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Articles by H. S Park
Total Records ( 5 ) for H. S Park
  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.

  H. S Park , S. A Roman and J. A. Sosa
 

Objective  To assess the effect of surgeon volume and specialty on clinical and economic outcomes after adrenalectomy.

Design  Population-based retrospective cohort analysis.

Setting  Healthcare Cost and Utilization Project Nationwide Inpatient Sample.

Participants  Adults (≥18 years) undergoing adrenalectomy in the United States (1999-2005). Patient demographic and clinical characteristics, surgeon specialty (general vs urologist), surgeon adrenalectomy volume, and hospital factors were assessed.

Main Outcome Measures  The 2 test, analysis of variance, and multivariate linear and logistic regression were used to assess in-hospital complications, mean hospital length of stay (LOS), and total inpatient hospital costs.

Results  A total of 3144 adrenalectomies were included. Mean patient age was 53.7 years; 58.8% were women and 77.4% white. A higher proportion of general surgeons were high-volume surgeons compared with urologists (34.1% vs 18.2%, P < .001). Low-volume surgeons had more complications (18.2% vs 11.3%, P < .001) and their patients had longer LOS (5.5 vs 3.9 days, P < .001) than did high-volume surgeons; urologists had more complications (18.4% vs 15.2%, P = .03) and higher costs ($13 168 vs $11 732, P = .02) than did general surgeons. After adjustment for patient and provider characteristics in multivariate analyses, surgeon volume, but not specialty, was an independent predictor of complications (odds ratio = 1.5, P < .002) and LOS (1.0-day difference, P < .001). Hospital volume was associated only with LOS (0.8-day difference, P < .007). Surgeon volume, specialty, and hospital volume were not predictors of costs.

Conclusion  To optimize outcomes, patients with adrenal disease should be referred to surgeons based on adrenal volume and laparoscopic expertise irrespective of specialty practice.

  J. S Kang , S Y.Bae , H R.Kim , Y. S Kim , D J.Kim , B. J Cho , H. K Yang , Y. I Hwang , K J.Kim , H. S Park , D H.Hwang , D J.Cho and W. J. Lee
 

Cancer cells metastasize to the other site after escaping from the immune system and CD70, CD44 and vascular endothelial growth factor (VEGF) play important roles in this process. It is recently reported that interleukin (IL)-18 is closely related with the pathogenesis of skin tumor. Therefore, we investigated the role of endogenous IL-18 from stomach cancer on the immune escape mechanism and metastasis via the regulation of CD70, CD44 and VEGF expression. IL-18 and IL-18R expressions were not only investigated on tumor tissues (n = 10), and sera (n = 20) from stomach cancer patients, but also on human stomach cancer cell lines. IL-18 and IL-18R expressions were found on stomach cancer cell lines and tumor tissues. In addition, IL-18 levels were elevated in sera from cancer patients (P < 0.05), compared with sera from normal individuals. Changes in CD70, CD44 and VEGF expression by flow cytometry, immunoblotting and enzyme-linked immunosorbent assay and immune susceptibility by 51Cr-release assay were investigated, after silencing or neutralization of endogenous IL-18. CD70 expression was increased and it increases immune susceptibility of cancer cells. In contrast, CD44 and VEGF expression was decreased and it suppresses neovascularization and the metastasis of stomach cancer. After inoculation of IL-18 small interfering RNA (siRNA)-transfected stomach cancer cells into Balb/C (nu/nu) mice, regression of tumor mass was determined by measuring of tumor size. And the number and location of metastatic lesions were investigated by hematoxylin and eosin staining. The regression of tumor mass and the suppression of metastasis were observed in the mice, which are injected with IL-18 siRNA-transfected cell lines. Our data suggest that endogenous IL-18 might facilitate stomach cancer cell immune escape by suppressing CD70 and increasing metastatic ability by upregulating CD44 and VEGF.

  M. J Betzenhauser , L. E Wagner , H. S Park and D. I. Yule
 

ATP is known to increase the activity of the type-1 inositol 1,4,5-trisphosphate receptor (InsP3R1). This effect is attributed to the binding of ATP to glycine rich Walker A-type motifs present in the regulatory domain of the receptor. Only two such motifs are present in neuronal S2+ splice variant of InsP3R1 and are designated the ATPA and ATPB sites. The ATPA site is unique to InsP3R1, and the ATPB site is conserved among all three InsP3R isoforms. Despite the fact that both the ATPA and ATPB sites are known to bind ATP, the relative contribution of these two sites to the enhancing effects of ATP on InsP3R1 function is not known. We report here a mutational analysis of the ATPA and ATPB sites and conclude neither of these sites is required for ATP modulation of InsP3R1. ATP augmented InsP3-induced Ca2+ release from permeabilized cells expressing wild type and ATP-binding site-deficient InsP3R1. Similarly, ATP increased the single channel open probability of the mutated InsP3R1 to the same extent as wild type. ATP likely exerts its effects on InsP3R1 channel function via a novel and as yet unidentified mechanism.

 
 
 
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