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Biomedical subjects

G C Fenn

Publications and source records attributed to G C Fenn.

27 records · Page 2Linked to original sources
PubMed1988

Double blind placebo controlled trial of low dose oxandrolone in the treatment of boys with constitutional delay of growth and puberty.

Nineteen boys, mean age 14.4 years (range 12.9-16.3), with constitutional delay of growth and puberty were randomised into two groups in a double blind fashion for a three month period. Ten boys received oxandrolone, 2.5 mg per day (mean dose 0.072 mg/kg/day), and nine boys were treated with placebo. Mean growth velocity increased from 4.5 cm/year in the oxandrolone treated group to 9.6 cm/year in three months, and this was sustained at 8.6 cm/year after cessation of treatment. In the placebo treated group, growth rate showed no alteration from 5.1 cm/year to 5.2 cm/year; boys in this group were then treated with oxandrolone, 2.5 mg a day (mean dose 0.073 mg/kg/day) for three months and growth velocity accelerated to 8.6 cm/year. Serum concentrations of insulin-like growth factor -1/somatomedin-C (IGF-1) increased during oxandrolone treatment and continued to rise after treatment had ceased. There was no change in serum IGF-1 concentration during treatment with placebo. Oxandrolone, when used in an appropriate regimen, is an effective, safe treatment for boys with constitutional delay of growth and puberty.

Adolescent↗
PubMed1988

Potential drug interactions with misoprostol: effects on the pharmacokinetics of antipyrine and propranolol.

First, the pharmacokinetics of antipyrine were studied in 12 healthy male and female volunteers (i) before misoprostol, (ii) after they had received misoprostol 400 micrograms twice daily for 28 days and (iii) after a further 28 days during which no misoprostol was taken. The plasma half-life and area under the plasma concentration-time curve of antipyrine were unchanged. The findings suggest that misoprostol is not an hepatic enzyme inducer. Second, 12 healthy male and female volunteers took propranolol 80 mg twice daily for four weeks; during the second and third of these weeks the volunteers also took misoprostol 400 micrograms twice daily. The plasma concentrations of propranolol under these steady state dosing conditions increased when misoprostol was added to propranolol. The mechanism underlying this finding should be clarified.

Adult↗
PubMed1983

Interactions of ethanol with ionophore A23187 in human platelets and erythrocytes and in rat brain slices.

The aggregation of gel-filtered human platelets induced by A23187 is very sensitive to inhibition by ethanol. Similarly when platelets preloaded with [3H]5-hydroxytryptamine ([3H]5HT) are studied in a superfusion system under conditions where aggregation is likely (high platelet density, presence of Ca2+) the rate of release of [3H]5HT induced by A23187 is reduced by the presence of ethanol. However when platelet aggregation is less likely (low platelet density, absence of Ca2+) ethanol does not reduce the rate of [3H]5HT efflux induced by A23187 in superfused platelets. In addition, in contrast to the effects of ethanol on platelet aggregation, the transformation of human red cells to echinocytes induced by A23187 is accelerated by the presence of ethanol. Similarly the increased efflux of 3H from superfused rat striatal slices preloaded with [3H]dopamine which is produced by A23187 is potentiated by ethanol. It is concluded that the inhibitory effect of ethanol on the action of A23187 may be confined to platelet aggregation. This may be because the mechanisms of action of either A23187 or ethanol on platelet aggregation differ from those on other cell functions.

Animals↗
PubMed1983

Comparison of effects of ethanol on platelet function and synaptic transmission.

Ethanol, at concentrations tolerated by man, is generally inhibitory to platelet function in vitro, producing significant inhibition of aggregation in response to most chemical aggregating agents. The calcium ionophore, A23187, is the agent which is most inhibited by ethanol, whereas aggregation induced by arachidonic acid is not inhibited even by concentrations of ethanol far in excess of the lethal range. This spectrum of inhibition found suggests that ethanol inhibits the platelet release reaction by a mechanism involving inhibition of Ca2+-activated phospholipase A2. These effects can be observed in superfused human platelets as well as in those suspended in buffer or in plasma. In superfused rat brain slices however, ethanol does not inhibit the A23187-induced release of radiolabelled neurotransmitter, although it can be shown to inhibit Ca2+-activated phospholipase A2 activity in rat synaptosomal preparations. It is concluded that, although there are many similarities between the effects of ethanol on the platelet and the synapse there may be differences between the way in which ethanol modifies release of intracellular contents in the two situations.

Adenosine Triphosphate↗
PubMedDate not supplied

Effect of ethanol on thrombin-induced platelet phospholipid breakdown and release of [3H]-5-hydroxytryptamine.

Ethanol has been reported previously to inhibit chemically-induced platelet aggregation and the release of platelet contents. In platelet suspensions the mechanical stimulus of stirring can induce slow aggregation and the loss of endogenous arachidonic acid from phospholipids by activation of platelet phospholipases. These changes are prevented by the presence of ethanol 20-100 mM, whereas, in unstirred suspensions, ethanol alone has no effect on platelet phospholipids. Under similar conditions of reduced platelet: platelet contact, chemical stimuli, such as thrombi, although unable to produce visible aggregation, still cause the release of [3H]-5-hydroxytryptamine from platelets and also initiate the breakdown of platelet phospholipids. Ethanol does not now inhibit the thrombin-induced release of platelet contents and has little effect on phosphatidylinositol breakdown, though it inhibits phosphatidylcholine breakdown. Ethanol may therefore inhibit platelet aggregation by reducing the effect of mechanical and chemical stimuli on the activation of phospholipase A2. In contrast ethanol has rather little effect on the receptor-mediated breakdown of phosphatidylinositol which is apparently sufficient to trigger the release of platelet contents.

Arachidonic Acid↗