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Articles by J. W Kim
Total Records ( 6 ) for J. W Kim
  C. H Lee , J. W Kim , H. J Lee , P. Y Yun , D. Y Kim , B. S Seo , I. Y Yoon and J. H. Mo

Objective  To quantitatively evaluate the effects of the mandibular advancement device (MAD) on changes in the upper respiratory tract during sleep using sleep videofluoroscopy (SVF) in patients with obstructive sleep apnea (OSA).

Design  Retrospective analysis.

Setting  Academic tertiary referral center.

Patients  Seventy-six patients (68 men and 8 women) who were treated with the MAD for OSA were included from September 1, 2005, through August 31, 2008.

Intervention  All patients underwent nocturnal polysomnography and SVF before and at least 3 months after receipt of the custom-made MAD. Sleep videofluoroscopy was performed before and after sleep induction and was analyzed during 3 states of awakeness, normoxygenation sleep, and desaturation sleep.

Main Outcome Measures  Changes in the length of the soft palate, retropalatal space, retrolingual space, and angle of mouth opening were evaluated during sleep events with or without the MAD.

Results  Without the MAD, the length of the soft palate and the angle of mouth opening increased during sleep events, especially in desaturation sleep, compared with the awake state. The retropalatal space and retrolingual space became much narrower during sleep compared with the awake state. The MAD had marked effects on the length of the soft palate, retropalatal space, retrolingual space, and angle of mouth opening. The retropalatal space and retrolingual space were widened, and the length of the soft palate was decreased. The MAD kept the mouth closed.

Conclusions  Sleep videofluoroscopy showed dynamic upper airway changes in patients with OSA, and the MAD exerted multiple effects on the size and configuration of the airway. Sleep videofluoroscopy demonstrated the mechanism of action of the MAD in patients with OSA. The MAD increased the retropalatal and retrolingual spaces and decreased the length of the soft palate and the angle of mouth opening, resulting in improvement of OSA.

  S. L Zheng , V. L Stevens , F Wiklund , S. D Isaacs , J Sun , S Smith , K Pruett , K. E Wiley , S. T Kim , Y Zhu , Z Zhang , F. C Hsu , A. R Turner , J. E Johansson , W Liu , J. W Kim , B. L Chang , D Duggan , J Carpten , C Rodriguez , W Isaacs , H Gronberg and J. Xu

Single nucleotide polymorphisms (SNP) at 11q13 were recently implicated in prostate cancer risk by two genome-wide association studies and were consistently replicated in multiple study populations. To explore prostate cancer association in the regions flanking these SNPs, we genotyped 31 tagging SNPs in a ~110 kb region at 11q13 in a Swedish case-control study (Cancer of the Prostate in Sweden), including 2,899 cases and 1,722 controls. We found evidence of prostate cancer association for the previously implicated SNPs including rs10896449, which we termed locus 1. In addition, multiple SNPs on the centromeric side of the region, including rs12418451, were also significantly associated with prostate cancer risk (termed locus 2). The two groups of SNPs were separated by a recombination hotspot. We then evaluated these two representative SNPs in an additional ~4,000 cases and ~3,000 controls from three study populations and confirmed both loci at 11q13. In the combined allelic test of all four populations, P = 4.0 x 10–11 for rs10896449 at locus 1 and P = 1.2 x 10–6 for rs12418451 at locus 2, and both remained significant after adjusting for the other locus and study population. The prostate cancer association at these two 11q13 loci was unlikely confounded by prostate-specific antigen (PSA) detection bias because neither SNP was associated with PSA levels in controls. Unlike locus 1, in which no known gene is located, several putative mRNAs are in close proximity to locus 2. Additional confirmation studies at locus 2 and functional studies for both loci are needed to advance our knowledge on the etiology of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1815–20)

  J. W Kim , A. R. M. R Amin and D. M. Shin

Recently, squamous cell carcinoma of the head and neck chemoprevention research has made major advances with novel clinical trial designs suited for the purpose, use of biomarkers to identify high-risk patients, and the emergence of numerous molecularly targeted agents and natural dietary compounds. Among many natural compounds, green tea polyphenols, particularly (–)-epigallocatechin-3-gallate (EGCG), possess remarkable potential as chemopreventive agents. EGCG modulates several key molecular signaling pathways at multiple levels and has synergistic or additive effects when combined with many other natural or synthetic compounds. This review will provide an update of the potential of green tea polyphenols, particularly EGCG, for the chemoprevention of squamous cell carcinoma of the head and neck. Cancer Prev Res; 3(8); 900–9. ©2010 AACR.

  A Kim , M. J Kim , Y Yang , J. W Kim , Y. I Yeom and J. S. Lim

Downregulation of the N-myc downstream-regulated gene 2 (NDRG2) gene is involved in the progression of aggressive forms of cancer, along with the poor prognosis of cancer patients. In the current study, we examined the effect of NDRG2 expression on the metastatic potential of HT1080 human fibrosarcoma and B16F10 murine melanoma cells in both in vitro and in vivo systems. In gelatin zymography, NDRG2 expression remarkably suppressed the matrix metalloproteinase (MMP)-9 activity and slightly inhibited MMP-2 activity of both cell lines. Tumor migration and invasion in vitro were significantly reduced by NDRG2 expression, and NDRG2 inhibited tumor cell proliferation in an anchorage-independent semisolid agar assay. Specifically, we found that NDRG2 affects invasion through suppression of nuclear factor kappa B (NF-B) activity. In animal experiments, subcutaneously injected B16F10-NDRG2 cells showed delayed tumor growth compared with B16F10-mock cells. Furthermore, severe metastasis from primary tumor mass into the draining lymph nodes was observed after injection of B16F10-mock cells, but not with B16F10-NDRG2 cells. Pulmonary metastasis after intravenous injection of B16F10 cells was also reduced by NDRG2 expression. Intra- and peritumoral angiogenesis that is critical for the tumor growth and metastasis was clearly found in tumors after injection with B16F10-mock cells, whereas it was impaired in tumors after injection with B16F10-NDRG2 cells. Collectively, our data show that NDRG2 expression significantly suppresses tumor invasion by inhibiting MMP activities, which are regulated through the NF-B signaling. Moreover, results from animal experiments provide evidence for the regulatory role of the NDRG2 gene in metastatic tumors.

  I Ueki , S. L Giesy , K. J Harvatine , J. W Kim and Y. R. Boisclair

Normal postnatal growth is dependent in part on overlapping actions of GH and IGF-I. These actions reflect GH stimulation of IGF-I production in liver and extrahepatic tissues, representing respectively the endocrine and autocrine/paracrine arms of the IGF system. Recent experiments in genetically modified mice show that each source of IGF-I can compensate for absence of the other but do not resolve their relative role in postnatal growth. In an effort to address this issue, we studied the GH responsiveness of mice harboring a null mutation of the acid-labile subunit (ALS). Null ALS mice have a substantial reduction in endocrine IGF-I but, unlike other models of plasma IGF-I deficiency, have no obvious additional endocrine defects. Wild type and null ALS mice of both sexes received daily sc injections of saline or recombinant bovine GH between d 35 and 63 of postnatal age. The GH-stimulated body weight gain of null ALS mice was reduced by more than 30% relative to wild type mice, irrespective of sex. Reductions in GH responsiveness were also seen for kidney and linear growth. Absence of ALS eliminated the ability of GH to increase plasma IGF-I despite intact GH-dependent stimulation of IGF-I expression in liver, adipose tissue, and skeletal muscle. GH treatment was also less efficient in antagonizing insulin action in null ALS mice. Overall, these results suggest that the GH effects mediated by endocrine IGF-I depends on ALS, and accordingly null ALS mice are less responsive to exogenous GH therapy.

  N Takeda , E. L O'Dea , A Doedens , J. w Kim , A Weidemann , C Stockmann , M Asagiri , M. C Simon , A Hoffmann and R. S. Johnson

Hypoxic response and inflammation both involve the action of the hypoxia-inducible transcription factors HIF-1 and HIF-2. Previous studies have revealed that both HIF- proteins are in a number of aspects similarly regulated post-translationally. However, the functional interrelationship of these two isoforms remains largely unclear. The polarization of macrophages controls functionally divergent processes; one of these is nitric oxide (NO) production, which in turn is controlled in part by HIF factors. We show here that the HIF- isoforms can be differentially activated: HIF-1 is induced by Th1 cytokines in M1 macrophage polarization, whereas HIF-2 is induced by Th2 cytokines during an M2 response. This differential response was most evident in polarized macrophages through HIF- isoform-specific regulation of the inducible NO synthase gene by HIF-1, and the arginase1 gene by HIF-2. In silico modeling predicted that regulation of overall NO availability is due to differential regulation of HIF-1 versus HIF-2, acting to, respectively, either increase or suppress NO synthesis. An in vivo model of endotoxin challenge confirmed this; thus, these studies reveal that the two homologous transcription factors, HIF-1 and HIF-2, can have physiologically antagonistic functions, but that their antiphase regulation allows them to coordinately regulate NO production in a cytokine-induced and transcription-dependent fashion.

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