Not wanted at thirty-five.
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Age Factors↗
Biomedical subjects
S Barlow
Publications and source records attributed to S Barlow.
Synthesis of carbonic anhydrase in rabbit and chicken reticulocyte lysates.
The synthesis of carbonic anhydrase, the second most abundant soluble protein of red blood cells, is shown to occur in rabbit and chicken reticulocyte lysates. This translation product was identified by chloroform/ethanol extraction, polyacrylamide gel electrophoresis in sodium dodecylsulphate and peptide mapping. In rabbit retic-locyte lysates, predominantly one of the two red cell isozymes, carbonic anhydrase I, is synthesised. The proportion of carbonic anhydrase synthesis (0.2-0.8% of total protein synthesis) in vitro is comparable to that (0.2-1.0%) in vivo for both rabbit and chicken reticulocytes.
Amino Acids↗
Some remaining problems in the reproductive toxicity testing of drugs.
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Abnormalities, Drug-Induced↗
Investigations into the mechanism of reduction of ethanol sleep by thyrotropin-releasing hormone (TRH).
Thyrotropin-releasing hormone (TRH), administered intraperitoneally, was found to antagonize ethanol-induced sleep and hypothermia in mice without affecting brain ethanol content. This reduction of the actions of ethanol was also apparent after oral or intracisternal administration of TRH. In addition, TRH reduced ethanol-induced sleep in rats, hamsters, gerbils and guinea pigs. Evidence that the pituitary-thyroid axis is not necessary for the effects of TRH was provided by observations that hypophysectomy did not reduce TRH antagonism of ethanol narcosis and findings that neither triiodothyronine nor thyrotropin mimicked its action. Certain analogs of TRH, which have little effect on the pituitary, were also found to antagonize ethanol-induced sleep and hypothermia. Pretreatment with the antiadrenergic drugs, alpha-methyltyrosine, phentolamine and propranolol did not antagonize the ability of TRH to reduce sleep induced by ethanol. However, after intracisternal administration of atropine methyl nitrate, TRH no longer caused a significant reduction of sleep, even though TRH antagonism of the ethanol-induced hypothermia was still apparent. In contrast, central administration of other anticholinergic drugs, such as delta-tobocurarine and hexamethonium, reduced ethanol-induced sleep and this effect was additive with TRH. Carbachol also reduced ethanol sleeping time and this effect was also blocked by atropine methyl nitrate. The antagonism of ethanol-induced sleep by dibutyryl cyclic adenosine 3', 5'-monophosphate was significantly reduced but not blocked by atropine methyl nitrate. Results provide evidence that TRH has a direct extrapituitary action on brain and that both TRH and ethanol may interact with central cholinergic systems.
Animals↗