By Giorgio Weber (auth.), Gustav R. V. Born, Alberico L. Catapano, Rodolfo Paoletti (eds.)
Interest within the box of atherosclerosis study has broadened in recent times. but the major concentration is still at the physiopathology of the arterial wall and on its interplay with blood ingredients. the aim of this NATO complex examine Institute on "Factors in Formation and Regression of the Atherosclerotic Plaque" used to be to debate the next issues: a) The physiopathology of the arterial wall; b) Animal types; c) equipment of learning the development and regression of atherosclerotic lesions quantitatively; d) The function of lipoproteins, platelets, smoke, alcohol, and so forth. within the formation of atherosclerotic lesions; e) The pharmacological and nutritional keep watch over of "risk factors." This quantity is a suite of the main correct displays on those subject matters. we are hoping it's going to supply a historical past for younger scientists in addition to a stimulus for additional examine to biologists and clinicians. we want to recognize the help of NATO and the foodstuff origin of Italy in organizing this complicated learn Institute.
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Extra info for Factors in Formation and Regression of the Atherosclerotic Plaque: Proceedings of a NATO Advanced Study Institute on the Formation and Regression of the Atherosclerotic Plaque, held September 3–13, 1980, in Belgirate, Italy
The 52 ELSPETH B. SMITH Table 3. 4 Thrombi: familiar "cauliflower-like encrustations" on ulcerated plaques also contained large amounts of bound lipoprotein; these structures contain masses of flat cholesterol crystals, packed on edge, and covered with endothelium and one or two thin strands of collagen. We do not really know if the LDL binding is primarily associated with invasion of collagen or with the presence of endothelium. In the non-endothelialized free lying fibrin thrombi, mural thrombi and prosthesis graft pseudo-intimas (in which there was no invasion of collagen or SMCs) the concentrations of bound LDL were very low, but so were the concentrations of free LDL and fibrinogen.
10. 11. 12. 13. L. Holman, Atherosclerosis - a pediatric nutrition problem? , 9: 565 (1961). C. , 18: 560 (1968). B. , 12: 1 (1974). D. Velican and C. Velican, Study of fibrous plaques occurring in the coronary arteries of children, Atherosclerosis, 33: 201 (1979). D. Velican and C. Velican, Atherosclerotic involvement of the coronary arteries of adolescents and young adults, Atherosclerosis, 36: 449 (1980). C. Velican and D. Velican, Incidence, topography and lightmicroscopic features of coronary atherosclerotic plaques in adults 26-35 years old, Atherosclerosis, 35: 111 (1980).
5%) Administration on Aortic Metabolism of Rabbits Fed an Atherogenic Diet* (4 Rabbits per Group; Fed 30 Days) B Diet~ Table 6. I ~ -< ~ < CJ) m ::I: (") =i ::c ~ o < o}> o 41 AORTIC LIPID METABOLISM Table 7. 0 - - - - - *Kritchevsky and Singer (30). ; BC t B plus 5% corn oil and 1% cholesterol; BCL, BC plus 1ipanthy1; BCR, BC plus pirinixil. ~(Arch plus Thoracic)+2. §S, nmo1es cholesterol esterified/mg protein/hour. H, nmo1es cholesterol liberated mg protein/hour. REFERENCES 1. 2. 3. 4. 5. A. Windaus, Uber den Gehalt norma1er und AtheromatBser Aorten an Cho1esterin und Cho1esterinestern, Hoppe-Seyler Z.