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Biomedical subjects

G M Wang

Publications and source records attributed to G M Wang.

81 records · Page 5Linked to original sources
PubMed1981

Absence of cholesterogenesis regulation in the liver and prostate of the BIO 87.20 hamster.

Normal, adult golden Syrian hamsters and the inbred stain BIO 87.20 Syrian hamsters were maintained on either control, cholesterol, candicidin or clofibrate diets for time periods of up to 4 months. The ventral prostate gland in both species was found to synthesize cholesterol at a greater rate than the liver. Also, our results show that, while hepatic cholesterol synthesis in the normal Syrian hamster is under feedback control with dietary cholesterol, hepatic cholesterol synthesis in the BIO 87.20 hamster, and prostatic cholesterol synthesis in either species, is under no such control. This apparent regulatory defect in the BIO 87.20 hamster, which results in a dramatic accumulation of cholesterol in the liver and serum, renders this animal a potentially valuable in vivo model for the study of cholesterol-related disorders.

Animals↗
PubMed1980

Effect of razoxane (ICRF 159) on daunomycin (NSC 82151) metabolism and DNA complexation.

Daunomycinol and deoxyaglycone were the two major metabolites obtained from daunomycin in vitro metabolism by rat and mouse liver preparations. Pretreatment with razoxane (ICRF 159) in these animals did not appear to alter these major metabolic enzymes. In an in vitro system, it was found that daunomycin reacted with DNA instantly and reached steady states within two minutes as evidenced by the diminishing, shifting or disappearance of certain and visible regions. Preincubation of razoxane with DNA did not alter the latter's capacity to interact with daunomycin. We suggest that the mode of razoxane-protected daunomycin-induced toxicities in mice is not mediated through an alteration in daunomycin metabolism or its complexation with DNA.

Animals↗
PubMed1976

Effect of candicidin and colestipol on the testes and prostate glands of BIO 87.20 hamsters.

The oral treatment of groups of aged BIO 87.20 male hamsters, an inbred line of Syrian hamsters that develops spontaneous cystic prostatic hypertrophy, with either the heptaene macrolide, candicidin, or the bile acid-sequestering anion exchange resin, colestipol, resulted in a significant reduction of prostate size and weight. The effect was most prominent in the high dosage (75 mg per kg per day) candicidin group and moderate in the high dosage (400 mg per kg per day) colestipol group. It was observed microscopically that the extreme dilation of the prostatic acini of the untreated control prostate glands was partially prevented by the treatment, resulting in much less distended prostatic acini. Concomitantly, there was a notable decrease of the total cholesterol content of the entire prostate gland and the plasma of the high dosage candicidin group. The relationship of certain aspects of sterol metabolism and the possible prevention of cystic prostatic hypertrophy in this new experimental animal disease model is discussed. The effect of these drugs on the nutritional state of the animal and on the synthesis and metabolism of androgens from the testis are questions that remain to be answered.

Animals↗
PubMedDate not supplied

Hypoxia-ischemia-induced apoptotic cell death correlates with IGF-I mRNA decrease in neonatal rat brain.

Hypoxia-ischemia induces apoptotic and necrotic cell death, which results partially from persistent alterations in cellular energy homeostasis. Insulin-like growth factor I (IGF-I) is an anabolic pleiotrophic factor required by developing neurons for their optimal proliferation, differentiation, and survival. To determine how cell death and changes in IGF-I gene expression relate to the extent of hypoxia-ischemia, we evaluated the time course of apoptosis in a neonatal hypoxia-ischemia model in relation to the cellular distribution of IGF-I and IGFBP5 mRNA. Severe hypoxia-ischemia results in an immediate decrease in neuronal IGF-I and IGFBP5 mRNA. The decrease in neuronal IGF-I mRNA was concurrent with an increase in the number of apoptotic cells. It is conceivable that the immediate decrease in IGF-I gene expression may contribute to the impending neuronal death and selective vulnerability of myelinogenesis during the perinatal period.

Animals↗