Using adjusted percentages for FEV1, values were significantly lower among obese compared to morbidly obese children at metacholine concentrations of 0.25, 1, and 4 mg/ml. The proportion of positive BHR (PC(20)16mg/ml) was higher in these two groups compared to normal-weight children (28.4%, 17.8%, and 12.5%, respectively), although differences were not significant.\n\nConclusionOur findings show that obesity by

itself is not a sufficient condition to alter airway responsiveness to methacholine in a group of adolescents. Pediatr Pulmonol. 2013; 48:1201-1205. (c) 2013 Wiley Periodicals, Inc.”
“Twenty genes involved in fatty acid metabolism Autophagy Compound Library were studied to reveal their effects on chicken fatness traits. To explore the interactions among these genes and evaluate their effects

on fat accumulation in chickens, a Bayesian network of candidate genes in fatty acid metabolism and growth was constructed in terms of these genes’ mRNA expression data derived from DNA microarray and the effects of these genes on fatness traits were analyzed. A full-sib family Beijing-You chicken population was raised and sampled for investigating the hepatic mRNA expression and measuring the fatness traits at 5 time points from 42 Angiogenesis inhibitor to 98 d. By using a Bayesian network toolbox, we obtained a Bayesian-directed acyclic network, which has 19 nodes and 28 edges. The results showed that the heart-type fatty acid-binding protein (H-FABP) was the hub of the network with connection to 7 other genes. The hepatic mRNA expression of H-FABP was significantly related to i.m. fat content (r = -0.44,

P < 0.05) at 70 d of age. The results indicated that the H-FABP gene plays the most important role among these genes associated with fatty acid metabolism and affects MGCD0103 datasheet i. m. fat content of chickens.”
“In utero smoke exposure has been shown to have detrimental effects on lung function and to be associated with persistent wheezing and asthma in children. One potential mechanism of IUS effects could be alterations in DNA methylation, which may have life-long implications. The goal of this study was to examine the association between DNA methylation and nicotine exposure in fetal lung and placental tissue in early development; nicotine exposure in this analysis represents a likely surrogate for in-utero smoke. We performed an epigenome-wide analysis of DNA methylation in fetal lung tissue (n = 85, 41 smoke exposed (48%), 44 controls) and the corresponding placental tissue samples (n = 80, 39 smoke exposed (49%), 41 controls) using the Illumina HumanMethylation450 BeadChip array. Differential methylation analyses were conducted to evaluate the variation associated with nicotine exposure. The most significant CpG sites in the fetal lung analysis mapped to the PKP3 (P = 2.94 x 10(-03)), ANKRD33B (P = 3.12 x 10(-03)), CNTD2 (P = 4.9 x 10(-03)) and DPP10 (P = 5.43 x 10(-03)) genes.