SMS scnews item created by Caroline Wormell at Thu 26 Feb 2026 1744
Type: Seminar
Distribution: World
Expiry: 4 Mar 2026
Calendar1: 4 Mar 2026 1200-1300
CalLoc1: Carslaw 451
CalTitle1: Myerscough: The mathematics of lipids and cells: modelling the development of atherosclerotic plaques
Auth: caro@10.136.88.81 (cwor5378) in SMS-SAML
Applied Maths Seminar: Myerscough -- The mathematics of lipids and cells: modelling the development of atherosclerotic plaques
This week, Mary Myerscough will be giving a talk (based on her Society of Mathematical
Biology plenary), on Wednesday 12pm in Carslaw 451.
Title: The mathematics of lipids and cells: modelling the development of atherosclerotic
plaques
Abstract: Atherosclerotic plaques are fatty accumulations in the inside of the
walls of major arteries. They are the principal cause of ischaemic heart attacks,
strokes and peripheral vascular disease. Their formation is driven by chronic
inflammation, which is initiated and fuelled by the presence of cholesterol-bearing
modified low density lipoproteins in the vessel wall. Atherosclerosis, like cancer, is
a major cause of death and disease world-wide. Unlike cancer, it has not, to date, been
well-studied by mathematical biologists and other modellers, and in particular the
cellular and immune processes, that drive plaque formation, maturation and ultimately
plaque fate, have not been widely modelled. In scientific research, plaques must be
grown inside an experimental animal and each plaque can be viewed at just one time
point, when the animal is sacrificed. In clinical practice, plaques in humans are
usually only observed at the late stage when clinical complications occur. Hence there
is a clear role for modelling and simulation in understanding the dynamics of plaques
and the factors that influence their growth or regression. In this talk, I will present
research on ODE and PDE models for immune cell populations and the lipid (cholesterol)
that they contain. In particular, I will present work exploring the effect of timing in
raising the level of high density lipoprotein (HDL which carries âgood
cholesterolâ); structured population models for macrophages that include lipid
trafficking; and a model to explore the outcomes of phenotypic changes in plaque smooth
muscle cells.
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