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Alan M. Fogelman
Researcher at University of California, Los Angeles
Publications - 294
Citations - 31891
Alan M. Fogelman is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Lipoprotein & Apolipoprotein B. The author has an hindex of 90, co-authored 287 publications receiving 30287 citations. Previous affiliations of Alan M. Fogelman include University of Alabama at Birmingham & University of California.
Papers
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Journal ArticleDOI
Atherosclerosis: basic mechanisms. Oxidation, inflammation, and genetics.
Judith A. Berliner,Mohamad Navab,Alan M. Fogelman,Joy S. Frank,Linda L. Demer,Peter A. Edwards,Andrew D. Watson,Aldons J. Lusis +7 more
TL;DR: Enzymes associated with HDL may play an important role in protecting against lipid oxidation in the artery wall and may account in part for the inverse relation between HDL and risk for atherosclerotic clinical events.
Journal ArticleDOI
Antiinflammatory Properties of HDL
Philip J. Barter,Stephen J. Nicholls,Kerry-Anne Rye,Gattadahalli M. Anantharamaiah,Mohamad Navab,Alan M. Fogelman +5 more
TL;DR: In this paper, HDL has been shown to have anti-atherogenic properties, which may explain the ability of HDL to promote the efflux of cholesterol from cells in the artery wall.
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Minimally modified low density lipoprotein induces monocyte chemotactic protein 1 in human endothelial cells and smooth muscle cells
Susan D. Cushing,Judith A. Berliner,Anthony J. Valente,Mary C. Territo,M Navab,Farhad Parhami,Ross G. Gerrity,Colin J. Schwartz,Alan M. Fogelman +8 more
TL;DR: After exposure to low density lipoprotein (LDL) that had been minimally modified by oxidation (MM-LDL), human endothelial cells (EC) and smooth muscle cells (SMC) cultured separately or together produced 2- to 3-fold more monocyte chemotactic activity than did control cells or cells exposed to freshly isolated LDL.
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Mice lacking serum paraoxonase are susceptible to organophosphate toxicity and atherosclerosis
Diana M. Shih,Lingjie Gu,Yu Rong Xia,Mohamad Navab,Wan Fen Li,Susan Hama,Lawrence W. Castellani,Clement E. Furlong,Lucio G. Costa,Alan M. Fogelman,Aldons J. Lusis +10 more
TL;DR: When fed on a high-fat, high-cholesterol diet, PON1 -null mice were more susceptible to atherosclerosis than their wild-type littermates.
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Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages
TL;DR: It is hypothesize that one modification of LDL in vivo may result from malondialdehyde which is released from blood platelets or is produced by lipid peroxidation at the site of arterial injury.