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Articles by K. W Park
Total Records ( 5 ) for K. W Park
  A Shin , E. R Cho , J Kim , J Sung , K. W Park , M. K Lim and H. R. Shin

Hepatitis B (HBV) and hepatitis C (HCV) viral infections are the most important risk factors for hepatocellular carcinoma (HCC), which is responsible for 17.5% of cancer deaths in Korea. The objectives of this study were to identify demographic characteristics that may affect hepatitis carriers' awareness of their infection status, and to assess whether health-related behaviors differed by awareness of the infection. Among 18,636 persons who were recruited from a cancer screenee cohort, 904 were HBV carriers and 146 were HCV carriers. Among the HBV carriers, 74.2% were aware of their infection status. Higher education (odds ratio, 1.8; college versus middle school or less), family history of liver cancer or disease, and marriage were associated with awareness of HBV infection status. Participants who were aware of their HBV carrier status were more likely to be former smokers or drinkers than those who were not aware of their status. Only 34.9% of HCV carriers were aware of their HCV infection status. No demographic characteristics were related to awareness of HCV infection status among HCV carriers. However, HCV carriers who were aware of their infection status were more likely to be former drinkers (odds ratio, 9.2; 95% confidence interval, 1.8-47.2). In conclusion, two thirds of HCV carriers and one fourth of HBV carriers in this study population were not aware of their infection status, and awareness of hepatitis infection status was significantly associated with other risk behaviors, such as alcohol consumption and cigarette smoking. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1894–8)

  J. Y Kim , H. J Cho , J. J Sir , B. K Kim , J Hur , S. W Youn , H. M Yang , S. I Jun , K. W Park , S. J Hwang , Y. W Kwon , H. Y Lee , H. J Kang , B. H Oh , Y. B Park and H. S. Kim

Inflammation, and the subsequent proliferative activity of vascular smooth muscle cells (VSMCs), is one of the major pathophysiological mechanisms associated with neointimal hyperplasia following vascular injury. Although sulfasalazine (SSZ) has been used as an anti-inflammatory and immune-modulatory agent in various inflammatory diseases, its primary targets and therapeutic effects on vascular disease have not yet been determined. We investigated whether SSZ could suppress VSMC growth and prevent neointimal hyperplasia.

Methods and results

SSZ was found to have pro-apoptotic and anti-proliferative activity in cultured VSMCs. Unexpectedly, these effects were not mediated by nuclear factor kappa B (NF-B) inhibition, which has been suggested to be the anti-inflammatory mechanism associated with the effects of SSZ. Instead, cell-cycle arrest of the VSMCs was observed, which was mediated by induction of haem oxygenase-1 (HO-1) followed by an increased expression of p21waf1/Cip1. The underlying mechanism for SSZ-induced HO-1 expression was by reactive oxygen species (ROS)-dependent nuclear translocation and activation of nuclear factor erythroid-2-related factor 2 (Nrf2). In a rat carotid artery balloon injury model, administration of SSZ significantly suppressed neointimal growth. In a series of reverse experiments, inhibition of HO-1 by shRNA, ROS by N-acetylcysteine (NAC) or Nrf2 by dominant-negative Nrf2 abrogated the beneficial effects of SSZ.


Our data demonstrate that SSZ inhibits VSMC proliferation in vitro and in vivo through a novel signalling pathway and may be a promising therapeutic option for the treatment of proliferative vascular disease.

  M. S Kim , C. S Lee , J Hur , H. J Cho , S. I Jun , T. Y Kim , S. W Lee , J. W Suh , K. W Park , H. Y Lee , H. J Kang , D. S Lee , G. Y Koh , H Nakagami , R Morishita , Y. B Park and H. S. Kim

Background— The low engraftment rate of stem/progenitor cells infused via the intracoronary route to the ischemic myocardium is one of the most important factors limiting the efficacy of cell therapy. We investigated the concept of priming peripheral blood stem cells enriched by granulocyte colony-stimulating factor mobilization and apheresis (mobPBSCs) with angiopoietin-1 (Ang1), to enhance the engraftment into the ischemic tissue and neovasculogenic potential.

Methods and Results— The expression of Tie2, the Ang1 receptor, was significantly higher in mobPBSCs than naïve peripheral blood mononuclear cells (19.2±3.0% versus 1.2±0.8% versus 1.2±0.2%; P<0.001 for mobPBSCs from acute myocardial infarction (AMI) patients with granulocyte colony-stimulating factor treatment for 3 days versus peripheral blood mononuclear cells from AMI patients versus peripheral blood mononuclear cells from stable angina patients). After 4 hours of cartilage oligomeric matrix protein (COMP)-Ang1 stimulation, mobPBSCs committed to the endothelial lineage with the induction of CD31 and VE-cadherin expression, mediated by Tie2/Ets-1 pathway. Priming of mobPBSCs with COMP-Ang1 induced the expression of 4β1 and 5β1 integrins, which are also Ets-1 downstream molecules, leading to enhanced adhesion to endothelial cells or fibronectin. In a rabbit ear ischemia/reperfusion model, priming of mobPBSCs with COMP-Ang1 improved first-pass engraftment to the distal vascular bed after intraarterial delivery. In a murine ischemic hind-limb model, intravascular delivery of primed mobPBSCs enhanced both engraftment and neovascularization.

Conclusions— The short-term priming with COMP-Ang1 may be a feasible and promising option to activate mobPBSCs by enhancing differentiation and adhesiveness and to improve the efficacy of cell therapy for ischemic diseases.

  J. W Chung , H. M Yang , K. W Park , H. Y Lee , J. S Park , H. J Kang , Y. S Cho , T. J Youn , B. K Koo , I. H Chae , D. J Choi , B. H Oh , Y. B Park and H. S. Kim

In the COREA-TAXUS trial ("Effect of Celecoxib On REstenosis after coronary Angioplasty with a TAXUS stent"), celecoxib reduced late luminal loss and adverse cardiac events at follow-up around 6 months. The objective of this study was to assess the long-term outcome of short-term adjunctive celecoxib treatment after paclitaxel-eluting stent implantation.

Methods and Results—

This is a 2-year clinical follow-up of the COREA-TAXUS trial, an open-label randomized controlled study. A total 274 patients were randomized to receive or not receive celecoxib (400 mg before the intervention and 200 mg twice daily for 6 months after the procedure), and 271 underwent successful paclitaxel-eluting stent implantation. All patients were given aspirin (100 mg daily indefinitely) and clopidogrel (75 mg daily for at least 6 months). Among the 271 patients, 267 (98.5%) completed the 2-year clinical follow-up. From the previous follow-up to 2 years, there was no difference in the rate of adverse cardiac events between the celecoxib and control groups (1.6% versus 4.3%, P=0.27). Thus, at 2 years, the rate of adverse cardiac events was consistently lower in the celecoxib group (6.9% versus 19.7%, P=0.002). A significant reduction in need for target lesion revascularization was observed (6.2% versus 18.2%, P=0.003). The efficacy benefit in the celecoxib group was not undermined by an increased risk for cardiac death or myocardial infarction at 2 years (1.5% versus 1.4%).


Six-month adjunctive celecoxib treatment after paclitaxel-eluting stent implantation was associated with durable long-term efficacy up to 2 years. However, the inconclusive evidence for the long-term safety of this treatment warrants caution.

Clinical Trial Registration—

URL: Unique identifier: NCT 00292721.

  W. K Kim , V Meliton , K. W Park , C Hong , P Tontonoz , P Niewiadomski , J. A Waschek , S Tetradis and F. Parhami

Hedgehog (Hh) signaling is indispensable in embryonic development, and its dysregulated activity results in severe developmental disorders as shown by genetic models of naturally occurring mutations in animal and human pathologies. Hh signaling also functions in postembryonic development and adult tissue homeostasis, and its aberrant activity causes various human cancers. Better understanding of molecular regulators of Hh signaling is of fundamental importance in finding new strategies for pathway modulation. Here, we identify liver X receptors (LXRs), members of the nuclear hormone receptor family, as previously unrecognized negative regulators of Hh signaling. Activation of LXR by specific pharmacological ligands, TO901317 and GW3965, inhibited the responses of pluripotent bone marrow stromal cells and calvaria organ cultures to sonic Hh, resulting in the inhibition of expression of Hh-target genes, Gli1 and Patched1, and Gli-dependent transcriptional activity. Moreover, LXR ligands inhibited sonic Hh-induced differentiation of bone marrow stromal cells into osteoblasts. Elimination of LXRs by small interfering RNA inhibited ligand-induced inhibition of Hh target gene expression. Furthermore, LXR ligand did not inhibit Hh responsiveness in mouse embryonic fibroblasts that do not express LXRs, whereas introduction of LXR into these cells reestablished the inhibitory effects. Daily oral administration of TO901317 to mice after 3 d significantly inhibited baseline Hh target-gene expression in liver, lung, and spleen. Given the importance of modulating Hh signaling in various physiological and pathological settings, our findings suggest that pharmacological targeting of LXRs may be a novel strategy for Hh pathway modulation.

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