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“Obese individuals are characterized by a chronic, low-grade inflammatory state. Increased levels Selleckchem JQ1 of C-reactive protein (CRP), a marker of inflammation, have been observed in subjects with the metabolic syndrome. We have previously reported that genes encoding proteins involved in

the anti-inflammatory and immune response are differentially expressed in visceral adipose tissue of obese men with or without the metabolic syndrome. Among these genes, the interferon-gamma-inducible protein 30 (IFI30), CD163 molecule (CD163), chemokine (C-X-C motif) ligand 9 (CXCL9) and thymic stromal lymphopoietin (TSLP), were selected for further genetic analyses. The aim of the study was to verify whether IFI30, CD163, CXCL9 and TSLP gene polymorphisms contribute to explain the inter-individual variability of the inflammatory profile of obesity assessed by plasma high-sensitivity CRP concentrations. A total of 1185 severely obese individuals were genotyped for single nucleotide polymorphisms (SNPs) covering most of the sequence-derived genetic variability at this website the IFI30, CD 163, CXCL9 and TSLP gene loci (total of 27 SNPs). Following measurement of plasma CRP levels, subjects were divided into two groups, low vs. high

using the median value of plasma CRP levels (8.31 mg/L) as a cutoff point. Genotype frequencies were compared between groups. Associations between genotypes and plasma CRP levels (continuous variable) were also tested after adjustments for age, sex, smoking and BMI. The rs11554159 and rs7125 IFI30 SNPs showed a significant difference in genotype frequencies (p < 0.05) between subgroups

of low vs. high plasma CRP levels (wild type homozygotes: rs11554159 = 47% vs. 55%, rs7125 = Bindarit mouse 31% vs. 24%, for low vs. high CRP groups, respectively). The association between rs11554159 and CRP levels as a continuous variable remained significant (p = 0.004). Both carriers of the GA and AA genotypes demonstrated, on average, a 13% lower CRP levels in comparison with GG homozygotes. No association was observed between SNPs in the CD163. CXCL9 and TSLP genes and CRP levels. The IFI30 rs11554159 polymorphism could partially explain the inter-individual variability observed in the inflammatory profile associated with obesity. (C) 2011 Elsevier Inc. All rights reserved.”
“To compare the outcome and complications of augmentation cystoplasty before or after renal transplantation in children with neurogenic bladders, with those after kidney transplantation in children with normal bladders.\n\nAugmentation cystoplasty preceded transplantation in 21 children (group 1) and after transplantation in 23 (group 2) operated from 1985 to 2006; these two groups were compared with a control group of 45 children with a normal bladder (group 3) who also received a transplant, for kidney function, episodes of urinary tract infection (UTI), surgical and medical complications.