[Partial gastric diverticula (author's transl)].
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Biomedical subjects
Publications and source records attributed to K Kitagawa.
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Hand-grip strength, elbow flexion strength, trunk extension strength and knee extension strength, and body composition (measured by densitometry) were measured in 59 male students (mean 19.2 years) in order to compare the muscle strength of obese men, in relation to fat storage rate (% fat), with those of non-obese men. Their % fat ranged from 6.2-35.6%. Correlations of body weight and lean body mass were found to be significant with each muscle strength. Our findings presented that obese men had lower muscle strengths for body weight and lean body mass than non-obese men do. This might be the result of two characteristics, inactivity and weak willpower, of obese men. Besides, the 20% fat of threshold of obesity for men proposed by Behnke and Wilmore was reasonable from the viewpoint of the muscle strength because of the differences between group D (18.8% fat) and group E (23.8% fat).
Experimental colitis was induced in rabbits either by immunizing the antigens which possess the cross-reacting antigenicity with colonic mucosa, and by infusing intravenously their own lymphocytes sensitized with E. coli 014 endotoxin which may contain a high concentration of common antigen (Kunin antigen). The hemorrhagic inflammatory changes were developed in the colon as follows; (1) three of fifteen rabbits immunized with rat colon, (2) one of three rabbits with their own E. coli, (3) six of fifteen rabbits with E. coli 014 and, (4) five of eight rabbits by infusing their own lymphocytes sensitized with E. coli 014 endotoxin. It was suggested that the cross-reacting antigenicity with the colonic mucosa and the sensitized lymphocytes implicate in the pathogenesis of chronic ulcerative colitis.
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Crude mitochondrial P2 fractions from bovine hypothalamus and substantia nigra, slices from rabbit spinal cord and mesencephalon and glial fractions from rabbit brain were incubated with [3H]-substance P and the uptake was measured and compared with those for 5-HT and GABA. Substance P was to some extent taken up into the fractions but this uptake was neither temperature nor time dependent and the pellet/medium ratios were less than 1. Similar results were obtained in high potassium treated slices from rabbit mesencephalon. The rate of uptake for [3H]-substance P increased linearly in proportion to the medium concentration, suggesting a non-saturable binding. These results, together with our previous observations provide strong evidence that nerve terminals and glial cells lack a temperature sensitive, active uptake system capable of terminating transmitter action of substance P at the synapse.
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Extracellular recordings were made from neurones in the mesencephalic reticular formation and substantianigra of the rat which was anaesthetized with urethane 1.5-2 g/kg i.p. Out of 44 cells tested 42 were excited by Substance P applied iontophoretically and in some cases this excitation was rapid. Evidence is presented for Substance P as a putative excitatory transmitter onto reticular and nigral neurones possibly released from primary sensory afferents.
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The mechanism of inactivation of a single-stranded DNA phage, deltaA of Escherichia coli, by AsA was investigated as a part of the study on the mechanism of inactivation of viruses by AsA. Bubbling air or oxygen gas through the reaction mixture, and the addition of oxidizing agents or transition metals into the reaction mixture enhanced the inactivation of the phage by AsA. In contrast, nitrogen gas bubling, and the addition of reducing agents, chelating agents or radical scavengers prevented inactivation. The rate of inactivation was faster in the AsA solution preincubated for several minutes than in the freshly prepared AsA solution. DAsA, an oxidized form of AsA, demonstrated little effect on the activity of the phage. Concentrations of hydrogen peroxide which were theoretically produced by the autoxidation of AsA had no effect on the phage. The results indicated that the free radical intermediates produced during the course of the autoxidation of AsA participated in the inactivation. The radicals attacked the DNA of the phage to introduce strand scissions in the DNA, which might be mainly responsible for the inactivation.
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