Retroperitoneal ectopic pregnancy.
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Biomedical subjects
Publications and source records attributed to M Harris.
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1. The effects of centrally acting drugs on the uptake of (3)H-gamma-aminobutyric acid (GABA) by slices of rat cerebral cortex have been studied.2. Many centrally acting drugs at concentrations of 0.1-1.0 mM significantly inhibited the uptake of (3)H-GABA by cortical slices, but the only classes of drugs in which all members consistently produced inhibition of uptake were the phenothiazines, tricyclic antidepressants, and butyrophenones.3. The receptor blocking drugs; phentolamine, propranolol, thymoxamine, mepyramine, and diphenhydramine at concentrations of 0.5-1 mM also significantly reduced the uptake of (3)H-GABA. However, atropine, hexamethonium and (+)-tubocurarine had little effect on the uptake of (3)H-GABA by cortical slices.4. Centrally acting drugs, which did not significantly inhibit (3)H-GABA uptake, included barbiturates, local anaesthetics, hallucinogens, monoamine oxidase inhibitors, anticonvulsants, and convulsants (except picrotoxin).5. Chlorpromazine, prochlorperazine, L-2,4,diaminobutyric acid, desmethylimipramine, and iprindole inhibited the uptake of (3)H-GABA by 50% (IC50) at concentrations of 30-100 muM. The most potent inhibitor of (3)H-GABA uptake was p-chloromercuriphenylsulphonate (IC50 = 18 muM).6. With the exception of L-2,4,diaminobutyric acid, an outstanding characteristic of these drugs was their complete lack of specificity. Thus at the IC50 for GABA, p-chloromercuriphenylsulphonate, chlorpromazine, prochlorperazine, iprindole, desmethylimipramine, apomorphine and diphenylhydramine also inhibited the uptake of radioactive glycine, alanine, noradrenaline, and 5-hydroxytryptamine. The uptake of the latter two compounds was often inhibited to a greater extent than GABA, glycine and alanine.7. Kinetic analysis indicated that the inhibition of (3)H-GABA by p-chloromercuriphenylsulphonate, chlorpromazine, and desmethylimipramine was noncompetitive. L-2,4,Diaminobutyric acid reduced the uptake of (3)H-GABA by a ;mixed' type of inhibition.8. The present results do not support the suggestion that some centrally acting drugs may produce their effects by reducing the uptake of GABA in the brain after its release from inhibitory nerve terminals. Conceivably, the design of compounds which interfere effectively with the mechanisms of GABA operated synapses may lead to the introduction of whole new groups of centrally acting drugs.
1. Twelve malnourished Jamaican children, aged 4-16 months, were studied before and after treatment, to see whether malnutrition impaired their response to cold.2. When they were studied in the post-absorptive state and in a neutral thermal environment, they had a lower rate of oxygen consumption per kg body weight, a slower pulse rate, lower body temperatures, lower R.Q., and evidence of a smaller peripheral blood flow on admission to hospital than they did after recovery.3. The malnourished children failed to increase their heat production above resting levels at 25 degrees C, and their rectal temperature fell at a rate of 1 degrees C/hr in spite of a further decrease in peripheral circulation.4. When they had recovered they maintained their body temperature within the normal range on exposure to this temperature, while increasing their heat production by 20%. The thermogenesis was apparently of the non-shivering type.5. There was evidence of increased metabolic activity in the interscapular brown fat pad at 25 degrees C both on admission and before discharge. In the malnourished children this activity was not sufficient to produce a measurable increase in total oxygen consumption.6. Interscapular brown fat was examined at autopsy in thirteen malnourished and fifteen well nourished children aged 1-24 months. Lipid depletion was found in this tissue in the former but not in the latter. This may explain the impaired response of the malnourished child to cold.
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The ultrastructure of a glomus tumour is described, and the implications of the findings with regard to the histogenesis of this type of tumour are briefly discussed.
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A case of florid rheumatoid heart disease with complete heart block is described, and the histopathology of the atrioventricular conducting tissue is described in detail.
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