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dc.contributor.authorPasqualino, Giuseppe
dc.date.accessioned2019-08-14T18:20:28Z
dc.date.available2019-08-14T18:20:28Z
dc.identifier.urihttp://hdl.handle.net/10222/76250
dc.description.abstractAtherosclerosis is a disease of the cardiovascular system of humans that can lead to myocardial infarction and stroke. It begins in the arterial walls (intima) as an inflammatory response to dysfunction of the endothelium and access of the intima by oxidized low-density lipoproteins (oxLDLs). In response to this, white blood cells, specifically monocytes, are recruited from the bloodstream. Trapped in the intima, the monocytes differentiate into macrophages which, after engulfing oxLDLs, become foam cells, leading to the production of inflammatory cytokines and further recruitment of white blood cells. This self-accelerating process results in an increase of the thickness of arteries, in the formation of atherosclerotic plaques and, possibly, in their rupture. We suggest a one-dimensional mathematical model of the initial events of atherosclerosis. This model consists of a reaction–diffusion system with Neumann boundary conditions, and describes the recruitment of monocytes as a function of the concentration of inflammatory cytokines.en_US
dc.language.isoenen_US
dc.subjectPattern Formation Atherosclerosisen_US
dc.subjectAtherosclerosis
dc.titlePattern Formation in Atherosclerotic Plaquesen_US
dc.date.defence2019-08-02
dc.contributor.departmentDepartment of Mathematics & Statistics - Math Divisionen_US
dc.contributor.degreeMaster of Scienceen_US
dc.contributor.external-examinern/aen_US
dc.contributor.external-examinern/aen_US
dc.contributor.graduate-coordinatorDr. David Ironen_US
dc.contributor.thesis-readerDr. Theodore Kolokolnikoven_US
dc.contributor.thesis-readerDr. Roman Smirnoven_US
dc.contributor.thesis-supervisorDr. David Ironen_US
dc.contributor.ethics-approvalNot Applicableen_US
dc.contributor.manuscriptsNot Applicableen_US
dc.contributor.copyright-releaseNot Applicableen_US
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