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

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Structure and Evolution of the Apolipoprotein and Lipase Gene Families,n, they capture some of the peripherally derived lipids and return them to the liver, where they are metabolized. Lipoprotein lipase (LPL) and hepatic triglyceride Lipase (HL) are enzymes located on the vascular endothelial surface that modify, through lipid hydrolysis, the circulating lipoprotein p

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A Gln to Arg Substitution in the Adducin Family of Proteins is a Necessary but not Sufficient Factose differences are determined within the stem cells, are genetically associated with the development of hypertension, and are similar to those found between the tubular cells of the two strains. This alteration seems to be associated with abnormalities of membrane skeleton (Bianchi et al. 1985; Ferr

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Receptor Regulation of Lipoprotein Metabolism,ide metabolism in the body. In addition fatty acid metabolism is partly dependent on the structure of lipoproteins. For these reasons it is obvious that the regulation of lipoprotein metabolism plays a major role in energy generation in the body. Next to these physiological functions defects in lipo

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The High-Density Lipoprotein Receptor,prised mostly of cholesteryl esters. The major cells that accumulate cholesterol in these lesions are macrophages which are derived from circulating monocytes that penetrate the endothelial barrier in response to inflammatory signals. Although the precise mechanism for subendothelial recruitment of

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Cholesterol-Lowering Clinical Trials: Where Do We Go From Here?,nd long term. The important information that has been gathered from clinical trials and the accomplishments of the late 1980s outline a highly impressive story. We now have firm evidence that the incidence of coronary heart disease (CHD) in the form of myocardial infarction and/or coronary death can

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