[Use of computer technology in drug supply in East Germany].
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Biomedical subjects
Publications and source records attributed to C Becker.
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Histologic evidence of intrarenal vasomotor changes were observed in the rat in the course of acute renal failure caused by the injection of HgCl2. Male Wistar rats injected s.c. with 2.5 or 4.7 mg HgCl2 per kg b. wt. developed fibrinoid damage in the media segments of preglomerular renal vessels, mostly in the arcuate and interlobular arteries. The lesions were patchy and irregularly scattered throughout the kidneys. 24 h post-injection the lesions were very rare and of only mild degree, whereas they were fully developed and regularly seen 48 h post-injection. A high percentage of similar changes was found in certain extrarenal vascular areas especially in the mesentery and pancreas. The damaged vascular segments were usually dilated. The results of various thichrome stains and histochemical reactions suggested edema of vascular smooth muscle cells and imbibition of the media by blood plasma substances, sometimes reaching the degree of fibrinoid necrosis. These findings were confirmed by electron microscopy. The imbibition of the smooth muscle cells by blood plasma material was clearly evidenced by the demonstration of intracellular fibrin precipitations. In connection with the degeneration of smooth muscle cells, accumulations of crystal-like fibrin formations could often be shown. Subendothelial fibrin formations were not observed. 96 h after the 2.5 mg injection the changes were already regressing, but edema of the vascular wall and signs of disturbed vasotonia persisted for several days. The maximum of the vascular changes usually coincided with the maximum of azotemia and the formation of debris cylinders in the renal tubules. However, no clear relationship was recognizable in individual cases between vascular damage, extent of tubular necrosis and renal function. The pathogenesis of the vascular changes is obscure, but neurogenic factors, increased release of catecholamines and/or vasoactive agents of renal origin in connection with other factors might play a decisive role. Arterial hypertension was absent. It is assumed that the structural damage of the vascular media is mainly brought about by prolonged or recurring vasospasms, or by alternating spasm and vasodilatation with local ischemia and increased tension of the vascular wall in the dilated segments. The altered function and structure of the vascular wall might, to a certain extent, contribute to renal insufficiency.
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Total mortality showed no association with heavy coffee consumption in the four race-sex groups of Evans County. Deaths from coronary heart disease in WM, WF and BM showed no statistically significant differences between the two coffee consuming groups. Sex differences in cerebrovascular death rates, consistent in both races, suggest the possibility for a female excess of stroke deaths among coffee drinkers, and a "protective" effect of coffee drinking among males. Thus, in an area of the United States which has been designated the "Stroke Belt", neither the cardiovascular nor the cerebrovascular death rates seem strongly nor consistently related to coffee drinking habits. Although the number of deaths (339) is fairly large, representing a 13% mortality in this community over a four and one-half year observation period, the classification in four race-sex groups with further division into the groups with different coffee drinking habits limits each stratum to rather small numbers. In addition, 86 cases of CHD and CVD were diagnosed during lifetime already and, therefore, were excluded from the prospective mortality study. Confidently to refute or confirm the allegations of a detrimental influence of high coffee intake on ischemic heart disease one would need larger numbers. But in the light of our most important finding--that mortality from all causes is not increased in the high coffee consuming group--the finding of increased ischemic heart disease death rates with high coffee consumption would have to be compensated by a provocative, lower rate for other causes of death.
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In 1961, blood pressure was measured in the 40-69-year-old segment of the population of Evans County, Georgia. Mortality was monitored for up to ten years. The relationship found between hypertension and mortality is characterized in this report by four parameters: attributable risk, prevalence, population attributable risk, and population attributable fraction. Attributable risk of death, a measure of the over-all impact of hypertension on those in each race-sex group with hypertension, is high in white males, black males, and black females, and is lowest in white females. Population attributable risk, a measure of the impact of hypertension on each entire race-sex group, is highest in black males and females due to the high prevalence of hypertension in blacks. It is somewhat lower in white males and lowest in white females. The fraction of all deaths attributable to hypertension (population attributable fraction) is highest in black females and lower in the other three groups. The population attributable fraction (ranging from 0.26 to 0.54 for systolic hypertension) is of such magnitude that if the 50% reduction in mortality achieved in the Veteran Administration Cooperative Study could be repeated in the general population, life expectancy after 40 years of age could be substantially increased.
During the past several years we have progressed from the use of perfluorinated substances, which were good gas solvents but often produced unexpected physiological reactions, to a point where emulsions of pure perfluorinated substances can be made in a reproducible way. A standardized method of making emulsions has now been developed. The physical properties of the perfluorinated substances needed to make useful emulsions have been defined. Specifically, perfluorinated substances having vapor pressures above about 40 torr must be avoided as they produce pulmonary gas embolism; also lower boiling components having vapor pressures above about 40 torr must be excluded. The relationship between chemical structure and several physiological and pharmacological effects has been delineated. Perfluorinated substances containing only carbon and fluorine, or those containing carbon, fluorine, and either bromine or iodine have reasonably short dwell times in the liver. Perfluorinated iodo- and bromo-compounds dissolve oxygen and are radiopaque. Present iodo-perfluorinates are unstable in the presence of light. Perfluorodecalin can enter and leave the liver without changing the liver's ultrastructure. Both egg phospholipid and Pluronic F68 are useful in making perfluorodecalin emulsions. Perfluorodimethyladamantane makes a fine-particle stable emulsion. There is a bright future for perfluorinated substances in a number of areas of research in biology and medicine.
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Perfluorinated organic liquids are useful as high capacity oxygen and carbon dioxide solvents. After intravenous infusion most of these perfluorinated emulsions are deposited in the liver and spleen in a matter of days, where they remain for the lifetime of the animal. Hence, while they may be useful as isolated organ perfusion media their value as artificial blood is limited. A family of perfluorocarbons has now been discovered, which, although deposited in the liver after circulation in the blood, leave the liver to be excreted via the lungs and skin in a matter of days without apparent harmn to the animal.
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