Atherosclerosis — is it reversible? by R. W. Wissler (auth.), Prof.Dr. Gotthard Schettler, Dr.

By R. W. Wissler (auth.), Prof.Dr. Gotthard Schettler, Dr. Eduard Friedrich Stange, Ph. D., M. D. Robert W. Wissler (eds.)

Even even though various questions in regards to the pathogenesis of athero­ sclerosis haven't but been responded, the gathered facts shows major regression of lesions in experimental animals. this can be mentioned largely during this monograph, as are the mechanisms curious about regression of lesions. even if human atherosclerosis has the possibility of regression seems to be an important, yet while the main tough query to respond to. opposite to experimental atherosclerosis in animals, which are produced and that may regress inside of a couple of months, human lesions more often than not advance slowly over a long time. accordingly, measures geared toward enhancing this method can also require decades to achieve success. additionally, repeated direct exam of lesions within the human is mostly impossible. however, fresh stories in sufferers with hyperlipoproteinemias point out that suggested and maintained keep watch over of hyperlipidemias could lead on, even inside of months, to regression as evidenced via angiography or subtle measurements of peripheral flow. The monograph is split into sections. the 1st will take care of of lipid deposition within the arterial wall, no matter if "atherogenesis": mechanisms or no longer there's proof of monoclonal starting place of human atherosclerosis plaques, cellphone tradition and components that stimulate delicate muscle proliferation, and animal types of atherogenesis. This part is concluded with a dialogue of nutritional elements except lipids in atherogenesis.

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31. : Hypercholesterolemia and atherosclerosis induced in vervet monkeys by cholesterol-free, semisynthetic diets. S. Afr. Med. J. ~, 2413-2414 (1974). 32. : Isocaloric, isogravic diets in rats. III. Effects of nonnutritive fiber (cellulose and alfalfa) on cholesterol metabolism. Nutr. Rep. Int. 9, 301-308 (1974). 33. : Hypercholesteremia and atherosclerosis induced in rabbits by purified high fat rations devoid of cholesterol. Proc. Soc. EXp. Biol. Med. 22, 544-549 (1958). 34. : Mechanism of the cholesteroldepressing effect of pectin in the cholesterol-fed rat.

It all depends on what we believe pathogenesis is. If we believe, that lipid deposition occurs because of intracellular esterification of cholesterol, we do not think that this occurs in lysosomes. , the endoplasmic reticulum. Lipid deposition occurs in the form of droplets, maybe in analogy to what is happening in the fatty liver, where you have formation of triglycerides. The lysosomes can be involved in degradation, but I really do not think that they are involved in the synthesis. 32 Regression Components ofthe Lesion and Regression S.

Exp. Biol. Med. 110, 580-582 (1962). 9. : Hypocholesterolemic activity of mucilaginous polysaccharides in white leghorn cockerels. Proc. Soc. Exp. Biol. Med. 123, 321-326 (1966). 27 10. : The retardation by pectin of cholesterol-induced atherosclerosis in the fowl. J. Atheroscler. Res. ~, 292-298 (1966). 11. : Effect of trivalent chromium on glucose tolerance. Metabolism 15, 510-520 (1966). 12. : Nutrition in the United States, 1900-1974. Cancer Res. 35, 3246-3253 (1975). 13. : Dietary carbohydrates and serum cholesterol.

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