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A Mixed Legal System in Transition
This collection of essays considers the work of Professor Sir Thomas Smith QC (1915-1988) and, through that work, the development of Scots law as a mixed legal system.
Factors in Formation and Regression of the Atherosclerotic Plaque
Interest in the field of atherosclerosis research has broadened in recent years. However the main focus remains on the physiopathology of the arterial wall and on its interaction with blood constituents. The purpose of this NATO Advanced Study Institute on "Factors in Formation and Regression of the Atherosclerotic Plaque" was to discuss the following points: a) The physiopathology of the arterial wall; b) Animal models; c) Methods of studying the progression and regression of atherosclerotic lesions quantitatively; d) The role of lipoproteins, platelets, smoke, alcohol, etc. in the formation of atherosclerotic lesions; e) The pharmacological and dietary control of "risk factors." This volume is a collection of the most relevant presentations on these topics. We hope it will provide a background for young scientists as well as a stimulus for further research to biologists and clinicians. We wish to acknowledge the support of NATO and the Nutrition Foundation of Italy in organizing this Advanced Study Institute.
Pathobiology of the Human Atherosclerotic Plaque
Seymour Glagov The last meeting, devoted exclusively to an examination of the atherosclerotic plaque, took place in Chicago 25 years ago under the joint auspices of the Council on Arteriosclerosis of the American Heart Association and the Chicago Heart Association. The proceedings were published subsequently in a volume entitled "Evolution of the Atherosclerotic Plaque", edited by Richard J. Jones (1). Both experimental and human lesions were considered and several provocative new approaches to the disorder were discussed. The electron microscope was being applied systematically to the study of blood vessels at that time, so that details of the infrastructure and cellular composition of the artery wall and of atherosclerotic lesions were presented in some detail. There was, as one result of these explorations, considerable discussion of morphologic evidence suggesting that the principal cell involved in the atherogenic process was neither the fibroblast nor the macrophage, as had been supposed, but the smooth muscle cell. In particular, the findings indicated that this cell could incorporate lipid and become a foam cell.
The Artery and the Process of Arteriosclerosis
Substantial progress toward reconciling disparate theories of the pathogenesis of arteriosclerosis was recorded in Volume I of this book. the proceedings of an interdisciplinary workshop conference held at Lindau. Germany, April 19-25, 1970. Strong evidence was ad duced that the early stages of arteriosclerosis consist of intimal proliferation similar to that associated with the increase in arteri al size and caliber that characterizes normal growth. The findings described recall a theory proposed by Richard Thoma (Thoma and Kaefer, 1889) of Heidelberg toward the end of the nineteenth century. He sug gested that the pathogenesis of arteriosclerosis began with intimal thickening that was init...
Atherogenesis
The Novartis Foundation Series is a popular collection of the proceedings from Novartis Foundation Symposia, in which groups of leading scientists from a range of topics across biology, chemistry and medicine assembled to present papers and discuss results. The Novartis Foundation, originally known as the Ciba Foundation, is well known to scientists and clinicians around the world.
Atherosclerosis III
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Atherosclerosis IV
The presence of monotypism in thick atherosclerotic lesions of black females with G-6-PD mosaicism first reported by the Benditts (1973) has been confirmed in two other laboratories. However, we believe that it is premature to conclude that the finding of monotypism necessarily indicates monoclonal origin of athero sclerotic lesions. We have suggested two alternative explanations for the obser vation of monotypism which we believe must be shown to be invalid before accept ing monoclonal origin as the only plausible way to account for the observed G-6-PD monotypism. One of these two alternatives relates to clonal heterogeneity of cell growth potential, i. e. , during the course of progressive...
