Sustained increase in microvessel permeability results in cell and tissue damage. To date, it has not been possible to safely and specifically block increased microvessel permeability in vivo. We showed that insulin stimulates angiogenesis and that the new microvessels are associated with more αSMA-producing cells, suggesting greater stability. In this study, we show that local injection of insulin under the skin of mice significantly inhibits thrombin-induced microvessel permeability and that insulin improves the barrier function of primary human endothelial cells under conditions that mimic endothelium in vivo. These findings indicate that insulin antagonizes thrombin-induced microvessel permeability. At the cell and molecular levels, we show that insulin interferes with thrombin-induced VE-cadherin signaling by decreasing the ability of thrombin to induce VE-cadherin translocation to the cytoskeleton/nuclear compartment, leading to microvessel leakage. Simultaneously, the rapid activation of Src by insulin followed by the activation of Rac1, a small GTPase involved in cytoskeletal reorganization, leads to the maintenance of endothelial barrier, short-circuiting the slower thrombin-induced Src-RhoA signaling that leads to endothelial permeability. This novel mechanism by which insulin inhibits thrombin-induced permeability provides support for the use of insulin treatment in pathological conditions that involve blood-barrier dysfunction, especially as resuscitation treatment methods for extensive burns, sepsis, and other severe pathological conditions.

The polyphenylene sulfide (PPS) Nonwoven was modified by grafting polymerization of the acrylic acid (AA) with the initiation of the low temperature plasma. Effects of different treatment conditions on the graft reaction and the hydrophility of the modified PPSs were investigated. Scanning electron microscopy (SEM) images showed that the graft polymerization only occurred on the surface of PPS. The hydrophility of the PPS nonwoven were examined by alkali absorption rate. The results show that the optimum modified conditions are 90s treating time, 50W plasma power and 1.5cm distance between of the electrodes.

The influences of jet flow rate and temperature on cathodic polarization of nickel deposits have been studied in this paper. The results indicate that increasing jet flow rate and temperature of the electrolyte make the equilibrium electrode potential decrease. When jet flow rate increases from 1.0 L/min to 6.0 L/min, the grain size of nickel deposits decreases from 22.6 nm to 18.9 nm. X-ray diffraction patterns show that increasing jet flow rate results in (111) preferred growth orientation for nickel deposits.