Anesthesia and von Hippel-Lindau disease associated with pheochromocytoma.
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Biomedical subjects
Publications and source records attributed to K Mikawa.
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A randomised, controlled, single blind trial was conducted in office workers with mild hypertension (systolic blood pressure (SBP) 140 to 180 mmHg, diastolic blood pressure (DBP) 90 to 110 mmHg) to determine the effect of decreasing alcohol consumption. After a baseline examination, 50 male volunteers aged 30 to 59 were randomised to two groups. Group A were told to abstain from or reduce alcohol consumption for two weeks, while group B were instructed to maintain their usual alcohol consumption. Complete records were obtained on 49 subjects. The daily alcohol consumption of groups A and B at baseline was similar, i.e. 71.9 ml and 72.5 ml of ethanol, respectively, and changed to 16.1 ml and 62.9 ml, respectively, during the experiment. After two weeks, group A were asked to resume their normal consumption whilst group B were asked to reduce or abstain (phase II). However in view of a treatment period interaction, statistical analysis was confined to phase I. During phase I, group A, whose alcohol consumption had reduced, showed decreases of 5.8 and 7.1 mmHg in SBP during the the first and second weeks, respectively. In group B, these decreases were only 0.6 and 1.9 mmHg, respectively. The difference between the falls in SBP in groups A and B was significant (P = 0.005) as judged by analysis of variance. The DBP also decreased, but there was no significant difference between the decreases in the two groups. Changes in gamma-glutamyl-transpeptidase, a biochemical marker of alcohol consumption, from the initial values to the end of phase I were significantly different in groups A and B.(ABSTRACT TRUNCATED AT 250 WORDS)
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The action of rennin on kappa-casein was studied as a function of time, employing turbidity measurements at 610 nm and the release of nonprotein nitrogen. kappa-Casein was converted to para-kappa-casein by the action of rennin. The para-kappa-casein aggregated to increase turbidity and then precipitated. Turbidity development was enhanced initially and then retarded severely by increasing concentrations of added alpha s- and beta-casein. The addition of selected amino acids and salts had variable effects on increase of turbidity.
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Sequential histochemical studies were conducted to determine the level of monoamine oxidase (MAO) activity in the infarcted tissue of the experimental myocardial infarction in dog. MAO activity was not found in the normal heart muscle, but the activities were present in the wall of the coronary artery histochemically. Fibroblasts and collagen fibers began to take the place of the destroyed heart muscles in the infarcted area from 10 days after the coronary occlusion in dogs, and MAO activities were noted sporadically in the fibroblasts and the interstices of the collagen fibers in the infarcted area. MAO activities increased histochemically in the fibroblasts and the fiber interstices in the infarcted area 10 days or more after the coronary occlusion. These findings suggested the presence of the active collagen metabolism outside the myocardial cells in the infarcted area in the recovery stage of the experimental myocardial infarction. It was also suggested that the interstices of the collagen fibers in the myocardial wall constituted the lymphatic ducts outside the blood vessels and that the MAO activity in serum determined by the method in which tryptamine hydrochloride was used as substrate might indicate the grade of fibrosis of the myocardial tissue in the infarcted areas.
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