Bernard Delfly
Pasteur Institute
4 Papers
270 Citations
Bernard Delfly is an academic researcher from Pasteur Institute. The author has contributed to research in topics: Reverse cholesterol transport & Cholesterol. The author has an hindex of 4, co-authored 4 publications.
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Papers
Alterations in the main steps of reverse cholesterol transport in male patients with primary hypertriglyceridemia and low HDL-cholesterol levels.
Fernando Brites,Carla D Bonavita,Catherine De Geitere,Marcelo Cloës,Bernard Delfly,Mario J Yael,Jean-Charles Fruchart,Regina Wikinski,Graciela Castro +8 more
TL;DR: Hypertriglyceridemia was found to induce quantitative and qualitative alterations in HDL and its subclasses and, consequently, in some steps of reverse cholesterol transport.
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Paraoxonase activity is reduced by a pro-atherosclerotic diet in rabbits.
Michael I. Mackness,Agnes Bouiller,Nathalie Hennuyer,Bharti Mackness,Maxine Hall,Anne Tailleux,Patrick Duriez,Bernard Delfly,Paul N. Durrington,Jean-Charles Fruchart,Nicolas Duverger,Jean-Michel Caillaud,Graciela Castro +12 more
TL;DR: The relationship between PON1 and atherosclerosis development in transgenic rabbits overexpressing human apolipoprotein (apo) A-I and nontransgenic littermates fed a pro-atherogenic diet is examined.
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Abnormal Reverse Cholesterol Transport in Controlled Type II Diabetic Patients Studies on Fasting and Postprandial LpA-I Particles
Elisabeth Cavallero,Fernando Brites,Bernard Delfly,Nathalie Nicolaı̈ew,Christelle Decossin,Catherine De Geitere,Jean-Charles Fruchart,Regina Wikinski,Bernard Jacotot,Graciela Castro +9 more
TL;DR: Different abnormalities found in the fasting state were further amplified in the postprandial situation and resulted in LpA-I particles with aberrant size and composition and decreased ability to accomplish their antiatherogenic role in type II diabetic patients.
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Apolipoprotein A-I-containing particles and reverse cholesterol transport: evidence for connection between cholesterol efflux and atherosclerosis risk.
TL;DR: The results in mice transgenic for apo A-I indicate that overexpression of apo C57BL/6 mice appears to decrease cholesterol efflux and to promote rather than retard aortic fatty streak development and the fact that LpA-I:A-II family can inhibit the Lp a-I promotedolesterol efflux strongly supports the role of apO A-II as an antagonist in the production of cholesterol eff Lux.
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