Choong Jae Lee

Chungnam National University Hospital, Sŏul, Seoul, South Korea

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Publications (41)72.87 Total impact

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    ABSTRACT: In this study, we investigated whether lobetyolin, lobetyol, and methyl linoleate derived from Codonopsis pilosula affect MUC5AC mucin secretion, production, and gene expression from airway epithelial cells. Confluent NCI-H292 cells were pretreated with lobetyolin, lobetyol, or methyl linoleate for 30 minutes and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 hours. The MUC5AC mucin gene expression, and mucin protein production and secretion were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Lobetyolin, lobetyol, and methyl linoleate inhibited the gene expression of MUC5AC mucin induced by PMA; lobetyolin did not affect PMA-induced MUC5AC mucin production. However, lobetyol and methyl linoleate inhibited the production of MUC5AC mucin; lobetyolin and lobetyol did not significantly affect PMA-induced MUC5AC mucin secretion from NCI-H292 cells. However, methyl linoleate decreased the MUC5AC mucin secretion. These results suggest that among the three compounds, methyl linoleate can regulate gene expression, production, and secretion of MUC5AC mucin by directly acting on the airway epithelial cells.
    Tuberculosis and Respiratory Diseases 11/2014; 77(5):203-208.
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    ABSTRACT: Luteolin, a flavonoidal compound derived from Lonicera japonica Thunb. and Chrysanthemum indicum L., has been reported to show anti-inflammatory, anti-oxidative and anti-carcinogenic effects. In this study, we investigated whether luteolin significantly affects the secretion, production and gene expression of airway mucin. Confluent NCI-H292 cells were pretreated with luteoiln for 30 min and then stimulated with EGF (epidermal growth factor) or PMA (phorbol 12-myristate 13-acetate) for 24 h or the indicated periods. The MUC5AC mucin gene expression was measured by RT-PCR. Production and secretion of MUC5AC mucin protein were measured by ELISA. To elucidate the action mechanism of luteolin, effect of luteolin on PMA-induced NF-κB signaling pathway was investigated by western blot analysis. The results were as follows: (1) Luteolin inhibited the secretion of MUC5AC mucin protein induced by EGF or PMA; (2) Luteoiln inhibited the production of MUC5AC mucin protein and the expression of MUC5AC mucin gene induced by EGF or PMA; (3) Luteolin inhibited PMA-induced phosphorylation and degradation of inhibitory kappa Bα (IκBα); (4) Luteolin inhibited PMA-induced phosphorylation and nuclear translocation of nuclear factor kappa B (NF-κB) p65. This result suggests that luteolin can regulate the secretion, production and gene expression of mucin by acting on airway epithelial cells via regulation of NF-kB signaling pathway.
    Pulmonary Pharmacology &amp Therapeutics 10/2014; · 2.54 Impact Factor
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    ABSTRACT: It is valuable to find the potential activity of regulating the excessive mucin secretion by the compounds derived from various medicinal plants. We investigated whether aqueous extract of the root bark of Morus alba L. (AMA), kuwanon E, kuwanon G, mulberrofuran G, and morusin significantly affect the secretion and production of airway mucin using in vivo and in vitro experimental models.
    Tuberculosis and Respiratory Diseases 08/2014; 77(2):65-72.
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    ABSTRACT: We investigated whether luteolin affects the gene expression, secretion and activity of matrix metalloproteinase-3 (MMP-3) in primary cultured rabbit articular chondrocytes, as well as production of MMP-3 in the rat knee to evaluate the potential chondro-protective effects of luteolin. Rabbit articular chondrocytes were cultured in a monolayer and IL-1β-induced gene expression levels of MMP-3, MMP-1, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4), ADAMTS-5 and type II collagen were measured by reverse transcription - polymerase chain reaction (RT-PCR). Effects of luteolin on interleukin-1β (IL-1β)-induced secretion and enzyme activity of MMP-3 in rabbit articular chondrocytes were investigated by western blot analysis and casein zymography, respectively. The effect of luteolin on MMP-3 protein production was also examined in vivo. The results were as follows: (1) luteolin inhibited the gene expression levels of MMP-3, MMP-1, MMP-13, ADAMTS-4 and ADAMTS-5. However, it increased the gene expression level of collagen in rabbit articular chondrocytes; (2) luteolin inhibited the secretion and activity of MMP-3; (3) luteolin inhibited in vivo production of MMP-3 protein. These results suggest that luteolin can regulate the gene expression, secretion and activity of MMP-3, by directly acting on articular chondrocytes.
    Biomolecules & therapeutics. 05/2014; 22(3):239-45.
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    ABSTRACT: In this study, we investigated whether natural products including coixol derived from Coix Lachryma-Jobi var. ma-yuen affect MUC5AC mucin gene expression, production and secretion from airway epithelial cells. Confluent NCI-H292 cells were pretreated with oleic acid, linoleic acid, glyceryl trilinoleate, beta-stigmasterol or coixol for 30 min and then stimulated with PMA (phorbol 12-myristate 13-acetate), EGF (epidermal growth factor) or TNF-α (tumor necrosis factor-α) for 24 h. The MUC5AC mucin gene expression, mucin protein production and secretion were measured by RT-PCR and ELISA. The results were as follows: (1) Oleic acid, linoleic acid, glyceryl trilinoleate, beta-stigmasterol and coixol inhibited the expression of MUC5AC mucin gene induced by PMA from NCI-H292 cells; (2) Oleic acid, linoleic acid, glyceryl trilinoleate, beta-stigmasterol and coixol also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI-H292 cells; (3) Coixol inhibited the expression of MUC5AC mucin gene and production of MUC5AC mucin protein, induced by EGF or TNF-α from NCI-H292 cells; (4) Coixol decreased PMA-induced MUC5AC mucin secretion from NCI-H292 cells. This result suggests that coixol, the characteristic component among the examined five natural products derived from C. Lachryma-Jobi var. ma-yuen, can regulate gene expression, production and secretion of mucin, by directly acting on airway epithelial cells.
    Archives of Pharmacal Research 04/2014; · 1.54 Impact Factor
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    ABSTRACT: We investigated whether wogonin and apigenin significantly affect the epidermal growth factor receptor (EGFR) signaling pathway involved in MUC5AC mucin gene expression, and production from cultured airway epithelial cells; this was based on our previous report that apigenin and wogonin suppressed MUC5AC mucin gene expression and production from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with wogonin or apigenin for 15 minutes or 24 hours and then stimulated with epidermal growth factor (EGF) for 24 hours or the indicated periods. We found that incubation of NCI-H292 cells with wogonin or apigenin inhibited the phosphorylation of EGFR. The downstream signals of EGFR such as phosphorylation of MEK1/2 and ERK1/2 were also inhibited by wogonin or apigenin. The results suggest that wogonin and apigenin inhibits EGFR signaling pathway, which may explain how they inhibit MUC5AC mucin gene expression and production induced by EGF.
    Tuberculosis and Respiratory Diseases 03/2014; 76(3):120-6.
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    ABSTRACT: We investigated whether aqueous extract of the root of Platycodon grandiflorum A. de Candolle (APG), platycodinD3 and deapi-platycodin significantly affect the production and secretion of airway mucin using in vivo and in vitro experimental models. Effect of APG was checked on hypersecretion of pulmonary mucin in sulfur dioxide-induced bronchitis in rats. Confluent NCI-H292 cells were pretreated with platycodinD3 or deapi-platycodin for 30min and then stimulated with PMA (phorbol 12-myristate 13-acetate) for 24h. The MUC5AC mucin production and secretion were measured by ELISA. The results were as follows: (1) APG stimulated the secretion of airway mucin in sulfur dioxide-induced bronchitis rat model; (2) platycodinD3 and deapi-platycodin inhibited the production of MUC5AC mucin induced by PMA from NCI-H292 cells, respectively; (3) however, platycodinD3 and deapi-platycodin did not inhibit but stimulated the secretion of MUC5AC mucin induced by PMA from NCI-H292 cells, respectively. This result suggests that aqueous extract of P. grandiflorum A. de Candolle and the two natural products derived from it, platycodinD3 and deapi-platycodin, can regulate the production and secretion of airway mucin and, at least in part, explains the traditional use of aqueous extract of P. grandiflorum A. de Candolle as expectorants in diverse inflammatory pulmonary diseases.
    Phytomedicine: international journal of phytotherapy and phytopharmacology 11/2013; · 2.97 Impact Factor
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    ABSTRACT: We investigated whether prunetin significantly affects tumor necrosis factor-α (TNF-α)-induced MUC5AC mucin gene expression, production, inhibitory kappa B (IκB) degradation and nuclear factor kappa B (NF-κB) p65 translocation in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with prunetin for 30 minutes and then stimulated with TNF-α for 24 hours or the indicated periods. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The effect of prunetin on TNF-α-induced degradation of IκB and translocation of NF-κB p65 was investigated by western blot analysis. We found that incubation of NCI-H292 cells with prunetin significantly inhibited mucin production and down-regulated the MUC5AC gene expression induced by TNF-α. Prunetin inhibited TNF-α-induced degradation of IκB and translocation of NF-κB p65. This result suggests that prunetin inhibits the NF-κB signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production regulated by the NF-κB signaling pathway.
    Tuberculosis and Respiratory Diseases 11/2013; 75(5):205-209.
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    ABSTRACT: In the present study, we investigated whether aqueous extract of Liriope Tuber, ophiopogonin D and spicatoside A derived from Liriope Tuber affect basal or phorbol ester (phorbol 12-myristate 13-acetate, PMA)-induced airway mucin production and secretion from airway epithelial cells. Confluent NCI-H292 cells were treated with each agent for 24h (basal production) or pretreated with each agent for 30min and then stimulated with PMA for 24h (PMA-induced production and secretion), respectively. MUC5AC airway mucin production and secretion were measured by ELISA. The results were as follows: (1) aqueous extract of Liriope Tuber stimulated basal mucin production and did not inhibit but increased PMA-induced mucin production; (2) ophiopogonin D and spicatoside A stimulated basal mucin production and did not inhibit but increased PMA-induced mucin production; (3) two compounds increased PMA-induced mucin secretion. These results suggest that ophiopogonin D and spicatoside A can increase mucin production and secretion, by directly acting on airway epithelial cells and, at least in part, explain the traditional use of aqueous extract of Liriope Tuber as expectorants in diverse inflammatory pulmonary diseases.
    Phytomedicine: international journal of phytotherapy and phytopharmacology 09/2013; · 2.97 Impact Factor
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    ABSTRACT: We developed a custom-made miniaturized neural stimulation system with a liquid crystal polymer (LCP)-based electrode array for animal experiments. In order to verify the feasibility of the system, motor cortex stimulation (MCS) was applied on the rat pain model induced by sciatic nerve injury. LCP is mechanically stable and chemically inert and has a much lower water absorption rate than other biocompatible polymers such as polyimide or parylene. In the present study, a film-type LCP substrate is used to microfabricate the cortical stimulation electrode array. A miniaturized electrical neuromodulation system is implemented using an application-specific integrated chip for generation of electrical stimulation current. In vivo experiment was performed using a rat neuropathic pain model induced by sciatic nerve injury. The electrodes were attached to the contralateral primary motor cortex, which processes the hind limb movement. Mechanical allodynia was measured before, during, and after electrical stimulation to determine the effects on pain threshold. Electrical stimulation into the brain structure processing pain perception was effective in alleviating neuropathic pain. The pain threshold of the rats increased more than fivefold during the electrical stimulation. We developed a miniaturized electrical stimulation system with a novel flexible LCP electrode array for MCS in rats. This system is expected to be used in studying various neurological diseases and examining in vivo brain function.
    Neuromodulation 08/2013; · 1.19 Impact Factor
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    ABSTRACT: In this study, we investigated whether wogonin significantly affects MUC5AC mucin gene expression and production in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with wogonin for 30 min and then stimulated with tumor necrosis factor-α (TNF-α) for 24 h or the indicated periods. The MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA, respectively. We found that incubation of NCI-H292 cells with wogonin significantly inhibited mucin production and down-regulated MUC5AC gene expression induced by TNF-α in a dose-dependent fashion. To elucidate the action mechanism of wogonin, effect of wogonin on TNF-α-induced NF-κB signaling pathway was investigated by western blot analysis. Wogonin inhibited NF-κB activation induced by TNF-α. Inhibition of IKK by wogonin led to the suppression of IκB phosphorylation and degradation, p65 nuclear translocation and NF-κB-regulated gene expression. This, in turn, led to the down-regulation of MUC5AC protein production in NCI-H292 cells. Wogonin also inhibited the gene products involved in cell survival (Bcl-2) and proliferation (cyclooxygenase-2). These results suggest that wogonin inhibits the NF-κB signaling pathway, which may explain its role in the inhibition of MUC5AC mucin gene expression and production. Copyright © 2013 John Wiley & Sons, Ltd.
    Phytotherapy Research 03/2013; · 2.40 Impact Factor
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    ABSTRACT: We investigated whether chrysin affected MUC5AC mucin production and gene expression induced by phorbol ester (phorbol 12-myristate 13-acetate, PMA) or epidermal growth factor (EGF) from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with varying concentrations of chrysin for 30 minutes, and were then stimulated with PMA and EGF for 24 hours, respectively. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Concentrations of 10µM and 100µM chrysin were found to inhibit the production of MUC5AC mucin protein induced by PMA; A concentration of 100µM chrysin also inhibited the production of MUC5AC mucin protein induced by EGF; 100µM chrysin inhibited the expression of MUC5AC mucin gene induced by PMA or EGF. The cytotoxicity of chrysin was checked by lactate dehydrogenase assay, and there was no cytotoxic effect observed for chrysin. These results suggest that chrysin can inhibit mucin gene expression and the production of mucin protein by directly acting on airway epithelial cells.
    Tuberculosis and respiratory diseases. 10/2012; 73(4):204-9.
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    ABSTRACT: In this study, we investigated whether apigenin and wogonin affect MUC5AC mucin production and gene expression induced by phorbol ester (phorbol 12-myristate 13-acetate, PMA) or epidermal growth factor (EGF) from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with PMA or EGF for 24 h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assay (ELISA). The results were as follows: (i) apigenin and wogonin were found to inhibit the production of MUC5AC mucin protein induced by PMA or EGF; (ii) both compounds also inhibited the expression of MUC5AC mucin gene induced by PMA or EGF. These results suggest that apigenin and wogonin can inhibit mucin gene expression and production of mucin protein, by directly acting on airway epithelial cells. Copyright © 2012 John Wiley & Sons, Ltd.
    Phytotherapy Research 03/2012; · 2.40 Impact Factor
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    ABSTRACT: We investigated whether silibinin significantly affects gene expression, production and secretion of mucin from cultured airway epithelial cells. Confluent NCI-H292 cells were pretreated with silibinin for 30 min and then stimulated with epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA) or TNF-α for 24 h. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The effect of silibinin on TNF-α-induced activation of NF-κB p65 was also examined. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then treated for 30 min in the presence of silibinin to assess the effect on mucin secretion using ELISA. The results were as follows: (i) silibinin inhibited the expression of the MUC5AC mucin gene induced by EGF, PMA or TNF-α from NCI-H292 cells; (ii) silibinin also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI-H292 cells; (iii) silibinin inhibited the activation of NF-κB p65 by TNF-α in NCI-H292 cells; (iv) silibinin significantly decreased ATP-induced mucin secretion from cultured RTSE cells. This result suggests that silibinin can regulate gene expression, production and secretion of mucin by directly acting on airway epithelial cells. Copyright © 2012 John Wiley & Sons, Ltd.
    Phytotherapy Research 01/2012; 26(9):1301-7. · 2.40 Impact Factor
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    ABSTRACT: The study investigated whether resveratrol significantly affects mucin gene expression, production and secretion from airway epithelial cells. Confluent NCI-H292 cells were pretreated with resveratrol for 30 min and then stimulated with EGF (epidermal growth factor), PMA (phorbol 12-myristate 13-acetate) and TNF-α (tumor necrosis factor-α) for 24 h, respectively. The MUC5AC gene expression and mucin protein production were measured by RT-PCR and ELISA. The effect of resveratrol on TNF-α- or PMA-induced activation of NF-κB p65 was also examined. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then treated for 30 min in the presence of resveratrol to assess the effect on mucin secretion using ELISA. The results were as follows: (1) resveratrol inhibited the expression of MUC5AC gene induced by EGF or PMA or TNF-α from NCI-H292 cells; (2) resveratrol also inhibited the production of MUC5AC mucin protein induced by the same inducers from NCI-H292 cells; (3) resveratrol inhibited the activation of NF-κB p65 by TNF-α or PMA in NCI-H292 cells; (4) resveratrol significantly decreased ATP-induced mucin secretion from cultured RTSE cells. This result suggests that resveratrol can regulate mucin gene expression, production and secretion, by directly acting on airway epithelial cells.
    Phytotherapy Research 12/2011; 26(7):1082-7. · 2.40 Impact Factor
  • Sun Goo Kim, Yu Jin Kim, Se Il Lee, Choong Jae Lee
    Dermatologic Surgery 12/2011; 37(12):1817-9. · 1.87 Impact Factor
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    ABSTRACT: In this study, the effects of oleanolic acid and ursolic acid on MUC5AC mucin production and gene expression induced by epidermal growth factor (EGF) and phorbol 12-myristate 13-acetate (PMA) from human airway epithelial cells were investigated. Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with EGF and PMA for 24 h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. Oleanolic acid and ursolic acid were found to inhibit the production of MUC5AC mucin protein induced by EGF and PMA, and both compounds also inhibited the expression of MUC5AC mucin gene induced by EGF and PMA. These results suggest that oleanolic acid and ursolic acid can regulate mucin gene expression, and production of mucin protein, by directly acting on airway epithelial cells.
    Phytotherapy Research 03/2011; 25(5):760-4. · 2.40 Impact Factor
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    ABSTRACT: In this study, we investigated whether daidzein significantly affects secretion, production and gene expression of mucin from cultured airway epithelial cells. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then chased for 30 min in the presence of daidzein to assess the effect on mucin secretion using ELISA. At the same time, confluent NCI-H292 cells were pretreated with daidzein for 30 min and then stimulated with EGF and PMA for 24 h, respectively. The MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. The results were as follows: (1) daidzein significantly decreased ATP-induced mucin secretion from cultured RTSE cells; (2) daidzein inhibited the production of MUC5AC mucin protein induced by EGF or PMA from NCI-H292 cells; (3) daidzein also inhibited the expression of MUC5AC mucin gene induced by EGF or PMA from NCI-H292 cells. This result suggests that daidzein can regulate secretion, production and gene expression of mucin, by directly acting on airway epithelial cells.
    Pulmonary Pharmacology &amp Therapeutics 02/2011; 24(1):128-32. · 2.54 Impact Factor
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    ABSTRACT: This study investigated whether prunetin significantly affects the secretion, production and gene expression of mucin from cultured airway epithelial cells. Confluent primary rat tracheal surface epithelial (RTSE) cells were pretreated with adenosine triphosphate (ATP) for 5 min and then chased for 30 min in the presence of prunetin to assess the effect on mucin secretion using enzyme-linked immunosorbent assay (ELISA). At the same time, confluent NCI-H292 cells were pretreated with prunetin for 30 min and then stimulated with epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA) for 24 h, respectively. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction (RT-PCR) and ELISA. The results were as follows: (1) prunetin significantly suppressed ATP-induced mucin secretion from cultured RTSE cells; (2) prunetin inhibited the production of MUC5AC mucin protein induced by EGF or PMA from NCI-H292 cells; (3) prunetin also inhibited the expression of MUC5AC mucin gene induced by EGF or PMA from NCI-H292 cells. This result suggests that prunetin can regulate the secretion, production and gene expression of mucin, by directly acting on airway epithelial cells.
    Phytotherapy Research 02/2011; 25(8):1196-200. · 2.40 Impact Factor
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    ABSTRACT: In this study, we investigated whether glycyrrhizin and carbenoxolone affect MUC5AC mucin production and gene expression induced by epidermal growth factor (EGF) or phorbol ester (PMA) from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with each agent for 30 min and then stimulated with EGF and PMA for 24h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. Glycyrrhizin and carbenoxolone were found to inhibit the production of MUC5AC mucin protein induced by EGF or PMA, and both compounds also inhibited the expression of MUC5AC mucin gene induced by EGF or PMA. These results suggest that glycyrrhizin and carbenoxolone can inhibit mucin gene expression and production of mucin protein, by directly acting on airway epithelial cells.
    Phytomedicine: international journal of phytotherapy and phytopharmacology 12/2010; 18(8-9):743-7. · 2.97 Impact Factor

Publication Stats

202 Citations
72.87 Total Impact Points

Institutions

  • 2012–2014
    • Chungnam National University Hospital
      Sŏul, Seoul, South Korea
    • Eulji University
      Daiden, Daejeon, South Korea
  • 2003–2014
    • Chungnam National University
      • Department of Pharmacology
      Daiden, Daejeon, South Korea
  • 2004–2013
    • Seoul National University
      • • School of Electrical Engineering and Computer Sciences
      • • School of Computer Science and Engineering
      • • Department of Electrical and Computer Engineering
      Seoul, Seoul, South Korea
  • 2011
    • Inje University
      • College of Medicine
      Kimhae, South Gyeongsang, South Korea
    • Gachon University
      Sŏngnam, Gyeonggi Province, South Korea
  • 2009
    • University of California, Santa Barbara
      • Department of Molecular, Cellular, and Developmental Biology
      Santa Barbara, CA, United States
  • 2004–2007
    • Inha University
      • College of Medicine
      Seoul, Seoul, South Korea