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Articles by W. J Wang
Total Records ( 3 ) for W. J Wang
  H. S Yao , Q Wang , W. J Wang and C. P. Ruan

Objective  To evaluate the hemostatic effects and safety of thyroidectomy performed using the LigaSure vessel-sealing device (Valleylab, Boulder, Colorado) or the conventional vessel ligation.

Data Sources  The MEDLINE, EMBASE, Elsevier, SpringerLink, Ovid, and Cochrane Library electronic databases as well as the LigaSure manufacturer's Web site were searched for studies published between 1996 and 2008. No language restrictions were applied.

Study Selection  Prospective, controlled clinical trials, both randomized and nonrandomized, comparing the hemostatic effects and safety of thyroidectomy using LigaSure and conventional vessel ligation were selected.

Data Extraction  Data regarding operative parameters, duration of the operation, amount of intraoperative blood loss, length of hospital stay, and any postoperative complications were entered and analyzed using dedicated software from the Cochrane Collaboration.

Data Synthesis  Four randomized and 5 nonrandomized trials that met selection criteria reported data from 927 patients, of whom 467 (50.4%) underwent LigaSure and 460 (49.6%) underwent conventional thyroidectomy. Operative duration (weighted mean difference [WMD], –11.97 minutes; 95% confidence interval [CI], –16.42 to –7.53 minutes) was significantly reduced with LigaSure thyroidectomy (P < .001). When LigaSure was used, operative time reductions of 20.32 minutes (95% CI, –33.86 to –6.79 minutes) for total thyroidectomy (P = .003) and 21.74 minutes (–38.32 to –5.16 minutes) for subtotal thyroidectomy (P = .01) were also confirmed with subgroup analysis. However, differences in the amount of intraoperative blood loss (WMD, –25.13 mL; 95% CI, –68.45 to 18.18 mL; P = .26), length of hospital stay (WMD, –0.08 days; 95% CI, –0.23 to 0.08 days; P = .31), and postoperative complication rates (odds ratio, 0.91; 95% CI, 0.61-1.04; P = .65) were not statistically significant for LigaSure vs conventional thyroidectomy.

Conclusions  The LigaSure technique may provide a safe, effective, and fast alternative to conventional vessel ligation in thyroidectomy and may result in a significant reduction in operative duration. However, it may not confer any advantage over conventional thyroidectomy in terms of the amount of intraoperative blood loss, length of hospital stay, and postoperative complication rates.

  T Tian , K. J Nan , S. H Wang , X Liang , C. X Lu , H Guo , W. J Wang and Z. P. Ruan

Hepatocellular carcinoma (HCC) is a typical hypervascular tumor, and increased levels of vascular endothelial growth factor (VEGF) are associated with progression of HCC. Tumor suppression gene PTEN (phosphatase and tensin homolog deleted on chromosome 10), an important antagonist of the phosphoinositide-3-kinase (PI3K)/adenosine triphosphate-dependent tyrosine kinase (Akt) pathway, is also commonly lost or mutated in HCC. However, the effect of PTEN on VEGF-mediated angiogenesis in HCC remains unknown. To explore this relationship, we expressed a panel of PTEN mutants in human HCC cells with low expression of PTEN (HepG2 cells). Overexpression of PTEN in HepG2 cells resulted in the downregulation of proliferation and migration of cocultured endothelial cells and decreased expression of hypoxia-inducible factor 1 (HIF-1) and VEGF. Similarly, using a nude mouse model, we demonstrated that PTEN decreased expression of HIF-1 and VEGF and suppressed HepG2-induced angiogenesis. This inhibitory effect was not observed in cells expressing a phosphatase-deficient PTEN mutant, suggesting that PTEN inhibits angiogenesis and VEGF through a phosphatase-dependent pathway. Strikingly, reintroducing the C2 domain of PTEN also resulted in a significant decrease in angiogenesis and VEGF expression, although it did not affect Akt phosphorylation or HIF-1 expression. In summary, this study suggests the novel viewpoint that PTEN suppresses angiogenesis and VEGF expression in HCC through both phosphatase-dependent and -independent mechanisms.

  C. C Lin , W. N Lin , W. J Wang , C. C Sun , W. H Tung , H. H Wang and C. M. Yang

Vascular smooth muscle cells (VSMCs) that function as synthetic units play important roles in inflammatory diseases such as atherosclerosis and angiogenesis. As extracellular nucleotides such as ATP have been shown to act via activation of P2 purinoceptors implicated in various inflammatory diseases, we hypothesized that extracellular nucleotides contribute to vascular diseases via upregulated expression of inflammatory proteins, such as cyclooxygenase (COX-2) and cytosolic phospholipase A2 (cPLA2) in VSMCs.

Methods and results

Western blotting, promoter assay, RT–PCR, and PGE2 immunoassay revealed that ATPS induced expression of COX-2 and prostaglandin (PGE2) synthesis through the activation of p42/p44 MAPK (mitogen-activated protein kinase), p38 MAPK, and nuclear factor-B (NF-B). These responses were attenuated by inhibitors of MAPK/ERK kinase (MEK1/2; U0126), p38 MAPK (SB202190), and NF-B (helenalin), or by tranfection with dominant negative mutants of p42, p38, IB kinase (IKK), and IKKβ. Furthermore, the ATPS-stimulated translocation of NF-B into the nucleus and degradation of IB was blocked by U0126 and helenalin. In addition, the ATPS-stimulated cPLA2 expression was inhibited by U0126, SB202190, helenalin, celecoxib (a selective COX-2 inhibitor), and PGE2 receptor antagonists (AH6809, GW627368X, and SC-19220). However, the inhibitory effect of celecoxib on cPLA2 expression was reversed by addition of exogenous PGE2.


Our results suggest that in VSMCs, activation of p42/p44 MAPK, p38 MAPK, and NF-B is essential for ATPS-induced COX-2 expression and PGE2 synthesis. Newly synthesized PGE2 was observed to act as an autocrine signal contributing to cPLA2 expression, which may be implicated in inflammatory responses. Collectively, our findings provide insights into the correlation between COX-2 and cPLA2 expression in ATPS-stimulated VSMCs with similar molecular mechanisms and functional coupling to amplify the occurrence of vessel disease-related vascular inflammation.

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