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Articles by X Tian
Total Records ( 2 ) for X Tian
  Y Tu , J Lu , J Fu , Y Cao , G Fu , R Kang , X Tian and B. Wang
  Objective

Neuroepithelial-transforming protein 1 is a member of the guanine nucleotide exchange factor family, a group of proteins which are known to activate and thereby regulate Rho family members. Deregulation of neuroepithelial-transforming protein 1 expression has been found in certain types of human tumors. To investigate its prognostic value in human gliomas, which is currently unknown, we examined the correlation between neuroepithelial-transforming protein 1 expression and prognosis in patients with gliomas.

Methods

Immunohistochemical staining was performed to detect neuroepithelial-transforming protein 1 expression patterns in the biopsies from 96 patients with primary gliomas. Kaplan–Meier survival and Cox's regression analyses were performed to evaluate the prognosis of patients.

Results

Immunohistochemical analysis with anti-neuroepithelial-transforming protein 1 antibody revealed that neuroepithelial-transforming protein 1 was significantly associated with the Karnofsky performance scale score and World Health Organization grades of patients with gliomas. Especially, the positive expression rates of neuroepithelial-transforming protein 1 were significantly higher in patients with higher grade (P = 0.001) and lower Karnofsky's performance scale score (P = 0.005). The median survival of patients with high neuroepithelial-transforming protein 1 expression was significantly shorter than that with low expression and without expression (316, 892 and 1180 days, respectively). Cox's multifactor analysis showed that the Karnofsky performance scale (P = 0.01), World Health Organization grade (P = 0.008) and neuroepithelial-transforming protein 1 (P = 0.006) were independent prognosis factors for human glioma.

Conclusions

Taken together, our study indicates for the first time that neuroepithelial-transforming protein 1 status may be a highly sensitive marker for glioma prognosis and suggest that the expression patterns of neuroepithelial-transforming protein 1 might be a potent tool for predicting the clinical prognosis of glioma patients.

  S. D Hingtgen , Z Li , W Kutschke , X Tian , R. V Sharma and R. L. Davisson
 

Recent studies from our laboratory and others have shown that increases in cytoplasmic superoxide (O2·–) levels and Akt activation play a key role in agonist-stimulated NF-B activation and cardiomyocyte hypertrophy in vitro. In this study, we tested the hypothesis that adenovirus (Ad)-mediated intramyocardial gene transfer of cytoplasmic superoxide dismutase (AdCu/ZnSOD) or a dominant-negative form of Akt (AdDNAkt) in mice would attenuate pressure overload-induced increases in activation of the redox-sensitive transcription factor NF-B and cardiac hypertrophy. Adult C57BL/6 mice were subjected to thoracic aortic banding (TAB) or sham surgery, and intramyocardial injections of viral vectors (AdCu/ZnSOD, AdDNAkt, or control) were performed. There was robust transgene expression in the heart, which peaked 6–7 days after injection and then declined to undetectable levels by 12–14 days. In mice injected with AdBgL II, TAB caused a significant increase in O2·– generation and cardiac mass at 1 wk, and these responses were markedly attenuated by AdCu/ZnSOD. In addition, TAB induced time-dependent activation of NF-B in the myocardium as measured longitudinally by in vivo bioluminescent imaging of NF-B-dependent luciferase expression. This was also abolished by intracardiac AdCu/ZnSOD or AdDNAkt, but not the control vector. The inhibition of Akt and O2·–-mediated NF-B activation in TAB hearts was associated with an attenuation of cardiac hypertrophy. Since a direct cause-and-effect relationship between NF-B activation and cardiomyocyte hypertrophy has been established previously, our data support the hypothesis that increased O2·– generation and Akt activation are key signaling intermediates in pressure overload-induced activation of NF-B and cardiac hypertrophy.

 
 
 
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