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Atherosclerosis: Cellular and Molecular Interactions in the by S. Fedoroff (auth.), Avrum I. Gotlieb, B. Lowell Langille,

By S. Fedoroff (auth.), Avrum I. Gotlieb, B. Lowell Langille, Sergey Fedoroff (eds.)

This quantity includes the papers that have been offered on the First Altschul Symposium, Atherosclerosis: mobile and Molecular Interactions within the Artery Wall. The symposium was once held in Saskatoon, on the college of Saskatchewan in could 1990 in reminiscence of Dr. Rudolph Altschul, a pioneer within the box of vascular biology and the prevention of atherosclerosis. Dr. Altschul was once Professor and Head of the dept of Anatomy on the collage of Saskatchewan from 1955 to 1963. The problem for biomedical scientists is to solve the multifactorial etiology of atherosclerosis. For the final hundred and sixty years, anatomical pathologists have conscientiously studied the morphological alterations of the human vascular wall in the course of the initiation and evolution of the fibrofatty atherosclerotic plaque. in keeping with those stylish morphological observations, theories on atherogenesis have been placed forth through pathologists within the 1840's. Rudolf Virchow recommended that the circulation of drugs from the blood into the vessel wall used to be very important for atherogenesis whereas Carl von Rokitansky felt that the deposition of drugs at the lumenal floor of the artery led to the formation of atherosclerotic plaque. due to the fact that those unique theories, it has turn into obvious that the pathogenesis of atherosclerosis is multifactorial and the disorder evolves in levels. it's also most likely that now not all plaques come up during the comparable series of occasions and that many steps are interested in the improvement of every plaque. at the present time, our knowing of the advanced methods of atherogenesis continues to be incomplete.

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134. M. F. 1984. Developmentally regulated production of platelet-derived growth factor-like molecules. Nature 311: 669-671. 135. N. K. 1988. Production of platelet-derived growth factor-like mitogen by smooth-muscle cells from human atheroma. N. Engl. J. Med. 318: 1493-1498. 136. P. M. 1988. Expression and developmental control of platelet-derived growth factor A-chain and B-chain/Sis genes in rat aortic smooth muscle cells. Proc. Natl. Acad. Sci. 85: 1524-1528. 137. , Thyberg, J. H. 1985. Arterial smooth muscle cells in primary culture produce a platelet-derived growth factor-like protein.

1976. Alterations in population dynamics of arterial smooth muscle cell during atherogenesis. IV. Evidence for a polyclonal origin of hypercholesterolemia dietinduced atherosclerotic lesions in young swine. Exp. Mol. Pathol. 24: 244-260. 116. A. F. 1979. Population dynamics of arterial cells during atherogenesis. VIII. Separation of the roles of injury and growth stimulation in early aortic atherogenesis in swine originating in preexisting intimal smooth muscle cell masses. Exp. Mol. Pathol. 31: 124-144.

Thus, tensile strain of arteries can vary by more than 25% with physiological adjustments of arterial pressure l , but physiological shear strains are below 1%2. Nonetheless, shear stress can elicit significant physiological and pathological responses from vascular tissues, primarily through their influence on endothelial cells, which are in direct contact with flowing blood. Arterial Responses to Shear Forces There is now much evidence that endothelial cells, which are in direct contact with blood flow, and are not embedded in matrix, are exquisitely sensitive to shear stress.

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