By R. W. Wissler (auth.), Prof.Dr. Gotthard Schettler, Dr. Eduard Friedrich Stange, Ph. D., M. D. Robert W. Wissler (eds.)
Even although a number of questions in regards to the pathogenesis of athero sclerosis haven't but been spoke back, the amassed facts shows major regression of lesions in experimental animals. this is often mentioned largely during this monograph, as are the mechanisms excited about regression of lesions. even if human atherosclerosis has the opportunity of regression seems to be an important, yet while the main tricky query to respond to. opposite to experimental atherosclerosis in animals, which are produced and which could regress inside a number of months, human lesions often advance slowly over a long time. for this reason, measures geared toward enhancing this method can also require decades to achieve success. additionally, repeated direct exam of lesions within the human is generally impossible. however, contemporary stories in sufferers with hyperlipoproteinemias point out that mentioned and maintained keep watch over of hyperlipidemias could lead on, even inside months, to regression as evidenced through angiography or subtle measurements of peripheral move. The monograph is split into sections. the 1st will take care of of lipid deposition within the arterial wall, even if "atherogenesis": mechanisms or no longer there's proof of monoclonal starting place of human atherosclerosis plaques, phone tradition and components that stimulate gentle muscle proliferation, and animal versions of atherogenesis. This part is concluded with a dialogue of nutritional components except lipids in atherogenesis.
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Extra resources for Atherosclerosis — is it reversible?
Although in smooth muscle cells only a small amount of lipid converted to membrane structures, most of the lipid inclusions of foam cells converted to membrane. Furthermore, conversion was slow in smooth muscle cells and rapid in foam cells. In smooth muscle cells, residual membrane-lipid complexes were retained in the cytoplasm for long periods of time, perhaps indefinitely. Macrophage-derived foam cells, on the other hand, soon became necrotic and membrane-lipid complexes were released into the interstitial space.
27. : Influence of dietary carbohydrate and protein on serum and liver cholesterol in germ-free chickens. Arch. Biochem. Biophys. ~, 444-451 (1959). 28 28. : Experimental atherosclerosis in rabbits fed cholesterol-free diets. 2. Influence of various carbohydrates. J. Atheroscler. Res. ~, 697-703 (1968). 29. : Experimental atherosclerosis in rabbits fed cholesterol-free diets. 3. Comparison of fructose and lactose with other carbohydrates. Nutr. Rep. Int. 2, 193-202 (1973). 30. : Lipid metabolism and experimental atherosclerosis in baboons: Influence of cholesterol-free, semi-synthetic diets.
Atherosclerosis and deficiency of essential fatty acids. Lancet 1959/11, 749-751. 39. : Cardiovascular mortality in relation to radio activity and hardness of local water supplies in the USA. Bull. WHO il, 687-697 (1970). 40. : Geochemical environments, trace elements and cardiovascular diseases. Bull. I, 139-150 (1972). 41. : Experimental atherosclerosis and high protein diets. Proc. Soc. EXp. Biol. Med. ~, 543-545 (1940). 42. : Effect of high protein diets on experimental atherosclerosis rabbits.
Atherosclerosis — is it reversible? by R. W. Wissler (auth.), Prof.Dr. Gotthard Schettler, Dr. Eduard Friedrich Stange, Ph. D., M. D. Robert W. Wissler (eds.)