[The place of puncture of sub-retinal fluid in the surgical treatment of retinal detachment].
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Biomedical subjects
Publications and source records attributed to A Wade.
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Normal, male Sprague-Dawley (S-D) rats and female, lean and obese Zucker rats were studied in the fed state and after 48 hours of food deprivation. Somatostatin-like immunoreactivity (SLI) was measured from acetic acid extracts of oesophagus-cardia, stomach, small and large intestine, pancreas, hypothalamus, pituitary and cerebellum. Within the CNS, the highest levels of SLI were found in the hypothalamus, while in the gut, these levels were highest in the stomach and pancreas. All Zucker rats displayed higher hypothalamic levels of SLI than did S-D rats. Obese Zucker rats in the fed state differed from their lean littermates in that SLI levels were lower in oesophagus-cardia, stomach and hypothalamus, while being higher in pancreas and pituitary. The response to starvation in both obese and lean Zucker rats was qualitatively similar, and included significant increases in stomach and oesophagus-cardia SLI, but with a significant fall hypothalamic SLI. We have concluded that the increase in gastrointestinal SLI with starvation in Zucker as well as in S-D rats may represent a significant regulatory mechanism in nutrient homeostasis. We postulate that gastric SLI may decrease the availability of intestinal insulin secretagogues in the fasting state. This adaptive mechanism appears to be intact in the obese Zucker rat.
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The pentagastrin acid-secretion test was used to teach medical students gastric investigation, the structure of a controlled trial, and the application of non-parametric statistics to the analysis of imperfect data. This teaching project also yielded considerable original data from 150 subjects on the extra-gastric effects of pentagastrin and histamine-receptor antagonists. Some, but not all, of the somatic symptoms induced by pentagastrin were abolished by cimetidine; however, the combination of pentagastrin and cimetidine induced a significant (p < 0.02) incidence of dizziness.
1. The metabolism of 4-ethynylbiphenyl has been studied in vitro with subcellular fractions of normal and induced rat liver, and rat intestinal microflora (caecal contents). 2. Oxidation was NADPH-dependent, was inhibited by CO and stimulated by pretreatment with phenobarbitone or 3-methylcholanthrene. 3. Oxidation of the ethynyl group occurred in washed microsomal preparations, but not significantly in soluble fractions. Oxidation of the ethynyl group by a microsomal fraction preceded aromatic hydroxylation and no metabolites containing the intact ethynyl group were detected. 4. The major metabolite in liver fractions was biphenyl-4-ylacetic acid. This was the only product produced by a modified Udenfriend system. 5. Metabolism of 4-ethynylbiphenyl by rat caecal contents under anaerobic conditions produced very small amounts of 4-vinylbiphenyl. 6. In a modified Ames test with Salmonella typhimurium TA98, 4-ethynylbiphenyl gave a weak positive result that was doubled after 'activation' with an induced rat S9 fraction.
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1. 4-Ethynylbiphenyl undergoes extensive metabolism in the rat and the rabbit, involving aromatic hydroxylation and oxidation of the ethynyl group. No metabolites containing the intact ethynyl group were detected. 2. In the rat unchanged 4-ethynylbiphenyl was concentrated initially in the adipose tissue. No other tissues accumulated significant amounts of radioactivity. 3. The major metabolites were the same in both the rat and the rabbit, namely 4'-hydroxybiphenyl-4-ylacetic acid (90-95% of dose) and biphenyl-4-ylacetic acid (2-10% of dose). 4. Excretion was slower in the rat than in the rabbit, probably because of greater biliary and faecal excretion in the rat. Biliary excretion and enterohepatic circulation of biphenyl-4-ylacetic acid and 4'-hydroxybiphenyl-4-ylacetic acid were demonstrated in the rat.
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