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Articles by J. H Nam
Total Records ( 2 ) for J. H Nam
  S. Y Ryu , S. I Park , B. H Nam , I Kim , C. W Yoo , J. H Nam , K. H Lee , C. H Cho , J. H Kim , S. Y Park , B. G Kim and S. B. Kang
 

Background: This study was to investigate the prognostic significance of clinicopathologic characteristics in patients with clear-cell carcinoma (CCC) of the ovary.

Materials and methods: Two hundred and one patients with CCC of the ovary were registered in the Korean Gynecologic Oncology Group. The Korean Gynecologic Pathology Study Group reviewed the pathological slides centrally, using a universal grading system. The prognostic significances of clinicopathologic factors were evaluated by multivariate analysis.

Results: Most of the patients were diagnosed at an early stage (stage I, 61.3%), and the overall 5-year survival rate was 57%. Early-stage disease showed a favorable prognosis, but advanced diseases showed poor prognosis. Stage of disease was the only significant prognostic factor on multivariate analysis (P < 0.001). However, universal grade and residual tumor also showed prognostic significance on the forward stepwise likelihood ratio test. There was no survival difference observed between patients treated with paclitaxel-based and those treated with platinum-based combination chemotherapy.

Conclusions: The stage, residual tumor, and universal grade were significant prognostic factors in patients with CCC of the ovary. The universal grading system is applicable in determining prognosis of CCC of the ovary. Further clinical trials for optimal chemotherapy are in need.

  H Zheng , J. H Nam , B Pang , D. H Shin , J. S Kim , Y. S Chun , J. W Park , H Bang , W. K Kim , Y. E Earm and S. J. Kim
 

Mouse B cells and their cell line (WEHI-231) express large-conductance background K+ channels (LKbg) that are activated by arachidonic acids, characteristics similar to TREK-2. However, there is no evidence to identify the molecular nature of LKbg; some properties of LKbg were partly different from the reported results of TREK type channels. In this study, we compared the properties of cloned TREK-2 and LKbg in terms of their sensitivities to ATP, phosphatidylinositol 4,5-bisphosphate (PIP2), intracellular pH (pHi), and membrane stretch. Similar to the previous findings of LKbg, TREK-2 showed spontaneous activation after membrane excision (i-o patch) and were inhibited by MgATP or by PIP2. The inhibition by MgATP was prevented by wortmannin, suggesting membrane-delimited regulation of TREKs by phosphoinositide (PI) kinase. The same was observed with the property of LKbg; the activation of TREK-2 by membrane stretch was suppressed by U73122 (PLC inhibitor). As with the known properties of TREK-2, LKbg were activated by acidic pHi and inhibited by PKC activator. Finally, we confirmed the expression of TREK-2 in WEHI-231 by using RT-PCR and immunoblot analyses. The amplitude of background K+ current and the TREK-2 expression in WEHI-231 were commonly decreased by genetic knockdown of TREK-2 using small interfering RNA. The downregulation of TREK-2 attenuated Ca2+-influx induced by arachidonic acid in WEHI-231. As a whole, these results strongly indicate that TREK-2 encodes LKbg in mouse B cells. We also newly suggest that the low activity of TREK-2 in intact cells is due to the inhibition by intrinsic PIP2.

 
 
 
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