Biomedical subjects
Publications and source records attributed to S Tsuruta.
A case of scleredema of Buschke associated with rheumatoid arthritis and Sjögren's syndrome is described. The onset of the skin changes and rheumatoid arthritis was almost simultaneous and the sicca syndrome developed 4 years later.
Since it has been reported that dopamine D2 receptors are elevated in the brain striatum of spontaneously hypertensive (SH) rats, and since both D1 and D2 receptors may interact with one another, we measured the densities of both these receptors in SH rat striatum, as well as those in the normotensive Wistar-Kyoto rat striatum. The D1 receptor density in both strains was virtually the same, 72.9 +/- 2.2 and 71.3 +/- 3.2 pmol/g, respectively (mean +/- SD). The D2 receptor densities were also almost identical, 16.3 +/- 0.6 and 16.8 +/- 1.0 pmol/g, respectively (mean +/- SD). Thus, these data do not support the concept of a dopamine receptor related role in spontaneous hypertension.
Diffused reflectance of dental casting alloys with low noble metal content by the spectrophotometer with an integrating sphere was used to determine the color of the alloy and the tarnish in 0.1% Na2S solution, to study whether or not the tarnish can be affected by the nobility and the microstructure of the alloy. The alloys which had a high atomic ratio of Au + Pt + Pd + In + Zn to Ag had higher tarnish resistance. However the alloys which had high content of In showed two phases, but these alloys had high tarnish resistance. This suggests that alloys which have only a small difference of nobility between the compound and the matrix, and in which the low tarnish resistance area is small, may have a high tarnish resistance.
Cobalt(II) chloride (CoCl2), non-mutagenic by itself, has been tested for mutagenic activity in the presence of 4-substituted pyridines in the test strains of Salmonella typhimurium. CoCl2 was found to be mutagenic in strains TA1537 and TA2637, when combined pyridine, with methyl isonicotinate, 4-methyl-pyridine, 4-ethylpyridine, 4-chloropyridine or 4-bromopyridine. Mixtures of CoCl2 and isonicotinic acid, 4-cyanopyridine, 4-aminopyridine, or 4-dimethylaminopyridine exhibited no mutagenicity. Judging from the spectral observations, such combined mutagenicity may be due to the formation of moderate to weak complexes between these compounds and the Co(II) cation.
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After four days of treatment with 10(-8) M TPA, differentiation of the human T-lymphoblastoid cell line MOLT-4 was induced along the T cell lineage, confirmed by a fall in adenosine deaminase and 5'-ectonucleotidase and a rise in purine nucleoside phosphorylase activity. TPA-treated cells became resistant to the cytotoxic effects of 1-beta-D-arabinofuranosylcytosine (Ara-C), 9-beta-D-arabinofuranosyladenine (Ara-A), and 2-chlorodeoxyadenosine. This was, in part, due to the altered cell cycle distribution (accumulation of cells in the G1 phase), since the toxicity of Ara-C and Ara-A is S phase specific. The diminished rate of Ara-C transport concomitant with Ara-CTP formation after TPA treatment is considered to be the biochemical basis for this acquired resistance.
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The present trial was designed to compare the effect of metoclopramide(MCP) + dexamethasone(DM) (Method A) with that of MCP + DM + lorazepam(Lor) (Method B) in the treatment of CDDP (cis-diamminedichloroplatinum)-induced nausea and vomiting in a randomized fashion. The results were collected by questionnaire given to 50 patients. The dosage of CDDP was 80-100 mg/m2. In addition, MMC and VDS, or VP-16 were used concurrently. Within 24 hours after the administration of CDDP, vomiting was not observed in 72% and 88% of the patients treated with Method A and Method B, respectively, and nausea was not noted in 48% and 68%, respectively. Marked malaise was observed in 36% of patients in the Method A group and in 12% in the Method B group. With respect to the extent of comfort, 16% of patients in the Method A group and 56% in the Method B group felt good. Sixteen percent in the Method A group and 56% in the Method B group were satisfied with the anti-emetic treatment. Thus, Method B was significantly superior to Method A with regard to the degree of comfort and treatment satisfaction.
Mutagenic activities of 4-aminopyridine (4AP), 4-aminoquinoline (4AQ), 9-aminoacridine (9AA) and harman (HM) were examined by the Salmonella test system in the presence of cobalt(II) chloride (CoCl2), which itself is non-mutagenic in this system. Mutagenic activity of the mixture of 9AA and CoCl2 was found to be much higher than that of 9AA alone in strains TA1537 and TA2637. A similar enhancing phenomenon was observed in 4AQ-CoCl2 and HM-CoCl2 mixtures but not in that of 4AP-CoCl2. Judging from visible and nuclear magnetic resonance spectral data, this increased mutagenicity may be attributable to the formation of moderate to weak complexes between these chemicals and the Co(II) cation. A survey of the mutagenicity of several Co(II) complexes supported this interpretation.
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A primary ovarian carcinoid composed of both trabecular and strumal types was studied by histochemical, immunocytochemical, and biochemical techniques. High contents of glucagon, secretin, and calcitonin were demonstrated in the tumor homogenate. All of the tumor cells, irrespective of histologic type, showed properties of argyrophilia and neurosecretory granules on electron microscopy. Glucagon-producing cells were positive in trabecular carcinoid by immunoperoxidase techniques. Bio-Gel P10 gel filtration showed that the molecular weight of major immunoreactive glucagon in tumor was 20,000. It migrated faster than true glucagon after polyacrylamide gel electrophoresis. No clinical symptoms of glucagonoma developed.
Aminopeptidase from dysgerminoma was purified and characterized using L-leucine-beta-naphthylamide as substrate. The enzyme was resistant to puromycin, methionine, amastatin, bastatin, and EDTA, and it was heat labile at 60 degrees C. The enzyme showed the same electrophoretic mobility as pregnant-patient serum oxytocinase CAP1 on polyacrylamide gel electrophoresis. Km value against S-benzylcysteine-p-nitroanilide was 4.2 X 10(-4) M. Oxytocin and vasopressin competitively inhibited the enzyme activity. Molecular weight of the enzyme was estimated to be 80,000 by Sephadex G-200 column chromatography. These results suggest that aminopeptidase from dysgerminoma is an oxytocinase-like enzyme, a placenta-specific protein.