[Influence on the cochlea of guinea pig by long termed exposure of band noise: observations by means of surface preparation technique (author's transl)].
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Biomedical subjects
Publications and source records attributed to N Yamada.
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Brain DNA synthesis was developmentally investigated in Gunn rat with marked cerebellar hypoplasia due to hereditary hyperbilirubinemia. In this mutant rat, the Purkinje cell was nearly selectively affected in the cerebellar cortex by bilirubin. The impaired DNA synthesis was observed in homozygous (jj) Gunn rat cerebellum, in which the DNA content and [3H]thymidine incorporation rate into DNA decreased after 10 days of age compared to those in the heterozygous (Jj)littermate. In contrast, these impairments were not found in the non-cerebellar parts of the brain and liver of jj Gunn rat. The activity of cerebellar thymidine kinase in jj Gunn rat decreased from a very early stae, being 80% of Jj rat at 6 days, and 50% at 10 days of age. The enzyme activity was not affected in the non-cerebellar parts of the brain. Although bilirubin competitively inhibited cerebellar thymidine kinase activity in vitro (15% at 10(-5) M), such bilirubin level was found to be about 1000-fold that in vivo. Moreover, photo-degradation of bilirubin in jj cerebellum exhibited no improvement in thymidine kinase activity, and the presence of an enzyme inactivator was not suggested in jj cerebellum. These results seem to indicate that the induction of thymidine kinase might be affected in jj Gunn rat cerebellum. The possibility that the impaired DNA synthesis in the external granular cells in jj cerebellum may be due to Purkinje cell damage is discussed.
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Thyroid-microsomal antibodies were quantitated by a new technique utilizing tanned sheep red blood cells coated with human thyroid microsomal antigens. This haemagglutination assay (MCHA) correlated with the immunofluorescent antibody (FAB) but not with the thyroglobulin haemagglutination antibodies (TGHA) assay. Of forty-one patients with Hasmimoto's thyroiditis, thirty-nine (95%) were MCHA but only twenty-four (59%) TGHA positive. Titres were similar for the hypothyroid and euthyroid patients. Patients less than 20 years of age had either negative (50%) or low titre (less than 1:160) TGHA but 100% positive MCHA at titres greater than 1:1280. Of twenty-one patients with Graves' disease eighteen (86%) were MCHA and six (29%) TGHA positive. Of thirty-two patients without thyroid disease eleven (34%) were MCHA and/or TGHA positive. On the basis of family history and associated abnormalities, in eight of eleven, positive antibodies may have been due to subclinical Hashimoto's thyroiditis. Fourteen subjects of a control group (10%) were MCHA positive. Seven of ten examined had goitres. MCHA is a simple and quantitative test, useful in the diagnosis of autoimmune thyroid diseases.
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