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10篇 您的检索式:作者名="Ryan Temel"
    题名 作者 年代 出处 被引量
1Polymersomes scalably fabricated via flash nano- precipitation are non-toxic in non-human primates and associate with leukocytes in the spleen and kidney following intravenous administration显示文摘Sean D. Allen Yu-Gang Liu Sharan Bobbala Lei Cai Peter I. Hecker Ryan Temel Evan A. Scott 2018Nano Research2018,11,10:3
2Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis显示文摘Rayner Katey J Sheedy Frederick J Esau Christine C Hussain Farah N Temel Ryan E Parathath Saj van Gils Janine M Rayner Alistair J Chang Aaron N Suarez Yajaira Fernandez-Hernando Carlos Fisher Edward A Moore Kathryn J 2011Journal of Clinical Investigation2011,,7:2
3A new framework for reverse cholesterol transport: Non-biliary contributions to reverse cholesterol transport显示文摘Reduction of low-density lipoprotein-cholesterol through statin therapy has only modestly decreased coronary heart disease (CHD)-associated mortality in developed countries, which has prompted the search for alternative therapeutic strategies for CHD. Major efforts are now focused on therapies that augment high-density lipoprotein (HDL)-mediated reverse cholesterol transport (RCT), and ultimately increase the fecal disposal of cholesterol. The process of RCT has long been thought to simply involve HDL-mediated delivery of peripheral cholesterol to the liver for biliary excretion out of the body. However, recent studies have revealed a novel pathway for RCT that does not rely on biliary secretion. This nonbiliary pathway rather involves the direct excretion of cholesterol by the proximal small intestine. Compared to RCT therapies that augment biliary sterol loss, modulation of non-biliary fecal sterol loss through the intestine is a much more attractive therapeutic strategy, given that excessive biliary cholesterol secretion can promote gallstone formation. However, we are at an early stage in understanding the molecular mechanisms regulating the non-biliary pathway for RCT, and much additional work is required in order to effectively target this pathway for CHD prevention. The purpose of this review is to discuss our current understanding of biliary and nonbiliary contributions to RCT with particular emphasis on the possibility of targeting the intestine as an inducible cholesterol secretory organ.Ryan E Temel J Mark Brown 2010World Journal of Gastroenterology2010,16,47:2
4Apolipoprotein A-I is necessary for the in vivo formation of high density lipoprotein competent for scavenger receptor BI-mediated cholesterol ester-selective uptake显示文摘Ryan E Temel Rosemary L Walzem Carole L 2002J Biol Chem2002,277,26:1
5Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis显示文摘Rayner Katey J Sheedy Frederick J Esau Christine C Hussain Farah N Temel Ryan E Parathath Saj van Gils Janine M Rayner Alistair J Chang Aaron N Suarez Yajaira Fernandez-Hernando Carlos Fisher Edward A Moore Kathryn J 2011Journal of Clinical Investigation2011,,7:1
6ACAT2 stimulates cholesteryl ester secretion in apoB-containing lipoproteins 显示文摘Ryan E Temel Li hou 2007Lipid Res2007,48,7:1
7A new model of reverse cholesterol transport: enTICEing strategies to stimulate intestinal cholesterol excretion显示文摘Ryan E. Temel J. Mark Brown 2015Trends in Pharmacological Sciences2015,,7:1
8Biliary Sterol Secretion Is Not Required for Macrophage Reverse Cholesterol Transport显示文摘Ryan E. Temel Janet K. Sawyer Liqing Yu Caleb Lord Chiara Degirolamo Allison McDaniel Stephanie Marshall Nanping Wang Ramesh Shah Lawrence L. Rudel J. Mark Brown 2010Cell Metabolism2010,,1:1
9ACAT2 stimulates cholesteryl ester secretion in apoB-containing lipoproteins显示文摘 Temel Li hou 2007Lipid Bes2007,48,7:1
10Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis显示文摘Rayner Katey J Sheedy Frederick J Esau Christine C Hussain Farah N Temel Ryan E Parathath Saj van Gils Janine M Rayner Alistair J Chang Aaron N Suarez Yajaira Fernandez-Hernando Carlos Fisher Edward A Moore Kathryn J 2011Journal of Clinical Investigation2011,,7:1
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