053-0.28 pmol/ ml plasma), and 80 times lower in urine (0.036, below detection 0.087 pmol/m1). Serum-ARGS and plasma-ARGS concentrations were similar, and correlated (rs = 0.773, P < 0.001). SF concentration correlated with serum concentrations (rs = 0.420, P = S3I-201 concentration 0.011). In blood, we identified 129-138 kDa aggrecan fragments containing the ARGS neoepitope.

Conclusions: This novel ARGS-aggrecan assay is highly sensitive and suited for analysis of SF and blood samples. Both SF and blood contains ARGS-aggrecan, and ARGS concentrations in

SF and serum are correlated. (C) 2013 Published by Elsevier Ltd on behalf of Osteoarthritis Research Society International.”
“p53 can mediate DNA damage-induced apoptosis in various cell lines treated with Benzo(a)pyrene (BaP). However, the potential role of p73, one of the p53

family members, in BaP-induced apoptotic cell death remains to be determined. In this study, normal fetal lung fibroblasts (MRC-5) and human lung adenocarcinoma cells (H1299, p53-null) were treated with BaP at concentrations of 8, 16, 32, 64, and 128 mu M for 4 and 12 h. The oxidative stress status, extent of DNA damage, expression of p53, p73, mdm2, bcl-2, and bax at the mRNA and protein levels, and the percentages of apoptosis and/or necrosis were assessed. In the two BaP-treated Entinostat ic50 cell lines, we observed increased malondialdehyde (MDA) formation and decreased superoxide buy Emricasan dismutase (SOD) and glutathione

peroxidase (GSH-Px) activity at 4 h after the treatment; furthermore, at the time points of 4 and 12 h, we observed extremely high levels of DNA damage. In addition, at 4 h after the treatment, BaP had induced necrosis in MRC-5 and H1299 cells, but it had inhibited apoptosis in MRC-5 cells (P < 0.01 for all). Furthermore, in BaP-treated H1299 cells, only the p73 mRNA level was up-regulated. The results suggested that BaP-induced DNA damage could trigger a shift from apoptotic cell death toward necrotic cell death and that necrotic cell death is independent of p53 and p73 in these cell lines. Future studies are needed to investigate the time course of changes in the type of BaP-induced cell death in more cell lines. (C) 2010 Wiley Periodicals, Inc. Environ Toxicol, 2012.”
“Background: The objective of this study was to assess the role of pulmonary fat embolism caused by intramedullary pressurization of the femoral canal in the development of acute lung injury in the setting of acute hemorrhagic shock and resuscitation.