Hye Sun Kim

Ajou University, Sŏul, Seoul, South Korea

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Publications (77)189.19 Total impact

  • Sung Ran Hong · Tae Jin Kim · In Ho Lee · Hye Sun Kim

    No preview · Article · Nov 2015
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    ABSTRACT: Metabolomic analysis of urinary polyamines (PAs) from rat exposed to 915 MHz radiofrequency identification (RFID) signal for 8 h/day for 2 weeks was performed by gas chromatography–mass spectrometry as N-ethoxycarbonyl/N-pentafluoropropionyl derivatives. Large alterations in nine PA levels including four aliphatic and five acetylated PAs were monitored in sham-exposed and RFID-exposed groups. Total PA and urinary levels of N 1-acetylputrescine, N 1-acetylcadaverine, putrescine, cadaverine, N 1-acetylspermidine, N 8-acetylspermidine, spermidine and spermine were reduced, whereas N 1-acetylspermine was significantly increased after sham and RFID exposure compared with those before exposure. Their levels were normalized to the corresponding group means before exposure and then plotted into star symbol patterns. N 1-Acetylspermine after RFID exposure was 54 % higher compared to the level before RFID exposure, while it was elevated by only 17 % in the sham group. The results suggest that 915 MHz RFID exposure may induce metabolic disturbance of PA. It may also elevate spermidine/spermine acetyltransferase (SSAT) activity. Thus, the present metabolic profiling combined with star pattern recognition method might be useful for understanding the complexity of biochemical events after exposure to RFID signal.
    No preview · Article · Aug 2015 · Amino Acids
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    ABSTRACT: Staphylococcus aureus plays an important role in sepsis, septic shock, pneumonia, and wound infections. Here, we demonstrate that Lactobacillus plantarum extracts inhibited S. aureus-induced cell death of human epithelial cell line, HT-29. In particular, we have shown that S. aureus-induced cell death was abolished by neutralization of alpha-toxin, indicating that α-toxin is the major mediator of S. aureus-induced cell death. DNA fragmentation experiment and caspase assay revealed that S. aureus-induced cell death was the apoptosis. L. plantarum extracts inhibited the generation of effector caspase-3 and the initiator caspase-9 in S. aureus- or α-toxin-induced cell death. Moreover, expression of Bcl-2, anti-apoptotic protein, was activated in L. plantarum extracts-treated cells as compared to the S. aureus- or α-toxin-treated only cells. Furthermore, S. aureus-induced apoptosis was efficiently inhibited by lipoteichoic acid (LTA) and peptidoglycan (PGN) of L. plantarum. Together, our results suggest that L. plantarum extracts can inhibit the S. aureus-mediated apoptosis, which associated with S. aureus spreading, in intestinal epithelial cells, and may provide a new therapeutic reagent to treat bacterial infections.
    No preview · Article · Jul 2015 · Journal of Microbiology and Biotechnology
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    ABSTRACT: We investigated the effects of whole-body exposure to the 915 MHz radiofrequency identification (RFID) on melatonin biosynthesis and the activity of rat pineal arylalkylamine N-acetyltransferase (AANAT). Rats were exposed to RFID (whole-body specific absorption rate, 4 W/kg) for 8 h/day, 5 days/week, for 2 weeks during the nighttime. Total volume of urine excreted during a 24-hour period was collected after RFID exposure. Urinary melatonin and 6-hydroxymelatonin sulfate (6-OHMS) was measured by gas chromatography-mass spectrometry (GC-MS) and enzyme-linked immunosorbent assay (ELISA), respectively. AANAT enzyme activity was measured using liquid biphasic diffusion assay. Protein levels and mRNA expression of AANAT was measured by Western blot and reverse transcription polymerase chain reaction (RT-PCR) analysis, respectively. Eight hours of nocturnal RFID exposure caused a significant reduction in both urinary melatonin (P = 0.003) and 6-OHMS (P = 0.026). Activity, protein levels, and mRNA expression of AANAT were suppressed by exposure to RFID (P < 0.05). Our results suggest that nocturnal RFID exposure can cause reductions in the levels of both urinary melatonin and 6-OHMS, possibly due to decreased melatonin biosynthesis via suppression of Aanat gene transcription in the rat pineal gland.
    No preview · Article · Jul 2015 · International Journal of Radiation Biology
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    Su Jin Choi · Ki Jung Jang · Jeong-A Lim · Hye Sun Kim
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    ABSTRACT: Hemophilia A is caused by heterogeneous mutations in F8. Coagulation factor VIII (FVIII), the product of F8, is composed of multiple domains designated A1-A2-B-A3-C1-C2. FVIII is known to interact with diverse proteins, and this characteristic may be important for hemostasis. However, little is known about domain-specific functions or their specific binding partners. To determine F8 domain-specific functions during blood coagulation, the FVIII domains A1, A2, A3, and C were cloned from Hep3B hepatocytes. Domain-specific recombinant polypeptides were glutathione S-transferase (GST)- or polyhistidine (His)-tagged, over-expressed in bacteria, and purified by specific affinity chromatography. Recombinant polypeptides of predicted sizes were obtained. The GST-tagged A2 polypeptide interacted with coagulation factor IX, which is known to bind the A2 domain of activated FVIII. Recombinant, domain-specific polypeptides are useful tools to study the domain-specific functions of FVIII during the coagulation process, and they may be used for production of domain-specific antibodies.
    Full-text · Article · Jun 2015 · Blood Research
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    ABSTRACT: Introduction: Whether exposure to the 848.5 MHz code division multiple access (CDMA) signal affects adult neurogenesis is unclear. Materials and methods: An animal experiment was performed with a reverberation chamber designed as a whole-body CDMA exposure system. Male Sprague-Dawley rats were assigned to three groups (n = 6 per group): Cage-control, sham-exposed, and CDMA-exposed groups. Rats in the CDMA-exposed group were exposed to the CDMA signal at a 2 W/kg whole-body specific absorption rate (SAR) for 1 or 8 h daily, 5 days per week, for 2 weeks. Rats received a single intraperitoneal injection of Bromodeoxyuridine (BrdU) to label proliferative cells daily for the last five consecutive days of CDMA signal exposure. An unbiased stereological method was used to estimate the number of BrdU(+) cells in the subventricular zone (SVZ) and dentate gyrus (DG). Results: We found no significant changes in the number of BrdU(+) cells in the SVZ or DG in the CDMA-exposed rats, compared with rats in the cage-control and sham-exposed groups (p > 0.05). Conclusion: Our results suggest that exposure to the CDMA signal does not affect neurogenesis in the adult rat brain, at least under our experimental conditions.
    No preview · Article · Dec 2014 · International Journal of Radiation Biology
  • Jae Kwan Lee · Hye Sun Kim · Suk Jin Yun
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    ABSTRACT: The synthesis and photovoltaic characteristics of a new organic dye, CU-L2, which has a unique and flexible alkylenesulfanyl-bridged bithienyl bridging framework between the phenylamino donor unit and cyanoacrylic acceptor unit, were demonstrated. CU-L2 exhibited better photovoltaic performance, with an enhanced photocurrent due to the redshifted optical absorption and reduced interfacial recombination, as compared to CU-L1, with its rigid dithienothiophene bridging motif between the same donor and acceptor units. The dye-sensitized solar cell fabricated with CU-L2 under optimized processing conditions presented a high power conversion efficiency of 6.63%.
    No preview · Article · Feb 2014 · Journal of Photochemistry and Photobiology A Chemistry
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    ABSTRACT: In this study, we investigated the molecular mechanisms underlying the anti-proliferative effects of Compound K, with specific reference to histone modification. Exposure of HT-29 human colon cancer cells to Compound K resulted in time-dependent inhibition of histone deacetylase (HDAC) activity, mRNA and protein expression. Compound K treatment induced unmethylation of the RUNX3 promoter region such as TSA treatment and an accumulation of acetylated histones H3 and H4 within the total cellular chromatin, resulting in an enhanced ability of these histones to bind to the promoter sequences of the tumor suppressor gene Runt-related transcription factor 3 (RUNX3). Treatment of cells with Compound K increased the mRNA and protein expression of RUNX3, as well as p21, a downstream target of RUNX3. These alterations were consistent with cell cycle arrest at the G0/G1 phases and induction of apoptosis. Our results provide new insights into the mechanisms of Compound K action in human colorectal cancer cells and suggest that HDAC inhibition presents a novel approach to prevent or treat colorectal cancer.
    Preview · Article · Oct 2013 · International Journal of Oncology
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    ABSTRACT: The modified guanine base 8-oxoguanine (8-oxoG) is abundantly produced by oxidative stress, can contribute to carcinogenesis, and can be removed from DNA by 8-oxoguanine DNA glycosylase-1 (OGG1), which acts as an 8-oxoG glycosylase and endonuclease. This study investigated the mechanism by which 7,8-dihydroxyflavone (DHF) inhibits oxidative stress-induced 8-oxoG formation in hamster lung fibroblasts (V79-4). DHF significantly reduced the amount of 8-oxoG induced by hydrogen peroxide (H2O2) and elevated the levels of OGG1 mRNA and protein. DHF increased the binding of nuclear factor erythroid 2-related factor 2 (Nrf2) to antioxidant response element sequences in the upstream promoter region of OGG1. Moreover, DHF increased the nuclear levels of Nrf2, small Maf proteins, and the Nrf2/small Maf complex, all of which are decreased by H2O2 treatment. Likewise, the level of phosphorylated Akt, which activates Nrf2, was decreased by H2O2 treatment but restored by DHF treatment. The levels of OGG1 and nuclear translocation of Nrf2 protein were decreased upon treatment with PI3K inhibitor or Akt inhibitor, and DHF treatment did not restore OGG1 and nuclear Nrf2 levels in these inhibitor-treated cells. Furthermore, PI3K and Akt inhibitors abolished the protective effects of DHF in cells undergoing oxidative stress. These data indicate that DHF induces OGG1 expression via the PI3K-Akt pathway and protects cells against oxidative DNA base damage by activating DNA repair systems.
    Full-text · Article · Sep 2013
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    ABSTRACT: Fucoxanthin is an important carotenoid derived from edible brown seaweeds and is used in indigenous herbal medicines. The aim of the present study was to examine the cytoprotective effects of fucoxanthin against hydrogen peroxide-induced cell damage. Fucoxanthin decreased the level of intracellular reactive oxygen species, as assessed by fluorescence spectrometry performed after staining cultured human HaCaT keratinocytes with 2',7'-dichlorodihydrofl uorescein diacetate. In addition, electron spin resonance spectrometry showed that fucoxanthin scavenged hydroxyl radical generated by the Fenton reaction in a cell-free system. Fucoxanthin also inhibited comet tail formation and phospho-histone H2A.X expression, suggesting that it prevents hydrogen peroxideinduced cellular DNA damage. Furthermore, the compound reduced the number of apoptotic bodies stained with Hoechst 33342, indicating that it protected keratinocytes against hydrogen peroxide-induced apoptotic cell death. Finally, fucoxanthin prevented the loss of mitochondrial membrane potential. These protective actions were accompanied by the down-regulation of apoptosispromoting mediators (i.e., B-cell lymphoma-2-associated x protein, caspase-9, and caspase-3) and the up-regulation of an apoptosis inhibitor (B-cell lymphoma-2). Taken together, the results of this study suggest that fucoxanthin defends keratinocytes against oxidative damage by scavenging ROS and inhibiting apoptosis.
    Preview · Article · Jul 2013 · Biomolecules and Therapeutics
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    ABSTRACT: Exposure of human skin to excessive ultraviolet B (UVB) radiation induces pathophysiological processes via the generation of reactive oxygen species (ROS) in skin cells, such as keratinocytes. This study investigated the ability of diphlorethohydroxycarmalol (DPHC) to protect human keratinocytes (HaCaT) against UVB-induced cell damage. DPHC restored cell viability that was reduced by UVB light. DPHC had an absorption maximum close to the UVB spectrum and decreased UVB-induced intracellular ROS levels, increased levels of reduced glutathione, activated superoxide dismutase and catalase. DPHC also decreased UVB-mediated damage to cellular components, including lipids, proteins, DNA, and attenuated UVB-induced apoptosis. These results suggest that DPHC safeguards human keratinocytes against UVB-induced cell damage by absorbing UVB ray, scavenging ROS and enhancing antioxidant system.
    Full-text · Article · Jun 2013
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    ABSTRACT: As a part of an investigation on the potential risks of radiofrequency identification (RFID) on human health, we studied whether exposure to 915 MHz RFID in rats significantly affected the secretory function of the thyroid system. A reverberation chamber was used as a whole-body exposure system. Male Sprague-Dawley rats were exposed for 8 h per day, 5 days per week, for a duration of 2, 4, 8, or 16 weeks. The estimated whole-body average specific absorption rate (SAR) varied from 3.2 to 4.6 W/kg depending on the age/mass of the animals for the field of the 915 MHz RFID reader. Plasma levels of triiodothyronine (T3), thyroxine (T4), and thyroid-stimulating hormone (TSH) were evaluated via enzyme-linked immunosorbent assay. Morphological changes in the thyroid gland were then analyzed. No changes in T3, T4, or TSH were observed over time between the sham- and RFID-exposed groups. We suggest that subchronic exposure to 915 MHz RFID at a SAR of 4 W/kg does not cause significant effects on thyroid secretory function. Bioelectromagnetics. 9999:XX-XX. © 2013 Wiley Periodicals, Inc.
    No preview · Article · Jun 2013 · Bioelectromagnetics
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    ABSTRACT: Ionizing radiation can induce cellular oxidative stress through the generation of reactive oxygen species, resulting in cell damage and cell death. The aim of this study was to determine whether the antioxidant effects of the flavonoid fisetin (3,7,3',4'-tetrahydroxyflavone) included the radioprotection of cells exposed to γ-irradiation. Fisetin reduced the levels of intracellular reactive oxygen species generated by γ-irradiation and thereby protected cells against γ-irradiation-induced membrane lipid peroxidation, DNA damage, and protein carbonylation. In addition, fisetin maintained the viability of irradiated cells by partially inhibiting γ-irradiation-induced apoptosis and restoring mitochondrial membrane potential. These effects suggest that the cellular protective effects of fisetin against γ-irradiation are mainly due to its inhibition of reactive oxygen species generation.
    Full-text · Article · May 2013 · Biomolecules and Therapeutics
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    ABSTRACT: The intestine-specific transcription factor, caudal type homeobox-1 (CDX1), is a candidate tumor suppressor gene that plays key roles in regulating intestinal epithelial differentiation and proliferation. It is aberrantly down-regulated in colorectal cancers and colon cancer-derived cell lines by promoter hypermethylation. Since the effects of oxidative stress on the transcription of tumor suppressor genes are largely unknown, this study explored the epigenetic alterations that occur during reactive oxygen species (ROS)-induced silencing of CDX1 in colorectal cancer cells. Oxidative stress by hydrogen peroxide (H2O2) down-regulated CDX1 mRNA levels and protein expression in the human colorectal cancer cell line, T-84. This down-regulation was abolished by pretreatment with the ROS scavenger, N-acetylcysteine. In addition, the DNA methylation inhibitor, 5-aza-2-deoxycytidine (5-Aza-dC) markedly attenuated the decrease in mRNA and protein expression levels induced by H2O2. Moreover, methylation-specific PCR data revealed that H2O2 treatment increased CDX1 promoter methylation, and treatment with 5-Aza-dC reversed this effect, suggesting that an epigenetic regulatory mechanism triggered by ROS-induced methylation may be involved in CDX1 expression. Furthermore, H2O2 treatment resulted in up-regulation of DNA methyltransferase 1 (DNMT1) and histone deacetylase 1 (HDAC1) expression and activity, and enhanced the association between DNMT1 and HDAC1. Taken together, these results suggest that ROS-induced oxidative stress silences the tumor suppressor CDX1 through epigenetic regulation, and may therefore be associated with the progression of colorectal cancer.
    No preview · Article · Apr 2013 · Gene
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    ABSTRACT: Purpose: We investigated the effect of whole-body exposure to 915-MHz radiofrequency identification (RFID) on rat cortical glucose metabolism by using (18)F-deoxyglucose positron emission tomography (FDG-PET). Materials and methods: Male Sprague-Dawley rats were divided into three groups: Cage-control, sham-exposed and RFID-exposed groups. Rats were exposed to the 915-MHz RFID for 8 h daily, 5 days per week, for 2 or 16 weeks. The whole-body average specific absorption rate (SAR) was 4 W/kg for the field of the 915 MHz RFID signal. FDG-PET images were obtained the day after RFID exposure, using micro-PET with a FDG tracer. With a Xeleris functional imaging workstation, absolute values in regions of interest (ROI) in the frontal, temporal and parietal cortexes and cerebellum were measured. Cortical ROI values were normalized to the cerebellar value and compared. Results: The data showed that the relative cerebral glucose metabolic rate was unchanged in the frontal, temporal and parietal cortexes of the 915 MHz RFID-exposed rats, compared with rats in cage-control and sham-exposed groups. Conclusion: Our results suggest that 915 MHz RFID radiation exposure did not cause a significant long lasting effect on glucose metabolism in the rat brain.
    Full-text · Article · Apr 2013 · International Journal of Radiation Biology
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    ABSTRACT: The consensus guideline development committee of Korean Society of Gynecologic Oncology was reconvened in March 2012. The committee consisted of 36 experts representing 12 university hospitals and professional organizations. The objective of this committee was to develop standardized guidelines for cervical cancer screening tests for Korean women and to distribute these guidelines to every clinician, eventually improving the quality of medical care. Since the establishment of the consensus guideline development committee, evidence-based guidelines have either been developed de novo considering specific Korean situations or by adaptation of preexisting consensus guidelines from other countries. Recommendations for cervical cancer screening tests, management of atypical squamous and glandular cells, and management of low-grade and high-grade squamous intraepithelial lesions were developed. Additionally, recommendations for human papillomavirus DNA testing and recommendations for adolescent and pregnant women with abnormal cervical screening test results were also included.
    Full-text · Article · Apr 2013 · Journal of Gynecologic Oncology
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    ABSTRACT: The cytotoxic effects and mechanism of action of clerosterol, isolated from the marine alga Codium fragile, were investigated in A2058 human melanoma cells. Clerosterol inhibited the growth of A2058 cells with an IC(50) of 150 µM and induced apoptotic cell death, as evidenced by DNA fragmentation, an increase in the number of sub-G(1) hypodiploid cells and the presence of apoptotic bodies. Clerosterol treatment caused the loss of mitochondrial membrane potential. Alterations in the expression of apoptosis-associated proteins in response to clerosterol treatment included upregulation of Bax, downregulation of Bcl-2 and activation of caspases 3 and 9. The pan-caspase inhibitor treatment attenuated the expression of the active form of caspases and cell death induced by clerosterol. The present results show that clerosterol exerts its cytotoxic effect in A2058 human melanoma cells by caspases-dependent apoptosis.
    Preview · Article · Feb 2013 · Marine Drugs
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    ABSTRACT: Previously, we reported that 20-O-(β-D-gluco-pyranosyl)-20(S)-protopanaxadiol (Compound K, a meta-bolite of ginseng saponin) induces mitochondria-dependent and caspase-dependent apoptosis in HT-29 human colon cancer cells via the generation of reactive oxygen species. The aim of the present study was to elucidate the mechanism underlying apoptosis induced by Compound K with respect to endoplasmic reticulum (ER) stress in HT-29 cells. In the present study, Compound K induced apoptotic cell death as confirmed by DNA fragmentation and apoptotic sub-G1 cell population. Compound K also induced ER stress as indicated by staining with ER tracker, cytosolic and mitochondrial Ca2+ overloading, phosphorylation of protein-kinase-like endoplasmic reticulum kinase (PERK), phosphorylation of eukaryotic initiation factor-2α (eIF-2α), phosphorylation of IRE-1, splicing of ER stress-specific X-box transcription factor-1 (XBP-1), cleavage of activating transcription factor-6 (ATF-6), upregulation of glucose-regulated protein-78 (GRP-78/BiP) and CCAAT/enhancer-binding protein-homologous protein (CHOP), and cleavage of caspase-12. Furthermore, downregulation of CHOP expression using siCHOP RNA attenuated Compound K-induced apoptosis. Taken together, these results support the important role of ER stress response in mediating Compound K-induced apoptosis in human colon cancer cells.
    No preview · Article · Feb 2013 · Oncology Reports
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    ABSTRACT: This study investigated the mechanisms underlying the cytotoxicity of the green algae Ulva fasciata Delile. U. fasciata extract (UFE) inhibited the growth of HCT 116 human colon cancer cells by 50% at a concentration of 200 μg/ml. In addition, UFE stimulated the production of intracellular reactive oxygen species, an effect that was abolished by pretreatment with N-acetyl cysteine, which also inhibited the cytotoxic effects of UFE. UFE also induced morphological changes indicative of apoptosis, such as the formation of apoptotic bodies, DNA fragmentation, an increase in the population of apoptotic sub-G(1) phase cells, and mitochondrial membrane depolarization. Concomitant activation of the mitochondria-dependent apoptotic pathway occurred via modulation of Bax and Bcl-2 expression, resulting in disruption of the mitochondrial membrane potential and activation of caspase-9 and caspase-3. This is the first report to demonstrate the cytotoxic effect of U. fasciata on human colon cancer cells and to provide a possible mechanism for this activity.
    No preview · Article · Jan 2013 · In Vitro Cellular & Developmental Biology - Animal
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    ABSTRACT: Oxidative stress caused by reactive oxygen species (ROS) induces DNA base modifications and DNA strand breaks. In this study, the protective effect of baicalein against H(2)O(2)-induced DNA damage was investigated in V79-4 Chinese hamster fibroblast cells. H(2)O(2) treatment increased the levels of intracellular ROS and DNA double-strand breaks (DSBs) and decreased the level of Ku70 protein and the phosphorylation (activation) of DNA-dependent protein kinase catalytic subunit (DNA-PKcs), which are involved in the repair of DSBs by nonhomologous end joining. Baicalein effectively scavenged intracellular ROS induced by H(2)O(2), reduced DSBs, and rescued Ku70 protein level and phosphorylation of DNA-PKcs. In cellular response to DNA base damage, 8-oxoguanine DNA glycosylase 1 (OGG1) plays a vital role in the removal of 8-oxoguanine (8-OxoG), which is formed mainly by oxidative stress. Baicalein significantly decreased the levels of 8-OxoG induced by H(2)O(2), and this correlated with increases in OGG1 promoter activity and OGG1 mRNA and protein expression. The phosphorylated form of Akt kinase, which is a regulator of OGG1, was sharply decreased by H(2)O(2), but was prevented by baicalein. A specific Akt inhibitor abolished the cytoprotective effects of baicalein, suggesting that OGG1 induction by baicalein involves the Akt pathway. In conclusion, baicalein exerted protective effects against DNA damage induced by oxidative stress by activating DNA repair systems and scavenging ROS.
    No preview · Article · Sep 2012 · Cell Biology and Toxicology

Publication Stats

1k Citations
189.19 Total Impact Points


  • 1997-2015
    • Ajou University
      • College of Natural Sciences
      Sŏul, Seoul, South Korea
  • 2013
    • Seoul National University Hospital
      Sŏul, Seoul, South Korea
  • 2008-2013
    • Catholic Kwandong University
      • College of Medicine
      Gangneung, Gangwon-do, South Korea
  • 1991-2013
    • Seoul National University
      • • College of Medicine
      • • Department of Medicine
      • • Department of Pharmacology
      • • College of Natural Sciences
      Sŏul, Seoul, South Korea
  • 2004-2012
    • Kyung Hee University
      • • Department of Dentistry
      • • Department of Biomedical Engineering
      Sŏul, Seoul, South Korea
  • 2011
    • Centro de Investigación del Cáncer
      Helmantica, Castille and León, Spain
  • 2009-2011
    • University of Texas MD Anderson Cancer Center
      • Department of Gynecologic Oncology
      Houston, Texas, United States
  • 2007-2010
    • Cheil General Hospital
      Sŏul, Seoul, South Korea
  • 2005-2009
    • Yonsei University Hospital
      • • Department of Internal Medicine
      • • Surgery
      Sŏul, Seoul, South Korea
  • 2005-2007
    • Sungkyunkwan University
      • Department of Pathology
      Sŏul, Seoul, South Korea
  • 2006
    • Korea University
      • Department of Pathology
      Seoul, Seoul, South Korea
    • Jeju National University
      • Department of Computer Education (College of Education)
      Tse-tsiu, Jeju, South Korea
  • 2005-2006
    • Cheju Halla University
      Tse-tsiu, Jeju, South Korea