Biomedical subjects
Publications and source records attributed to K Stalter.
We have described a technique for elevating the injured pediatric hand for the patient who is nursed in a crib. This system allows full movement of the patient throughout the length of the crib with little danger for the potential of shoulder dislocation.
In experiments designed to study the mechanism of glucocorticoid hormone induced reductions in rat thymic transcription, adrenalectomized rats were injected with hydrocortisone (50 mg/kg) or control vehicle 12 h prior to sacrifice. Thymic nuclei were used to prepare soluble nuclear extracts containing RNA polymerase II. Nuclear extract RNA polymerases II were then partially purified (600-fold) on DEAE-Sephadex columns and characterized. The responses of partially purified thymic RNA polymerases II from rats treated in vivo with hydrocortisone or vehicle were similar to: pH, temperature, ionic strength, trypsin proteolysis, and inhibition by alpha-amanitin; however, RNA polymerase II from hydrocortisone treated animals was consistently reduced in activity compared to control RNA polymerase II. Determination of the apparent specific activities of peak RNA polymerase II fractions from DEAE-Sephadex columns suggested that the specific activity of RNA polymerase II from hydrocortisone treated animals was reduced compared to RNA polymerase II activity from control animals. The fact that both nuclear extract and partially purified RNA polymerases II from hydrocortisone treated rats were reduced in activity when assayed in reconstituted transcriptive systems suggests a denatured, defective or modified RNA polymerase II molecule acting as a transcription inhibitor. Thermally denatured nucleoplasmic RNA polymerase II fractions were shown to interfere with transcription by native nucleoplasmic RNA polymerase II in vitro, but did not appear to inhibit transcription to he degree observed in vitro following in vivo hydrocortisone administration.
In experiments to determine the mechanism of glucocorticoid induced decreases in thymic transcription, adrenalectomized rats were injected with hydrocortisone (50 mg/kg) or vehicle. Thymic nuclei were used to prepare chromatins and soluble nuclear extracts containing RNA polymerase II for cross-over experiments. With calf thymus DNA or rat thymic chromatins as templates limiting RNA polymerase II from rats treated with hydrocortisone 3 h previously had 130% of the [3H]UMP incorporating activity of RNA polymerase II from control vehicle treated rats. In contrast, limiting RNA polymerase II from rats treated with hydrocortisone 12 h previously had 40-50% of the [3H]UMP incorporating activity of RNA polymerase II from controls. When limiting calf thymus DNA or rat thymic chromatins were used in 12 h cross-over experiments. Individual RNA polymerases II produced equal [3H]UMP incorporations, but RNA polymerase II activity from hydrocortisone treated rats was again only 50% of control values. Thus with template saturation, RNA polymerase II from hydrocortisone treated rats could not transcribe rat thymic chromatin templates to the level achieved by RNA polymerase II from control rats. This suggests that the activity, rather than the amount, of RNA polymerase II from hydrocortisone treated rats is reduced. Double reciprocal plots of [3H]UMP incorporation on rat chromatins with increasing concentrations of RNA polymerases II were made at 12 h. The apparent Km for RNA polymerase II from animals treated with hydrocortisone was identical to that of RNA polymerase II from controls, but the Vmax of RNA polymerase II from hydrocortisone treated animals was reduced. These data suggest the presence of an inhibitor of transcription or an RNA polymerase II defective in its capacity to initiate and/or elongate RNA transcripts. Further experiments demonstrated that these effects were not due to steroid induced changes in ribonuclease or protease activities.
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Rifampicin produces a dose-dependent decrease in protein synthesis in rat thymocytes. At concentrations up to 200 micrograms per milliliter, rifampicin does not alter rat thymic transcription. Rifampicin causes a direct inhibition of protein synthesis in rat thymic and hepatic microsomes, and in cadaveric human hepatic microsomes. Protein synthesis inhibition could explain the toxicity of rifampicin in man.