“
“Background Previous studies suggested that mechanical

intervention during early reperfusion, or ischemia postconditioning (IPo), could protect kidneys against renal ischemia reperfusion injury (RIRI). However, the mechanisms responsible for this protection remain unclear. This study therefore investigated the protection afforded by IPo in rat kidneys in vivo, and the roles of mitochondrial K(ATP) channels (mitoK(ATP)) and mitochondrial permeability transition pores (MPTPs), by inhibiting mitoK(ATP) with 5-hydroxydecanoate (5-HD), and by directly detecting open MPTPs using calcein-AM and CoCl(2).\n\nMethods Thirty-five male Sprague-Dawley rats were randomly assigned to sham-operation (S), ischemia-reperfusion (I/R), IPo, ischemia reperfusion with 5-HD (I/R+5-HD), or IPo with 5-HD (IPo +5-HD) groups. Rats in each group were Dibutyryl-cAMP molecular weight sacrificed after 6 hours of reperfusion by heart exsanguination or cervical dislocation under anesthesia. RIRI was assessed by determination of creatinine and blood urea nitrogen (BUN), and by examination of histologic sections. The roles of mitoK(ATP) and MPTP were investigated by analyzing fluorescence intensities of mitochondria, mitochondrial membrane potential, intracellular reactive oxygen species (ROS) and intracellular calcium, using

appropriate selleckchem fluorescent markers. The relationship between apoptosis and RIRI was assessed by determining the apoptotic index (Al) of kidney tubular epithelial cells.\n\nResults The RIRI model was shown to be successful. Significantly higher levels of creatinine and BUN, and abnormal pathology of histologic

sections, were observed in group I/R, compared with group S. 5-HD eliminated the renoprotective effects of IPo. Mitochondrial and mitochondrial membrane potential fluorescence intensities increased, and intracellular calcium, ROS fluorescence intensities and Al decreased in group IPo, compared with group I/R. However, mitochondrial and selleck products mitochondrial membrane potential fluorescence intensities decreased, and intracellular calcium and ROS fluorescence intensities and Al increased in group IPo+5-HD, compared with group IPo.\n\nConclusions mitoK(ATP) and MPTPs participated in IPo-induced renoprotective mechanisms in rat kidneys subjected to RIRI, possibly through decreased renal tubular epithelial cell apoptosis. Chin Med J 2011;124(14):2191-2195″
“In a continuous anaerobic-anoxic-aerobic (A(2)O) process treating domestic wastewater at ambient temperatures, nitritation was achieved through a combination of short aerobic actual hydraulic retention time (AHRT) and low dissolved oxygen (DO) levels (0.3-0.5 mg/L). The nitrite accumulation rate was about 90% and ammonia removal efficiency was over 95%. With respect to total nitrogen removal, nitritation-denitritation at low DO levels of 0.3-0.5 mg/L was essentially equal to the complete nitrification-denitrification at DO levels of 1.5-2.5 mg/L with the addition of external carbon sources.