A SHORT COURSE IN THE MODELING OF CHEMOTAXIS

to be characterized by a change in the permeability of the endothelial layer that al-
lows lipids to migrate into the subendothelial layer followed by an influx of the cells
that comprise the immune response. The change in permeability is also accompanied
by an increase in the adhesiveness of the endothelial layer and a change from an-
ticoagulant to procoagulant properties. A number of factors have been considered
as possible causes of endothelial dysfunction. These include multiple typical and
atypical CVD risk factors such as cigarette smoking, diabetes mellitus and hyper-
tension (all of which generate free radicals), elevated LDL cholesterol blood levels,
and possibly even infection by microorganisms (e.g. herpes viruses or chlamydia
pneumonae) [23]. It is observed that certain sites, in particular the opposing wall
at an arterial bifurcation, are especially vulnerable to endothelial injury and subse-
quent dysfunction resulting in plaque formation. This pattern suggests that blood
flow changes including increased turbulence, decreases in shear stress, flow reversal,
and stagnation zones occurring at these sites may also contribute to the dysfunction.
Endothelial cells are known to be sensitive to shear stress, and recirculation due to
flow separation can deprive the vessel wall of fresh, nutrient rich blood resulting in
dysfunctional cells.
Lipoprotein Oxidation
Lipoproteins are micellar particles produced by the liver and intestines which
contain regulatory proteins that direct the blood trafficking of cholesterol and other
lipids to various cells in the body. There are four major classes of lipoprotein–
very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-
density lipoprotein (LDL, the ”bad cholesterol” containing particle), and high-
density lipoprotein (HDL, the ”good cholesterol” containing particle). The bulk
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