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Articles by W Shen
Total Records ( 4 ) for W Shen
  P Liu , W Chen , H Zhu , B Liu , S Song , W Shen , F Wang , S Tucker , B Zhong and D. Wang

The purpose of this study was to specifically investigate the clinicopathological role of expression of vascular endothelial growth factor-C (VEGF-C) as well as the correlation with clinical outcomes in esophageal squamous cell carcinomas (ESCCs).


Seventy-three patients with ESCC resected in our institute were included in this study. Formalin-fixed paraffin-embedded specimens were stained for VEGF-C and the correlation between the staining, its clinicopathological parameters and its prognostic power were analyzed statistically.


Of the 73 ESCC patients studied, 39 cases (53.4%) were strongly positive for VEGF-C. Six cases (8.2%) were negative and 28 cases (38.4%) revealed unclear weak reactions. All 34 cases were included in the negative group (46.6%). VEGF-C expression correlated with histological grade (P = 0.005), depth of tumor invasion (pT) (P = 0.021), lymph node metastasis (pN) (P = 0.002) and lymphatic invasion (P = 0.008). The median overall survival of 39 patients who had positive staining for tumor cell VEGF-C and 34 patients who had negative staining were 10.4 months (95% CI, 6.9–13.9 months) and 28.5 months (95% CI, 12.6–44.4 months), respectively (P = 0.003). In univariate analysis by log-rank test, histological grade, pN, stage, lymphatic invasion and VEGF-C were significant prognostic factors (P = 0.047, 0.007, 0.018, 0.002 and 0.003, respectively.). In multivariate analysis, high VEGF-C expression (P = 0.0451) maintained its independent prognostic influence on overall survival, as well as pN status (P = 0.0029).


Expression of VEGF-C is related to histological grade, pT, pN and lymphatic invasion, and is a prognostic indicator for ESCC.

  T Iriuchishima , G Tajima , S. J. M Ingham , W Shen , P Smolinski and F. H. Fu

Background: Although the literature has extensively discussed impingement after anterior cruciate ligament (ACL) reconstruction, the definition of impingement is vague, and impingement pressure has not been well investigated as a function of tunnel position.

Purpose: To determine the amount of impingement pressure between the ACL and posterior cruciate ligament (PCL) and between the ACL and notch roof in the native ACL, the single-bundle ACL reconstruction with different tunnel placements, and the anatomical double-bundle ACL reconstruction.

Study design: Controlled laboratory study.

Methods: Fifteen fresh-frozen nonpaired human cadaver knees were used. In each knee, different femoral and tibial tunnels were created, which allowed different graft placements. A single graft was placed in 3 positions: tibial anteromedial (AM) to femoral AM (anatomical), tibial posterolateral (PL) to femoral high AM (nonanatomical/mismatch), and tibial AM to femoral high AM. Double grafts were placed in an anatomical fashion (AM to AM and PL to PL). In each case, pressure-measuring films were inserted between the ACL and roof, the ACL and PCL, and the AM and PL bundles (for double-bundle group only). Knees were then moved with 40 N of force and from full flexion to full extension, and the pressure pattern on the film was analyzed.

Results: Compared with other groups, only the AM–high AM group showed significantly higher roof impingement pressure (P < .05). There was no significant difference in PCL impingement pressure between the intact ACL group and any of the reconstructed groups. No impingement pressure was observed between the grafts in the anatomical double-bundle ACL reconstruction.

Conclusion: This study evaluated the effect of different tunnel placements on the impingement pressure after ACL reconstruction. Anatomical single- or double-bundle ACL reconstruction and nonanatomical tibial PL–femoral high AM ACL reconstruction do not cause roof, PCL, and interbundle impingement.

Clinical relevance: Surgeons can perform the anatomical double-bundle ACL, anatomical single-bundle, and nonanatomical tibial PL–femoral high AM reconstructions as impingement-free reconstructions.

  X. p Tong , X. y Li , B Zhou , W Shen , Z. j Zhang , T. l Xu and S. Duan

NG2 cells originate from various brain regions and migrate to their destinations during early development. These cells express voltage-gated Na+ channels but fail to produce typical action potentials. The physiological role of Na+ channels in these cells is unclear. We found that GABA induces membrane depolarization and Ca2+ elevation in NG2 cells, a process requiring activation of GABAA receptors, Na+ channels, and Na+/Ca2+ exchangers (NCXs), but not Ca2+ channels. We have identified a persistent Na+ current in these cells that may underlie the GABA-induced pathway of prolonged Na+ elevation, which in turn triggers Ca2+ influx via NCXs. This unique Ca2+ signaling pathway is further shown to be involved in the migration of NG2 cells. Thus, GABAergic signaling mediated by sequential activation of GABAA receptors, noninactivating Na+ channels, and NCXs may play an important role in the development and function of NG2 glial cells in the brain.

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