An X-ray evidence for the ring-stacking interaction between indole ring ad the pyrimidine moiety of thiamin: crystal structure of thiamin indole-3-propionate.
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Biomedical subjects
Publications and source records attributed to T Ishida.
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The ability of sulfhydryl compounds to provide protection against the acute toxicity of morphinone was investigated in mice. Subcutaneous administration of morphinone produced a reduction of hepatic non-protein sulfhydryl concentration. Pretreatments of mice with glutathione or cysteine significantly increased the survival rate of mice given a lethal dose of morphinone, whereas morphinone lethality was markedly potentiated by diethyl maleate. On the other hand, the administration of morphine produce a dose dependent reduction of hepatic non-protein sulfhydryl contents. However, neither glutathione nor cysteine protected mice from the acute toxicity of morphine. A possible explanation for these observations was proposed as follows: morphine is oxidized by morphine 6-dehydrogenase to morphinone, and the morphinone thus produced decreases the sulfhydryl contents in the liver. This mechanism is supported by the fact that morphinone reacts easily with glutathione and cysteine in vitro.
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Fibrin contains a factor which promotes growth of the mesenchymal cells and such may be related tissue repair. Effects of fibrin and fibrinogen degradation products (FDP) on the growth of smooth muscle cells (SMC) of rabbit aortas in culture were investigated, in relation to atherogenesis. Fibrin, free from plasminogen enhanced the proliferation of SMC during the experimental period of 48 h. Fibrin, rich in plasminogen also stimulated the proliferation of SMC within 24 h, but inhibited it after 48 h. FDP (fragments D and E) inhibited the proliferation of SMC. SMC of rabbit aortas demonstrated plasminogen activator activity. Thrombin and urokinase exhibited no promoting effects on the growth of SMC. These results support the hypothesis that the proliferation of SMC is stimulated by fibrin and later inhibited by FDP, as produced by the fibrinolytic activity of SMC. It is proposed that the metabolism of fibrin in the arterial wall may be of importance in the regulation of SMC proliferation and that the coagulation-fibrinolysis system may play a significant role in atherogenesis.
A case of teratoma of the neck in a newborn is presented. Teratoma of the neck is a rare lesion and is mostly found in the newborn, but in some cases in the fetus and stillborn infant. Although in this case prenatal diagnosis was possible via ultrasonography, the infant did not survive because of respiratory distress. Hence, urgent surgery is imperative in such cases.
In addition to six metabolites of oxycodone which were reported previously, 7 beta-hydroxy-6 beta-oxycodol was further isolated as one of the major metabolites in rabbits. The structure of this novel metabolite was characterized by mass and nuclear magnetic resonance spectra. Such a metabolite possessing vicinal hydroxyl groups in aliphatic ring is very new in the metabolism of narcotic analgesics.
Determination of oxycodone metabolites excreted in urines and feces of several mammalian species was studied by use of the tritium labeled compound. It was found that the radioactivity was excreted more in the urines than in the feces in rabbits, guinea pigs and mice, but not in rats, who eliminated it equally into the urines and feces. Most of the radioactivity was excreted in 48 h after the administration. Seven metabolites, oxymorphone, 6 alpha-oxycodol, 6 beta-oxycodol, 7 beta-hydroxy-6 beta-oxycodol, noroxycodone, oxycodone N-oxide, and 6 alpha-oxycodol, N-oxide, as well as well as unchanged oxycodone, were found to be excreted into urines of rabbits in both free and conjugated forms except two N-oxides, which were found only in the free form. It was discussed that analgesic effect of oxycodone would mainly be attributable to the oxycodone itself, but not to the metabolites.
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Adult female ICR mice were able to produce high titered neutralizing antibodies to mouse hepatitis virus (MHV) by repeated intraperitoneal injections of formalin-inactivated virus. Offspring sucklings born to the immunized dams resisted to MHV causing fatal diarrhea, when their dams had a complement fixing antibody titer of 1:5 or higher. The protection was found to be mediated mainly through neutralizing IgG antibodies in the milk. Sucklings from non-immune dams were also protected by foster-nursing by immune mothers.
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