PubMed Health⌕ Search

Biomedical subjects

S C Cheng

Publications and source records attributed to S C Cheng.

151 records · Page 9Linked to original sources

Characterization of 7,12-dimethylbenz[a]anthracene-adenine nucleoside adducts.

Chromatographic comparisons were made between radioactive adducts derived from the DNA of cells treated with [3H]7,12-dimethylbenz[a]anthracene and adducts derived from calf thymus DNA or nucleotides which had been treated in vitro with the synthetic syn 3,4-dihydrodiol 1,2-epoxide of this same carcinogen. This confirmed that three of the adducts formed in cells were derived from reaction of this particular dihydrodiol epoxide with deoxyadenosine while a fourth adduct was derived from its reaction with deoxyguanosine. After reaction of the dihydrodiol epoxide with polyadenylic acid, two ribonucleoside adducts were characterized by spectroscopic methods and were shown to have arisen from the cis opening of the epoxide ring at C1 by the amino group of adenine residues.

9,10-Dimethyl-1,2-benzanthracene↗

DNA adducts from carcinogenic and noncarcinogenic enantiomers of benzo[a]pyrene dihydrodiol epoxide.

The characterization of eight benzo[a]pyrene-deoxyribonucleoside adducts derived from reaction of the anti-dihydrodiol epoxide and deoxyguanylic and deoxyadenylic acids is described. It is reported that the epoxide ring is opened by the purine amino groups to yield similar amounts of both cis and trans products. NMR data show that the 7- and 8-hydroxyl groups are pseudodiaxial in the cis products and pseudodiequatorial in the trans products, and we suggest that these products arise from reaction with the diaxial and diequatorial conformers of the dihydrodiol epoxides, respectively. The chiral nature of the interactions of these metabolites with DNA restricts the range of products formed with this macromolecule, and a trans product with deoxyguanosine is the major product formed with either enantiomer of the anti-dihydrodiol epoxide.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

Chemosensitivity of human hepatocellular carcinoma cell line QGY-7703 is related to bcl-2 protein levels.

Bcl-2 protein is one of the major apoptosis regulators. The study examines the effect of Bcl-2 protein on the chemosensitivity of a human hepatocellular carcinoma cell line, QGY-7703. Western blot analysis showed that Bcl-2 and Bax proteins were expressed in QGY-7703 cells. Characteristic features of Taxol- and doxorubicin-induced apoptosis were evidenced by the Annexin-V binding assay, TUNEL and DAPI staining. At constant Bax protein levels, stable sense and antisense gene-transfected QGY-7703 cells showed that constitutive expression of Bcl-2 could render the cells more resistant to Taxol and doxorubicin. Contrarily, decreased Bcl-2 levels caused the cells to be more sensitive to the drugs. As Bcl-2 levels are directly proportional to the resistance of QGY-7703 cells to Taxol and doxorubicin, manipulation of Bcl-2 could be performed to enhance the sensitivity of liver cancer to chemotherapeutic agents.

Annexin A5↗

A neurochemical hypothesis for halothane anesthesia.

We hypothesize that anesthetic agents exert their effects through an inhibition of oxidation of reduced nicotinamide adenine dinucleotide (NADH) in the synaptic regions of the brain. This inhibition could lead to gamma-amino-butyric acid (GABA) accumulation in the synaptic cleft and to hyperpolarization of the post-synaptic membrane. The resulting reduction in synaptic transmission then would manifest itself as the anesthetic state, reducing the work performed by the brain so that cerebral respiration is reduced and cerebral metabolite energy is conserved.

Acetates↗

Association of hypertriglyceridemia and insulin resistance in uremic patients undergoing CAPD.

OBJECTIVE: Hyperlipidemia is frequently encountered in uremic patients and may be worsened by continuous ambulatory peritoneal dialysis (CAPD) treatment. The lipid abnormalities in these patients may be multifactorial. Insulin resistance (or its compensatory hyperinsulinemia) is commonly observed in uremic patients, but its association with hyperlipidemia in these patients has not been studied. PATIENTS AND METHODS: Lipid profiles of 35 nondiabetic nonobese patients undergoing CAPD for more than 1 year (mean 52.3 months) were studied. Current laboratory data and parameters related to peritoneal dialysis (PD) within the previous 3 months were recorded. After overnight fasting and interruption of PD, an oral 75-g glucose tolerance test (OGTT) was examined. RESULTS: After CAPD treatment for more than 12 months, these patients had higher serum triglyceride (TG) (p = 0.001) and total cholesterol (p = 0.0058) levels than their values before commencing CAPD. Twelve of 14 patients with serum TG higher than 200 mg/dL (high-TG) were diagnosed de novo, in contrast with only 1 patient diagnosed of de novo hypercholesterolemia (total cholesterol > 240 mg/dL). There was no difference in age, gender, body mass index (BMI), duration of PD treatment, serum albumin, hematocrit, intact serum parathyroid hormone (iPTH), peritoneal glucose load, solute transport, or weekly Kt/V urea between normal-TG and high-TG patients. After adjusting for age, gender, BMI, weekly Kt/V urea, and iPTH, the high-TG patients had higher levels of area under the curve for glucose (AUC(Glu)), area under the curve for insulin (AUC(Ins)), and AUC(Ins)/AUC(Glu) ratios (F = 10.63, 10.14, and 8.65; p = 0.0029, 0.0035, and 0.0065, respectively), indicating that the high-TG patients were more insulin resistant. There were 24 patients with normal glucose tolerance (NGT), and 11 patients with impaired glucose tolerance (IGT). The IGT group had higher serum TG (F = 10.43, p = 0.003) and total cholesterol (F = 8.05, p = 0.009) than the NGT group, after adjusting for BMI, duration of CAPD treatment, peritoneal glucose load, solute transport, serum albumin, and lipid levels before PD treatment. TheTG levels after CAPD treatment were positively correlated with AUC(Glu), AUC(Ins), and AUC(Ins)/AUC(Glu) ratio (r = 0.48, 0.53, and 0.49; p = 0.0037, 0.001, and 0.0028, respectively). CONCLUSIONS: These results indicate that insulin resistance is an important factor in the development of hypertriglyceridemia in CAPD patients.

Adult↗