pylori lysates increased the proliferation of HSCs, which was boosted by the addition of transforming growth factor-beta1 (TGF-beta 1). Furthermore, the treatment of H. pylori lysates promoted the translocation of nuclear factor kappa-light-chain enhancer of activated B cells (NF-kappa B) into the nucleus based on an increase in the degradation of NF-kB inhibitor alpha, in the presence of TGF-beta 1, as did H(2)O(2) treatment. In conclusion, H. pylori PD-0332991 nmr infection along with an elevated TGF-beta 1 may accelerate hepatic fibrosis through increased TGF-beta

1-induced pro-inflammatory signaling pathways in HSCs. Moreover, H. pylori infection might increase the risk of TGF-beta 1-mediated tumorigenesis by disturbing the balance between apoptosis and proliferation of hepatocytes. Laboratory Investigation (2010) 90, 1507-1516; doi: 10.1038/labinvest.2010.109; published online 7 June 2010″
“Toxic lead (Pb) exposure poses serious risks to human health, especially to children at developmental stages, even at low exposure levels. Neural cell adhesion molecule (NCAM) is considered to be a potential early target in the neurotoxicity of Pb due to its role in cell adhesion, neuronal migration, synaptic plasticity, and learning and memory. However, the effect of low-level Pb exposure on the specific expression

of NCAM isoforms has not been reported. In the present click here study, we found that Pb could concentration-dependently

(1-100 nM) inhibit the expression of three major NCAM isoforms (NCAM-180, -140, and -120) Rho in primary cultured hippocampal neurons. Furthermore, it was verified that levels of all three major isoforms of NCAM were reduced by Pb exposure in human embryonic kidney (HEK)-293 cells transiently transfected with NCAM-120, -140, or -180 isoform cDNA constructs. In addition, low-level Pb exposure delayed the neurite outgrowth and reduced the survival rate of cultured hippocampal neurons at different time-points. Together, our results demonstrate that developmental low-level Pb exposure can attenuate the expression of all three major NCAM isoforms, which may contribute to the observed Pb-mediated neurotoxicity. (C) 2010 Elsevier Inc. All rights reserved.”
“Exposure to non-physiological solutions during peritoneal dialysis (PD) produces structural alterations to the peritoneal membrane and ultrafiltration dysfunction. The high concentration of glucose and glucose degradation products in standard PD fluids induce a local diabetic environment, which leads to the formation of advanced glycation end products (AGEs) that have an important role in peritoneal membrane deterioration. Peroxisome proliferator-activated receptor g (PPAR-g) agonists are used to treat type II diabetes and they have beneficial effects on inflammation, fibrosis, and angiogenesis.