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J Math Biol ; 85(5): 58, 2022 10 22.
Article in English | MEDLINE | ID: mdl-36271960

ABSTRACT

Atherosclerosis, one of the leading causes of death in USA and worldwide, begins with a lesion in the intima of the arterial wall, allowing LDL to penetrate into the intima where they are oxidized. The immune system considers these oxidized LDL as a dangerous substance and tasks the macrophages to attack them; incapacitated macrophages become foam cells and leads to the formation of a plaque. As the plaque continues to grow, it progressively restricts the blood flow, possibly triggering heart attack or stroke. Because the blood vessels tend to be circular, two-space dimensional cross section model is a good approximation, and the two-space dimensional models are studied in Friedman et al. (J Differ Equ 259(4):1227-1255, 2015) and Zhao and Hu (J Differ Equ 288:250-287, 2021). It is interesting to see whether a true three-space dimensional stationary solution can be developed. We shall establish a three-space dimensional stationary solution for the mathematical model of the initiation and development of atherosclerosis which involves LDL and HDL cholesterols, macrophages and foam cells. The model is a highly nonlinear and coupled system of PDEs with a free boundary, the interface between the plaque and the blood flow. We establish infinite branches of symmetry-breaking stationary solutions which bifurcate from the annular stationary solution in the longitude direction.


Subject(s)
Atherosclerosis , Plaque, Atherosclerotic , Humans , Plaque, Atherosclerotic/pathology , Foam Cells/pathology , Foam Cells/physiology , Macrophages/pathology , Arteries
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