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Viewing February 1981 — 3 paper(s) from the local store. (Local view only — run without --view to fetch new papers.)
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Also flagged:bile acidtaurinebiosynthesisextracellularbile acidscysteic acid decarboxylase
Journal Article 1981-02-01 No Snippets Ohtomo T, Yoshida K, San Clemente CL.
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Various bile acids were added to cultures of encapsulated strains of Staphylococcus aureus growing in serum-soft agar medium of brain heart infusion broth. We examined effects of these compounds on cellular characteristics such as growth type, cell volume index, clumping factor reaction, slime yield, taurine content, and L-(--)-cysteic acid decarboxylase activity. Upon addition to the medium of either taurochenodeoxycholic acid, taurocholic acid (25 to 50 microgram/ml), or cholic acid (10 to 25 microgram/ml), the colonial morphology of taurine-positive cells (strain S-7) was altered from the diffuse to the compact type in serum-soft agar. Also, the titer of the clumping factor reaction increased, while the cell volume index and slime yield were markedly decreased. Tauro-bile acids, including taurocholic acid, taurochenodeoxycholic acid, taurodehydrocholic acid, and taurodeoxycholic acid (50 microgram/ml) inhibited the synthesis of taurine and resulted in decreased L-(--)-cysteic acid decarboxylase activity. Among all of the derivatives cholic acid itself was found to inhibit slime production and L-(--)-cysteic acid decarboxylase activity to the greatest extent. Glyco-bile acid derivatives and taurolicholic acid (50 to 100 microgram/ml) had no effect on L-(--)-cysteic acid decarboxylase activity. Compounds such as glycodeoxycholic acid (50 to 100 microgram/ml) had no effect upon any of the cellular characteristics tested. No effect was observed upon addition of any of these compounds to cultures of the taurine-negative strain (T-26-B). We did find a correlation between the inhibition of taurine biosynthesis and decreased slime production. Electron micrographs indicated that this encapsulated strain was converted to an unencapsulated state in the presence of bile acids.

Also flagged:estrogen receptorsbreast cancerERestradiolalbuminfluorescein
Journal Article 1981-02-01 ✓ 3 Snippets Tominaga T, Kitamura M, Saito T, Itoh I, Takikawa H.
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Estrogen receptors (ER) in breast cancer tissue were determined in 51 patients by a histochemical method with estradiol-17 beta-bovine serum albumin-fluorescein isothiocyanate conjugate and were compared with those in the adjacent tissue determined by biochemical method, i.e., the sucrose density gradient (SDG) and dextran-coated charcoal (DCC) methods.

The percentage of fluorescent cells to all cancer cells was not related to the number of binding sites of ER determined by the DCC method.

…determined by theDCCmethod.…

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Estrogen receptors (ER) in breast cancer tissue were determined in 51 patients by a histochemical method with estradiol-17 beta-bovine serum albumin-fluorescein isothiocyanate conjugate and were compared with those in the adjacent tissue determined by biochemical method, i.e., the sucrose density gradient (SDG) and dextran-coated charcoal (DCC) methods. Excluding one non-evaluable case, 26 specimens were ER(+) and 24 were ER(-) in histochemical assay. The presence of ER(+) cells in histochemical assay was not related to menopause or to the molecular pattern of ER determined by the ASG method, or to the histological type of cancer. The percentage of fluorescent cells to all cancer cells was not related to the number of binding sites of ER determined by the DCC method. As determined by the histochemical assay, breast cancer cells having ER accounted for 20 to 100% of all cancer cells examined and ER(+) cells were in clumps or intermixed with ER(-) cells in cancer tissue. The co-existence of Er(+) and Er(-) cells may be one reason for the fact that surgical ablation of breast cancer rarely results in complete tumor regression.

Also flagged:antithrombin IIIdeficiencycoagulation inhibitorsthrombotic diseasesynthesis
Journal Article 1981-02-01 ✓ 1 Snippet Scully MF, De Haas H, Chan P, Kakkar VV.
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…decreased antithrombin III (ATIII) measured by a…

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A family including four members with decreased antithrombin III (ATIII) measured by a biological and an immunological method is described. Immunologically measured levels of other coagulation inhibitors were normal. In the antithrombin III deficient family members there was a history of thrombotic disease. Turnover of 125I-antithrombin III in a deficient individual showed the lower plasma levels probably to be due to a deficiency in the rate of synthesis rather than to an increased catabolic rate.