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Articles by W. Jiang
Total Records ( 3 ) for W. Jiang
  X. Zou , Z. Deng , M. Ge , G. Dick , W. Jiang and J. Liu
  In order to obtain crustal deformations of higher spatial resolution, existing GPS networks must be densified. This densification can be carried out using single-frequency receivers at moderate costs. However, ionospheric delay handling is required in the data processing. We adapt the Satellite-specific Epoch-differenced Ionospheric Delay model (SEID) for GPS networks with mixed single- and dual-frequency receivers. The SEID model is modified to utilize the observations from the three nearest dual-frequency reference stations in order to avoid contaminations from more remote stations. As data of only three stations are used, an efficient missing data constructing approach with polynomial fitting is implemented to minimize data losses. Data from large scale reference networks extended with single-frequency receivers can now be processed, based on the adapted SEID model. A new data processing scheme is developed in order to make use of existing GPS data processing software packages without any modifications. This processing scheme is evaluated using a sub-network of the German SAPOS network. The results verify that the new scheme provides an efficient way to densify existing GPS networks with single-frequency receivers.
  L Wang , B Wu , Y Sun , T Xu , X Zhang , M Zhou and W. Jiang
  Background

Previous studies have indicated that protein kinase C (PKC) may enhance endothelial nitric oxide synthase (eNOS) activation, although the detailed mechanism(s) remains unclear. In this study, we investigated the roles of PKC isoforms in regulating propofol-induced eNOS activation in human umbilical vein endothelial cells (HUVECs).

Methods

We applied western blot (WB) analysis to investigate the effects of propofol on Ser1177 phosphorylation-dependent eNOS activation in HUVECs. Nitrite (NO2) accumulation was measured using the Griess assay. The phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway was examined by WB assay. Propofol-induced translocation of individual PKC isoforms in subcellular fractions in HUVECs was analysed using WB assay.

Results

In HUVECs, protocol treatment (1–100 µM) for 10 min induced a concentration-dependent increase in phosphorylation of eNOS at Ser1177. The NO production was also increased accordingly. PKC inhibitors, bisindolylmaleimide I (0.1–1 µM), and staurosporine (20 and 100 nM), effectively blocked propofol-induced eNOS activation and NO production. Further analyses in fractionated endothelial lysate showed that short-term propofol treatment (50 µM) led to translocation of PKC-, PKC-, PKC-, PKC-, and PKC- from cytosolic to membrane fractions, which could also be inhibited by both PKC inhibitors. These data revealed that the differential redistribution of these isozymes is indispensable for propofol-induced eNOS activation. In addition, Akt was not phosphorylated in response to propofol at Ser473 or Thr308.

Conclusions

Propofol induces the Ser1177 phosphorylation-dependent eNOS activation through the drug-stimulated translocation of PKC isoforms to distinct intracellular sites in HUVECs, which is independent of PI3K/Akt-independent pathway.

  Y. Liu , W. Jiang , S. Li , Z.P. Cheng , D. Song , X.J. Zhang and F.S. Li
  Novel Fe3O4/carbon nanotubes (CNTs) nanocomposites were prepared by a polyol-medium solvothermal method using oleate as an interlinker molecule and characterized via X-ray diffractometry, X-ray photoelectron spectroscopy, transmission electron microscopy and vibration sample magnetometry. Results indicated that the Fe3O4 nanoparticles were successfully attached on the surface of CNTs and the nanocomposites were proved to be superparamagnetic with saturation magnetization of 50.0 emu g−1. A proposed formation mechanism of the magnetic nanocomposites was presented.
 
 
 
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