[Heritability and genetic correlation of body mass index and coronary heart disease in Chinese adult twins].

Objective: To examine the heritability of body mass index (BMI) and coronary heart disease (CHD), and to explore whether genetic factors can explain their correlation. Methods: Participants were from 11 provinces/municipalities reqistered in the Chinese National Twin Registry (CNTR) from 2010 to 2018. Participants data were collected from face-to-face questionnaire survey. Bivariate structure equation model was used to estimate the heritability and the genetic correlation of BMI and CHD. Results: A total of 20 340 pairs of same-sex twins aged ≥25 years were included in this study. After adjusting for age and gender, the heritability of BMI and CHD was 0.52 (95%CI: 0.49-0.55) and 0.76 (95%CI: 0.69-0.81), respectively. Further, a genetic correlation was identified between BMI and CHD (rA=0.10, 95%CI:0.02-0.17). Conclusion: In Chinese adult twin population, BMI and CHD are affected by genetic factors, and their correlation can be attributed to the common genetic basis.

[Analysis of association between gene polymorphisms of microsomal epoxide hydrolase (EPHX1) and infant birthweight].

We investigated association between genetic polymorphisms of EPHX1 in mother and infant birthweight. Data of 342 female workers were collected in textile mill. A total of 342 mothers were genotyped for the His139Arg polymorphism of EPHX1 by a polymerase chain reaction-restriction fragment length polymorphism assay. Using multiple linear regression models, we estimated the adjusted association between polymorphisms of EPHX1 and birthweight, with adjusted for potential confounders. We found that polymorphisms of EPHX1 were closely associated with reduced birthweight (beta +/- SE = -149 g +/- 56, P = 0.0083) after adjustment for major cofounders. In subgroup of passive smoking analysis, the polymorphisms of EPHX1 were highly associted with birthweight for those with passive smoking (beta +/- SE = -234 g +/- 88, P = 0.0088); The significant association of EPHX1 polymorphisms with reduced birthweight were showed for those with working stress (beta +/- SE = -157 g +/- 59, P = 0.0079). Our data provide polymorphisms of EPHX1 in mothers were significant association with birthweight of their infant, and showed gene-environmental interaction in relation to birthweight.

Effects of anticholinergic drugs on rabbit efferent phrenic discharges.

In conscious, vagotomized, curarized, and artificially-ventilated rabbits, the efferent phrenic discharges were recorded. When scopolamine, atropine, pirenzepine or AF-DX 116 (11-2[[2-[(diethylamino)methyl]-1-piperidinyl]acetyl]-5,11-dihydro- 6H[2,3-6] [1,4]benzodiazepine-6-one) was injected into the cerebello-medullary cistern, the frequency and voltage of phrenic discharges were decreased (P less than 0.05) by scopolamine (0.5 mg.kg-1) and pirenzepine (0.5 mg.kg-1), but were increased (P less than 0.01) by atropine (0.05 mg.kg-1) and AF-DX 116 (0.1 mg.kg-1). It is probable that scopolamine inhibits the respiratory center by blocking the M1 cholinergic receptors while atropine excites the respiratory center blocking the M2 cholinergic receptors.

Increased phospholipid fatty acid remodeling in human and rat prostatic adenocarcinoma tissues.

PURPOSE: To study the mechanism of diminished arachidonic acid levels in malignant prostatic tissues. MATERIALS AND METHODS: Benign and malignant prostate tissues were obtained from human radical prostatectomy specimens and from rats using Pollard's Lobund/Wistar rat prostate cancer model. Fatty acid composition and a variety of enzyme activities involved in maintaining phospholipid fatty acid composition were compared in malignant and benign prostatic tissues. RESULTS: Decreased arachidonic acid levels, previously reported in human prostate cancer, were present in malignant rat as well as in human tissues. There were 21% and 26% decreases of arachidonic acid levels in the rat and human malignant tissues compared with benign tissues. Fatty acid desaturase activity was undetectable. Fatty acyl-CoA hydrolase and synthetase activities were not altered in the malignant tissues. However, there was a 2-fold increase in phospholipase A2 activity and a 4- to 12-fold increase in fatty acyl-CoA lysophosphatidylcholine acyltransferase activity in malignant rat and human prostatic tissues. CONCLUSIONS: These data indicate that, in malignant prostate tissues, the fatty acid remodeling mechanism is activated through the deacylation-reacylation cycle. This process may be a result of increased use of arachidonic acid for the formation of prostaglandins that may be crucial for the further development and growth of the malignant tissues.