It can be used to assess perceived rehabilitation needs for individuals with schizophrenia in Hong Kong. Upon further validations, it may be applied in other Chinese societies such as Singapore and the mainland. Similar research

methodology can also be used for assessing needs in other types of psychiatric disability groups.”
“The mechanisms underlying the neurotoxicology of endemic fluorosis still remain obscure. To explore lactate dehydrogenase (LDH) leakage, intracellular Ca2+ concentration ([Ca2+]i) and reactive oxygen species (ROS) production induced by fluoride, human neuroblastoma (SH-SY5Y) cells Smad inhibitor were incubated with sodium fluoride (NaF, 20, 40, 80 mg/L) for 24 h, with 40 mg/L NaF for 3, 6, 12, 18, 24 h, and N-acetyl-L-cysteine (NAC), ethyleneglycol-bis-(-aminoethyl ether)-N,N,N,N-tetraacetic acid (EGTA), 1,2-bis(O-aminophenoxy)ethane-N,N,N,N-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM) alone or combined with fluoride (40 mg/L) respectively for 12 h in vitro. The results showed that the LDH levels in the 40 and 80 mg/L fluoride-treated groups were significantly CT99021 purchase higher than that of the control group (in the test level of 0.05, the difference were statistical significance). [Ca2+]i and ROS reached a peak at 3 h and 12 h respectively after exposure to 40 mg/L fluoride. Fluoride coincubated with NAC (antioxidant) dramatically decreased ROS and LDH

levels compared with the fluoride only group (in the test level of 0.05, the difference were statistical significance). However, fluoride-induced increase in [Ca2+]i was not affected by NAC. BAPTA-AM (intracellular calcium chelator) markedly lowered fluoride-induced increase of [Ca2+]i, ROS 3-MA mouse and LDH levels while EGTA (extracellular calcium chelator) have no effects on them. These results indicate that fluoride-related Ca2+ release from the site of intracellular calcium storage causes the elevation of ROS contributing to the cytotoxicity in SH-SY5Y cells. (c) 2011 Wiley Periodicals, Inc. Environ

Toxicol, 2013.”
“Recent and compelling investigation has expanded our view of the biological settings in which the products of nonenzymatic glycation and oxidation of proteins and lipids – the advanced glycation endproducts (AGEs) – form and accumulate. Beyond diabetes, natural ageing and renal failure, AGEs form in inflammation, oxidative stress and in ischaemia – reperfusion. The chief signal transduction receptor for AGEs – the receptor for AGEs (RAGE) – is a multiligand-binding member of the immunoglobulin superfamily. In addition to AGEs, RAGE binds certain members of the S100/calgranulin family, high-mobility group box 1 (HMGB1), and beta-amyloid peptide and beta-sheet fibrils. Recent studies demonstrate beneficial effects of RAGE antagonism and genetic deletion in rodent models of atherosclerosis and ischaemia reperfusion injury in the heart and great vessels.