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Biomedical subjects

J A Vale

Publications and source records attributed to J A Vale.

At least 127 records · Page 7Linked to original sources
PubMed1982

Effects of oestrogen administration on vitamin B6 and tryptophan metabolism in the rat.

1. In order to assess the effects of oestrogens on the metabolism of tryptophan and vitamin B6, ovariectomized rats have been maintained on diets providing known amounts of tryptophan, nicotinamide and vitamin B6. They received oestrone sulphate, 210 micrograms/kg body-wt per d, either incorporated in the diet for 8 weeks, or by daily intraperitoneal injection for periods of 1-3 d. 2. Oestrone sulphate administration caused a slight reduction in the concentration of pyridoxal phosphate in plasma. It had no effect on the concentration of pyridoxal phosphate in liver or kidney, the urinary excretion of 4-pyridoxic acid, the activation of erythrocyte aspartate aminotransferase (L-aspartate:2-oxo-glutarate aminotransferase, EC 2. 6. 1. 1) by incubation with added pyridoxal phosphate, or the activity of pyridoxal oxidase (aldehyde:oxygen oxido-reductase, EC 1.2.3.1) in the liver. 3. Oestrone sulphate administration caused an increase in the urinary excretion of kynurenine and a reduction in the activity of liver kynureninase (L-kynurenine hydrolase, EC 3.7.1.3). It had no effect on the urinary excretion of N1-methyl nicotinamide or the concentrations of nicotinamide nucleotides in blood, liver or kidney. 4. There was a considerable excess of the apoenzyme of kynureninase in the liver. Incubation of liver homogenates with added pyridoxal phosphate led to a 4- to 5-fold increase in activity. 5. We conclude that there is no evidence of any significant effect of oestrogens on vitamin B6. It is suggested that abnormalities of tryptophan metabolism in women receiving oestrogens, which have been widely attributed to drug-induced vitamin B6 depletion, can be accounted for by inhibition of kynureninase by oestrogen metabolites.

Animals↗
PubMed1981

Extracorporeal treatment of salicylate or acetaminophen poisoning--is there a role?

Hemodialysis or sorbent hemoperfusion has been used in the management of clinical overdose of salicylates or acetaminophen. Hemodialysis offers considerable benefit in severe salicylate poisoning and is preferred to hemoperfusion or peritoneal dialysis, since it more rapidly corrects acid-base and electrolyte abnormalities than does hemoperfusion, and since it is clearly more efficient than is peritoneal dialysis for the removal of salicylates. Charcoal hemoperfusion in animal studies and hemodialysis in man have been shown to accelerate acetaminophen elimination from the body. Hemodialysis and hemoperfusion are of questionable benefit in clinical acetaminophen overdose. However, our clinical experience to date with charcoal hemoperfusion in "late" acetaminophen overdose has been associated with a less notable increase in liver enzyme concentrations in comparison with results of retrospective studies of series of patients treated or not treated with sulfhydryl donors.

Acetaminophen↗
PubMed1981

Treatment of acetaminophen poisoning. The use of oral methionine.

One hundred thirty-two cases of severe acetaminophen (paracetamol) poisoning were treated with oral methionine. Seven of 96 patients who received the antidote within ten hours of ingestion of the overdose had severe liver damage (aspartate transaminase level, greater than 1,000 IU/L), but none of these patients died. Thirty-six patients received methionine between ten and 24 hours of ingestion; severe liver damage occurred in 47%, and two patients died. The treatment protocol for oral methionine is simple, and therapy is complete within 12 hours as compared with three days for oral acetylcysteine and 20 hours for intravenous acetylcysteine. Side effects from methionine were unimportant. Oral methionine is as effective as acetylcysteine in preventing severe liver damage and death after acetaminophen overdose. However, as with acetylcysteine, it must be given within ten hours of ingestion to be effective.

Acetaminophen↗
PubMed1981

The epidemiology of acute acetaminophen poisoning in England and Wales.

The mortality from analgesic poisoning in England and Wales has risen markedly during the last five years, but only a small increase in mortality from acetaminophen poisoning has been seen in the same period. Two separate epidemiologic studies of acetaminophen-overdose patients were undertaken during the two years from 1977 to 1978. Eighty-five percent of 1,644 patients and 95% of 341 patients arrived at the hospital within 12 hours of ingestion of an acetaminophen overdose. Although most patients who ingested hepatotoxic doses of acetaminophen were asymptomatic--347 (66%) of 667 and 26 (51%) of 51 patients--the absence of symptoms did not adversely affect the time of their arrival at the hospital.

Acetaminophen↗
PubMed1977

Corynebacterium bovis as a cause of human disease.

Corynebacterium bovis is a gram-positive rod which can cause bovine mastitis and rancidity in cream. On only one occasion has this organism been reported to cause human disease. Six further cases are described in which infections were caused by C. bovis. In two patients the nervous system was involved; two patients had bacterial endocarditis; one had chronic otitis media; and one had a persistent leg ulcer. Five patients recovered completely from the infection; the other died from endocarditis.

Acute Disease↗