P
Peter Brecher
Researcher at Boston University
Publications - 109
Citations - 5904
Peter Brecher is an academic researcher from Boston University. The author has contributed to research in topics: Angiotensin II & Nitric oxide synthase. The author has an hindex of 46, co-authored 109 publications receiving 5813 citations. Previous affiliations of Peter Brecher include Cardiovascular Institute of the South & Boston Medical Center.
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AMP-activated protein kinase is required for the lipid-lowering effect of metformin in insulin-resistant human HepG2 cells.
Mengwei Zang,Adriana Zuccollo,Xiuyun Hou,Daisuke Nagata,Kenneth Walsh,Haya Herscovitz,Peter Brecher,Neil B. Ruderman,Richard A. Cohen +8 more
TL;DR: Results indicate that AMPKα negatively regulates ACC activity and hepatic lipid content, which may contribute to lipid accumulation induced by high concentrations of glucose associated with insulin resistance.
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Superoxide Anion From the Adventitia of the Rat Thoracic Aorta Inactivates Nitric Oxide
Hui Di Wang,Patrick J. Pagano,Yue Du,Antonio J. Cayatte,Mark T. Quinn,Peter Brecher,Richard A. Cohen +6 more
TL;DR: Results indicate that NADPH oxidase located in the adventitia of rat thoracic aorta generates sufficient extracellular superoxide anion to constitute a barrier capable of inactivating nitric oxide and suggests that adventitial superoxideAnion can play a role in the pathophysiology of the arterial wall.
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Rapid expression of heat shock protein in the rabbit after brief cardiac ischemia.
TL;DR: The effect of brief myocardial ischemia on the expression of heat shock protein (HSP 70) was examined in an in vivo rabbit model of myocardia using Northern blotting and Measurements with the piezoelectric crystals showed mildMyocardial dysfunction concomitant with the increase in HSP 70.
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Angiotensin II induces fibronectin expression associated with cardiac fibrosis in the rat.
TL;DR: The data indicate that angiotensin II induces an acute fibrotic response within the heart and suggests that Ang II stimulates fibronectin expression within nonmyocytic cardiac cells by a direct action.
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Growth factor expression in aorta of normotensive and hypertensive rats.
TL;DR: The hypothesis that synthesis and release of growth factors in the arterial wall are involved in autocrine and/or paracrine regulatory mechanisms is supported and the increased expression of TGF-beta in vivo may have a role in mediating the aortic changes induced by hypertension.