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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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:20201031T003138Z
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