Eun Young Park

Catholic University of Korea, Sŏul, Seoul, South Korea

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Publications (157)301.48 Total impact

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    ABSTRACT: To investigate the role of α3 and α7 nicotinic acetylcholine receptor subunits (nAChRs) in the bladder, using a rat model with detrusor overactivity induced by partial bladder outlet obstruction (BOO). Forty Sprague-Dawley rats were used: 10 were sham-operated (control group) and 30 were observed for 3 weeks after partial BOO. BOO-induced rats were further divided into 3 groups: Two groups of 10 rats each received intravesicular infusions with hexamethonium (HM group; n=10) or methyllycaconitine (MLC group; n=10), which are antagonists for α3 and α7 nAChRs, respectively. The remaining BOO-induced rats received only saline infusion (BOO group; n=10). Based on the contraction interval measurements using cystometrogram, the contraction pressure and nonvoiding bladder contractions were compared between the control and the three BOO-induced groups. Immunofluorescent staining and Western blotting were used to analyze α3 and α7 nAChRs levels. The contraction interval of the MLC group was higher than that of the BOO group (P<0.05). Nonvoiding bladder contraction almost disappeared in the HM and MLC groups. Contraction pressure increased in the BOO group (P<0.05) compared with the control group and decreased in the HM and MLC groups compared with the BOO group (P<0.05). Immunofluorescence staining showed that the α3 nAChR signals increased in the urothelium, and the α7 nAChR signals increased in the urothelium and detrusor muscle of the BOO group compared with the control group. Western blot analysis showed that both α3 and α7 nAChR levels increased in the BOO group (P<0.05). Alpha3 and α7 nAChRs are associated with detrusor overactivity induced by BOO. Furthermore, nAChR antagonists could help in clinically improving detrusor overactivity.
    International neurourology journal 03/2015; 19(1):12-8. DOI:10.5213/inj.2015.19.1.12
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    ABSTRACT: Mercury is a well-known environmental pollutant that can cause nephropathic diseases, including acute kidney injury (AKI). Although quercetin (QC), a natural flavonoid, has been reported to have medicinal properties, its potential protective effects against mercury-induced AKI have not been evaluated. In this study, the protective effect of QC against mercury-induced AKI was investigated using biochemical parameters, new protein-based urinary biomarkers, and a histopathological approach. A 250 mg/kg dose of QC was administered orally to Sprague-Dawley male rats for 3 days before administration of mercury chloride (HgCl2). All animals were sacrificed at 24 h after HgCl2 treatment, and biomarkers associated with nephrotoxicity were measured. Our data showed that QC absolutely prevented HgCl2-induced AKI, as indicated by biochemical parameters such as blood urea nitrogen (BUN) and serum creatinine (sCr). In particular, QC markedly decreased the accumulation of Hg in the kidney. Urinary excretion of protein-based biomarkers, including clusterin, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and vascular endothelial growth factor (VEGF) in response to HgCl2 administration were significantly decreased by QC pretreatment relative to that in the HgCl2-treated group. Furthermore, urinary excretion of metallothionein and Hg were significantly elevated by QC pretreatment. Histopathological examination indicated that QC protected against HgCl2-induced proximal tubular damage in the kidney. A TUNEL assay indicated that QC pretreatment significantly reduced apoptotic cell death in the kidney. The administration of QC provided significant protective effects against mercury-induced AKI.
    Journal of Medicinal Food 02/2015; DOI:10.1089/jmf.2014.3242 · 1.70 Impact Factor
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    ABSTRACT: Transparent Pb(Zr,Ti)O3 (PZT) capacitors were fabricated using cost-effective solution process.•Photovoltaic response was investigated by introducing ultra-thin Pt layer between bottom electrode and PZT.•Introduction of Pt layer reduces the leakage current and enhances ferroelectric and PV response.•The transmittance of the capacitors were 45–50% in visible region.
    Solar Energy 01/2015; 111. DOI:10.1016/j.solener.2014.10.037 · 3.54 Impact Factor
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    Korean journal of anesthesiology 12/2014; 67(Suppl):S3-4. DOI:10.4097/kjae.2014.67.S.S3
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    ABSTRACT: The aim of this study was to investigate the effect of a 1.8-GHz continuous electromagnetic field (EMF) on wound healing in a human airway cell-culture system. In vitro study using a cell line. Immortalized human bronchial epithelial cells (a BEAS-2B cell line) were exposed to a 1.8-GHz EMF (specific absorption rate = 1.0 W/kg). We evaluated the effect of EMF on the cells using an 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide (MTT) viability assay, by cell counting, and by using fluorescence-activated cell sorting (FACS) analysis of cell cycle dynamics and apoptosis. Inhibition of migration was tested by a wound-healing assay on scratched cell cultures. Cell migration in the wound-healing assay was decreased by the EMF treatment compared with controls. The MTT assay and cell counting consistently showed that the EMF used was not cytotoxic and did not inhibit cell proliferation. FACS analysis showed no alterations in the cell-cycle phase distribution or in apoptosis after EMF exposure. EMF can inhibit wound healing in vitro by inhibiting cell migration. N/A. Laryngoscope, 2014. © 2014 The American Laryngological, Rhinological and Otological Society, Inc.
    The Laryngoscope 12/2014; DOI:10.1002/lary.25109 · 2.03 Impact Factor
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    ABSTRACT: Human breast cancers include cancer stem cell populations as well as non-tumorigenic cancer cells. Breast cancer stem cells have self-renewal capability and are resistant to conventional chemotherapy. MicroRNAs (miRNAs) regulate the expression of many target genes; therefore, dysregulation of miRNAs have been associated with the pathogenesis of human diseases, including cancer. However, a role for miRNA dysregulation in stemness and drug resistance has yet to be identified. Members of the miR-34 family are reportedly tumor-suppressor miRNAs and are associated with various human cancers. Our results confirm that miR-34a expression was downregulated in MCF7/ADR cells compared with MCF7 cells. We hypothesized that this reduction was due to the p53 (TP53) mutation in MCF7/ADR cells. In this study, we found that primary and mature miR-34a were suppressed by treatment with p53 RNAi or the dominant negative p53 mutant in MCF7 cells. Ectopic miR-34a expression reduced cancer stem cell properties and increased sensitivity to doxorubicin treatment, by directly targeting NOTCH1. Furthermore, tumors from nude mice treated with miR-34a were significantly smaller compared to those of mice treated with control lentivirus. Our research suggests that the ectopic expression of miR-34a represents a novel therapeutic approach in chemoresistant breast cancer treatment.
    Cancer Research 11/2014; 74(24). DOI:10.1158/0008-5472.CAN-14-1140 · 9.28 Impact Factor
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    ABSTRACT: In nature, there exist a wide repertoire of dsRNA-binding proteins that have different binding modes for siRNA as well as structural differences, and some of these proteins have the potential as the effective siRNA delivery carriers. For delivering siRNA into cancer cells, a dsRNA-binding 2b protein derived from Tomato aspermy virus was genetically modified by fusing the integrin-targeting RGD peptide to its C-terminus, and biosynthesized. The resulting 2b-RGD protein possesses distinct characteristics favorable to biomedical applications of siRNA: (1) high affinity for siRNA, (2) siRNA protection against RNases in serum, (3) low cytotoxicity compared to the polycationic polymers often employed in the conventional siRNA carriers, (4) specific binding to integrins on cancer cells, and passing through the cell membrane via endocytosis, (5) ability to facilitate cytosolic release of siRNA. Here, we demonstrate the 2b-RGD/siRNA complexes have the high potential as a tumor-targeting siRNA delivery carrier and suggest their possible therapeutic applications for cancer treatment.
    Acta Biomaterialia 11/2014; 10(11). DOI:10.1016/j.actbio.2014.07.014 · 5.68 Impact Factor
  • Eun Young Park, Yoo Im Choi
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    ABSTRACT: [Purpose] The purpose of this study was to investigate the psychometric properties of the lower extremity subscale of the Fugl-Meyer Assessment lower extremity (FMA-LE) for community-dwelling hemiplegic stroke patients. [Subjects] The participants were 140 community-dwelling hemiplegic stroke patients. [Methods] To determine the psychometric properties of the FMA-LE, we examined construct validity, response characteristics, item discrimination, and internal consistency. [Results] Factor analysis of the FMA-LE revealed that the first factor explained 61.73% of the variance and provided evidence of unidimensionality. The FMA-LE did not show ceiling or floor effects; Cronbach's α was 0.935 (95% CI: 0.919-0.950). [Conclusion] Because the FMA-LE seems to be both valid and reliable, we conclude that it is appropriate for the measurement of the lower extremity motor impairment of community-dwelling hemiplegic stroke patients.
    Journal of Physical Therapy Science 11/2014; 26(11):1775-1777. DOI:10.1589/jpts.26.1775 · 0.20 Impact Factor
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    ABSTRACT: Previously, we showed that retinol (vitamin A) decreased both colorectal cancer cell invasion and phosphatidylinositol 3-kinase (PI3K) activity through a retinoic acid receptor-independent mechanism. Here, we determined if these phenomena were related by using parental HCT-116 cells that harbor 1 allele of wild-type PI3K and 1 allele of constitutively active (ca) PI3K and 2 mutant HCT-116 cell lines homozygous for caPI3K. In vitro, treatment of parental HCT-116 cells with 10 μM retinol reduced cell invasion whereas treatment of mutant HCT-116 cell lines with retinol did not. Treatment with 10 μM retinol also decreased the activity of matrixmetalloproteinase-9 and increased tissue inhibitor of matrixmetalloproteinase-I levels in parental, but not mutant, HCT-116 cells. Finally, parental or mutant cells were intrasplenically injected into athymic mice consuming diets with or without supplemental vitamin A. As expected, vitamin A supplementation tended (P = 0.18) to reduce the incidence of metastases in mice injected with the parental cell line and consuming the supplemented diet. In contrast, metastatic incidence was not affected (P = 1.00) by vitamin A supplementation in mice injected with mutant cells. These data indicate that the capacity of retinol to inhibit PI3K activity confers its ability to decrease colorectal cancer metastasis.
    Nutrition and Cancer 10/2014; 66(8):1-10. DOI:10.1080/01635581.2014.956258 · 2.47 Impact Factor
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    ABSTRACT: The aim of this study was to investigate urinary metabolomic profiles associated with cadmium (Cd)-induced nephrotoxicity and their potential mechanisms. Metabolomic profiles were measured by high-resolution (1)H-nuclear magnetic resonance (NMR) spectroscopy in the urine of rats after oral exposure to CdCl2 (1, 5, or 25 mg/kg) for 6 wk. The spectral data were further analyzed by a multivariate analysis to identify specific urinary metabolites. Urinary excretion levels of protein biomarkers were also measured and CdCl2 accumulated dose-dependently in the kidney. High-dose (25 mg/kg) CdCl2 exposure significantly increased serum blood urea nitrogen (BUN), but serum creatinine (sCr) levels were unchanged. High-dose CdCl2 (25 mg/kg) exposure also significantly elevated protein-based urinary biomarkers including osteopontin, monocyte chemoattractant protein-1 (MCP-1), kidney injury molecules-1 (Kim-1), and selenium-binding protein 1 (SBP1) in rat urine. Under these conditions, six urinary metabolites (citrate, serine, 3-hydroxyisovalerate, 4-hydroxyphenyllactate, dimethylamine, and betaine) were involved in mitochondrial energy metabolism. In addition, a few number of amino acids such as glycine, glutamate, tyrosine, proline, or phenylalanine and carbohydrate (glucose) were altered in urine after CdCl2 exposure. In particular, the metabolites involved in the glutathione biosynthesis pathway, including cysteine, serine, methionine, and glutamate, were markedly decreased compared to the control. Thus, these metabolites are potential biomarkers for detection of Cd-induced nephrotoxicity. Our results further indicate that redox metabolomics pathways may be associated with Cd-mediated chronic kidney injury. These findings provide a biochemical pathway for better understanding of cellular mechanism underlying Cd-induced renal injury in humans.
    Journal of Toxicology and Environmental Health Part A 10/2014; 77(22-24):1384-98. DOI:10.1080/15287394.2014.951755 · 1.83 Impact Factor
  • Myungsun Yi, Keeho Park, Eun Young Park
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    ABSTRACT: The purpose of the study was to investigate significant psychosocial needs of low-income people with cancer in Korea and the extent to which these needs are unmet and which factors influence them.
    European journal of oncology nursing: the official journal of European Oncology Nursing Society 10/2014; DOI:10.1016/j.ejon.2014.07.005 · 1.79 Impact Factor
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    ABSTRACT: Excessive reactive oxygen species (ROS) production plays a crucial role in causing various diseases, including inflammatory disorders. The activation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappaB (NF-κB) signaling is implicated in stimulating inflammatory response and cytokines. Peroxiredoxin 2 (Prx2) is a 2-cysteine (Cys) peroxiredoxin capable of removing endogenous hydrogen peroxide (H2O2). PEP-1 peptide, a protein transduction domain, consists of three domains which are used to transduce exogenous therapeutic proteins into cells. The correlation between effectively transduced PEP-1-Prx2 and ROS-mediated inflammatory response is not clear. In the present study, we investigated the protective effects of cell permeable PEP-1-Prx2 on oxidative stress-induced inflammatory activity in Raw 264.7 cells and in a mouse ear edema model after exposure to lipopolysaccharides (LPS) or 12-O-tetradecanoylphorbol-13-actate (TPA). Transduced PEP-1-Prx2 suppressed intracellular ROS accumulation and inhibited the activity of MAPKs and NF-κB signaling that led to the suppression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and cytokines in LPS-induced Raw 264.7 cells and TPA-induced mouse ear edema model. Given these results, we propose that PEP-1-Prx2 has therapeutic potential in the prevention of inflammatory disorders.
    International Immunopharmacology 09/2014; 23(2). DOI:10.1016/j.intimp.2014.09.008 · 2.71 Impact Factor
  • Su Yeon Kye, Eun Young Park, Kyounghee Oh, Keeho Park
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    ABSTRACT: The aims of the present study were to assess the prevalence of perceived risk for cancer; to explore associations between sociodemographics and family history of cancer and perceived cancer risk; to identify perceived cause of cancer risk; and to examine the associations between sociodemographics and family history of cancer and perceived cause of cancer risk. This cross-sectional study was conducted among 1,009 participants aged 30-69 years, selected from a population-based database in October 2009 through multiple-stratified random sampling. Information was collected about the participants' perceived cancer risk and perceived cause of cancer risk. Overall, 59.5% of the respondents thought they had the chance of developing cancer. Female sex, younger age, lower income, and family history of cancer were positively associated with perceived cancer risk. The most important perceived cause of cancer risk was stress. There was a difference between sociodemographics and family history of cancer and perceived cause of cancer risk. Factors affecting perceptions of cancer risk and cause of cancer risk need to be addressed in risk communications. The results provide important directions for the development of educational strategies to promote awareness and self-appraisal of cancer risk and risk factors.
    Cancer Research and Treatment 09/2014; DOI:10.4143/crt.2014.024 · 2.98 Impact Factor
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    ABSTRACT: Porphyrias are inherited metabolic disorders resulting from a specific enzyme defect in the heme biosynthetic pathway. Porphyrias are induced by various precipitants. Clinical features include abdominal pain, neurologic manifestations, autonomic neuropathy, and mental disturbance. Diagnosis may be delayed because of variable symptoms that mimic other diseases and because of the rarity of of porphyrias. Although most patients with known porphyria can complete anesthesia and surgery safely, undiagnosed porphyric patients are in danger of porphyric crisis due to inadvertent exposure to precipitating drugs and environment. We report a case of a patient who experienced delayed emergence with neurological disturbance after general anesthesia, ultimately diagnosed as acute intermittent porphyria.
    Korean journal of anesthesiology 09/2014; 67(3):217-20. DOI:10.4097/kjae.2014.67.3.217
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    ABSTRACT: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by abnormal proliferation of renal tubular epithelial cells resulting in loss of renal function. Despite identification of the genes responsible for ADPKD, few effective drugs are currently available for the disease. Thus, finding additional effective drug targets is necessary. The functions of MRP3 have been reported only in the field of drug-resistance, and the renal functions of multidrug-resistance associated protein 3 (MRP) are mostly unknown. In this study, we found that MRP3 was significantly downregulated in kidneys of human patients with ADPKD and polycystic kidney disease (PKD) mouse models. Our results suggest that downregulated MRP3 stimulated renal epithelial cell proliferation through the B-Raf/MEK/ERK signaling pathway. In contrast, we found that restoring MRP3 reduced cell proliferation and cystogenesis in vitro. These results suggest that the renal function of MRP3 is related to renal cell proliferation and cyst formation and that restoring MRP3 may be an effective therapeutic approach for PKD.
    American journal of physiology. Renal physiology 08/2014; DOI:10.1152/ajprenal.00159.2014 · 3.30 Impact Factor
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    ABSTRACT: The recent proliferation of data on large collections of well-characterized cancer cell lines linked to therapeutic drug responses has made it possible to identify lineage- and mutation-specific transcriptional markers that can help optimize implementation of anticancer agents. Here we leverage these resources, to systematically investigate the presence of mutation-specific transcription markers in a wide variety of cancer lineages and genotypes. Sensitivity and specificity of potential transcriptional biomarkers were simultaneously analyzed in 19 cell lineages grouped into 228 categories based on the mutational genotypes of 12 cancer-related genes. Among a total of 1,455 category-specific expression patterns, the expression of cAMP phosphodiesterase-4D (PDE4D) with 11 isoforms, one of the PDE4(A-D) sub-families, was predicted to be regulated by a mutant form of Serine/threonine kinase 11 (STK11)/liver kinase B1 (LKB1) present in lung cancer. STK11/LKB1 is the primary upstream kinase of adenine monophosphate-activated protein kinase (AMPK). Subsequently, we found that the knockdown of PDE4D gene expression inhibited proliferation of STK11-mutated lung cancer lines. Furthermore, challenge with a panel of PDE4 specific inhibitors was shown to selectively reduce the growth of STK11-mutated lung cancer lines. Thus we show that multidimensional analysis of a well-characterized large-scale panel of cancer cell lines provides unprecedented opportunities for identification of unexpected oncogenic mechanisms and mutation-specific drug targets.
    Molecular Cancer Therapeutics 08/2014; 13(10). DOI:10.1158/1535-7163.MCT-14-0297 · 6.11 Impact Factor
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    ABSTRACT: Background Epithelial-mesenchymal transition (EMT) is associated with tumor hypoxia. EMT is regulated, in part, by the action of TWIST, which inhibits of E-cadherin expression and may interfere with the p53 tumor-suppressor pathway. Methods We examined the expression of TWIST, E-cadherin, hypoxia-inducible factor 1α (HIF1α), and p53 by immunohistochemistry in 123 cases of ovarian epithelial cancers (OEC) to evaluate the role of TWIST in OEC. We assessed the association between protein expression and clinicopathologic parameters. Results The expression of TWIST, E-cadherin, HIF1α, and p53 proteins was found in 28.5%, 51.2%, 35.0%, and 29.3% of cases, respectively. TWIST expression was associated with higher histologic grade and unfavorable survival. TWIST expression was correlated with HIF1α expression and reduced E-cadherin expression. The altered HIF1α/TWIST/E-cadherin pathway was associated with lower overall survival (OS), while the co-expression of TWIST and p53 was correlated with lower progression-free survival. In the multivariate analyses, TWIST expression was an independent prognostic factor for OS. Conclusions Our data imply that TWIST expression could be a useful predictor of unfavorable prognosis for OEC. TWIST may affect the p53 tumor-suppressor pathway. Moreover, hypoxia-mediated EMT, which involves the HIF1α/TWIST/E-cadherin pathway may play an important role in the progression of OEC.
    The Korean Journal of Pathology 08/2014; 48(4):283-91. DOI:10.4132/KoreanJPathol.2014.48.4.283 · 0.17 Impact Factor
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    ABSTRACT: Soft tissue sarcomas (STS) are rare. We evaluated the WT1 protein expression level in various types of STS and elucidated the value of WT1 as a prognostic factor and a possible therapeutic target.
    World Journal of Surgical Oncology 07/2014; 12(1):214. DOI:10.1186/1477-7819-12-214 · 1.20 Impact Factor
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    ABSTRACT: Objective. We assessed the extent to which self-reported exposure to SHS underestimates the actual exposure to SHS and what factors are associated with a tolerance for SHS exposure in the Korean setting where the smoke-free policy is incomplete. Methods. Information on socio-demographic characteristics, alcohol drinking nd smoking was collected for 7948 nonsmokers aged >= 19 years from the fourth Korea National Health and Nutrition Examination Survey, 2008-2009. Self-reported and cotinine verified SHS exposures were compared. Potential factors associated with cotinine verified but not self-reported SHS exposures were assessed using a logistic regression model. Results. Self-reported SHS exposure significantly underestimated the actual SHS exposure as determined by cotinine verification (kappa coefficient: 0.1066). At younger age, frequent alcohol drinking in females and a longer smoking duration in males were positively associated with cotinine verified exposure but not with the self-reported SHS exposure; they were also positively associated with cotinine verified exposure irrespective of self-reported SHS exposure. Conclusions. Our findings show a tolerance for smoking in Korea The current partial ban on smoking does not fully protect people from exposure to SHS. Smoking should be banned in all public places. In addition, efforts to "de-normalize smoking in the Korean culture need to be strengthened.
    Preventive Medicine 07/2014; 67. DOI:10.1016/j.ypmed.2014.07.003 · 2.93 Impact Factor
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    ABSTRACT: As it is known that FK506 binding proteins (FK506BPs) play an important role regulating a variety of biological processes for cell survival, this study was designed to examined the protective effects of FK506 binding protein 12 (FK506BP) on low humidity air flow induced dry eye in a rat model using transduced PEP-1-FK506BP. After the topically application of PEP-1-FK506BP tear volumes were markedly increased and cornea damage was significantly prevented compared with dry eye rats. Further, immunohistochemical analysis demonstrated that PEP-1-FK506BP markedly prevented damage to the cornea, the bulbar conjunctiva, and the palpebral conjunctiva epithelial lining compared with dry eye rats. Also this decreased caspase-3 and PARP expression levels. These results demonstrated that topically applied PEP-1-FK506BP significantly ameliorates dry eye injury in an animal model. Thus, we suggest that PEP-1-FK506BP can be developed as a new ophthalmic drop to treat dry eye diseases.
    BMB reports 07/2014; · 1.99 Impact Factor

Publication Stats

1k Citations
301.48 Total Impact Points


  • 2005–2015
    • Catholic University of Korea
      • • Department of Urology
      • • College of Medicine
      • • Department of Internal Medicine
      Sŏul, Seoul, South Korea
    • Seoul National University Hospital
      • Department of Nuclear Medicine
      Sŏul, Seoul, South Korea
  • 2012–2014
    • Hallym University Medical Center
      • Department of Anesthesiology and Pain Medicine
      Sŏul, Seoul, South Korea
    • Pusan National University
      • • Department of Pathology
      • • Department of Surgery
      Tsau-liang-hai, Busan, South Korea
    • Chungnam National University
      • Department of Horticultural Science
      Daiden, Daejeon, South Korea
  • 2011–2014
    • Gachon University
      • Department of Nursing (College of Nursing)
      Sŏngnam, Gyeonggi-do, South Korea
    • Jeonju University
      • Department of Secondary Special Education
      Sŏul, Seoul, South Korea
  • 2007–2014
    • Sookmyung Women's University
      • Department of Biological Science
      Sŏul, Seoul, South Korea
  • 2004–2014
    • National Cancer Center Korea
      Kōyō, Gyeonggi Province, South Korea
  • 2013
    • Ajou University
      • Department of Otolaryngology
      Sŏul, Seoul, South Korea
    • Kyungpook National University
      • Green-Nano Materials Research Center
      Daikyū, Daegu, South Korea
  • 2011–2013
    • Hallym University
      • College of Medicine
      Seoul, Seoul, South Korea
  • 2004–2013
    • Korea University
      • • College of Nursing
      • • Department of Life Sciences
      Sŏul, Seoul, South Korea
  • 2009–2011
    • Hannam University
      • Department of Advanced Materials
      Daiden, Daejeon, South Korea
  • 2010
    • Korea Institute of Radiological & Medical Sciences
      Sŏul, Seoul, South Korea
  • 2004–2009
    • Ewha Womans University
      • • Department of Pediatrics
      • • Center for Cell Signaling Research (CCSR)
      Sŏul, Seoul, South Korea
  • 2008
    • Dong Seoul College
      Sŏul, Seoul, South Korea
    • Chonnam National University
      • Department of Pediatrics
      Gwangju, Gwangju, South Korea
  • 2007–2008
    • Hanyang University
      • Division of Chemical Engineering and Bioengineering
      Sŏul, Seoul, South Korea
  • 2002–2008
    • Seoul National University
      • • Department of Preventive Medicine
      • • Research Institute of Pharmaceutical Sciences
      • • College of Pharmacy
      • • Department of Biological Sciences
      Sŏul, Seoul, South Korea
    • Hankuk University of Foreign Studies
      • Department of Bioscience and Biotechnology
      Sŏul, Seoul, South Korea
  • 2006
    • Kangbuk Samsung Hospital
      Sŏul, Seoul, South Korea