodiversity patterns therein. In this metapopulation system\, we simulate dispersal o f individuals based on the probabilities given by a dispersal connectivity matrix\, and measure resulting biodiversity. \n\nDifficulties with this a pproach include the variety of possible network structures and the increas ing complexity of networks as they become larger. To deal with this proble m\, we analyze and compare 1) theoretical networks of relatively small siz e\, which vary in complexity\, and 2) realistic large and complex networks that represents coral larval dispersal connectivities in a marine system. Through this approach\, we will be better able to understand the possible contribution of geographical structure to biodiversity for metapopulation s.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/481/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/481/ END:VEVENT BEGIN:VEVENT SUMMARY:Elasticity analysis of random matrices in matrix population model s DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-247@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Takenori Takada (Hokkaido University)\nProjection ma trix models are known to provide us with a plenty of population statistics \, such as population growth rate\, steady size-class distribution\, and s ensitivity and elasticity for population growth rate. Hundreds of academic papers using the model have been published these last forty years and a d atabase on many of their matrices is now available on the internet (COMPAD RE and COMADRE)\, which contains the demographic data on more than a thous and species. Silvertown *et al*. (1996) published a famous paper\, where t hey mapped elasticity vectors of survival\, growth and fecundity for 84 pl ant species in a triangle simplex and found that they are located in a spe cific region. The same trend is found on the map for 1230 plant population s in the above plant database. To understand and clarify why they are loca ted in a specific region\, we constructed five types of random matrices. 4 by 4 random matrices were composed of two parts: fecundity and transition probabilities from a stage to another. The distribution of fecundities fo llowed a Poisson distribution. The transition probabilities range from zer o to one\, whose row sums are less than 1. The elasticities for survival\, growth and fecundity were calculated using 3000 random matrices and the e lasticity vectors were plotted in the triangle map. The five types of matr ices were as follows: (1) random matrices with no zero-element\, (2) rando m matrices with no zero-element and the survival probabilities increase as individuals grow\, (3) random matrices which have non-zero elements only on diagonal and sub-diagonal positions\, (4) random matrices which have no n-zero elements only on diagonal and sub-diagonal positions and the surviv al probabilities increase as individuals grow\, (5) random matrices in sem elparous species. The results are: (a) the distribution of the elasticity vectors moves to upper-left region of the triangle map as average of fecun dity increases\, (b) In the third and fourth types of random matrices\, th e distribution is located on a line whose slope is equal to 46 degrees. Th e slope can be described by a formula depending on the matrix dimension\, *n* and ranges from 30 to 60 degrees with *n* = 2 to infinity. (c) In seme lparous species\, the distribution moves to the upper left along the 46-de gree line. (d) There are no elasticity vectors in the bottom half of the t riangle map.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribution s/247/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/247/ END:VEVENT BEGIN:VEVENT SUMMARY:What sort of interspecific interactions leads to deviation from a neutral community? DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-484@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hisashi Ohtsuki ()\nThe neutral theory in community ecology attempts to explain its species-abundance composition by the balan ce between local extinction of species due to demographic stochasticity an d immigrational supply of new species from a meta-community. The original neutral theory is described by two parameters\; the one (“theta”) that represents biodiversity in the meta-community\, and the other (m) is the immigration rate. Quite surprisingly\, such a two-parameter model often sh ows a good fit to real community data\, leading to the impression that man y real communities significantly look “neutral”. Inspired by the metho dology in evolutionary game theory\, here I try to reveal whether non-neut ral communities with intra- and inter-specific interactions really look “neutral”\, and if not\, under what condition. My random community mod el explicitly incorporates those interactions and has new parameters that control the proportions of mutualistic (+/+)\, competitive (-/-)\, and exp loitative (+/-) interactions in the community. Extensive computer simulati ons have revealed that communities that are rich with mutualistic interact ions\, or those with exploitative ones tend to look neutral although they are not\, whereas those communities that have a mixture of competitive and exploitative interactions are often deemed non-neutral. Those results tel l us limited statistical power in existing neutrality tests.\n\nhttps://co nferences.maths.unsw.edu.au/event/2/contributions/484/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/484/ END:VEVENT BEGIN:VEVENT SUMMARY:Theoretical study of interaction between allergy and intestinal mi crobiome DTSTART;VALUE=DATE-TIME:20180711T005000Z DTEND;VALUE=DATE-TIME:20180711T011000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-397@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Akane Hara (Kyushu University)\nRecent studies show that human immune system interacts with intestinal microbiome. A certain g roup of intestinal bacteria is known to be possible suppressor of undesira ble immune response [1]. They produce short chain fatty acid such as butyr ate and induce regulatory T cells [1]. Regulatory T cells are suppressor o f exaggerated immune responses [2]. Therefore\, collapse of the ecological balance of intestinal microbiome may cause dysregulation of immune system . On the other hand\, mutant mice with regulatory T cells that have limite d diversity of T cell receptor repertoire cause inflammation to commensal intestinal microbiome driven by T helper cells [3]\, suggesting that immun e cells develop hypersensitive response to commensal microbiome and that r egulatory T cells suppress the reactions.\n\nThis suggests us that interve ntion targeting intestinal microbiome may provide a novel strategy for tre atment of allergic symptoms. In this talk\, we develop a simple mathematic al model that describes interaction between intestinal microbiome and immu ne system. We consider dynamics of T helper cells (trigger of allergic res ponse)\, regulatory T cells (suppressor of allergy)\, and intestinal micro biome. Differentiation process of these two types of T cells is described as a model of immune system\, the structure of which was developed in our previous study [4].\n\nAnalysis shows that the model has results of three different types differing in stable steady states: (1) the case with a sin gle stable positive steady state representing “healthy condition”\, (2 ) the case with a single stable steady state representing “allergic cond ition”\, and (3) the case with two stable steady states\, representing “healthy” and “allergic” conditions\, respectively. Steady states representing healthy condition has a low level of helper T cells\, a high level of regulatory T cells\, and bacteria\; whilst those representing all ergic condition has opposite features (high helper T cells\, low regulator y T cells and bacteria). Considering these three different situations\, no w we have two strategies for allergy treatment. The first strategy is to e liminate steady state which corresponds to allergy\, by realizing the cond ition for case (1). We derived a formula for the absence of allergic state . The second strategy is to reduce the abundance of helper T cells at the steady state. We tested bacteria-related parameters for their effectivenes s in suppressing the level of helper T cells. This study is the first atte mpt in modelling association between intestinal microbiome and immune syst em and in finding out a therapy method for allergy by intervention of inte stinal microbiome. \n\n[1] Furusawa\, Y. *et al*. 2013. *Nature* 504\, 446 -50. \n[2] Sakaguchi\, S *et al*. 2008. *Cell* 133\, 775-787. \n[3] Nishio \, J. *et al*. 2015. *Proc Natl Acad Sci U S A* 112\, 12770-5. \n[4] Hara\ , A and Iwasa\, Y. 2017. *J. Theor. Biol*.425\, 23-42.\n\nhttps://conferen ces.maths.unsw.edu.au/event/2/contributions/397/ LOCATION:University of Sydney New Law School/--020 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/397/ END:VEVENT BEGIN:VEVENT SUMMARY:Adaptive partner recruitment by hosts can help maintain a diversit y in mutualistic systems DTSTART;VALUE=DATE-TIME:20180711T054000Z DTEND;VALUE=DATE-TIME:20180711T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-485@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Hideo Ezoe (Osaka Prefecture University)\nMutualisms are reciprocally beneficial interactions between heterospecific organisms . Theoretical studies have predicted that genetic diversity in mutualistic systems should decrease over time because of innate positive feedback str ucture of the interaction. Negative feedback due to asymmetry in the excha nge of benefits can maintain the diversity and stabilize multi-strain mutu alistic systems\, but partner preference for more beneficial partners migh t reduce such asymmetry and strengthen the positive feedback. Here I devel op a replicator dynamics model for a mutualistic system between two host a nd two symbiont strains to clarify conditions that can stabilize multi-str ain mutualisms in which the positive interspecies feedback is dominant. I assume that one symbiont strain is mutualistic for one host strain but par asitic for the other\, whereas the other symbiont strain is the opposite. Hosts choose multiple symbiont individuals from the environment and discri minately offer them resources (e.g. photosynthates in legume–rhizobium m utualisms)\, and only mutualistic symbionts spend a fraction of the resour ces on producing beneficial products for their hosts (e.g. nitrogen fixati on by rhizobium). The fitness of a host is proportional to the product of the amount of remaining resources and that of receiving beneficial product s\, while the fitness of a symbiont is proportional to the amount of the r est of resources offered by its host. I assume that proportions of resourc es to spend for hosts are different between the two symbionts\, and values of other parameters including the partner preference are identical betwee n the two mutualistic associations of the hosts and symbionts. \n\nI show that two host and symbiont strains can coexist stably under strong partner preference by hosts if hosts adaptively adjust the number of associating symbionts\, even when the intra-strain competition among hosts is not stro ng enough for coexistence of the strains by itself. They can also coexist under weak partner preference. However\, under moderate partner preference the coexistent equilibrium is dissolved and the strains cannot coexist.\n \nhttps://conferences.maths.unsw.edu.au/event/2/contributions/485/ LOCATION:University of Sydney New Law School/--022 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/485/ END:VEVENT BEGIN:VEVENT SUMMARY:Comparing age- and stage-structured matrix models for declining sp ecies: case study with marine mammals DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-494@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Lia Hemerik (Wageningen University and Research)\nIU CN criteria are the most authoritative and objective to assess the conserv ation status of animal species. Although IUCN criteria are purely descript ive in nature\, they can be interpreted as e.g. the relative size of the a nnual population growth factor (λ\, the dominant eigenvalue of a projecti on matrix). This enables quantitative assessment based on demographic data (survival and reproduction). However\, such an assessment for many specie s is hampered since demographic data are often incomplete. To facilitate a ssessment when demographic data are incomplete we extended an existing fra mework (developed for species with a pre-adult stage of one year) to apply to species with pre-adult stages (=juvenile and sub-adult together) longe r than one year. We develop both Leslie-matrices and stage-structured matr ices and compare these with respect to eigenvalues\, and both sensitivity and elasticity of underlying parameters. We illustrate our work with life history data and conservation status of a few marine mammal species.\n\nht tps://conferences.maths.unsw.edu.au/event/2/contributions/494/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/494/ END:VEVENT BEGIN:VEVENT SUMMARY:A geometric model to explore multiple macroecological patterns acr oss scales DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-462@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Nao Takashina (Okinawa Institute of Science and Tech nology)\nMacroecological patterns\, such as the species area relationship (SAR)\, relative species abundance (RSA)\, and endemic area relationship ( EAR) provide us useful information of ecosystem structures that can be app lied to\, for example\, ecosystem conservations. To understand these patte rns across spatial scales is one of the central challenges recent years. T o tackle the challenge\, we develop a spatially explicit geometric model w here a set of species distribution ranges and individual distributions the rein are described by spatial point processes. Essentially by calculating the number of individuals or distribution ranges given a sampling region\, several well-known macroecological patterns are recovered including the t ri-phasic SAR on a log-log plot with its asymptotic slope\, and various RS As such as Fisher’s logseries and the lognormal distribution. In a simpl e manner\, the EAR is also calculated in our framework. These multiple mac roecological patterns can be derived with a single set of biological param eters\, and therefore it may provide us a convenient way to discuss the mu ltiple patterns in a consistent manner.\n\nhttps://conferences.maths.unsw. edu.au/event/2/contributions/462/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/462/ END:VEVENT BEGIN:VEVENT SUMMARY:Menopause with a cause: The evolution of monogamy in response to f emale fertility loss DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-489@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Katrina Milliner (University of Sydney)\, Viney Kuma r (University of Sydney)\nThe human species is unique in its tendency towa rds monogamy\, a trait which can be traced back to hunter-gathering societ ies. Traditional explanations for this evolution have focused on the prese nce of paternal care and the needs of our offspring. However\, recent rese arch has challenged this claim\, contending that the significant effects o f mating competition on male choice result in evolutionary equilibria with little male care. This paper models the population dynamics of a rudiment ary hunter-gathering society\, and determines sufficient conditions for mo nogamy to supersede pure mating strategies as the optimal allocation of ma le reproductive effort. Utilising an approach based on the graphical analy sis of systems of nonlinear ordinary differential equations\, various situ ations were considered including the variation of reproduction rate\, sex ratio and fertility loss. While our results concur with previous findings that male pair bonding triumphs in response to partner scarcity and male-b iased populations\, a dynamic expected gain model extended this reasoning to explicitly show that menopause and the age of menopause occurrence dire ctly cause the evolutionary bias sufficient to cause a shift away from the multiple mating strategy.\n\nhttps://conferences.maths.unsw.edu.au/event/ 2/contributions/489/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/489/ END:VEVENT BEGIN:VEVENT SUMMARY:Effects of population size and social connectedness on cumulative cultural evolution: A gene-culture coevolutionary model DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-254@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yutaka Kobayashi (Kochi University of Technology)\nT he demographic hypothesis of cumulative cultural evolution claims that pop ulation size has been a crucial determinant of the rate of cumulative cult ural evolution in humans rather than other factors such as environmental r isk. The original version of this hypothesis does not distinguish the role of population size from that of social connectedness\, i.e. the degree to which individuals in a population are socially connected with each other. Recently\, one of our models showed that social connectedness may actuall y have a larger impact on the rate of cumulative cultural evolution than p opulation size. However\, these models all assume that the mode of learnin g which underlies cultural transmission is fixed and does not evolve\, so that they cannot deal with the time scale of genetic evolution. In the pre sent study\, we extend previous models of cumulative cultural evolution by assuming that the allocations of the individual lifetime into two modes o f learning\, social and individual learning\, co-evolve with the level of culture in the population. We derive the evolutionarily stable learning st rategy\, assuming that cultural evolution occurs on a faster time scale th an genetic evolution. The results suggest that population size may have on ly a minor effect on the equilibrium level of culture realized by the evol utionarily stable learning strategy\, while social connectedness may have a relatively large effect\, conforming with the results of models without evolution of learning. These results indicate the importance of distinguis hing different aspects of demography when modelling cumulative cultural ev olution.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/25 4/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/254/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling and optimal policy for decreasing Japanese empty homes\, Akiya\, due to an aging society DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-223@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Masaaki Nomata (Hiroshima University)\nEmpty homes\, called Akiya in Japanese\, due to an aging population and declining birth rate is very serious problem in the aging society of modern Japan. The cur rent proportion of empty home in Japan is 13.5%\, but it is expected to be increased up to 30.2% nationwide in 2033\, implying that Akiya will have a serious impact on the economy as well as the national finance. Indeed\, Detroit city in USA was financially collapsed by 29.3% empty homes caused by the decline of the automobile industry. Currently\, the Japanese govern ment has started a countermeasure for decreasing the empty homes\, but the effect is completely uncertain. Therefore\, we here develop a mathematica l model including an effective utilization of empty homes and consider the future transition of empty homes. Using the model\, we suggest optimal po licies by which we can reduce empty homes most effectively\, with regard t o government tax system and subsidy for the effective utilization of empty homes. This study shows a new framework of mathematical model to be appli ed for solving a social and economic problem in real world.\n\nhttps://con ferences.maths.unsw.edu.au/event/2/contributions/223/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/223/ END:VEVENT BEGIN:VEVENT SUMMARY:Optimising and understanding new HIV therapies DTSTART;VALUE=DATE-TIME:20180710T020000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-58@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Deborah Cromer (UNSW Sydney)\nOne of the main focuse s of HIV research today concerns allowing people living with HIV to experi ence prolonged periods where they do not need to remain on treatment. Curr ent therapies are able to suppress HIV to undetectable levels\, however as soon as therapy is interrupted the virus “rebounds” to pre-treatment levels and this leads to increased morbidity from HIV. This rebound likely occurs as a result of long-lived latently infected cells\, which persist in spite of therapy as part of a ‘latent reservoir’. Recent work has f ocused on reducing the size of the latent reservoir in the hope this will increase the time subjects can remain off therapy.\n\nWe set up a model of HIV remission and viral reactivation and used this to estimate both the p robability of viral rebound even with a reduced latent reservoir\, and als o the optimal reduction in reservoir size that both minimises drug exposur e\, and maximises treatment effect.\n\nUsing a stochastic model we show th at a treatment that achieves an average of a one-year viral remission will still lead to nearly a quarter of subjects experiencing viral rebound wit hin the first three months and give rise to an expected 39 (95%UI 22-69) h eterosexual transmissions and up to 262 (95%UI 107-534) homosexual transmi ssions per 1\,000 treated subjects over a 10-year period. \n\nAdditionally \, using a deterministic model we investigated the trade-off between incre asing the average duration of remission\, versus the risk of treatment fai lure (viral recrudescence) and the need for re-treatment. To minimise drug exposure\, we find that the optimal treatment would increase the average time of viral rebound to 30 years. Interestingly\, this is a significantly lower level of reduction than that required for complete elimination of t he viral reservoir\, but significantly longer than is currently being targ eted. We show that when shorter periods are targeted\, there is a real pro bability of viral transmission occurring in between the times at which sub jects would be tested for viral rebound.\n\nOur work shows that while ther apies designed to reduce the size of the latent reservoir present a promis ing avenue of research\, prior to widespread implementation of such strate gies\, the possibilities and consequences of viral reactivation from laten cy must be adequately considered.\n\nhttps://conferences.maths.unsw.edu.au /event/2/contributions/58/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/58/ END:VEVENT BEGIN:VEVENT SUMMARY:Global stability of some continuous and nonstandard discretization models for the Ebola virus disease with fast and slow transmissions DTSTART;VALUE=DATE-TIME:20180709T060000Z DTEND;VALUE=DATE-TIME:20180709T063000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-122@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jean Lubuma (University of Pretoria)\nMathematical m odels for the Ebola Virus Disease (EVD) were\, until recently\, mostly bas ed on the fast/direct transmission route\, which involves contact with blo od or body fluid and objects that have been contaminated by body fluid. Th e fact that in almost all outbreaks of the EVD in Africa\, the index case became infected through contact with infected animals\, such as fruit bats and primates\, makes the environment a no negligible channel for slow/ind irect transmission of the disease. \n\nIn this talk\, we incorporate both direct and indirect transmission routes in the setting of SIR-type models that are developed gradually. Firstly\, we add two compartments (for dead individuals and for the environment) in order to capture infection through the manipulation of deceased individuals before burial as well as contami nated environment. Secondly\, we enrich the first model with self-protecti on measures reflected by the addition of classes of vaccinated and trained individuals. \n\nFor the two models\, we prove that the disease-free equi librium is globally asymptotically stable (GAS) whenever the basic reprodu ction number is less than or equal to unity\, and unstable when this thres hold number is greater than 1. In the latter case\, the existence of at le ast one endemic equilibrium (EE) (for the second model) and of a unique EE (for the first model)\, which are locally asymptotically stable (LAS) is shown\, together with the fact that the unique EE is GAS in the absence of shedding and manipulation of deceased human individuals before burial. At the endemic level\, it is shown that the number of infectious individuals is much smaller than that obtained in the absence of any intervention. \n \nIn a final step\, we construct nonstandard finite difference schemes tha t are dynamically consistent with respect to the above features of the con tinuous models.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribut ions/122/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/122/ END:VEVENT BEGIN:VEVENT SUMMARY:Dengue dynamics in Southern Mexico: an approximation to its popula tion dynamics and the role of population movement DTSTART;VALUE=DATE-TIME:20180709T063000Z DTEND;VALUE=DATE-TIME:20180709T070000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-194@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jorge Velasco-Hernandez (UNAM)\nUsing a data base o n Dengue incidence available for four different states of the country we d evelop mathematical models that describe the recurrent dynamics of cases a t different geographical/regional levels. We present preliminary results.\ n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/194/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/194/ END:VEVENT BEGIN:VEVENT SUMMARY:Models for thrombopoiesis with bifurcation analysis DTSTART;VALUE=DATE-TIME:20180710T020000Z DTEND;VALUE=DATE-TIME:20180710T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-184@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Joseph Mahaffy (San Diego State University)\nThrombo poiesis is the process for producing platelets\, which uses a negative fee dback to maintain homeostasis in normal individuals. However\, pathologica l states exist where platelet concentrations in the body oscillate. An age -structured model for thrombopoiesis was developed and fitted to clinical data for subjects with normal and pathological platelet production. Variat ions on this model are described to obtain more details on how this system undergoes a Hopf bifurcation. Our study explores parameter sensitivity an d which model features are most significant in the bifurcation to periodic solutions. We observed that near the Hopf bifurcation there is a very rap id transition of the stationary solution along with the change in the real part of the leading pair of eigenvalues. The creation and analysis of the characteristic equations from these models provide some interesting new i deas. Certain model reductions decrease the complexity of the characterist ic equation and allow a better understanding of the source of the Hopf bif urcation. Our modelling efforts might improve insight into the primary pro blems underlying the diseased state\, where levels of platelets and thromb opoietin vary periodically.\n\nhttps://conferences.maths.unsw.edu.au/event /2/contributions/184/ LOCATION:University of Sydney New Law School/--102 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/184/ END:VEVENT BEGIN:VEVENT SUMMARY:A mechanism for metacommunity-scale biodiversity regulation DTSTART;VALUE=DATE-TIME:20180712T050000Z DTEND;VALUE=DATE-TIME:20180712T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-493@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Jacob Dinner O'Sullivan (Queen Mary University of Lo ndon)\nThere exists a growing body of empirical evidence that suggests bio diversity regulation – the emergence of dynamic equilibrium diversity – may be a common or even general feature of ecosystems. However a mech anistic understanding of what tends to constrain diversity in nature remai ns elusive. Here we introduce a metacommunity assembly model in which reg ional diversity converges on dynamic equilibria\, despite continuous speci es turnover (temporal β -diversity). We build on previous theoretical st udies of local biodiversity regulation by arguing that the mechanism contr olling these temporal diversity patterns is the loss of Ecological Structu ral Stability – a diversity dependent measure of the sensitivity of an e cological assemblage to perturbation. As the limit of structural stabilit y is approached\, macroecological patterns characteristic of natural assem blages emerge in model metacommunities. In particular\, the species abund ance distribution\, range size distribution\, species co-occurrence profil e\, and species area relation all match patterns observed robustly in the field. These results suggest that structural instability is an important macroecological organising principle.\n\nhttps://conferences.maths.unsw.ed u.au/event/2/contributions/493/ LOCATION:University of Sydney New Law School/--104 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/493/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling Human African Trypanosomiasis and the effects of domesti c animals on transmission DTSTART;VALUE=DATE-TIME:20180712T013000Z DTEND;VALUE=DATE-TIME:20180712T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-193@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Meghan Burke (Kennesaw State University)\nThe Human African Trypanosomiasis (HAT) parasite\, which causes African Sleeping Sic kness\, is transmitted by the tsetse fly as a vector. It has several poss ible hosts\, including wild and domestic animals\, who are not as negative ly impacted by the disease as the human host. It has long been assumed th at because domestic animals can be hosts for the parasite\, that keeping d omestic animals near human populations increases the spread of the disease . However\, several parameters found in the literature\, including the sh orter lifespan of the male vector\, and the female vector's preference for domestic animals\, made us question this assumption. \n\n We developed a differential equation compartmental model to examine whether increasing th e domestic animal population can be used to deflect the infection from hum ans and reduce its impact. We have used numerical simulations and have ex amined the Basic Reproduction Number ($R_0$) for the model to quantify the effect of the domestic animal population on human infection. These analy ses allow us to propose novel methods of controlling the impact of the dis ease on humans.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribut ions/193/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/193/ END:VEVENT BEGIN:VEVENT SUMMARY:Marriage decision-making models based on male’s willingness to c ooperate on housework and childcare DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-234@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Manon Morita (Nara Women's University)\nThe unmarrie d rate of Japanese people is rising year by year\, and countermeasures are required. We modelled male and female marriage decision-making models bas ed on male’s willingness to cooperate on housework and childcare. We ass ume that male marriage utility function decreases as male’s willingness to cooperate on housework and childcare increases\, while female marriage utility function increases. We also assume that a male decides to marry a female when his marriage utility function is nonnegative\, while a female does so when her partner’s willingness to cooperate is at least the valu e that she demands. When both male’s and female’s conditions are satis fied\, they get married. If they don’t get married\, the utility functio n is 0 for both males and females. Male’s strategy is the value of his w illingness to cooperate\, and female’s strategy is the value that she de mands. There are Nash equilibria with marriage and without marriage. At Na sh equilibria with marriage\, both male and female marriage utility functi ons are positive and male’s strategy is equal to female’s.When the uti lity function changes by individuals\, increase of marriage utility raises male’s marriage fraction slowly in the all range and female’s sharply in the range of large female marriage utility. We conclude that we should take countermeasures to all males and females with greater marriage utili ty to increase the rate of marriage.\n\nhttps://conferences.maths.unsw.edu .au/event/2/contributions/234/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/234/ END:VEVENT BEGIN:VEVENT SUMMARY:Comparing malaria surveillance with periodic spraying in the prese nce of insecticide-resistant mosquitoes: Should we spray regularly or base d on human infections? DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-9@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Robert Smith? (The University of Ottawa)\nThere is a n urgent need for more understanding of the effects of surveillance on mal aria control. Indoor residual spraying has had beneficial effects on globa l malaria reduction\, but resistance to the insecticide poses a threat to eradication. We develop a model of impulsive differential equations to acc ount for a resistant strain of mosquitoes that is entirely immune to the i nsecticide. The impulse is triggered either due to periodic spraying or wh en a critical number of malaria cases are detected. For small mutation rat es\, the mosquito-only submodel exhibits either a single mutant-only equil ibrium\, a mutant-only equilibrium and a single coexistence equilibrium\, or a mutant-only equilibrium and a pair of coexistence equilibria. Bistabi lity is a likely outcome\, while the effect of impulses is to introduce a saddle-node bifurcation\, resulting in persistence of malaria in the form of impulsive periodic orbits. If certain parameters are small\, triggering the insecticide based on number of malaria cases is asymptotically equiva lent to spraying periodically.\n\nhttps://conferences.maths.unsw.edu.au/ev ent/2/contributions/9/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/9/ END:VEVENT BEGIN:VEVENT SUMMARY:Investigating the mechanisms of influenza viral interference using within-host models based on a ferret re-exposure experiment DTSTART;VALUE=DATE-TIME:20180710T003000Z DTEND;VALUE=DATE-TIME:20180710T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-60@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Pengxing Cao (School of Mathematics and Statistics\, University of Melbourne)\nViral interference\, whereby infection with one type of virus may temporarily “protect” the host from subsequent infe ction with another virus has been described for a number of influenza stra ins and in a number of different host species. In particular\, experiments performed in ferrets with influenza A(H1N1)pdm09\, A(H3N2) and B have dem onstrated strong levels of interference dependent upon the particular viru s pair\, order of infection and precise timing of re-exposure. Mathematica l modelling\, which aims to capture the viral time course of the re-exposu re behaviour based on plausible immunological mechanisms\, is a particular ly useful tool to study viral interference\, opening up a new approach to advancing our understanding of viral dynamics and the host immune response .\n\nIn this talk\, I will first briefly describe the ferret re-exposure e xperiments performed by our collaborators. In the experiments\, naïve fer rets were inoculated with one virus (i.e. primary infection) and subsequen tly exposed to another (to induce the secondary infection) after a certain time interval (1 – 14 days). Viral interference was observed when the i nter-exposure interval was less than a week. Furthermore\, viruses differe d in their ability to induce a protective immune response against subseque nt exposure. \n\nI will then introduce the model-based approaches that we have used to investigate immune-mediated viral interference. We begin with a qualitative approach by introducing and analysing a family of within-ho st models of re-exposure viral kinetics which differ in their hypothesised mechanisms of action for the non-specific innate immune response. We assu med that different viruses stimulate the innate immune response to differe nt degrees and demonstrate the models’ ability to qualitatively reproduc e the observed viral shedding profile in the secondary infection for short inter-exposure intervals (less than 5 days). We then extend the models by incorporating cross-reactive adaptive immunity (in particular CD8+ T cell s)\, which provides an explanation of the viral shedding profile of the se condary infection for longer inter-exposure intervals (5-14 days).\n\nFina lly\, I will briefly describe our most recent efforts to calibrate the pro posed models to the re-exposure data in a Bayesian framework\, providing q uantitative insight. Through this approach\, we have shown that models fit ted to the re-exposure data are able to predict the outcome of viral inter ference more accurately than models fitted only to the data from a single infection.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 60/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/60/ END:VEVENT BEGIN:VEVENT SUMMARY:Understanding age-specific differences in immune cell dynamics DTSTART;VALUE=DATE-TIME:20180709T010000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-150@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Arnold Reynaldi (UNSW Sydney)\nAge plays an importan t role on immunity across the lifespan\, as both very young and very old i ndividuals are at higher risk of severe infection. CD8 T cells are importa nt for controlling a number of viral and bacterial infections\, and both t he number and phenotype of CD8 T cells change with age. Various mathematic al and experimental methods have been used to analyse T cell kinetics\, an d most of them assume a homogeneous population of cells. This assumption h as been challenged experimentally and theoretically\, that cells produced early in life may have different behaviour to those produced recently. We have recently developed a novel experimental model to ‘timestamp’ CD8 T cells in mice. More specifically\, double positive CD8 T cells can be la beled in the thymus (using CD4 promoter tamoxifen-inducible cre to drive t he expression of RFP permanently)\, thus the survival of these cells can b e tracked over time. \n\nCells produced early in life show a faster decay\ , which then slows with time-since-production of the cell. Cells produced at later ages show a more stable behaviour\, and their rate of decay also slows with time-since production of the cell. Comparing various mathematic al models (based on the AIC values)\, we found that the population of T ce ll can be described by a model with three parameters. The model has an ini tial decay rate of cells made at birth\, how the decay rate changes with t he age of the host\, and how the decay changes with the age of cell (since cell production). \n\nUsing the best-fit parameters from the model\, we c an develop another model about the ‘layering’ of cells made at differe nt ages\, and how this contributes to the total T cell pool. Based on our model\, in a 300-day-old mouse\, only 20% of the cells were made recently. We also modelled the process of cellular differentiation\, and how this c hanges with age. The model can be described by a system of differential eq uations with non-constant parameters. We found that cells made early in li fe show a higher rate of differentiation.\n\nOverall\, this reveals an age -dependent heterogeneity in *in vivo* survival of CD8 T cells.\n\nhttps:// conferences.maths.unsw.edu.au/event/2/contributions/150/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/150/ END:VEVENT BEGIN:VEVENT SUMMARY:Predicting mechanism of action and quantifying anti-viral effects of cytokines against hepatitis B virus DTSTART;VALUE=DATE-TIME:20180710T010000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-100@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Yusuke Kakizoe (Systems Life Sciences\, Graduate sch ool of Kyushu University)\nHepatitis B Virus (HBV) is widespread infectiou s disease and more than 240 million people are chronic infected so far. Al though some patients can suppress the viral load under detection limits by current drug treatments\, these are not effective for over 60% of patient s. The obstacles for developing effective drugs are the existence of a res ervoir in infected cells\, which is known as covalently closed circular DN A (cccDNA). Because cccDNA remains in infected cells for a long time\, the replication of HBV is not completely inhibited. We need new effective dru g that can decrease the concentration of cccDNA persistently. In this stud y\, we carried out cell culture experiments that can be measured the time course of the concentration of cccDNA\, intracellular HBV DNA and extracel lular DNA. Then\, we added several kinds of cytokines in this experiment\, and measured the same time course data. Furthermore\, to investigate mech anism of action and quantify the anti-viral effect of each cytokine\, we e stablished a mathematical model that can capture the dynamics of intracell ular HBV replication and fitted this model to the our time course data. Fi nally\, we investigated which cytokines can decrease the concentration of cccDNA. This framework that combining viral experiment and mathematical mo del would be helpful to find a chemical that have desired mechanism of act ion.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/100/ LOCATION:University of Sydney New Law School/--106 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/100/ END:VEVENT BEGIN:VEVENT SUMMARY:Signatures of within-host dynamics of dengue at a population level DTSTART;VALUE=DATE-TIME:20180709T003000Z DTEND;VALUE=DATE-TIME:20180709T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-67@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Lauren Childs (Virginia Tech)\nVector-borne diseases cause worldwide concern with hundreds of millions of new cases and over a million deaths reported annually. Mathematical models are a key tool in t he study of the spread of diseases such as malaria and dengue. In particul ar\, transmission models have been successful at determining the most prom ising intervention strategies\, despite the fact that many of these models assume all individuals experience identical infections. Within-host dynam ics of infections\, however\, vary widely among individuals. In the case o f dengue\, within-host dynamics differ between primary and secondary infec tions\, where secondary infections with a different virus serotype typical ly last longer\, produce higher viral loads\, and induce more severe disea se. Here\, we build upon models of variable within-host dengue virus dynam ics resulting in mild dengue fever and severe dengue hemorrhagic fever by coupling them to a population-level model. The resulting multiscale model examines the dynamics of between-host infections in the presence of two ci rculating virus strains that involves feedback from the within-host and be tween-hosts scales. We analytically determine a threshold under which infe ctions persist in the population.\n\nhttps://conferences.maths.unsw.edu.au /event/2/contributions/67/ LOCATION:University of Sydney New Law School/--101 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/67/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling of immune dynamics in disease and treatment DTSTART;VALUE=DATE-TIME:20180711T003000Z DTEND;VALUE=DATE-TIME:20180711T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-51@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Lisette dePillis (Harvey Mudd College)\nImmune syste m dynamics in the context of a number of diseases\, including certain canc ers and type I diabetes\, continues to play an increasingly central role i n the development of new treatment strategies. The critical importance of the immune system in fighting such diseases has been verified clinically\ , as well as through mathematical models.\n\nMany open questions remain\, however\, including what may lead to non-uniform patient responses to trea tments\, and how to optimize and personalize therapy protocols. Mathemati cal models can help to provide insights into the mechanisms that may be in fluencing patient outcomes\, and provide a way to investigate questions th at that are difficult\, if not impossible\, to address in any other way. In this talk\, we will present a sampling of mathematical models we have d eveloped that help us to simulate immune system interactions\, disease dyn amics\, and treatment approaches that may slow\, or even stop\, disease pr ogression.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/ 51/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/51/ END:VEVENT BEGIN:VEVENT SUMMARY:Target product profiles for second-generation childhood malaria va ccines DTSTART;VALUE=DATE-TIME:20180709T013000Z DTEND;VALUE=DATE-TIME:20180709T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-56@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Alexandra Hogan (Imperial College London)\nClinical trials of the four-dose RTS\,S/AS01 vaccine for *P. falciparum* malaria de monstrated a protective effect in young children and\, beginning in 2018\, the vaccine will be evaluated through a large-scale pilot implementation program in Ghana\, Kenya and Malawi. Recent evidence from a phase 2a chall enge study indicates that varying the timing and amount of the fourth dose could further improve the public health impact.\n\nWe used a dynamic mode lling approach to inform target product profiles (TPPs) for a second-gener ation malaria vaccine\, focussing on the vaccine properties of initial eff icacy\, duration of protection\, dosing schedules and coverage. We simulat ed the changing anti-circumsporozoite antibody titre following vaccination \, related titre to vaccine efficacy\, and then implemented this efficacy profile within an individual-based model of malaria transmission. We devel oped a range of efficacy profiles for different vaccine schedules and used these to evaluate the relative impact of initial efficacy\, duration\, an d fourth dose characteristics. We ran the simulations across a range of ep idemiological strata\, measuring clinical cases averted children younger t han five years.\n\nWe found that in the first decade of delivery\, a vacci ne with high initial efficacy vaccine resulted in more clinical cases aver ted\, compared to a longer duration vaccine\, and that the effect was more pronounced in high malaria prevalence settings. However\, the low initial efficacy and long duration schedule averted more cases across all age coh orts if a longer time horizon was considered. We also observed that a high er antibody titre resulting from the fourth dose was always advantageous\, and that a longer delay between doses three and four averted more cases i n older age classes. \n\nOur results indicate that an imperfect malaria va ccine\, initial efficacy may be more important than vaccine duration. An o ptimised malaria vaccine may outperform the current RTS\,S\, but timing of the fourth dose determines the age group that benefits most. This TPP ana lysis could provide insight for vaccine developers and policy-makers into how distinct characteristics of a malaria vaccine may translate to public health outcomes.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contribu tions/56/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/56/ END:VEVENT BEGIN:VEVENT SUMMARY:Climate change and the equine infectious anemia virus epidemic DTSTART;VALUE=DATE-TIME:20180709T053000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-168@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Morenikeji Deborah Akinlotan (Queensland University of Technology)\nEquine Infectious Anemia Virus (EIAV)\, a retrovirus that establishes a persistent lifelong infection in horses and ponies\, and whi ch can be transmitted by vectors (biting flies)\, is endemic in regions wi th warm climates. With the advent of global warming\, research have shown that vector-borne diseases may be on the rise. This study seeks to unders tand how climate change will affect the EIAV epidemic\, especially in ende mic regions. We developed two vector-host mathematical epidemic models of EIAV infection that describe the direct transmission of EIAV between wild and domestic horses\, and also through vectors: a basic model and a patch model. The models are rigorously analysed mathematically. The effects of v ariability in the model parameters are also investigated. Results of disea se thresholds give conditions necessary for the control of the infection. We hypothesise that climate change to warmer temperatures may increases th e time that the virus can thrive in the vector. Model results\, which are underway\, could be significant for the control of any or all fly-borne pa thogens.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/16 8/ LOCATION:University of Sydney New Law School/--105 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/168/ END:VEVENT BEGIN:VEVENT SUMMARY:A systems immunology approach to study immune responses against vi ral infection DTSTART;VALUE=DATE-TIME:20180709T053000Z DTEND;VALUE=DATE-TIME:20180709T060000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-132@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Preston Leung (Kirby Institute\, UNSW)\nCD8+ T (CTL) cells play a pivotal role in protection from viral infection. Better unde rstanding of the heterogeneous phenotypes of T cell subsets evolving durin g an immune response is timely needed for development of T cell based vacc ines that can provide long-term immune protection. Viruses causing chronic infections such as HIV and HCV\, trigger a T cell response characterised by functional exhaustion\, and accumulation of immune escape variants. We have developed a single cell approach to identify and link functional phen otype\, gene expression profile\, TCR diversity and T cell avidity with th e onset of exhaustion and its relationship with immune escape. \n\nWe anal ysed a cohort of prospectively followed subjects from acute primary HCV in fections to disease outcome (clearance and chronicity). Antigen specific ( Ag-) CTL were identified via epitope discovery and functional validation v ia IFNγ-ELISPOT. Index sorting was utilised to link surface phenotyping w ith gene expression profile. Full length TCRαβ repertoire was identified from scRNAseq data using novel tools. Exhaustion was detected early on in the acute phase of infection and in CTL targeting conserved but also immu ne escape epitopes. Single cell RNAseq showed a distinct gene expression p rofile of exhausted T cells compared to the less differentiated subsets. I n contrast\, Ag-CTL in subjects that cleared HCV\, polyfunctional (IFNγ\, granzyme\, and perforin) responses were found\, with a highly diverse TCR repertoire. We discovered a novel T cell clone\, characterised by high av idity for viral epitope\, elevated IFNγ productions and polyfunctional ph enotype. \n\nThis systems immunology approach provides new routes to inves tigate complex T cell dynamics and to identify new mechanisms to exploit i n vaccine and immunotherapy.\n\nhttps://conferences.maths.unsw.edu.au/even t/2/contributions/132/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/132/ END:VEVENT BEGIN:VEVENT SUMMARY:Evidence for independent fate competition within B lymphocytes: CD 40 signal strength regulates the rate of B cell differentiation to plasmab lasts by altering their time to divide only DTSTART;VALUE=DATE-TIME:20180709T050000Z DTEND;VALUE=DATE-TIME:20180709T053000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-172@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Philip Hodgkin (Walter and Eliza Hall Institute)\nDu ring the adaptive immune response\, T and B lymphocytes receive and integr ate signals from different sources that determine the strength and type of response they follow. Here we asked how reducing stimulation strength thr ough the CD40 receptor could lead to an accelerated division-linked B cell differentiation\, as noted in an earlier study [Hawkins *et al.*\, Nat Co mms 2014]. We observed using flow cytometry that reducing CD40 stimulation strength had two effects on B cell fates in vitro: it slowed down B cell division\, and produced a greater proportion of differentiated plasmablast s in each subsequent generation. We studied this system with direct time-l apse imaging to observe division\, death\, and differentiation to Blimp-1+ plasmablasts\, after 3-4 days in culture. We found that strength of stimu lation by CD40 affected division times\, as predicted\, whereas times to d ie and times to differentiate to plasmablasts were unaffected. We could a lso show\, by fitting mathematical models\, that simple fate competition b etween division and differentiation could explain the accelerated differen tiation by slowing division alone. Thus\, our data suggest that weakly CD4 0 stimulated B cells divide slowly\, and as a consequence\, have more time to undergo differentiation before their next mitotic event. By understand ing how different components of the B cell response are controlled and aff ected by regulatory signals\, we aim to build up models of complex signal integration by cells that can predict net immune outcome. Successful model s built in this way have many potential applications such as rational immu notherapy design.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contrib utions/172/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/172/ END:VEVENT BEGIN:VEVENT SUMMARY:Modelling the mammalian circadian clock: from molecular mechanism to sleep-wake cycle disorders and jet lag DTSTART;VALUE=DATE-TIME:20180712T003000Z DTEND;VALUE=DATE-TIME:20180712T010000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-106@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Albert Goldbeter (Université LIbre de Bruxelles (UL B))\nCircadian rhythms originate at the cellular level from feedback proce sses in genetic regulatory networks. Based on experimental observations\, computational models of have been proposed for the molecular mechanism of circadian rhythms\, which occur spontaneously with a period of the order o f 24 h in all eukaryotic organisms\, as well as in cyanobacteria. Mathemat ical models were initially proposed for circadian rhythms in *Drosophila* and *Neurospora*\, and were later extended to the mammalian circadian cloc k [1]. The mammalian clock model\, based on the intertwined positive and n egative regulatory loops involving the *Per*\, *Cry*\, *Bmal1*\, *Clock* a nd *Rev-Erb* genes\, can give rise to sustained circadian oscillations of the limit cycle type. These oscillations correspond to circadian rhythms s pontaneously generated by suprachiasmatic nuclei and some peripheral tissu es. The results pertain not only to the molecular bases of circadian rhyth ms but also to physiological disorders of the sleep-wake cycle linked to p erturbations of the human circadian clock [2]. Among such disorders are th e familial advanced or delayed sleep phase syndromes\, and the non-24 h sl eep-wake syndrome associated with a loss of entrainment of the circadian c lock by the periodic environment. Jet lag that follows delays or advances of the circadian clock can also be studied by means of a computational app roach. The latter reveals the existence of critical conditions which might considerably slow down circadian clock recovery after jet lag [3].\n\n[1] Leloup\, J.-C. & Goldbeter\, A.\, 2003. *Proc. Natl. Acad. Sci. USA* 100\ , 7051-56\n[2] Leloup\, J.-C. & Goldbeter\, A.\, 2008. *BioEssays* 30\, 59 0-600\n[3] Leloup\, J.-C. & Goldbeter\, A. 2013. *J. Theor. Biol.* 333\, 4 7-57\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/106/ LOCATION:University of Sydney New Law School/--026 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/106/ END:VEVENT BEGIN:VEVENT SUMMARY:Host control of malaria infection is rarely mediated by host clear ance DTSTART;VALUE=DATE-TIME:20180711T020000Z DTEND;VALUE=DATE-TIME:20180711T023000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-54@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: David Khoury (UNSW Sydney)\nInfections with the mala ria parasite can lead to severe illness and mortality\, with nearly half a million deaths attributed to malaria globally each year. Adults from mala ria endemic regions often have immunity to malaria and are much less susce ptible to disease\, compared with children. Understanding how a host can c ontrol malaria infections is critical in guiding the development of a much need efficacious vaccine. Infected individuals are thought to clear infec ted red blood cells (RBCs) from circulation via organs such as the spleen - and this clearance is thought to play a major role in controlling malari a infections. However\, no work has directly quantified clearance of infec ted RBCs or studied the extent to which parasite clearance is improved in\ , for example\, immune hosts. \n\nIn this study\, we developed a unique ex perimental approach to directly track the loss of a single cohort of infec ted RBCs in mice. We used this system to study the loss of infected RBCs i n naïve\, immune deficient\, acutely infected\, drug treated and immune m ice. Modelling data from these experiments enabled us determine the baseli ne clearance half-life of infected RBCs in naïve mice (14.4 h)\, which su ggests that about one third of infected cells are cleared every parasite r eplication cycle. Further\, we found that this half-life was approximately doubled when phagocytes (a certain host immune cell) were depleted (33.8 h)\, suggesting host immune cells are important in removing infected cells . Surprisingly\, with the exception of treatment with a high dose of a par ticular antimalarial (sodium artesunate)\, we did not observe an increase in the rate of clearance of infected RBCs in acutely infected mice\, immun e mice\, or after drug treated\, despite observing effective control of in fection in all scenarios. Instead\, of elevated host removal of infected\, we observed an array of other factors that caused the control of infectio n\, and in particular\, this work revealed a novel mechanism of host contr ol in acute infection\, that is\, slowing the development of parasites.\n\ nThis work has revealed that the basal rate of removal of infected RBCs in murine malaria infection is very high\, but this rate cannot easily be im proved by host responses or drug treatment.\n\nhttps://conferences.maths.u nsw.edu.au/event/2/contributions/54/ LOCATION:University of Sydney New Law School/--024 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/54/ END:VEVENT BEGIN:VEVENT SUMMARY:Multiscale methods for modelling intracellular processes DTSTART;VALUE=DATE-TIME:20180709T010000Z DTEND;VALUE=DATE-TIME:20180709T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-20@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Radek Erban (University of Oxford)\nI will discuss m athematical and computational methods for spatio-temporal modelling in mol ecular and cell biology\, including all-atom and coarse-grained molecular dynamics (MD)\, Brownian dynamics (BD)\, stochastic reaction-diffusion mod els and macroscopic mean-field equations. \n\nMicroscopic (BD\, MD) models are based on the simulation of trajectories of individual molecules and t heir localized interactions (for example\, reactions). Mesoscopic (lattice -based) stochastic reaction-diffusion approaches divide the computational domain into a finite number of compartments and simulate the time evolutio n of the numbers of molecules in each compartment\, while macroscopic mode ls are often written in terms of mean-field reaction-diffusion partial dif ferential equations for spatially varying concentrations. \n\nI will discu ss the development\, analysis and applications of multiscale methods for s patio-temporal modelling of intracellular processes\, which use (detailed) BD or MD simulations in localized regions of particular interest (in whic h accuracy and microscopic details are important) and a (less-detailed) co arser model in other regions in which accuracy may be traded for simulatio n efficiency [1\,2\,3]. I will discuss error analysis and convergence prop erties of the developed multiscale methods\, their software implementation [4] and applications of these multiscale methodologies to modelling of in tracellular calcium dynamics [5]\, actin dynamics [6\,7] and DNA dynamics [8]. I will also discuss the development of multiscale methods which coupl e MD and coarser stochastic models in the same dynamic simulation [3\,9].\ n \n[1] M. Flegg\, S.J. Chapman and R. Erban (2012). Two Regime Method for optimizing stochastic reaction-diffusion simulations. *Journal of the Roy al Society Interface* **9**: 859-868.\n[2] B. Franz\, M. Flegg\, S.J. Chap man and R. Erban (2013). Multiscale reaction-diffusion algorithms: PDE-ass isted Brownian dynamics. *SIAM Journal on Applied Mathematics* **73**: 122 4-1247.\n[3] R. Erban (2014). From molecular dynamics to Brownian dynamics . *Proceedings of the Royal Society A* **470**: 20140036.\n[4] M. Robinson \, S. Andrews and R. Erban (2015). Multiscale reaction-diffusion simulatio ns with Smoldyn. *Bioinformatics* **31**: 2406-2408. \n[5] U. Dobramysl\, S. Rudiger and R. Erban (2016). Particle-based multiscale modeling of calc ium puff dynamics. *Multiscale Modelling and Simulation* **14**: 997-1016. \n[6] R. Erban\, M. Flegg and G. Papoian (2014). Multiscale stochastic r eaction-diffusion modelling: application to actin dynamics in filopodia. * Bulletin of Mathematical Biology* **76**: 799-818.\n[7] U. Dobramysl\, G. Papoian and R. Erban (2016). Steric effects induce geometric remodeling of actin bundles in filopodia. *Biophysical Journal* **110**: 2066-2075. \n[ 8] E. Rolls\, Y. Togashi and R. Erban (2017). Varying the resolution of th e Rouse model on temporal and spatial scales: application to multiscale mo delling of DNA dynamics. *Multiscale Modelling and Simulation* **15**(4): 1672-1693.\n[9] R. Erban (2016). Coupling all-atom molecular dynamics simu lations of ions in water with Brownian dynamics. *Proceedings of the Royal Society A* **472**: 20150556.\n\nhttps://conferences.maths.unsw.edu.au/ev ent/2/contributions/20/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/20/ END:VEVENT BEGIN:VEVENT SUMMARY:The spatial dynamics of selfish genetic elements in ${\\textit Ae des~aegypti}$ arbovirus vector populations DTSTART;VALUE=DATE-TIME:20180710T013000Z DTEND;VALUE=DATE-TIME:20180710T020000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-99@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Penelope Hancock (Oxford University)\nNovel strategi es for controlling mosquito vectors of human diseases involve introduction s of selfish genetic elements (SGEs)\, or elements that spread through the mosquito population by means of non-Mendelian inheritance. The releases of the endosymbiotic bacteria *Wolbachia* into *Aedes aegypti* populations in order to reduce their capacity for arbovirus transmission are the firs t application of an SGE introduction strategy in a field setting. Gene dr ive technologies for creating SGEs that reduce vectorial capacity are also being developed. SGEs are vertically transmitted between mosquito hosts\ , and their spread dynamics have complex interactions with natural mosquit o population dynamics\, population structure and fitness components. We d evelop a model of an *Ae. aegypti* metapopulation that incorporates empiri cal relationships linking variation in mosquito abundance to density-depen dent fitness components. We first show that our model can produce pattern s of demographic variation similar to those found in natural populations\, and predict rates of spatial spread of *Wolbachia* matching those observe d following field releases. We then explore different SGE release strateg ies over an operationally relevant spatial scale\, and compare the spread dynamics of *Wolbachia* and gene drive. We find that the spatial release distribution strongly affects the rate of spread of both SGEs\, with widel y dispersed release distributions out-performing spatially aggregated dist ributions\, especially when the SGE incurs fitness costs. Our results dem onstrate how spatial and demographic structure in the mosquito host popula tion impacts SGE spread\, with implications for the design of effective re lease strategies.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contrib utions/99/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/99/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical modelling of CRISPR gene drives for exotic vertebrate pest eradication DTSTART;VALUE=DATE-TIME:20180710T010000Z DTEND;VALUE=DATE-TIME:20180710T013000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-130@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Joshua Ross (The University of Adelaide)\nSynthetica lly-constructed gene drives\, that use CRISPR-Cas9 technology to bias inhe ritance of a particular gene\, have been proposed for exotic pest eradicat ion. This is a controversial idea\, as there is an apparent potential risk in the use of such technologies\, for example to non-target populations o f the species. Further\, the basic question — Is the technology actually able to achieve its goal in practice? — is vexed. I will discuss some o f our work which has developed stochastic\, individual-based models of a n umber of gene drive strategies that have been proposed for the possible er adication of exotic vertebrate pests. I will discuss some of the issues su rrounding their likely effectiveness for eradication\, explore the potenti al risks to non-target populations\, along with considering options for al leviating these issues.\n\nhttps://conferences.maths.unsw.edu.au/event/2/c ontributions/130/ LOCATION:University of Sydney New Law School/--100 URL:https://conferences.maths.unsw.edu.au/event/2/contributions/130/ END:VEVENT BEGIN:VEVENT SUMMARY:Estimation of model parameters used to predict treatment response in breast cancer from dynamic contrast-enhanced MRI data using novel mathe matical software DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-285@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: David Ekrut (University of Texas at Austin)\nSpecifi c biomarkers can be identified in dynamic contrast-enhanced magnetic reson ance imaging (DCE-MRI) breast scans and quantified using pharmacokinetic m odels that return estimates of parameters related to tissue physiology inc luding vessel perfusion and permeability ($K^{trans}$)\, the extravascular -extracellular volume fraction ($v_e$)\, the plasma volume fraction ($v_p$ )\, and the efflux constant ($k_{ep}$). In particular\, $K^{trans}$ and $k _{ep}$ have been shown to be effective at predicting the response of cance r patients to treatment. Two fundamental issues in the field of DCE-MRI is the lack of standardization of the analysis and characterizing the time r ate of change of the concentration of contrast agent in the vascular (the so-called “arterial input function” or AIF). We have recently develope d a method for estimating accurate AIFs for the individual patients and as sociated software to automate the estimation of model parameters from DCE- MRI data taken from breast cancer patients using data that can be acquired routinely in community-based imaging centres.\n\nhttps://conferences.math s.unsw.edu.au/event/2/contributions/285/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/285/ END:VEVENT BEGIN:VEVENT SUMMARY:Effects of different discretisations of the Laplacian in stochasti c simulations DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-457@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Bartosz Bartmanski (University of Oxford)\nA determi nistic model of biochemical reaction networks is not always appropriate. G ene expression\, for example\, often involves a small number of molecules which means that noise can significantly influence the dynamics. By discre tising space into voxels and letting the molecule dynamics be governed by the reaction-diffusion master equation\, it is possible to model the react ion and diffusion of individual molecules on an arbitrary domain. Followin g on from the work of Meinecke and Lötstedt we apply a variety of numeric al methods to the Laplacian operator in order to derive the jump rates tha t simulate the diffusion of molecules. We discuss how pattern formation wi thin a Turing model might be influenced by the geometry of the spatial dis cretisation and the numerical method.\n\nhttps://conferences.maths.unsw.ed u.au/event/2/contributions/457/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/457/ END:VEVENT BEGIN:VEVENT SUMMARY:Polarity-dependent folding of epithelial cell sheets in three dime nsions DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-458@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Fu-Lai Wen (RIKEN)\nThe apical-basal cell polarity e ndows epithelial tissues with distinct biochemical and mechanical properti es at the apical\, basal\, and lateral sides of tissues. Mounting evidence shows that remodelling of epithelial cell polarity\, where polarity regul ators redistribute their locations on the cell membrane\, causes changes o f cell shapes that drives tissue morphogenesis during embryonic developmen t. However\, the principles underlying epithelial tissue morphology format ion regulated by remodelling of intracellular polarity remain elusive. Usi ng mathematical modelling and computer simulations\, we first show how epi thelial cell polarity is established\, maintained\, and remodelled by the interactions among the polarity regulators in the model system of fruit fl y (*Drosophila melanogaster*). Then\, based on a geometrical modelling for epithelial tissue deformation in three dimensions\, we further demonstrat e how tissue morphology is determined by its constituent cell mechanics. F inally\, taking into account the polarity-dependent cell mechanics\, we sh ow that the feedback between cellular mechanics and polarity can lead to a self-organizing tissue morphogenesis in the absence of sustained external stimuli.\n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/4 58/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/458/ END:VEVENT BEGIN:VEVENT SUMMARY:Simulation study to obtain biological circadian clocks that have a feature of predicting future DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-271@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Motohide Seki (Faculty of Design\, Kyushu University )\nMany species of animals\, plants\, cyanobacteria\, and fungi are report ed to have circadian clocks\, that is\, gene regulatory and biochemical ne twork in a cell exhibiting endogenous oscillatory dynamics with a period c lose to 24 hours. There is diversity in the members of the circadian syst em\, but all clocks share similar features such as temperature-compensated circadian period. Therefore\, theoretical studies on a general (and abst ract) network are as important as studies focusing on a specific network f ound in each species. Previous simulation studies using evolutionary algo rithm have established a method to obtain networks that follow an autonomo usly oscillating dynamics. In those simulations the degree of deviation f rom the demanded period was defined as the cost function to be minimized b y the optimization process because natural selection apparently favours a clock with a certain period\, namely\, 24 hours. However\, if the ultimat e goal is to implement the 24-hour period\, it may be easier and more reli able to refer to external cues such as sunlight. Indeed\, the circadian c locks are reported to have sensitivity to the light signal\, and their pha ses are adjusted by sunlight. In addition\, empirical studies have sugges ted that the circadian clocks play more sophisticated roles such as predic ting timing of the next dawn (respectively\, the next dusk) and preparing molecules required during the day (resp. during night) in advance. In the present study\, we first examine the effect of sunlight as an external os cillator represented by a binary function (1 = light\; 0 = dark). We compa re the proportions of regulatory networks that exhibit and do not exhibit an oscillation autonomously (i.e.\, without the external force) among thos e oscillating with the same period as the external force. We also found t hat even the non-autonomous oscillators have an adaptive feature of the da y-length compensation\, showing 24-hour oscillation regardless of the prop ortion of the light period. Next\, we introduce a novel cost function tha t reflects the merit of predicting future\, and report shared features of networks optimized based on this cost function.\n\nhttps://conferences.mat hs.unsw.edu.au/event/2/contributions/271/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/271/ END:VEVENT BEGIN:VEVENT SUMMARY:Effects of the physiological parameter evolution on the dynamics o f tonic-clonic seizure DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-407@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Farah Deeba (Ph. D. Candidate)\nThe temporal and spe ctral characteristics of tonic-clonic seizures are investigated by using a neural field model of the corticothalamic system in the presence of a tem porally varying connection strength between the cerebral cortex and thalam us. Increasing connection strength drives the system into 10 Hz seizure os cillations once a threshold is passed and a subcritical Hopf bifurcation o ccurs. \n\nIn this study\, the spectral and temporal characteristics of to nic-clonic seizures are explored as functions of the relevant properties o f physiological connection strengths\, such as maximum connection strength \, time above threshold\, and the rate at which the connection strength in creases or decreases (ramp rate). Dynamical analysis shows that the seizur e onset time decreases with the maximum connection strength and time above threshold\, but increases with the ramp rate. Seizure offset time and dur ation increase with maximum connection strength\, time above threshold\, a nd rate of change. Spectral analysis reveals that the power of nonlinear h armonics and the duration of the oscillations increase as the maximum conn ection strength and the time above threshold increase. A secondary limit c ycle\, termed a saddle cycle in previous studies\, is also seen in this st udy. A detailed analysis of the saddle cycle oscillations shows that these oscillations become more prominent and robust with maximum connection str ength and rate of change of the ramp. However\, for a small ramp rate\, th e system does not exhibit any saddle cycle oscillations. We also find that if the time above the threshold is too small and the ramp rate is too lar ge\, the system does not reach to the larger limit cycle attractor of 10 H z oscillation\, and only exhibits the saddle cycle oscillations. It is als o seen that the times to reach the saturated large amplitude limit-cycle s eizure oscillation from both the instability threshold and from the end of the saddle cycle oscillations are inversely proportional to the square ro ot of the ramp rate\, as is the time to reach the seizure offset from the bifurcation from the saturated limit cycle oscillations.\n\nhttps://confer ences.maths.unsw.edu.au/event/2/contributions/407/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/407/ END:VEVENT BEGIN:VEVENT SUMMARY:Mathematical model for the effects of Aβ on calcium signalling DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-413@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Joe Latulippe (Norwich University)\nAlzheimer’s di sease (AD) is a devastating illness affecting over 40 million people globa lly. The accumulation of AD associated Amyloid beta (Aβ) oligomers can tr igger aberrant intracellular calcium signals by disrupting calcium regulat ory mechanism within neurons. These disruptions can cause changes in homeo stasis levels that can have detrimental effects on cell function and survi val. Although studies have shown that Aβ can interfere with various calci um fluxes\, the complexity of these interactions remains elusive. In order to better understand the impact of Aβ on calcium dynamics\, we use a mat hematical model to simulate calcium patterns under the influence of Aβ. M ore specifically\, we assume that Aβ affects individual flux contribution s through inositol triphosphate receptors\, ryanodine receptors\, and the plasma membrane. We show that the inclusion of Aβ can increase regions of mixed-mode oscillations leading to aberrant signals under various conditi ons. We use single and double parameter bifurcation structures to predict model solutions for various levels of Aβ. We further demonstrate that con trolling certain biophysically relevant parameters can help control aberra nt signalling. These results can be used to suggest possible targets for e stablishing therapeutic strategies in AD pathology.\n\nhttps://conferences .maths.unsw.edu.au/event/2/contributions/413/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/413/ END:VEVENT BEGIN:VEVENT SUMMARY:Predicting ecosystem responses to species eradications and reintro ductions: an uncertain future? DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-471@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Matthew Adams (The University of Queensland)\nSpecie s eradications and reintroductions are drastic management actions that alt er ecosystem structure with the end goal of conserving or restoring one or more species of interest. Because of the complexity of ecosystem food web s\, these actions can have unintended consequences on other parts of the e cosystem. Even with the best available data\, predicting future trajectori es of the ecosystem with high precision is not always possible. In this ta lk\, I demonstrate the situations where ordinary differential equation (OD E) models of the ecosystem food web\, calibrated to species abundance data \, can or cannot be used to accurately predict future responses of the eco system to species eradications and/or reintroductions.\n\nhttps://conferen ces.maths.unsw.edu.au/event/2/contributions/471/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/471/ END:VEVENT BEGIN:VEVENT SUMMARY:Sex differences in hepatic one-carbon metabolism DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-451@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Farrah Sadre-Marandi (Mathematical Biosciences Insti tute)\nThere are large differences between men and women of child-bearing age in the expression level of 5 key enzymes in one-carbon metabolism almo st certainly caused by the sex hormones. These male-female differences in one-carbon metabolism are greatly accentuated in during pregnancy. Thus\, understanding the origin and consequences of sex differences in one-carbon metabolism is important for precision medicine.\n\nWe have created a math ematical model of hepatic one-carbon metabolism\, based on the underlying physiology and biochemistry. We use the model to investigate the consequen ces of sex differences in gene expression. We use the model to give a mech anistic understanding of observed concentration differences in one-carbon metabolism and explain why women have lower S-andenosylmethionine\, lower homocysteine\, and higher choline and betaine. We give a new explanation o f the well known phenomenon that folate supplementation lowers homocystein e and we show how to use the model to investigate the effects of vitamin d eficiencies\, gene polymorphisms\, and nutrient input changes.\n\nOur mode l of hepatic one-carbon metabolism is a useful platform for investigating the mechanistic reasons that underlie known associations between metabolit es. In particular\, we explain how gene expression differences lead to met abolic differences between males and females.\n\nhttps://conferences.maths .unsw.edu.au/event/2/contributions/451/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/451/ END:VEVENT BEGIN:VEVENT SUMMARY:Single cohort vaccination can be cost-effective. Paradox in HPV mi tigation model for Moldova. DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-257@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Andrzej Jarynowski (Interdisciplinary Research Insti tute in Wroclaw)\nHuman papillomavirus\, or HPV\, is a sexually transmissi ble virus infection\, which is necessary risk factor for developing cervic al cancer\, most common type of cancer in working age women in Moldova. We observe both behavioural change (increase in sexual partner acquisition rates) and demographical change (population ageing and massive emigration \, but still very young)\, which both corresponding to second demographic transition since Soviet Union collapse (yearly expenditure on health limit ed to 150 EUR-per-capita). Moldova will spend around 400\,000 EUR on 'si ngle cohort' vaccination in 2018\, which cost effectiveness is questionab le\, because vaccinating a single cohort may not have a substantial effect in other countries. Thus we examine such a single vaccination scenario to show its conditional cost-effectiveness.\n\nWe have run computer simulati on to prepare cost-benefit/effectivness analysis for different vaccination strategies\, various screening programs and preventive programs for Mold ova in low resource settings\, based on its own demography and sexual beha viour. We used data since 1998 to 2017 to adjust model parameter and we project till around 2038. Model aggregated the most important paths of i nfection\, cancer development\, uncertainty in healthcare capacity and sex uality and prevention scenarios with around 100 differential equations (st ochasticity introduced in sexual partner change rates).\n\nSingle cohort v accination could be both cost-beneficial (total cost reduction balance int ervention cost before 2037) and cost-effective (with incremental impact in 20 years perspective on the level of 2300 EUR/QALY). \n\nThe possible ex planation of this nonintuitive behaviour is transitional situation in Mold ova ($R_0$~1)\, still small change of conditions could cause strong effec t in epidemiology. Main effect of intervention is via men\, which avoid in fection and will not infect other women. This can have effect probably whi le changing partners is still not as common as in other countries. However \, even slight change in initial conditions and parameter values could d iminish positive effect (e.g. faster partner acquisition rate increase). \n\nhttps://conferences.maths.unsw.edu.au/event/2/contributions/257/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/257/ END:VEVENT BEGIN:VEVENT SUMMARY:Can we future-proof phylogenetic consensus trees? DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-474@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Andrew Francis (Western Sydney University)\nConsensu s methods are widely used for combining phylogenetic trees into a single e stimate of the evolutionary tree for a group of species. But how robust a re these methods to future information? If additional species are added t o the original set of trees\, will the expanded consensus tree simply be a n expansion of the original consensus tree? In this talk I will formalise and answer this question. Joint work with David Bryant (Otago\, NZ) and Mike Steel (Canterbury\, NZ).\n\nhttps://conferences.maths.unsw.edu.au/eve nt/2/contributions/474/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/474/ END:VEVENT BEGIN:VEVENT SUMMARY:Network inference of circadian clock DTSTART;VALUE=DATE-TIME:20180709T094500Z DTEND;VALUE=DATE-TIME:20180709T100000Z DTSTAMP;VALUE=DATE-TIME:20210223T074715Z UID:indico-contribution-2-488@conferences.maths.unsw.edu.au DESCRIPTION:Speakers: Seokjoo Chae (Department of Mathematical Sciences\, KAIST)\nThe mammalian circadian rhythm is governed by the principal clock which is located in the suprachiasmatic nucleus (SCN). This clock is compo sed of tens of thousands of neurons and their connection to one another is essential to important roles of SCN: synchronization\, entrainment to lig ht\, etc. Previous studies about the SCN network used the maximal informat ion coefficient (MIC) statistic to oscillating time course data during res ynchronization after desynchronization by TTX. Since this method requires desynchronization and resynchronization\, it takes a long time and the rec overed structure may not be similar to the normal SCN network. Finally\, e ven though numerous studies argued that the connection between SCN cells a re asymmetric\, MIC cannot detect directionality. \n\nWe develop our own m ethod\, which can detect causality. This method does not require desynchro nization by TTX\, so it takes shorter time and one can obtain the normal n etwork structure of the SCN. Moreover\, it is able to obtain main results of previous studies: small-world network\, exponential distribution of nod e degree. Finally\, as our method can diagnose causality\, our method can also be used to verify the asymmetry of the SCN.\n\nhttps://conferences.ma ths.unsw.edu.au/event/2/contributions/488/ LOCATION:University of Sydney Holme Building/--The Refectory URL:https://conferences.maths.unsw.edu.au/event/2/contributions/488/ END:VEVENT END:VCALENDAR