H
H. Bryan Brewer
Researcher at MedStar Washington Hospital Center
Publications - 215
Citations - 61956
H. Bryan Brewer is an academic researcher from MedStar Washington Hospital Center. The author has contributed to research in topics: Cholesterol & Apolipoprotein B. The author has an hindex of 75, co-authored 215 publications receiving 60497 citations. Previous affiliations of H. Bryan Brewer include American College of Cardiology & MedStar Health.
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Journal ArticleDOI
Evacetrapib alone or in combination with statins lowers lipoprotein(a) and total and small LDL particle concentrations in mildly hypercholesterolemic patients
Stephen J. Nicholls,Giacomo Ruotolo,H. Bryan Brewer,Ming Dauh Wang,Liping Liu,Mark B. Willey,Mark A. Deeg,Kathryn A. Krueger,Steven E. Nissen +8 more
TL;DR: Evaluating the effects of the cholesteryl ester transfer protein (CETP) inhibitor evacetrapib on atherogenic apolipoprotein B (apoB)-containing lipoproteins in mildly hypercholesterolemic patients found that Evacetrapib, alone or with statins, significantly increased LDL-P size.
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Hemoglobin Switching in Sheep and Goats: III. CELL-FREE INITIATION OF SHEEP GLOBIN SYNTHESIS
TL;DR: The mechanism of sheep globin initiation is similar to that of rabbit and human Globin initiation; this conclusion suggests a pretranslational control for hemoglobin switching in the sheep.
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Characterization of plasma lipids and lipoproteins in patients with β2-glycoprotein I (apolipoprotein H) deficiency
Jeffrey M. Hoeg,Pesach Segal,Richard E. Gregg,Y.S. Chang,Frank T. Lindgren,Gerald L. Adamson,Michael M. Frank,C M Brickman,H. Bryan Brewer +8 more
TL;DR: It is concluded that the lack of apolipoprotein H does not result in a significant perturbation of normal lipoprotein metabolism as reflected by analysis of fasting plasma lipoproteins.
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Vitamin A and Vitamin E Replacement in Abetalipoproteinemia
TL;DR: Patients with abetalipoproteinemia are unable to secrete apolipoprotein B, they cannot normally transport lipids in their circulation and thus have depressed plasma concentrations, and their plasma concentrations are depressed.
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Homozygous familial hypobetalipoproteinemia. Increased LDL catabolism in hypobetalipoproteinemia due to a truncated apolipoprotein B species, apo B-87Padova.
Carlo Gabelli,Claudio Bilato,Scipione Martini,Gregory E. Tennyson,Loren A. Zech,Alberto Corsini,Marco Albanese,H. Bryan Brewer,Gaetano Crepaldi,G Baggio +9 more
TL;DR: Results indicate that apoB-87 LDL has an enhanced ability to interact with the LDL receptor, the increasedApoB catabolism contributes to the hypobetalipoproteinemia and may explain the mild expression of the disease in the two homozygous individuals.