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Biomedical subjects

F Allison

Publications and source records attributed to F Allison.

At least 19 recordsLinked to original sources
PubMed1988

Acylcoenzyme A dehydrogenase deficiency in heart tissue from infants who died unexpectedly with fatty change in the liver.

Heart muscle from infants who died unexpectedly and who showed fatty changes in the liver at necropsy was analysed for long chain and medium chain acylcoenzyme A dehydrogenase activities by using the natural electron acceptor. In two of the seven cases investigated a deficiency in acylcoenzyme A dehydrogenase activity was found. In one case the deficiency was in medium chain acylcoenzyme A dehydrogenase activity and in the other long chain acylcoenzyme A dehydrogenase activity. These findings emphasise the importance of investigating fatty acid oxidation in infants who have died unexpectedly.

Acyl-CoA Dehydrogenase↗
PubMed1988

The oxidation of octanoic acid by cultured amniotic fluid cells: the effect of cell type and passage number.

We have measured the rate of oxidation of [1(-14)C]octanoate in cultured amniotic fluid (AF) cells at various passages and in AF cell lines with different clonal morphology. It is possible that both the passage number and the cell type may influence the outcome of prenatal diagnosis of fatty acid oxidation defects using this technique. We found that there was no significant difference between the three major AF cell types (epithelial, large epithelial, and fibroblast) when analysed at identical passage number but there was a significant reduction in octanoate oxidation in all cell types with increasing passage. For reliable prenatal diagnosis, cell lines of similar low passage number should be used.

Acyl-CoA Dehydrogenase↗
PubMed1987

Prenatal diagnosis of medium-chain acyl-coenzyme A dehydrogenase deficiency.

A fatal case of medium-chain acyl-coenzyme A dehydrogenase deficiency is described in a patient who presented with hypoglycaemia and a gross non-ketotic dicarboxylic aciduria. Cultured skin fibroblasts released 14CO2 from [1-14C] octanoic acid at half the normal rate. Prenatal diagnosis was undertaken in a subsequent pregnancy in which cultured amniotic fluid cells revealed a marked reduction in octanoate oxidation indicative of an affected fetus. The pregnancy was terminated and the diagnosis was confirmed by enzyme analysis of skin fibroblasts taken from the fetus. The high residual octanoate oxidation by affected fibroblasts together with the absence of any characteristic abnormality of amniotic fluid organic acids are a potential limitation to the reliability of this type of prenatal diagnosis.

Acyl-CoA Dehydrogenase↗
PubMed1970

Studies on the pathogenesis of acute inflammation. IX. The influence of hyperosomolality secondary to hyperglycemia upon the acute inflammatory response induced by thermal injury to ear chambers of rabbits.

The inflammatory reaction induced in ear chambers of rabbits by heat injury was studied in nondiabetic animals made hyperglycemic with continuous infusions of glucose. Hypertonic solutions of glucose administered intravenously to rabbits induced the following triad: hyperglycemia, hyperosmolality, and metabolic lactic acidosis. It was found that relatively short periods of this metabolic abnormality were associated with a significant reduction in the intensity of the inflammatory reaction. There was no evidence microscopically of circulatory impairment within ear chambers; and since neither arterial hypotension nor oxygen deficit was recorded during experiments, it appeared most likely that decreased leucocytic margination per se best explained the inhibited exudative response. Hyperglycemia seemed the dominant factor responsible for this anti-inflammatory effect. It was found subsequently that hyperglycemia and hyperosmolality without metabolic acidosis impaired cellular exudation just as well.

Acidosis↗
PubMed1969

Histoplasmosis.

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Amphotericin B↗