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

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S. Guiducci,G. Martinelli,M. A. Pregeras 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

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S. Guiducci,G. Martinelli,M. A. Pregeroma.. 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

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Nuclear Physics with Polarized ParticlesCs and SMCs in atherosclerotic plaques.. These similarities have led to the suggestion that SMCs in atherosclerosis and hypertension may recapitulate certain aspects of earlier developmental events.. To permit a critical analysis of this possibility, it is crucial that we obtain a better understandi

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Lipid Accumulation and Plaque Disruption: Processes Triggering Clinical Instability in Coronary Diseept that there are acute “triggering” risk factors for plaque disruption has been described in detail elsewhere (., ., .) and we will summarize the salient aspects of this approach to understanding coronary artery disease.

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Expression of 92 KDA Gelatinase in Human Atherosclerotic Lesions Following Recent Plaque Rupturetion and sudden cardiac death. These disparate syndromes occur along a clinical continuum linked by a common pathophysiologic event, intracoronary thrombosis (.–.). Thrombosis is initiated by rupture of atherosclerotic plaque and exposure of highly thrombogenic plaque constituents to coronary blood