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Articles by K. U. Lee
Total Records ( 2 ) for K. U. Lee
  E. H Koh , M Kim , K. C Ranjan , H. S Kim , H. S Park , K. S Oh , I. S Park , W. J Lee , M. S Kim , J. Y Park , J. H Youn and K. U. Lee
 

Nitric oxide (NO) stimulates mitochondrial biogenesis. We recently reported that adiponectin synthesis is regulated by mitochondrial function in adipocytes. This study was undertaken to test the hypothesis that endothelial NO synthase (eNOS) plays an important role in adiponectin synthesis by producing NO and enhancing mitochondrial function in adipocytes. We examined the effects of eNOS knockdown on adiponectin synthesis in 3T3-L1 adipocytes and also examined plasma adiponectin levels and the mitochondria in adipose tissue of eNOS knockout (eNOS–/–) mice with and without chronic administration of a NO donor. In cultured 3T3-L1 adipocytes, eNOS siRNA decreased rosiglitazone-induced adiponectin secretion, which was associated with decreases in mitochondrial proteins and biogenesis factors. Plasma adiponectin concentrations were reduced in adult eNOS–/– mice compared with age-matched wild-type mice. Mitochondrial contents in adipose tissue were reduced in eNOS–/– mice, and this was associated with decreased expression of mitochondrial biogenesis factors, increased levels of 8-hydroxyguanosine, a biomarker of oxidative stress, and morphological abnormalities in mitochondria. Rosiglitazone-induced increases in adiponectin expression and mitochondrial content were also reduced significantly in eNOS–/– mice. Chronic administration of a NO donor reversed mitochondrial abnormalities and increased adiponectin expression in adipose tissue of eNOS–/– mice. eNOS plays an important role in adiponectin synthesis in adipocytes by increasing mitochondrial biogenesis and enhancing mitochondrial function.

  S. H Hwang , D. J Park , Y. S Jee , M. C Kim , H. H Kim , H. J Lee , H. K Yang and K. U. Lee
 

Objective  To analyze 3-year actual disease-free survival after laparoscopy-assisted gastrectomy for gastric cancer on the assumption that 3-year disease-free survival may represent 5-year overall survival.

Design  Retrospective analysis.

Setting  Department of surgery of a university hospital.

Patients  A total of 197 patients who underwent laparoscopy-assisted gastrectomy for gastric cancer from May 1998 to September 2007 and who were followed up for more than 3 years.

Main Outcome Measures  Feasibility and long-term survival rate with survival analysis by the Kaplan-Meier method.

Results  Subtotal and total gastrectomies were performed in 178 and 19 patients, respectively. The scope of the lymph node dissections were D1 + β (n = 152) and D2 (n = 45). There were 153, 28, 8, 6, 1, and 1 patients in stages Ia, Ib, II, IIIa, IIIb, and IV, respectively. The median follow-up was 45 months (range, 1-113 months), and there were 7 recurrences. Multivariate analysis of disease-specific survival showed that depth of invasion and lymph node metastasis influenced the prognosis independently. The actual 3-year disease-free survival rate for all patients was 96.9%. The 173 patients with early gastric cancer and 24 with advanced gastric cancer showed 98.8% and 79.1% actual 3-year disease-free survival rates, respectively.

Conclusions  Laparoscopy-assisted gastrectomy is acceptable oncologically in early gastric cancer if 3-year disease-free survival represents 5-year overall survival. Laparoscopy-assisted gastrectomy may also play an important role in the treatment of advanced gastric cancer.

 
 
 
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