Search PubMed⌕ Search

Biomedical subjects

P Edwards

Publications and source records attributed to P Edwards.

At least 163 records · Page 9Linked to original sources
PubMed1977

A high prevalence of affective disorder discovered in a "schizophrenia clinic".

Fifty outpatients in a "schizophrenia clinic" were examined, and sixteen were found to be suffering from periodic affective disorders. Nine of these were given lithium carbonate, and eight responded well. Case histories illustrate three separate reasons for incorrect diagnosis. Examination of extensive old clinical notes of five of these patients suggests that the problems of diagnosis which have been described in the literature in the past, continue to represent obstacles to correct diagnosis. Suggestions for improvement are offered.

Adult↗
PubMed1975

Prostaglandin E2 effects on cation flux in sickle erythrocyte ghosts.

Prostaglandin E2 has previously been shown to enhance the shape transformation of sickle prone erythrocytes (8) and to reduce the oxygen resaturation of Hemoglobin SS within intact sickle cell erythrocytes after deoxygenation (15). In view of the recent importance attributed to calcium transport in maintaining erythrocyte shape and viability (10) and the suggestion that prostaglandins may act via a calcium ionophore mechanism (9) on cell membranes, erythrocyte ghosts were prepared following the method of Lepke and Passow (12) from normal and sickle cell anemia erythrocytes. These two classes of ghosts are shown to display differing patterns of sodium and calcium transport, whith calcium influx being preferentially stimulated by prostaglandin E2 in sickle cell ghosts. It is suggested that in hypoxic, stasis conditions in vivo, prostaglandins may play a role in accelerating sickling of sickle prone erythrocytes via stimulation of calcium influx.

Anemia, Sickle Cell↗
PubMed1975

Comparison of 125-I-insulin binding and degradation to isolated rat hepatocytes and liver membranes.

UNLABELLED: We have compared the ability of rat liver plasma membranes and isolated hepatocytes to bind and degrade insulin. Isolated cells were prepared in two different ways: by mechanical separation of cells and by collagenase digestion of extracellular matric. In all studies the binding and degradative characteristics of both types of hepatocyte preparations were identical. Furthermore, with one exception, the binding characteristics of membranes and cells were also quite similar. The only exception concerned the amount of insulin bound by hepatocytes as compared to liver membranes. Thus, at concentrations of cells (1.2 times 10(6) cells per milliliter) and membranes (150 mug. protein per milliliter) that gave equal binding at insulin concentrations less than 100 ng./ml., the amount of insulin specifically bound at insulin concentrations greater than 100 ng./ml. was greater with use of hepatocytes. Additional studies indicated that, in contrast to membranes, at the higher insulin concentration only 75 per cent of the previously bound insulin could be recovered from hepatocytes. Thus, a nondissociable component exists; which probably represents intracellular radioactivity and appears to account for the higher specific insulin binding by cells at higher insulin concentrations. When insulin degradation was studied at the above hepatocyte and plasma membrane concentrations, cells degraded 30 per cent more insulin than did membranes. Kinetic analysis of these data revealed that the Km for insulin degradation (5 times 10(-7) M at 37 degrees) was the same for both systems wereas the Vmax was greater with use of hepatocytes. IN CONCLUSION: (1) Preparation of hepatocytes by collagenase digestion does not appear to alter insulin binding or degradation; (2) studies of liver membranes and isolated hepatocytes obtained from normal rats should yield similar information about insulin-receptor interaction as long as insulin concentrations less than 100 ng./ml. are used; (3) at very high insulin concentrations, some of the radioactivity appears to enter the cells; (4) the kinetics of insulin degradation by hepatocytes and liver membranes are similar; and (5) insulin degradation appears to be primarily a membrane phenomenon.

Animals↗
PubMed1971

Paracetamol and renal damage.

Renal function was assessed in 18 patients who had consumed 2 to 30 kg of paracetamol. No relationship was found between the total amount of paracetamol taken and any aspect of renal function studied. No patient had clinically significant renal impairment. Thirteen of the patients showed no significant deterioration of renal function over a period of about one year during which they consumed an additional mean 2 kg of paracetamol.

Acetaminophen↗