Development of gastrin activity.
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Biomedical subjects
Publications and source records attributed to O Gregor.
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The hypothesis upon which this study was based is that there is a relationship between mortality from gastrointestinal cancer and living standards. On this basis we found significant correlations between the intake of animal proteins and the mortality rates for gastric and intestinal cancer. The negative correlation coefficient (r = - 0.85) is an expression of the inverse relationship between gastric and intestinal cancer mortality rates. This inverse relationship is also expressed as the correlation between the food intake, expressed by the intake of animal protein, and the respective mortality rates. The higher the food intake, the lower the gastric cancer mortality rate but the higher the intestinal cancer mortality rate. We do not claim that this relationship discovered by correlation analysis is a causal one. On the basis of this study it cannot therefore be said that food intake has a direct effect on the development of gastrointestinal cancer. In this respect our findings can only be a signal for further studies. Secondly no time lag has been proved between food intake and the mortality rate for intestinal cancer. The findings relating to gastric cancer do not contradict the hypothesis of a time lag.
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When tested with isolated, calcium-resistant resting rat cardiocytes in an in vitro assay system, adriamycin exerted a dose-dependent cytotoxic effect which could easily be assessed by the ATP depletion of the heart cells and the loss of vitality as monitored by morphological changes (blebbing, spherical contraction). Apart from extremely high non pharmacological concentrations of verapamil and diltiazem, both calcium antagonists left the cardiocytes intact and without loss of internal ATP when given alone to the medium. Coincubation of adriamycin and verapamil or diltiazem did not increase adriamycin toxicity to the cardiocytes; instead a remarkable ATP preservation by verapamil could be demonstrated when both drugs (adriamycin and verapamil) were incubated simultaneously with the heart cells. This acute protective effect was limited in time and could no longer be detected after 9 hours. Diltiazem in coincubation experiments exerted neither a toxic nor an acute protective effect on adriamycin-exposed heart cells.