[Visit with a midwife: Ms. Toshi Sone, marriage counselor at the Welfare Center for the Disabled, Tokyo].
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Biomedical subjects
Publications and source records attributed to M Fujiwara.
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The effects of 14 guanidino compounds on the activity of rabbit brain choline acetyltransferase (CAT) and acetylcholine esterase (ACE) have been studied, comparatively with that of pentylentetrazol. No guanidino compound examined nor pentylentetrazol had an effect on CAT activity. 4 of them showed a moderate inhibitory effect on ACE, of the same order of magnitude as that of pentylentetrazol, but significantly lower than that of the specific inhibitors eserine and mytelase.
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Effects of catecholamines on the contraction of isolated guinea-pig gallbladder induced by transmural stimulation (TM) were investigated. Tetrodotoxin and atropine prevented the TM-induced contraction. Atropine, but not tetrodotoxin, blocked the acetylcholine-induced contraction. Furthermore, the TM-induced contraction was sharply reduced during a cold storage for 1 to 4 days and then abolished 4 to 7 days later. Norepinephrine (5 X 10(-6) M) and epinephrine (4.5 X 10(-6) M) did not affect acetylcholine-induced contraction, but reduced the contractile response to TM by about 40% and 60%, respectively. Phentolamine, but not propranolol, abolished the inhibitory effects of norepinephrine and epinephrine on the contraction induced by TM. Isoproterenol and phenylephrine did not significantly modify the TM-induced contraction. These observations suggest that TM-induced contraction is produced by the release of acetylcholine from the ending of postganglionic cholinergic fibers. The possibility that norepinephrine and epinephrine act on the inhibitory alpha-adrenoreceptors in the ending of cholinergic neuron is discussed.
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Tolerance inducibility was examined in various strains of mice by injecting aggregate-free HGG, followed by challenge with aggregated HGG plus LPS and by assessing spleen PFC numbers. Marked differences were shown between C57BL/6 and DDD mice. The antibody response to HGG was totally suppressed in C57BL/6 mice injected with 0-1 to 1 mg of aggregate-free HGG whereas little suppresssion was observed in DDD mice. Cellular mechanisms of the resistance to tolerance induction in DDD mice were explored. On the injection of 1 mg of aggregate-free HGG, spleen cells were only partially tolerized (at minimum, 21 per cent of control level on 5th day) and thymus cells were suppressed to 40 per cent of the normal responsiveness. No suppression was observed in bone marrow cells. Macrophages do not seem to play a decisive role in the resistance to tolerance induction in DDD mice as the injection of biofiltered HGG or the pretreatment with carrageenan did not ease the resistance. From these data, it was suspected that the resistance to tolerance induction to HGG in DDD mice might be due to the raised threshold of T cells for tolerance.
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Protocatechuate 3,4-dioxygenase (EC 1.13.11.3) has been reported to have a molecular weight of 700,000 and to consist of eight identical subunits, each containing one atom of ferric iron and a substrate binding site. This subunit has now been found to dissociate further into four smaller subunits of two nonidentical types (alpha2beta2), upon sodium dodecyl sulfate gel electrophoresis. The molecular weights of the alpha and beta subunits were estimated to be 22,500 and 25,000, respectively. Isoelectric focusing of the enzyme in 6 M urea revealed that the isoelectric points of the alpha and beta subunits were 5.2 and 9.5, respectively. Separation of the two subunits was achieved by chromatography on sulfopropyl (SP)-Sephadex in 6 M urea after treatment of the enzyme with 8 M urea at 37 degrees C for 6 h. The NH2-terminal sequence of the alpha subunit was determined to be Pro-Ile-Glu-Leu-Leu-Pro-Glu-Thr-Pro-Ser-Glx-Thr-Ala-Gly and that of the beta subunit, Pro-Ala-Gln-Asp-Asn-Ala-Arg-Phe-Val-Ile-Arg-Asx-Arg-Asx. Phenylalanine was found as the COOH-terminal residue of the alpha subunit. However, the COOH terminus of the beta subunit was not detected by any of three methods employed.
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Strain differences in the antibody response to human IgG (HGG) were observed when aggregated HGG was injected intravenously. Lipopolysaccharide (LPS) administered subsequently markedly enhanced the antibody response to HGG in low responder C57BL/6 mice as compared with that in high responder DDD, C3H/He or (C57BL/6 X DDD)F1 mice. Aggregate-free preparation of HGG at a dose of 0.5 mg induced immunological tolerance in all strains of mice tested. LPS injected subsequently converted tolerogenic, aggregate-free HGG into immunogen in DDD mice but not in C57BL/6 mice. To determine the correlation between adjuvanticity and mitogenicity of LPS, spleen cells from normal mice were cultured in the presence of LPS and 3H-thymidine uptake was measured. Spleen cells of DDD mice incorporated three times as much 3H-thymidine as those of C57BL/6 mice. There seems no strong correlation between both activities of LPS. The data obtained are discussed in terms of strain differences in the macrophage function for processing the antigen.