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Biomedical subjects

B S Kilgore

Publications and source records attributed to B S Kilgore.

7 recordsLinked to original sources
PubMed1979

Impaired growth in hyperkinetic children receiving pemoline.

Decreased longitudinal growth was observed in 24 hyperkinetic children receiving pemoline therapy. Mean height velocity was 3.67 +/- 0.25 cm/year during therapy but 5.35 +/- 0.42 cm/year after treatment had been discontinued (P less than 0.01). There appeared to be an inverse relationship between growth velocity and drug dosage. All patients receiving less than the median dose of 3.72 mg/kg grew 4 cm/year or more, while seven of 12 patients receiving more than this dose grew at a slower rate. Body weight, basal and stimulated growth hormone values, and plasma somatomedin concentrations were not significantly altered by pemoline treatment, suggesting that this drug may have a direct effect on cartilage metabolism.

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PubMed1979

Alterations in cartilage metabolism by neurostimulant drugs.

Suppression of growth without significant alterations in hormonal patterns has been demonstrated for the neurostimulant drug pemoline. Comparison of the in vitro effect of pemoline, methylphenidate, and methamphetamine on somatomedin-stimulated sulfate uptake by cartilage showed all three drugs to be inhibitory. Sulfate uptake by cartilage can be directly related to growth and glycosaminoglycan biosynthesis. Assay of two of the enzymes involved in the glycosaminoglycan biosynthetic pathway showed that methamphetamine and methylphenidate caused a marked depression of xylosyl- and galactosyltransferase enzyme activity. These data suggest an interference with cartilage metabolism as one possible mechanism for the growth retardation observed in children on neurostimulant drug therapy.

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PubMed1979

Alteration of cartilage glycosaminoglycan protein acceptor by somatomedin and cortisol.

The effect of somatomedin and cortisol on embryonic chick cartilage in vitro indicates that somatomedin stimulates 35SO4 uptake while cortisol decreases it with no effect on glycosaminoglycan turnover. Xylosyltransferase activity is increased in crude fractions of somatomedin-treated cartilage but decreased in cortisol-treated cartilage. By using a Smith-degraded proteoglycan as an exogenous acceptor, xylosyltransferase activities from both treatments were equivalent, suggesting that the enzyme was not rate limiting. The results of xylosyltransferase assays conducted by mixing enzyme and endogenous acceptor from control, cortisol-treated and somatomedin-treated cartilage, suggest both effects to be at the level of the acceptor protein.

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PubMed1976

Uridine diphosphate xylosyltransferase activity in cartilage from manganese-deficient chicks.

The glycosaminoglycan content of cartilage is decreased in manganese deficiency in the chick (perosis). The activity of xylosyltransferase, the first enzyme in the biosynthetic pathway of sulphated glycosaminoglycans, was studied in the epiphysial cartilage of 4-week-old chicks which had been maintained since hatching on a manganese-deficient diet. Enzymic activity was measured by the incorporation of [14C]xylose from UDP-[14C]xylose into trichloroacetic acid precipitates. Optimal conditions for the xylosyltransferase assay were established and shown to be the same for both control and manganese-deficient cartilage. Assay of the enzyme by using an exogenous xylose acceptor showed no difference in xylosyltransferase activity between control and manganese-deficient tissue. Further, the extent of xylose incorporation was greater in manganese-deficient than in control cartilage preparations, suggesting an increase in xylose-acceptor sites on the endogenous acceptor protein in the deficient cartilage. 35S turnover in the manganese-deficient cartilage was also increased. The data suggest that the decreased glycosaminoglycan content in manganese-deficient cartilage is due to decreased xylosylation of the acceptor protein plus increased degradation of glycosaminoglycan.

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PubMedDate not supplied

Glucocorticoid effects on the embryonic chick heart. I. Glucocorticoid enlargement of the heart.

Cortisol increases the heart weight relative to body weight following injection of growth suppressing amounts of the hormone on incubation days 9, 10, 13, and 15. Hormone administration increases glycogen, glycosaminoglycan (GAG), and total lipid concentration in the embryonic myocardium. Deoxyribonucleic acid (DNA) and protein concentration are decreased proportionally. Glycogen synthetase and radiosulphate incorporation into GAG are increased by the glucocorticoid. Lack of growth inhibition of the embryonic myocardium by glucocorticoids is not due to absence of glucocorticoid receptors. [3H]-Dexamethasone was shown to bind to a cytoplasmic and nuclear fraction of the chick heart. Binding to a cytoplasmic protein could be demonstrated in the heart at nine days of embryonic development and increased with developmental age. The increase in cardiac mass appears to be specific for the glucocorticoid hormones when compared with epinephrine and deoxycorticosterone. The latter two hormones did not increase cardiac mass.

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PubMedDate not supplied

Somatomedin activity in cystic fibrosis and reserpinized rats: possible explanation for growth retardation.

Somatomedin activity in children who have cystic fibrosis is reduced to approximately 50 percent of the levels found in normal children. In contrast, the growth hormone concentration in these patients, both the resting and the stimulated levels, was found to be no different from normal children (17.2 and 18.4 ng per ml, respectively). Reserpinized rats have been proposed as a model for cystic fibrosis. Serum somatomedin activity in rats treated with reserpine (0.50 mg per kg per d x 7 days) was reduced to 30 percent of the levels measured in control rats. Reserpine also decreased radiosulfate incorporation into cartilage glycosaminoglycan (GAGS) in vivo and in vitro. Fasting decreased serum somatomedin activity as well as the concentration of GAGS in rat cartilage. Refeeding for 24 hours restored these parameters to normal. These data suggest that one mechanism for the growth retardation occurring in patients who have cystic fibrosis may be explained by decreased serum somatomedin activity.

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