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SUMMARY:Exploring differential regulation of blood clot degradation
DTSTART;VALUE=DATE-TIME:20180712T052000Z
DTEND;VALUE=DATE-TIME:20180712T054000Z
DTSTAMP;VALUE=DATE-TIME:20210228T011219Z
UID:indico-contribution-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/
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