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Michael Aviram

Researcher at Technion – Israel Institute of Technology

Publications -  489
Citations -  32705

Michael Aviram is an academic researcher from Technion – Israel Institute of Technology. The author has contributed to research in topics: Cholesterol & Lipoprotein. The author has an hindex of 94, co-authored 479 publications receiving 31141 citations. Previous affiliations of Michael Aviram include University of Tromsø & Steward Health Care System.

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Chronic ataluren (PTC124) treatment of nonsense mutation cystic fibrosis.

TL;DR: Chronic ataluren administration produced time-dependent improvements in CFTR activity and clinical parameters with generally good tolerability and CFTR function was greater with time and was accompanied by trends toward improvements in pulmonary function and CF-related coughing.
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Licorice extract and its major polyphenol glabridin protect low-density lipoprotein against lipid peroxidation: in vitro and ex vivo studies in humans and in atherosclerotic apolipoprotein E-deficient mice.

TL;DR: In this paper, the authors investigated the antioxidative activity against low-density-lipoprotein (LDL) oxidation of a not yet studied subclass of polyphenols, the isoflavans, which are present in licorice alcoholic extract.
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Phagocytosis of aggregated lipoprotein by macrophages: low density lipoprotein receptor-dependent foam-cell formation

TL;DR: Results indicate that macrophages internalize PLC-LDL by LDL receptor-dependent phagocytosis, and methylation of 125I- LDL (125I-MeLDL) prior to treatment with phospholipase C decreased its subsequent uptake and degradation by human macrophage.
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Paraoxonase 1 (PON1) enhances HDL-mediated macrophage cholesterol efflux via the ABCA1 transporter in association with increased HDL binding to the cells: a possible role for lysophosphatidylcholine.

TL;DR: It is concluded that HDL-associated PON1 may contribute to the attenuation of atherosclerosis development by its ability to act on macrophage phospholipids, to form LPC, which stimulates HDL binding and HDL-mediated macrophages cholesterol efflux via the ABCA1 transporter.