Measurement of the branching fractions for D0--> pi -e+ nu e and D0-->K-e+ nu e and determination of ||Vcd/Vcs||2.
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Biomedical subjects
Publications and source records attributed to C Simopoulos.
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The growth of cultured epithelium like cells from human normal embryonic intestine was studied in response to various hormones using a method that quantifies the number of cells by the amount of dye that they bind after fixation. Gastrin and neurotensin in the pg/ml range and higher caused small increases in cell growth. Glucagon and VIP were stimulatory in the low ng/ml range, whereas somatostatin and bombesin had no effect at the lower concentrations but were stimulatory at the highest concentration tested (10 and 100 ng/ml respectively). Secretin and pancreozymin (cholecystokinin) seemed to be ineffective.
The present study involved evaluation of the role played by cyclic AMP on the secretion and mechanism of action of gastrin in man. On the basis of the results obtained, gastrin secretion induced by an excessive rise in gastric pH is accompanied by a simultaneous increase in plasma cyclic AMP concentrations (p less than 0.05) as well as a tissue cyclic AMP in the region of the fundus (p less than 0.001). By contrast, no significant change was seen regarding antropyloric AMP. As a result, it is felt that cyclic AMP does not play a direct role in the secretion of gastrin by G cells but is a mediator of the mechanism of action of gastrin in terms of the secretion of HCl by the parietal cell.
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Changes on levels gastric acidity, on serum gastrin, cAMP and cGMP levels were studied in 18 healthy volunteers after either stimulation (injection of 0.2 IU of soluble insulin/kg body weight to a group of 9 subjects) or stimulation and inhibition (injection of insulin plus atropine per os to the other group of 9 subjects) of the vagus nerve. After vagus nerve stimulation, gastric acid levels, serum gastrin and cGMP were raised and cAMP reduced. After stimulation and inhibition of vagus nerve, gastrin and cAMP were increased, cGMP reduced and gastric acid levels remained unchanged. These findings suggest that the vagus nerve, and more particularly the acetylcholine released from its metaganglionic fibers, stimulate parietal cells provoking acid secretion, and also stimulate G cells with subsequent gastrin secretion through cGMP.