D
David E. Bowyer
Researcher at University of Cambridge
Publications - 60
Citations - 2821
David E. Bowyer is an academic researcher from University of Cambridge. The author has contributed to research in topics: Cholesterol & Low-density lipoprotein. The author has an hindex of 26, co-authored 60 publications receiving 2786 citations.
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Journal ArticleDOI
C-Reactive Protein Frequently Colocalizes With the Terminal Complement Complex in the Intima of Early Atherosclerotic Lesions of Human Coronary Arteries
Jan Torzewski,Michael Torzewski,David E. Bowyer,Margit Fröhlich,Wolfgang Koenig,Johannes Waltenberger,Colin M. Fitzsimmons,Vinzenz Hombach +7 more
TL;DR: The data suggest that CRP may promote atherosclerotic lesion formation by activating the complement system and being involved in foam cell formation as well as in the deep fibroelastic layer and in the fibromuscular layer of the intima adjacent to the media.
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Human Blood-Derived Macrophages Induce Apoptosis in Human Plaque-Derived Vascular Smooth Muscle Cells by Fas-Ligand/Fas Interactions
TL;DR: It is concluded that human macrophages potently induce human VSMC apoptosis, which requires direct cell-cell interactions and is in part dependent on Fas/Fas-L interactions, and may therefore directly promote plaque rupture.
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Inhibitory effect of calcium antagonists on balloon catheter-induced arterial smooth muscle cell proliferation and lesion size
TL;DR: Results show that nifedipine and other antihypertensive agents inhibit smooth muscle cell proliferation and selectively reduced arterial DNA synthesis in balloon catheterised rabbits.
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Processes in atherogenesis: complement activation.
TL;DR: Subendothelial deposition of low density lipop protein appears to be an important stimulus in these events and substantial evidence suggests that complement activation may be a link between lipoprotein deposition and subsequent lesion development.
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Atherosclerosis induced in hypercholesterolaemic baboons by immunological injury; and the effects of intravenous polyunsaturated phosphatidyl choline
TL;DR: It is concluded that immunological injury hastens the onset of Atherosclerosis produced by feeding a hypercholesterolaemic diet and that changes in aortic lipolytic enzymes may be the mechanism by which Lipostabil reduces atherosclerosis.