Human Phospho-Tie-2 (Y992) ELISA Kit

Fast decline of groundwater levels in Pakistan requires the use of artificial recharging techniques to minimize the adverse effect of over pumping. A study was conducted in the Toba Tek Singh district, Punjab, Pakistan, to investigate aquifer storage and recovery (ASR) technology to recharge groundwater. The facility was developed by drilling a pumping/injection well and constructing the water storage tank along with developing the recharge mechanism. Three treatments of 51, 71, and 99 m(3) of treated canal water were injected into the aquifer under gravity and were retained for 7 days. Another three treatments of 100 m(3) each were injected for retention times of 14, 28, and 56 days. The recovery efficiency (RE) was found to be 83, 91, and 98% for injected volumes of 51, 71, and 99 m(3), respectively, for retention time of 7 days. Similarly, the RE for an injected volume of 100 m(3) was found to be 73, 62, and 52% for retention times of 14, 28, and 56 days, respectively. These results indicated that RE improved with increase in injected volume and decreased with increase in retention time; however, the technology was found to have potential for storing and recovering of water injected into the aquifer.

Endothelial cells participate in the pathophysiology of ischemic AKI by increasing the expression of cell adhesion molecules and by recruiting inflammatory cells. We previously showed that endothelial Kruppel-like factor 4 (Klf4) regulates vascular cell adhesion molecule 1 (Vcam1) expression and neointimal formation after carotid injury. In this study, we determined whether endothelial Klf4 is involved in ischemic AKI using endothelial Klf4 conditional knockout (Klf4cKO) mice generated by breeding Tek-Cre mice and Klf4floxed mice. Klf4 cKO mice were phenotypically normal before surgery. However, after renal ischemia-reperfusion injury, Klf4 cKO mice exhibited elevated serum levels of urea nitrogen and creatinine and aggravated renal histology compared with those of Klf4 floxed controls. Moreover, Klf4 cKO mice exhibited enhanced accumulation of neutrophils and lymphocytes and elevated expression of cell adhesion molecules, including Vcam1 and Icam1, in injured kidneys. Notably, statins ameliorated renal ischemia-reperfusion injury in control mice but not in Klf4 cKO mice. Mechanistic analyses in cultured endothelial cells revealed that statins increased KLF4 expression and that KLF4 mediated the suppressive effect of statins on TNF-alpha-induced VCAM1 expression by reducing NF-kappa B binding to the VCAM1 promoter. These results provide evidence that endothelial Klf4 is renoprotective and mediates statin-induced protection against ischemic AKI by regulating the expression of cell adhesion molecules and concomitant recruitment of inflammatory cells.