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 a number of questions with reference to the pathogenesis of athero­ sclerosis haven't but been replied, the accrued proof shows major regression of lesions in experimental animals. this is often mentioned generally during this monograph, as are the mechanisms all in favour of regression of lesions. even if human atherosclerosis has the possibility of regression seems to be crucial, yet even as the main tough query to reply to. opposite to experimental atherosclerosis in animals, that are produced and which may regress inside of a couple of months, human lesions regularly improve slowly over decades. as a result, measures geared toward enhancing this method can also require a long time to achieve success. additionally, repeated direct exam of lesions within the human is mostly impossible. however, fresh experiences in sufferers with hyperlipoproteinemias point out that said and maintained keep an eye on of hyperlipidemias could lead on, even inside months, to regression as evidenced by means of 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, even if "atherogenesis": mechanisms or now not there's proof of monoclonal foundation of human atherosclerosis plaques, mobile tradition and components that stimulate tender muscle proliferation, and animal versions of atherogenesis. This part is concluded with a dialogue of nutritional elements except lipids in atherogenesis.

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Atherosclerosis — is it reversible?

Even supposing various questions in regards to the pathogenesis of athero­ sclerosis haven't but been replied, the collected proof shows major regression of lesions in experimental animals. this is often mentioned widely during this monograph, as are the mechanisms all for regression of lesions.

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Am. J. Clin. Nutr. 20, 176-184 (1967). 14. : "Sugars in cardiovascular disease". In: Sugars in nutrition. ). New York: Academic Press 1974, pp. 401-437. 15. : Effect of dietary sucrose and glucose on plasma cholesterol in chicks and rabbits. Proc. Soc. Exp. Biol. Med. 100, 250-252 (1959). 16. : Effect of bread in the diet on serum cholesterol. Am. J. Clin. Nutr. 20, 191-197 (1967). 17. : "Epidemiological data on dietary fat intake and atherosclerosis with an appendix on possible side effects". ).

STRONG. We induced coronary artery and aortic lesions in rhesus monkeys with an atherogenic highcholesterol diet described previously (2, 4). We gave the high-cholesterol diet to 12 groups of monkeys for 12 weeks. Then one group of animals was killed and the diet of 11 groups was changed to lowcholesterol food. We then killed and studied groups of monkeys at intervals of 2, 3, 4, 8, 12, 16, 24, 32, 40 and 64 weeks. One group, still alive, will be killed after 2 years of regression. Mean serum cholesterol levels during the 12-week high-cholesterol diet varied from animal to animal, ranging from 260 to 830 mg/dl.

24. : Factors affecting atherosclerosis in rabbits fed cholesterol-free diets. Life Sci. 4, 1467-1471 (1965) • 25. : Experimental atherosclerosis in rabbits fed cholesterol-free diets: Influence of chow components. J. Atheroscler. Res. ~, 357-369 (1968). 26. : Effect of dietary carbohydrate on the metabolism of cholesterol-4-C14 in chickens. Arch. Biochem. Biophys. 75, 142-147 (1958). 27. : Influence of dietary carbohydrate and protein on serum and liver cholesterol in germ-free chickens. Arch.

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