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Biomedical subjects

J A SMITH

Publications and source records attributed to J A SMITH.

At least 19 recordsLinked to original sources
PubMed1976

Density-dependent regulation of proliferation rate in cultured, androgen-responsive, tumour cells.

Short-term cultures of androgen-responsive Shionogi 115 (S115) cells exhibited density-dependent regulation of proliferation rate in the presence or absence of testosterone. The average surface area per cell exposed to the growth medium was inversely proportional to population density. By contrast, long-term cultures (serially passaged in testosterone-containing medium for several months) did not exhibit density-dependent regulation of proliferation rate when grown in testosterone-containing medium. In this medium, cells became elongated and no longer exhibited any obvious decrease in exposed surface area with increasing density. Nevertheless, when subcultured into testosterone-free medium, these cells reverted to an epithelial morphology and exhibited density-dependent regulation of proliferation rate. These relationships suggested that the proliferation rate of cells decreased with density in proportion to the decrease in exposed surface area...

Aminoisobutyric Acids↗
PubMed1964

STRUCTURAL CHANGES IN ISOLATED LIVER MITOCHONDRIA OF RATS DURING ESSENTIAL FATTY ACID DEFICIENCY.

Liver mitochondria isolated in 0.44 M sucrose from rats deficient in essential fatty acids (EFA) oxidized citrate, succinate, alpha-ketoglutarate, glutamate, and pyruvate at a faster rate than did mitochondria isolated from normal rats; however, the oxidation of malate, caprylate, and beta-hydroxybutyrate was not significantly increased. The mitochondria from deficient rats exhibited an increased ATPase activity and extensive structural damage as revealed by electron microscope examination of thin sections. An increase in citrate oxidation and ATPase activity, together with some structural damage, could be demonstrated as early as the 4(th) week in rats on a fat-free diet. Saturated fat in the diet did not prevent the change in mitochondrial structure but accelerated its appearance. Both the biochemical and structural defects could be reversed within three weeks after feeding deficient rats a source of EFA. In the presence of a phosphate acceptor the effect of EFA deficiency on substrate oxidation was largely eliminated. A trend toward a reduced efficiency of oxidative phosphorylation was noted in mitochondria from EFA-deficient rats, but significant uncoupling was found only in the case of citrate, beta-hydroxybutyrate, and glutamate in the presence of malonate. Together with the increased ATPase activity, the uncoupling of phosphorylation could account for the poor respiratory control found with the deficient preparation. However, EFA deficiency was without effect on the respiration of liver slices, which supports the belief that the observed changes in oxidation and phosphorylation are an artifact resulting from damage sustained by the deficient mitochondria during their isolation.

Adenosine Triphosphatases↗