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Allen D. Cooper

Researcher at Stanford University

Publications -  109
Citations -  5855

Allen D. Cooper is an academic researcher from Stanford University. The author has contributed to research in topics: Cholesterol & Chylomicron remnant. The author has an hindex of 45, co-authored 109 publications receiving 5704 citations. Previous affiliations of Allen D. Cooper include Royal London Hospital & United States Department of Veterans Affairs.

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Journal ArticleDOI

Hepatic uptake of chylomicron remnants.

TL;DR: In humans, delayed removal of chylomicron remnants has been documented in diabetes, renal failure, and familial combined hyperlipemia and is the abnormality resulting in type III hyperlipidemia.
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Cloning of a unique lipase from endothelial cells extends the lipase gene family

TL;DR: Its tissue-restricted pattern of expression and its ability to be expressed by endothelial cells, suggests that endothelial cell-derived lipase may have unique functions in lipoprotein metabolism and in vascular disease.
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Endothelial lipase is a major determinant of HDL level.

TL;DR: Analysis of lipoprotein particle composition indicated that this increase was due primarily to an increased number of HDL particles, and phospholipase assays indicated that EL is a primary contributor to phospholIPase activity in mouse.
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Very low and low density lipoprotein synthesis and secretion by the human hepatoma cell line Hep-G2: effects of free fatty acid.

TL;DR: It is concluded that human liver-derived cells can secrete distinct VLDL and LDL-like particles, and the relative amounts of these lipoproteins are determined, at least in part, by the availability of free fatty acid.
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Endothelial lipase modulates susceptibility to atherosclerosis in apolipoprotein-E-deficient mice.

TL;DR: Endothelial lipase (EL) expression correlates inversely with circulating high density lipoprotein (HDL) cholesterol levels in genetic mouse models, and human genetic variation in this locus has been linked to differences in HDL cholesterol levels, suggesting a role for EL in the development of atherosclerotic vascular disease.