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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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Macrophage paraoxonase 2 (PON2) expression is upregulated by unesterified cholesterol through activation of the phosphatidylinositol 3-kinase (PI3K) pathway.

TL;DR: Macrophage PON2 expression is upregulated in UC-enriched macrophages through activation of the PI3K signal pathway, indicating a progressive increase in the unesterified cholesterol content and a decrease in its cholesteryl ester content in atherosclerotic lesions.
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Apolipoprotein E and lipoprotein lipase reduce macrophage degradation of oxidized very-low-density lipoprotein (VLDL), but increase cellular degradation of native VLDL.

TL;DR: Results showed that LPL and apo E, two important regulatory substances in cellular metabolism of plasma lipoproteins, increased macrophage degradation of native VLDL, but reduced the degradation of Ox-VLDL.
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LDL oxidation is associated with increased blood hemoglobin A1c levels in diabetic patients.

TL;DR: Increased tendency of LDL to undergo lipid peroxidation in diabetic patients contributes to increased levels of blood HbA1c, mainly in those with Hb a1c<7.3.
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Familial homozygous hypercholesterolemia: clinical and cardiovascular features in 18 patients.

TL;DR: It is concluded that coronary artery disease is prevalent in patients with HFH and the performance of noninvasive technique, coronary arteriography and supravalvular aortography at an early age is recommended to detect and to follow the progression of the disease.
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Proteins derived from platelet α granules modulate the uptake of oxidized low density lipoprotein by macrophages

TL;DR: PDGF, thus, may represent the protein-like factor present in PCM which stimulates Ox-LDL degradation by macrophages, whereas B-TG may have a role in the recognition of PCM particles by the macrophage scavenger receptor.