Serum gamma glutamyl transferase activities in epileptic patients receiving carbamazepine monotherapy.
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Biomedical subjects
Publications and source records attributed to P T Lascelles.
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A patient with progressive neurological disease resembling Wilson's disease but in whom Kayser-Fleischer rings were absent, was given 67Cu and 64Cu, orally and intravenously, to measure the rate of absorption of copper using a convolution integral. The data show an abnormal distribution of body copper resulting in low copper concentrations in plasma, urine and liver but with an accumulation in the lower bowel probably due to a defect in mucosal transport. The importance of differentiating this condition from Wilson's disease is stressed.
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In vivo and in vitro experimental data are presented in support of the hypothesis that sodium valproate displaces diphenylhydantoin (DPH) from plasma protein binding sites. This interaction could have important practical implications in the management of patients on combined therapy with these two drugs. Acute neurological features of DPH intoxication may be precipitated as a result of an increased free (pharmacologically active) fraction, which would not be detected by routine plasma DPH estimations since these reflects largely the bound fraction.
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An imporved method is described for measuring low levels of prostaglandin F2alpha in small volumes of cerebrospinal fluid. Single ion monitoring of the ion at m/e 423, derived from the methyl ester tri-TMS ether derivatives of prostaglandin F2alpha and the internal standard, w-trinor-16-cyclohexyl prostaglandin F2alpha, is employed. Injection of 2 pg of prostaglandin F2 alpha derivative gave a standard deviation of +/- 9%. The majority of patients had cerebrospinal fluid levels of up to 2 ng ml-1 of prostaglandin F2 alpha, whereas in certain neurological conditions with progressive disease, elevated levels were encountered, some of which were higher than 10 ng ml-1.
A polarographic technique has been used to study the oxygen uptake of rat brain homogenates incubated with metabolites known to accumulate in uraemia and hepatic coma. In general, results with individual metabolites were in agreement with those previously obtained with brain slices using the Warburg technique. Inhibition was induced at higher concentrations with urea, creatine, indoxysulphate, guanidine, dimethylamine hydrochloride, ammonium chloride, taurocholate, glycodeoxycholate, sodium deoxycholate, skalote and indole. Serum and ultrafiltrate from drowsy uraemic patients also caused inhibition, and this was reversed by renal dialysis. Similarly serum and ultrafiltrate from patients in hepatic coma inhibited oxygen uptake but in this instance reversal of the inhibition was not demonstrated following exchange blood transfusion to the patients.
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