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Atherogenesis: Lipid Accumulation and Plaque Disruption: Processes Triggering Clinical Instability in Coronary Disease-An Overview; B.G. Brown. Expression of 92 kDa Gelatinase in Human Atherosclerotic Lesions Following Recent Plaque Rupture; D.L. Brown. Atherogenic Lipoproteins: Current Concepts of the Plasma Lipoproteins and Their Role in Atherosclerosis-An Overview; H.B. Brewer, Jr. Homeostasis of Lipid Oxidation in the Artery Wall; A.M. Fogelman, et al. Antiatherogenesis/Cholesterol Removal Mechanisms: The Role of HDL Receptors in Removal of Cellular Cholesterol; J.F. Oram, et al. Signal Transduction in Vascular Proliferation: Identification of FGF1-Inducible Genes by Differential Display; J.A. Winkles, et al. Adhesion Pathobiology: Molecular Basis and Pathological Consequences of Neutrophil Adherence to Endothelium; J.M. Harlan, et al. Thrombosis/Fibrinolysis: Regulation of Vascular Fibrinolysis by Type 1 Plasminogen Activator Inhibitor (PAI1): D. Seiffert, et al. Modified Gene Expression/Clues to Cause, Prevention, and Treatment of Atherosclerosis: Genetic Factors Contributing to Atherosclerosis: From Humans to Mice and Back Again; C.H. Warden, A.J. Lusis. Atherosclerosis Prevention and Public Policy: Cholesterol and Mortality: What Can Metaanalysis Tell Us? D.J. Gordon. 35 additional articles. Index.
The Fourteenth Washington International Spring Symposium, held in Washington, D.C., in June 1994, brought together over 400 leading scientists from 21 countries to review and update research on cardiovascular disease. This group satisfied the symposium goals of formulating a more comprehensive and integrated picture of the events contributing to atherosclerosis and of exploring modified gene expression as an to understanding the causes of atherosclerosis and providing clues to the approach prevention and treatment. This volume contains most of the papers presented at the eight plenary sessions together with selected contributions from the special sessions. The multidisciplinary nature of the chapters and their authors should stimulate the interests of biochemists, cell and molecular biologists, pathologists, pharmacologists, epidemiologists, nutritionists, and clinicians. The volume 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 lipoproteins. The introductory paper reviews the current view of the role of plasma lipoproteins in atherosclerosis. With respect to the newer members on the list,: [oxidized LDL, Lp(a)] evidence is provided that suggests the involvement of one major gene in the development of oxidized LDL lipids. the expression of inflammatory genes, and the development of aortic fatty streaks.
The Sixth Annual International Spring Symposium on Health Sciences, held in Washington, D. C., in May 1986, brought together over 650 scientists from 19 countries to review and update research on cardiovascular disease. In this volume, which contains 59 chapters, an internationally recognized group of authors con tribute up-to-date accounts of molecular and cellular processes occurring in the vessel wall in atherogenesis and describe approaches to the prevention and treatment of atherosclerosis. The volume is divided into six major sections. Two sections deal with current aspects of lipoprotein metabolism. In Part I, we are alerted to the impact on li poprotein metabolism of structural heterogeneity within the four broad lipoprotein classes. Attention then turns to the components that orchestrate lipoprotein metab olism. Apolipoprotein identities, processing, and functions are described, as are the roles of lipid transfer proteins in plasma lipoprotein remodeling. Hepatic lipase synthesis and secretion are described. In Part II, Nobel Laureates Michael S. Brown and Joseph L. Goldstein describe mutations in the LDL receptor that reveal the functions of its various domains and point out how understanding the LDL receptor has provided a rational basis for its regulation. A discussion of the role of receptors in regulating cholesterol uptake by tissues follows, with emphasis on receptor-ligand interactions. Additional pathways for cholesterol delivery to cells are explored, as are pathways for cholesterol egress."
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