[Reevaluation of the clinical parameters of experimental gingivitis in man].
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Biomedical subjects
Publications and source records attributed to M Iwata.
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T lymphocytes of rats treated with Bordetella pertussis vaccine (BP) formed a soluble factor that enhanced the glycosylation of IgE-binding factors during their biosynthesis, and provided the latter factors with the biologic activity to potentiate the IgE response. The present experiments demonstrated that pertussigen (leukocytosis-promoting factor) from BP induced normal rat spleen cells to form the glycosylation-enhancing factor. The same factor was obtained by incubation of normal spleen cells with 5 micrograms/ml, but not 2 micrograms/ml, concanavalin A. When normal rat mesenteric lymph node cells were incubated with the glycosylation-enhancing factor together with IgE, IgE-binding factors formed by the cells selectively potentiated the IgE response. The IgE-binding factors formed by the same cells upon incubation with IgE alone neither enhanced nor suppressed the IgE response. The glycosylation-enhancing factor changed the nature of IgE-binding factors formed by the rat-mouse T cell hybridoma, 23A4. IgE-binding factors induced by IgE alone lacked affinity for lentil lectin, whereas those induced by IgE in the presence of the glycosylation-enhancing factor had affinity for the lectin. The cell source of the glycosylation-enhancing factor appeared to be W 3/25+ Fc gamma R+ T cells. The glycosylation-enhancing factor was protein in nature and had a m.w. of about 25,000. The factor had affinity for acid-treated Sepharose and could be recovered from the beads by elution with lactose. The factor was different from interleukin 2 with respect to both its affinity for galactose and its isoelectric point.
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A study was made of the possibility that the maltose infusion, which had good clinical results against intrauterine growth retardation, can change the amino acid composition in maternal and, or fetal blood. We have done a comparative study with maltose-infusion and non-infusion groups in spontaneous delivery. Amino acid, maltose, glucose, glutamine dehydrogenase (GLDH), isocitrate dehydrogenase (ICDH), gamma-glutamyl transpeptidase (GGTP) and blood urea nitrogen were analyzed in maternal venous (MV), umbilical venous (UV) and umbilical arterial blood (UA). The following results were obtained: Blood glucose were significantly higher in MV and UV in the infusion group. Maltose had a significant correlation only between UV and UA. Glucose and maltose had no significant correlation. Valine, tyrosine and ethanolamine were significantly lower in MV with infusion. Aspartic acid in UA was significantly lower with infusion. Phenylalanine in UV had a significant correlation (r = -0.58) with the maltose level. Activities of GLDH, ICDH, GGTP and BUN did not change significantly following maltose infusion. These results suggest that clinical efficiency of maltose infusion can be based not only in the increased supply of glucose but also the efficient use of transported amino acid in the fetus.
HeLa cells grown in a monolayer culture and in nude mice were exposed to graded dose rates (37, 55 or 200 rad/hour) and doses (500-2,000 rad) of radiation and analyzed in terms of their cell cycle distribution using flow-microfluorometry. In the case of the cultured HeLa cells, dose-survival curves were constructed using colony formation as the end-point. The HeLa cells, both in vitro and in vivo, accumulated in G2-M phases after both acute and chronic irradiation. The dose rate of 37 rad/hour proved to be the most effective in producing G2-M accumulation, which is the sensitive phase of the cell cycle. In comparing the G2-M accumulation to the irradiation time, 55 and 37 rad/hour proved to be similarly efficient in producing G2-M accumulation, both in vitro and in vivo. When survival of HeLa cells in vitro was studied, the radiation-induced changes in cell distribution correlated with cell survival and accounted for the change in the dose rate effect above 1,000 rads. In the case of in vivo HeLa cells, the decrease in the number of G0+G1 stage cells was demonstrated during chronic irradiation (37 and 55 rad/hour). The two low dose rates were equally efficient in producing a decrease in the number of G0 + G1 cells. These data indicate that chronic irradiation induces redistribution and recruitment more effectively than acute irradiation.
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Petroleum benzine is one of the mixtures of organic solvents containing n-hexane. The occurrence of polyneuropathy in the workers using petroleum benzines is attributed mainly to n-hexane, though other hydrocarbons present are also suspected of having some neurotoxicity or some potential which could modify the neurotoxicity of n-hexane. The present experiment was performed in order to clarify the toxicity of petroleum benzine to the peripheral nerve and compare it with that of n-hexane. Forty rats were randomly divided into five groups. The groups were exposed to 200 ppm n-hexane, 500 ppm n-hexane, and petroleum benzine vapor containing 200 ppm n-hexane or 500 ppm n-hexane, together with aliphatic and aromatic hydrocarbons for 12 h a day for 24 weeks. The body weight, motor nerve conduction velocity, motor distal latency, and mixed nerve conduction velocities were measured before exposure and every 4 weeks of exposure. A rat from each exposed group was histopathologically examined after 24 weeks' exposure. The function of the peripheral nerve was conspicuously impaired by 500 ppm n-hexane, slightly impaired by 200 ppm n-hexane and petroleum benzine containing 500 ppm n-hexane, and even less impaired by petroleum benzine containing 200 ppm n-hexane. Degenerations of the myelin sheaths and axons were demonstrated in all exposed groups upon examination of the revealed tail nerves. Thus, the experiment revealed that petroleum benzine could impair the peripheral nerves, while some components of petroleum benzine were considered to inhibit the neurotoxicity of n-hexane.
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The anterior sacral horns and external anal sphincter muscle were examined histologically with special reference to Onuf's nucleus in amyotrophic lateral sclerosis (ALS) and Shy-Drager syndrome. Onuf's nucleus and the external anal sphincter muscles were well preserved in ALS, but in Shy-Drager syndrome both structures showed marked degenerative changes. These findings suggest that Onuf's nucleus does not belong to the autonomic neurons, but to the motoneurons in anterior sacral horn, and it innervates the external sphincter muscles of the anus and urethra.
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BALB/C mice were immunized with conjugate of benzylpenicillin or ampicillin with Ascaris suum extract. The mice developed IgE antibodies to penicillin, which were found to react with commercially available penicillin preparations in the PCA system. Elimination of polymerized penicillin by Sephadex chromatography from tested preparations could not diminish their activities to elicit PCA. High pressure liquid chromatographic (HPLC) separation of PcG preparation yielded fractions unable to elicit PCA. On the other hand, all fractions from ABPC retained the activity even after the HPLC purification. A comparative estimation of cross-reactivity of IgE and IgE antipenicillin antibodies showed that IgE antibodies cross-reacted with a variety of beta-lactam antibiotics in a high degree.
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Carcinogenicity study of cholestyramine, an anti-hypercholesterolemic agent, was carried out by feeding B6C3F1 mice of both sexes with the pellet diet in which cholestyramine was admixed at the rates of 1.25, 2.5 and 5%. The animals were fed on the drug-admixed diet for 18 months and on a normal diet for subsequent 3 months. After 32 weeks the mortality of male mice began to increase in the 5% cholestyramine group and the number of dead or moribund mice increased markedly after 60 weeks. Hemorrhage recognized in pleural cavity, heart and other organs, was suggested to be the main cause of death. Some kinds of tumors occurred in each group, but the tumor-incidences seen in mice of 1.25 and 2.5% cholestyramine groups were similar to those in mice of the control group and the occurrence of the specific tumor or an acceleration of tumor-development by feeding cholestyramine were not observed. Furthermore, the tumor-incidence in mice fed on the 5% cholestyramine diet was less than that in mice of the other three groups.
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