Gut flora in HLA B27 related reactive arthropathy.
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Biomedical subjects
Publications and source records attributed to R Kumar.
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A broad area of C-kinase inhibitory activity was detected after DEAE-cellulose chromatography of 20,000 g supernatant of rat stomach homogenate. Attempts to characterize the inhibitory moiety indicated that it was a non-protein, low molecular weight substance which eluted immediately after C-kinase activity. Similar inhibition was observed in the presence of KC1, the salt used in the elution buffer. Several other salts examined also displayed inhibition of C-kinase activity. Kinetic analysis showed that both KC1 and the inhibitor displayed competitive inhibition of histones and gave identical inhibitor constants.
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We have shown previously that the 3-beta-D-glucopyranosides of vitamin D3, 1 alpha-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3 and 25-hydroxyvitamin D3 are biologically active in vivo. In order to determine whether the presence of the beta-D-glucopyranoside moiety linked to either the C-3, the C-25 or the C-1 hydroxyl function of the molecule affected the biological activity of the conjugates 1, 2, or 3 derived from 1,25-dihydroxyvitamin D3, we administered increasing amounts of compounds to vitamin D-deficient rats maintained on a low calcium diet. The aglycone, 1,25-dihydroxyvitamin D3 (4), also was administered to another group of such animals. When administered i.v., all three beta-D-glucopyranosides increased intestinal calcium transport in doses as low as 50 pmol/rat. A dose of approximately 500 pmol/rat was required to increase bone calcium mobilization in these same animals. The three glucosides were found to be equally active in both biological responses. A dose of only 5 pmol of 1,25-dihydroxyvitamin D3 (4) increased both intestinal calcium transport and bone calcium mobilization. We also performed similar experiments after the p.o. administration of these compounds to vitamin D-deficient rats maintained on a low calcium diet. The glucopyranosides 1, 2 and 3 were able to increase calcium transport in the intestine, as well as mobilize bone calcium at doses of between 500 and 5000 pmol/rat. Once again, the compounds were equipotent, but were less active than 1,25-dihydroxyvitamin D3 (4). After the i.v. or p.o. doses of the glucosides, plasma concentrations of 1,25-dihydroxyvitamin D3 increased in a dose-dependent manner. We conclude that: The C-3, C-25 and C-1 beta-D-glucopyranosides of 1,25-dihydroxyvitamin D3 are biologically active and equipotent in vivo, most likely as a result of hydrolysis to the free aglycone and they are less active than the aglycone in this respect.
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The molecular species of ether-linked lipids in the phosphatidylcholine (PC) fraction of the pulmonary surfactant obtained from the lavage fluid of dog were characterized. A combination of base-catalyzed methanolysis, phospholipase C treatment, gas-liquid chromatography, and mass spectrometry procedures were applied. The phospholipid composition of the surfactant, obtained by phosphorus assay of lipids separated by silica gel G thin-layer chromatography (TLC), was: PC (75%), phosphatidylglycerol (10%), phosphatidylethanolamine (7%), plus small amounts of sphingomyelin, phosphatidylinositol, and phosphatidylserine. The major components of the PC were 1,2-diacylPC (95%), and 1-O-alkyl-2-acylPC (5%). No detectable amounts of 1-O-alkyl-1'-enyl-2-acylPC or di-alkyl-1-enylPC were observed. The acyl groups present in the diacylPC were 14:0 (5%), 16:0 (68%), 16:1 (12%), 18:0 (6%), 18:1 (7%) and 18:2 (2%). The predominant alkyl ether chains located at the carbon 1 position of the 1-O-alkyl-2-acylPC were 16:0 (84%), 18:0 (5%) and 18:1 (14%). At the carbon 2 position only a 16:0 fatty acyl residue was detected. In three out of seven animals platelet-activating factor-like activity, as determined by a platelet aggregation assay, was isolated by TLC. This aggregating activity was lost upon base-catalyzed methanolysis, but was restored by functional levels after acetylation.
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By electron diffraction pattern the presence of metallic elements, particularly chromium-nickel, chromium phosphide, copper, aluminum-copper and zinc has been shown in the pineal organ of a freshwater teleost, M. vittatus. It is likely that their occurrence within the pineal is due to binding with the neurosecretory material fractions/ligands.
By sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), the protein profile and autophosphorylation of plasma membranes of red cells from 3-, 9-, 18-, and 30-month-old rats was examined. No major changes in SDS-PAGE protein profiles were noticeable. However, endogenous (auto) and exogenous phosphorylation in the presence of (gamma-32P)ATP showed an age-dependent increase in 32P uptake. pH optimum was between 8.0 and 9.0 for all age groups. Cyclic AMP was without effect on either endogenous or exogenous phosphorylation. Further analysis of the autophosphorylation reaction by quantification of autoradiograms obtained from SDS-PAGE gels displayed an age-dependent increase in phosphorylation of bands 2, 3, 4.1, and 4.5 [nomenclature of Fairbanks et al. Biochemistry 10:2606, 1971] and of several other minor bands. The data imply that alteration in red cell membranes may occur during aging of rats causing an enhancement in endogenous kinase activity and possibly in the number of phosphate acceptor sites as well.
Skin from hairless mice was incubated with two synthetic retinoids, isotretinoin and etretinate, and the cAMP content as well as the activity of cAMP-dependent protein kinase were determined. A crude plasma membrane preparation was used to measure adenylyl cyclase activity. Neither isotretinoin (10(-6) and 10(-5)M) nor etretinate (10(-6)-10(-4)M) produced any significant changes in adenylyl cyclase activity. Tissue cAMP levels also remained unaltered after treatment with these retinoids. Although the protein kinase activity ratios remained constant over the concentration range of each retinoid, absolute protein kinase activity was stimulated by treatment with etretinate. These data suggest that cAMP may not mediate the action of retinoids in skin, and that the stimulation of protein kinase activity caused by etretinate probably involves an alternative mechanism.
The role of humoral antibodies and the effect of BCG vaccination were studied in the experimental candidiasis in mice. The antibody suppressed, B-cell deficient animals were prepared by repeated administration of rabbit anti-mouse-mu-antiserum to the new born mice from birth onwards. Such immunodeficient animals along with controls were infected intravenously with Candida albicans, to study the course of candidal infection. It was observed that B-cell-deficient animals were found to be more susceptible to candidal infection than the controls, as indicated by their steady loss of body weight, longer mean time to death and higher viable counts of candidal cells in different organs. The anti-candidal antibodies were absent in all B-cell-deficient animals but present in the controls. These results suggest that antibodies make a contribution in protection against candidal infection in mice. The BCG vaccinated animals were prepared by repeated intravenous administration of BCG to mice and these vaccinated animals along with unvaccinated controls were challenged intravenously with C. albicans, to study the course of candidal infection. It was observed that BCG vaccination prolonged meantime to death and reduced the number of candidal cells in their kidneys.
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