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Titlebook: Cellular and Molecular Biology of Atherosclerosis; Antonio M. Gotto Book 1992 Springer-Verlag London Limited 1992 Arterien.Arterienverkalk

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楼主: Maudlin
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Genetic Control of Plasma Lipid, Lipoprotein and Apolipoprotein Levels: From Restriction Fragment Lroaches to investigate the problem, including epidemiology, dietary and metabolic studies and more recently the techniques of cellular and molecular biology have been used. This review focuses on the identification of genetic factors that contribute to the between-individual differences in plasma LDL-C levels seen in the general population.
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Morphological Findings in the Coronary Arteries in Fatal Coronary Artery Disease,sclerotic CAD. In the USA alone, about 6 million persons have symptomatic myocardial ischemia because of atherosclerotic CAD. About 250000 coronary artery bypass grafting operations were performed in 1990 in the USA and about 300000 coronary angioplasty procedures. The cause of atherosclerosis is no
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The ,-Arginine: Nitric Oxide Pathway in Physiology and Pathology,t only explains the biological properties of the so-called endothelium-derived relaxing factor (EDRF) but is also the stimulator of the soluble guanylate cyclase in a number of tissues such as the platelet and the brain. Furthermore, NO is a cytotoxic factor released by activated murine macrophages
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Basic Fibroblast Growth Factor in Vascular Development and Atherogenesis,logies, such as restenosis after angioplasty and intimal proliferation in vessels of transplanted organs. Clearly, the rationale is that the development of these lesions involves the migration and proliferation of smooth muscle cells and monocyte-macrophages, and secretion of large amounts of extrac
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The Monocyte and Endothelial Injury in Atherogenesis,blood monocyte in atherosclerosis was first pointed out by Leary as late as 1941. Poole and Florey (1958) later discussed the blood as a source of lesion foam cells in hypercholesterolemic rabbits, and demonstrated a macrophage traversing the endothelium. Still and O’Neal (1962) were the first to de
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Lp [a]: A Lipoprotein Class with Atherothrombotic Potential,e (ASGVD) (Utermann 1989; Scanu and Fless 1990; Berg 1990). At this time this notion rests predominantly on epidemiological data although emerging experimental evidence is now permitting to formulate hypotheses on the possible mechanism(s) of this pathogenicity. This experimental evidence will be re
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Modified Lipoproteins and Atherogenesis,erosclerotic plaque (Palinski et al. 1989; Haberland et al. 1988; Ylä-Herttuala et al. 1989; Clevidence et al. 1983). Low-density lipoprotein (LDL) isolated from the vessel wall has been shown to contain oxidized lipids and protein (Ylä-Herttuala et al. 1989; Clevidence et al. 1983) and monoclonal a
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The Molecular Biology of Apolipoprotein B,lipoprotein (LDL). LDL is an oily droplet, containing a core of hydrophobic cholesteryl esters and a surface monolayer of phospholipid and free cholesterol at the surface. The particle is stabilized and made soluble in the water of the blood by the presence at its surface of a huge protein apolipopr
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