Titlebook: Cardiovascular Disease; Cellular and Molecul Linda L. Gallo Book 1995 Springer Science+Business Media New York 1995 Lipid.Oxidation.cardiov

visceral-fat

Apolipoprotein E: Paradoxes Aboundensity lipoproteins [IDL], and high density lipoproteins [HDL]) except low density lipoproteins (LDL) (though traces of apo E may be found in more buoyant LDL particles, especially in animal species other than the human). Like apo B, it serves as a ligand for the E/B (LDL) receptor, and its binding

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Cholesterol Efflux from Cells in Culture: Studies with Lipid-Free Acceptors, Reconstituted Particlesthe release of radiolabeled cholesterol from the cells. In the studies using lipid-free peptides or reconstituted particles the release of the labeled cholesterol reflects the net movement of cholesterol from cells to acceptors, since the acceptors were initially free of cholesterol and no significa

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Identification of FGF-1-Inducible Genes by Differential Displayas also been detected in human platelets. and T lymphocytes.. Direct evidence for the involvement of FGF-2 in rat balloon injury-induced medial smooth muscle cell proliferation was reported by Lindner and Reidy.. Therefore, it is possible that inhibition of FGF expression or action may be of therape

致敬

Mechanisms of Potentiation of Pdgf in Atherosclerosisoma.. Its protein product, the homodimeric PDGF A-chain, is a chemoattractant for monocytes, fibroblasts, and smooth muscle cells and a mitogen for fibroblasts and smooth muscle cells . In addition, PDGF A upregulates its own transcription (and thus is autoregulatoryll) and transcription of a number

debris

召集

Book 1995ivided into eight sections which reflect the focus of the plenary sessions. Part I focuses on the pathophysiology of atherosclerotic plaques and predicts that the nature of the fibrous cap of atheroma determines plaque disruption and clinical events. Papers in Part II deal with atherogenic lipoprote

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olume is divided into eight sections which reflect the focus of the plenary sessions. Part I focuses on the pathophysiology of atherosclerotic plaques and predicts that the nature of the fibrous cap of atheroma determines plaque disruption and clinical events. Papers in Part II deal with atherogenic lipoprote978-1-4613-5805-3978-1-4615-1959-1

CAMP

哎呦

The Lebedev Physics Institute Seriesensity lipoproteins [IDL], and high density lipoproteins [HDL]) except low density lipoproteins (LDL) (though traces of apo E may be found in more buoyant LDL particles, especially in animal species other than the human). Like apo B, it serves as a ligand for the E/B (LDL) receptor, and its binding

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