Zobrazeno 1 - 10
of 558
pro vyhledávání: '"A M, LEFER"'
Publikováno v:
Journal of Cardiovascular Pharmacology. 41:649-656
The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been shown to upregulate endothelial nitric oxide synthase in isolated endothelial cells in a manner that is independent of their lipid-lowering effects. Nitric oxide inhib
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a040016130bbb8662fdf4c2ccecd62a7
https://doi.org/10.1097/00005344-200304000-00019
https://doi.org/10.1097/00005344-200304000-00019
Publikováno v:
Diabetes. 51:1556-1564
Inhibition of protein kinase C (PKC) activity has been shown to improve the endothelial dysfunction associated with hyperglycemia and diabetes. The mechanisms by which inhibition of PKC activity ameliorates endothelial dysfunction in diabetes are not
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6bd95423d4fd1822c749ca04646f34a7
https://doi.org/10.2337/diabetes.51.5.1556
https://doi.org/10.2337/diabetes.51.5.1556
Publikováno v:
British Journal of Pharmacology. 133:406-412
Recent studies have reported that hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have vasculoprotective effects independent of their lipid-lowering properties, including anti-inflammatory actions. We used intravital microscopy of the
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::b44e1a53d62d822cf892ca4f92c376ec
https://doi.org/10.1038/sj.bjp.0704070
https://doi.org/10.1038/sj.bjp.0704070
Publikováno v:
American Journal of Physiology-Endocrinology and Metabolism. 280:E848-E856
We employed intravital microscopy of the rat mesenteric microvasculature to study the effects of local hyperglycemia on leukocyte-endothelial cell interactions. Intraperitoneal injection of 6, 12.5, and 25 mmol/ld-glucose to the rat significantly and
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2a24490012da0fb06b223f4bd7fa8f79
https://doi.org/10.1152/ajpendo.2001.280.6.e848
https://doi.org/10.1152/ajpendo.2001.280.6.e848
Autor:
David J. Lefer, Michaela R. Hoffmeyer, David M. Rimmer, Michael E. Gooszen, Steven D. Trocha, Paul L. Huang, Steven P. Jones, Allan M. Lefer, Rosario Scalia, Melanie B. Smith
Publikováno v:
Circulation. 103:2598-2603
Background —Simvastatin attenuates ischemia and reperfusion in normocholesterolemic animals by stabilizing endothelial nitric oxide synthase activity and inhibiting neutrophil-mediated injury. Because endothelial dysfunction is a detrimental effect
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1e0f032fe38fed60857197537473bd93
https://doi.org/10.1161/01.cir.103.21.2598
https://doi.org/10.1161/01.cir.103.21.2598
Publikováno v:
The FASEB Journal. 14:2357-2364
C-peptide is a cleavage product that comes from processing proinsulin to insulin that induces nitric oxide (NO) -mediated vasodilation. NO modulates leukocyte-endothelium interaction. We hypothesized that C-peptide might inhibit leukocyte-endothelium
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::369da9f516e3f532bbe3721aa80173ba
https://doi.org/10.1096/fj.00-0183com
https://doi.org/10.1096/fj.00-0183com
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 279:H1453-H1459
Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in cardiac dysfunction. C-peptide, a cleavage product of proinsulin to insulin processing, induces nitric oxide (NO)-mediated vasodilation. NO is reported
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::19ad42287073df62bab471573e97f224
https://doi.org/10.1152/ajpheart.2000.279.4.h1453
https://doi.org/10.1152/ajpheart.2000.279.4.h1453
Publikováno v:
Arteriosclerosis, Thrombosis, and Vascular Biology. 20:1033-1039
Abstract —Endothelial dysfunction is a major pathophysiological consequence of hypercholesterolemia and other conditions. We examined whether a synthetic mediator of lipid transport from peripheral tissues to the liver (ie, the “reverse” pathwa
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3953049495493e23a3c78d4ebf08e6ef
https://doi.org/10.1161/01.atv.20.4.1033
https://doi.org/10.1161/01.atv.20.4.1033