By B. Greg Brown, Xue Qiao Zhao, Drew Poulin, John J. Albers (auth.), Linda L. Gallo (eds.)
The Fourteenth Washington foreign Spring Symposium, held in Washington, D.C., in June 1994, introduced jointly over four hundred prime scientists from 21 nations to study and replace examine on heart problems. This crew happy the symposium pursuits of formulating a extra complete and built-in photograph of the occasions contributing to atherosclerosis and of exploring transformed gene expression as an to figuring out the motives of atherosclerosis and offering clues to the technique prevention and therapy. This quantity comprises lots of the papers provided on the 8 plenary classes including chosen contributions from the certain periods. The multidisciplinary nature of the chapters and their authors should still stimulate the pursuits of biochemists, mobile and molecular biologists, pathologists, pharmacologists, epidemiologists, nutritionists, and clinicians. the amount is split into 8 sections which replicate the focal point of the plenary periods. half I makes a speciality of the pathophysiology of atherosclerotic plaques and predicts that the character of the fibrous cap of atheroma determines plaque disruption and scientific occasions. Papers partially II take care of atherogenic lipoproteins. The introductory paper reports the present view of the function of plasma lipoproteins in atherosclerosis. With admire to the more moderen contributors at the list,: [oxidized LDL, Lp(a)] facts is equipped that implies the involvement of 1 significant gene within the improvement of oxidized LDL lipids. the expression of inflammatory genes, and the advance of aortic fatty streaks.
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Additional resources for Cardiovascular Disease: Cellular and Molecular Mechanisms, Prevention, and Treatment
A separate approach to the evaluation of the antiatherogenic properties of LpAI and LpA-I:A-1I using transgenic mouse models. A comparison of the ability of LpA-I and LpA-I:A-II to protect against the development of diet induced atherosclerosis has been performed in transgenic mice on a high fat and cholesterol diet (46). Transgenic mice overexpressing human apoA-I and apoA-I + apoA-1I were developed and the degree of atherosclerosis induced by a diet enriched in cholesterol and fat quantitated.
These act synergistically with PDGF to induce intimal hyperplasia, and are capable of self-perpetuating their own mitogenic stimulation and SMC proliferation. Therefore, once SMC transform from a quiescent state (contractile phenotype) to a proliferative state (synthetic phenotype) and migrate to the intima, their continued activity may be self-perpetuated beyond the phase of platelet deposition. 17 ,24,25 There is evidence that direct injury of the SMC itself can initiate the biological process leading to restenosis.
Fogelman, The ultrastructure of the intima in WHHL and cholesterol-fed rabbit aortas prepared by ultra-rapid freezing and freeze-etching, J Lipid Res 30:967 (1989). 2. M. M. Fogelman, G. S. Frank, Lipid accumulation in rabbit aortic intima two hours after bolus infusion of low density lipoprotein: A deep-etch and immuno-Iocalization study for ultra-rapidly frozen tissue, Arteriosclerosis and Thrombosis 11: 1795 (1994). 3. P. Nievelstein-Post, G. M. S. Frank, An ultrastructural study of lipoprotein accumulation in cardiac valves of the rabbit, Arteriosclerosis and Thrombosis 14:1151 (1994).