Eun Young Choi

University of Wisconsin–Madison, Madison, Wisconsin, United States

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Publications (218)694.16 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: An unusual 1D-to-3D transformation of a coordination polymer based on organic linkers containing highly polar push–pull π-conjugated side chains is reported. The coordination polymers are synthesized from zinc nitrate and an organic linker, namely, 2,5-bis{4-[1-(4-nitrophenyl)pyrrolidin-2-yl]butoxy}terephthalic acid, which possesses highly polar (4-nitrophenyl)pyrrolidine groups, with high dipole moments of about 7 D. The coordination polymers exhibit an unusual transformation from a soluble, solvent-stabilized 1D coordination polymer into an insoluble, metal–organic framework (MOF)-like 3D coordination polymer. The coordination polymer exhibits good film-forming ability, and the MOF-like films are insoluble in conventional organic solvents.
    Chemistry - A European Journal 09/2015; DOI:10.1002/chem.201502128 · 5.73 Impact Factor
  • Hee Young Kang · Eun Young Choi
    08/2015; 21(3):289-297. DOI:10.5977/jkasne.2015.21.3.289
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    ABSTRACT: Despite recent advances in therapeutic strategies for lung cancer, mortality still is increasing. In the present study, we investigated the anti-cancer effects of KMU-193, 2-(4-Ethoxy-phenyl)-N-{5-[2-fluoro-4-(4-methyl- piperazine-1-carbonyl)-phenylamino]-1H-indazol-3-yl}-acetamide in a human non-small cell lung cancer cell line A549. KMU-193 strongly inhibited the proliferation of A549 cells, but it did not have anti-proliferative effect in other types of cancer cell lines. KMU-193 further induced apoptosis in association with activation of caspase-3 and cleavage of PLC-γ1. However, KMU-193 had no apoptotic effect in untransformed cells such as TMCK-1 and BEAS-2B. Interestingly, pretreatment with z-VAD-fmk, a pan-caspase inhibitor, strongly abrogated KMU- 193-induced apoptosis. KMU-193 treatment enhanced the expression levels of p53 and PUMA. Importantly, p53 siRNA transfection attenuated KMU-193-induced apoptosis. Collectively, these results for the first time demonstrate that KMU-193 has strong apoptotic effects on A549 cells and these are largely mediated through caspase-3- and p53-dependent pathways.
    Asian Pacific journal of cancer prevention: APJCP 08/2015; 16(14):5883-7. · 2.51 Impact Factor
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    ABSTRACT: CD8(+) T cells activated without CD4(+) T-cell help are impaired in memory expansion. To understand the underlying cellular mechanism, here we track the dynamics of helper-deficient CD8(+) T-cell response to a minor histocompatibility antigen by phenotypic and in vivo imaging analyses. Helper-deficient CD8(+) T cells show reduced burst expansion, rapid peripheral egress, delayed antigen clearance and continuous activation, and are eventually exhausted. Contrary to the general consensus that CD4 help encodes memory programmes in CD8(+) T cells and helper-deficient CD8(+) T cells are abortive, these cells can differentiate into effectors and memory precursors. Importantly, accelerating antigen clearance or simply increasing the burst effector size enables generation of memory cells by CD8(+) T cells, regardless of CD4 help. These results suggest that the memory programme is CD8(+) T-cell-intrinsic, and provide insight into the role of CD4 help in CD8(+) T-cell responses.
    Nature Communications 08/2015; 6:7994. DOI:10.1038/ncomms8994 · 11.47 Impact Factor
  • Bong‐Hee Kim · Hee‐Young Kang · Eun‐Young Choi
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    ABSTRACT: Aims and objectivesThis study evaluated the effects of handholding and spoken information provided on the anxiety of patients undergoing percutaneous vertebroplasty under local anaesthesia.BackgroundA surgical intervention usually entails physical discomfort and psychological burden. Furthermore, patients under local anaesthesia are conscious during the surgical intervention, which leads to more anxiety, as patients are aware of their surroundings in the operating theatre.DesignA quasi-experimental design with a nonequivalent control group was utilised.Methods Amsterdam preoperative anxiety scale assessed psychological anxiety, while blood pressure and pulse were measured to evaluate physiological anxiety. Participants were 94 patients undergoing percutaneous vertebroplasty in a spine hospital in Gwangju Metropolitan City, South Korea. Thirty patients were assigned to Experimental Group I, 34 to the Experimental Group II and 30 to the control group. During a surgical intervention, nurses held the hands of those in Experimental Group I and provided them with spoken information. Patients in Experimental Group II experienced only handholding.ResultsPsychological anxiety in Experimental Group I was low compared to those in Experimental Group II and the control group. In addition, there were significant decreases in systolic blood pressure in both Experimental Groups compared to the control group.Conclusions Handholding and spoken information provided during a surgical intervention to mitigate psychological anxiety, and handholding to mitigate physiological anxiety can be used in nursing interventions with patients undergoing percutaneous vertebroplasty.Relevance to clinical practiceHandholding and providing nursing information are possibly very useful interventions that are easily implemented by circulating nurses during a surgical intervention. In particular, handholding is a simple, economical and appropriate way to help patient in the operating theatre.
    Journal of Clinical Nursing 08/2015; DOI:10.1111/jocn.12928 · 1.26 Impact Factor
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    ABSTRACT: To identify significant fluorescein angiographic (FA) characteristics associated with visual acuity (VA) in Behçet retinal vasculitis. Retrospective review of 86 eyes of 48 patients (age: 35.6±10.2 years) with Behçet retinal vasculitis were performed. VA and FA findings as well as correlation between them were assessed. The mean initial VA of eyes with posterior pole-involved vasculitis (63 eyes; 73.3%) was significantly worse than that of those with peripheral vasculitis (23 eye; 26.7%) (logarithm of the minimum angle of resolution VA: 0.554±0.572 vs. 0.078±0.148; p<0.0001). Subgroup analysis revealed a more severe and diffuse pattern of vascular leakage in posterior pole-involved vasculitis compared to peripheral vasculitis (p<0.0001). Retinal vascular leakage (β=0.345; p<0.0001), optic disc hyperfluorescence (β=0.147; p=0.032), and macular leakage (β=0.107; p=0.047) were significantly associated with worse initial VA. During the follow up (mean: 33.3±17.9 months), the change of leakage showed no significant correlation with change of VA in posterior pole-involved vasculitis (τ=0.199, p=0.092). Posterior pole involvement, the degree of retinal vascular leakage, optic disc hyperfluorescence, and macular leakage are significantly associated with VA in Behçet retinal vasculitis.
    Yonsei medical journal 07/2015; 56(4):1087-1096. DOI:10.3349/ymj.2015.56.4.1087 · 1.29 Impact Factor
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    ABSTRACT: Upregulation of microRNA-21 (miR-21) is known to be strongly associated with the proliferation, invasion, and radio-resistance of glioma cells. However, the regulatory mechanism that governs the biogenesis of miR-21 in glioma is still unclear. Here, we demonstrate that the DEAD-box RNA helicase, DDX23, promotes miR-21 biogenesis at the post-transcriptional level. The expression of DDX23 was enhanced in glioma tissues compared to normal brain, and expression level of DDX23 was highly associated with poor survival of glioma patients. Specific knockdown of DDX23 expression suppressed glioma cell proliferation and invasion in vitro and in vivo, which is similar to the function of miR-21. We found that DDX23 increased the level of miR-21 by promoting primary-to-precursor processing of miR-21 through an interaction with the Drosha microprocessor. Mutagenesis experiments critically demonstrated that the helicase activity of DDX23 was essential for the processing (cropping) of miR-21, and we further found that ivermectin, a RNA helicase inhibitor, decreased miR-21 levels by potentially inhibiting DDX23 activity and blocked invasion and cell proliferation. Moreover, treatment of ivermectin decreased glioma growth in mouse xenografts. Taken together, these results suggest that DDX23 plays an essential role in glioma progression, and might thus be a potential novel target for the therapeutic treatment of glioma. © The Author (2015). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email:
    Brain 06/2015; 138(Pt 9). DOI:10.1093/brain/awv167 · 9.20 Impact Factor
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    ABSTRACT: Activation of IκB kinase (IKK) and NF-κB by genotoxic stresses modulates apoptotic responses and production of inflammatory mediators, thereby contributing to therapy resistance and premature aging. We previously reported that genotoxic agents induce nuclear localization of NEMO (NF-κB essential modulator) via an undefined mechanism to arbitrate subsequent DNA damage-dependent IKK/NF-κB signaling. Here we show that a nonclassical nuclear import pathway via IPO3 (importin 3, transportin 2) mediates stress-induced NEMO nuclear translocation. We found putative nuclear localization signals (NLS) in NEMO whose mutations disrupted stress-inducible nuclear translocation of NEMO and IKK/NF-κB activation in stably reconstituted NEMO-deficient cells. RNAi screening of both importin α and β family members, as well as co-immunoprecipitation analyses, revealed that a nonclassical importin β family member, IPO3, was the only importin that was able to associate with NEMO and whose reduced expression prevented genotoxic stress-induced NEMO nuclear translocation, IKK/NF-κB activation, and inflammatory cytokine transcription. Recombinant IPO3 interacted with recombinant NEMO but not NLS-mutant version and induced nuclear import of NEMO in digitonin-permeabilized cells. We also provide evidence that NEMO is disengaged from IKK complex following genotoxic stress induction. Thus, the IPO3 nuclear import pathway is an early and crucial determinant of the IKK/NF-κB signaling arm of the mammalian DNA damage response. Copyright © 2015, The American Society for Biochemistry and Molecular Biology.
    Journal of Biological Chemistry 06/2015; 290(29). DOI:10.1074/jbc.M115.645960 · 4.57 Impact Factor
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    ABSTRACT: Acute graft-versus-host-disease (GVHD) is characterized by selective damage to the liver, the skin, and the gastrointestinal tract. Following allogeneic hematopoietic stem cell transplantation, donor bone marrow (BM) cells repopulate the immune system of the recipient. We previously demonstrated that the acute intestinal GVHD (iGVHD) mortality rate was higher in MyD88-deficient BM recipients than that in the control BM recipients. In the present study, the role of MyD88 (expressed by donor BM) in the pathophysiology of hepatic GVHD (hGVHD) was examined. Unlike iGVHD, transplantation with MyD88-deficient T-cell depleted (TCD) BM attenuated hGVHD severity and was associated with low infiltration of T cells into the liver of the recipients. Moreover, GVHD hosts, transplanted with MyD88-deficient TCD BM, exhibited markedly reduced expansion of CD11b(+)Gr-1(+) myeloid-derived suppressor cells (MDSC) in the liver. Adoptive injection of the MDSC from wild type mice, but not MyD88-deficient mice, enhanced hepatic T cell infiltration in the MyD88-deficient TCD BM recipients. Pre-treatment of BM donors with LPS increased MDSC levels in the liver of allogeneic wild type BM recipients. In conclusion, hGVHD and iGVHD may occur through various mechanisms based on the presence of MyD88 in the non-T cell compartment of the allograft.
    Immune Network 06/2015; 15(3):125-34. DOI:10.4110/in.2015.15.3.125
  • Jinkyeong Park · Eun Young Choi
    Journal of Parenteral and Enteral Nutrition 05/2015; 39(4):383-4. DOI:10.1177/0148607114556842 · 3.15 Impact Factor
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    ABSTRACT: Desmopressin is used for treating nocturnal polyuria, but hyponatremia is an associated concern in the elderly due to impaired urinary dilution. This study was undertaken to characterize hyponatremia occurring in adults using desmopressin for nocturnal polyuria. Data from 172 patients who were prescribed desmopressin for nocturnal polyuria at a urology clinic from September 2010 through February 2013 were retrospectively analyzed. Demographic and laboratory parameters were investigated to examine the risk factors for desmopressin-associated hyponatremia. The average follow-up serum sodium measured 21 ± 22 days after using desmopressin was 138 ± 5 mmol/l. Hyponatremia (<135 mmol/l) was found in 24 patients (14%), and it was severe in 7 (<126 mmol/l). In the hyponatremic patients, serum sodium decreased by 11 ± 6 mmol/l. Patients with hyponatremia were older than those with normonatremia (78 ± 7 vs. 68 ± 9 years, p < 0.0001). The presence of either hyponatremia-predisposing comorbidities or concurrent medications was associated with hyponatremia. Patients with hyponatremia had lower basal hemoglobin (11 ± 2 vs. 13 ± 2 g/dl, p < 0.001) and serum sodium (139 ± 2 vs. 140 ± 2 mmol/l, p < 0.05) than those with normonatremia. Multivariate logistic regression after adjustment for basal serum sodium showed that advanced age (OR 1.15; 95% CI 1.03-1.27) and lower hemoglobin level (OR 0.64; 95% CI 0.43-0.94) were independently associated with hyponatremia. Hyponatremia is not infrequently associated with desmopressin use. Those with advanced age (≥65 years) and lower hemoglobin are at risk of desmopressin-associated hyponatremia and need to be carefully monitored. © 2015 S. Karger AG, Basel.
    American Journal of Nephrology 04/2015; 41(3):183-190. DOI:10.1159/000381562 · 2.67 Impact Factor
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    ABSTRACT: Objectives The aim of this study was to evaluate HA coated with different ratios of TCP as a carrier for hABMSCs obtained during implant osteotomy in comparison to slowly-resorbing biomaterial, Bio-Oss, as a negative control, using in vitro and in vivo experiments.Materials and Methods Human ABMSCs (hABMSCs) harvested during implant osteotomy were transplanted using HA/TCP or Bio-Oss as carriers in a murine ectopic transplantation model (n = 12). Pore size and cell affinity were evaluated in vitro. The area of newly formed bone was analyzed histometrically, the number of osteocytes was counted, and immunohistochemical staining was conducted against several markers of osteogenesis, including alkaline phosphatase (ALP), runt-related transcription factor 2 (RUNX-2), osteocalcin (OCN), and osteopontin (OPN). Osteoclast formation was evaluated by tartrate-resistant acid phosphatase staining.ResultsThe carrier materials had comparable pore sizes. The cell affinity assay resulted in a high proportion of cell adhesion (>90%) in all experimental groups. Substantial new bone and osteocyte formation was observed on both HA/TCP carriers, whereas it was minimal with Bio-Oss. Positive immunostaining for ALP, RUNX-2, OCN, and OPN was observed with HA/TCP, but only limited expression of osteogenic markers with Bio-Oss. Conversely, there was a minimal osteoclast presence with Bio-Oss, but a significant presence of osteoclasts with both HA/TCP carriers.Conclusions Both types of scaffolds, BCP and Bio-Oss, showed high stem cell-carrying potential, but the in vivo healing patterns of their complexes with hABMSC could be affected by the microenvironment on the surfaces of the scaffolds. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2015.
    Journal of Biomedical Materials Research Part B Applied Biomaterials 04/2015; DOI:10.1002/jbm.b.33416 · 2.76 Impact Factor
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    ABSTRACT: NF-κB essential modulator, NEMO, plays a key role in canonical NF-κB signaling induced by a variety of stimuli, including cytokines and genotoxic agents. To dissect the different biochemical and functional roles of NEMO in NF-κB signaling, various mutant forms of NEMO have been previously analyzed. However, transient or stable overexpression of wild-type NEMO can significantly inhibit NF-κB activation, thereby confounding the analysis of NEMO mutant phenotypes. What levels of NEMO overexpression lead to such an artifact and what levels are tolerated with no significant impact on NEMO function in NF-κB activation are currently unknown. Here we purified full-length recombinant human NEMO protein and used it as a standard to quantify the average number of NEMO molecules per cell in a 1.3E2 NEMO-deficient murine pre-B cell clone stably reconstituted with full-length human NEMO (C5). We determined that the C5 cell clone has an average of 4 x 105 molecules of NEMO per cell. Stable reconstitution of 1.3E2 cells with different numbers of NEMO molecules per cell has demonstrated that a 10-fold range of NEMO expression (0.6-6x105 molecules per cell) yields statistically equivalent NF-κB activation in response to the DNA damaging agent etoposide. Using the C5 cell line, we also quantified the number of NEMO molecules per cell in several commonly employed human cell lines. These results establish baseline numbers of endogenous NEMO per cell and highlight surprisingly normal functionality of NEMO in the DNA damage pathway over a wide range of expression levels that can provide a guideline for future NEMO reconstitution studies.
    PLoS ONE 03/2015; 10(3):e0116374. DOI:10.1371/journal.pone.0116374 · 3.23 Impact Factor
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    Il Kang · Yoo · Ji Yeong Jeon · Su Jeong Ryu · Giri Nam · Hyewon Youn · Eun Young Choi
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    ABSTRACT: In allogeneic transplantation, including the B6 anti-BALB.B settings, H60 and H4 are two representative dominant minor histocompatibility antigens that induce strong CD8 T-cell responses. With different distribution patterns, H60 expression is restricted to hematopoietic cells, whereas H4 is ubiquitously expressed. H60-specific CD8 T-cell response has been known to be dominant in most cases of B6 anti-BALB.B allo-responses, except in the case of skin transplantation. To understand the mechanism underlying the subdominance of H60 during allogeneic skin transplantation, we investigated the dynamics of the H60-specific CD8 T cells in B6 mice transplanted with allogeneic BALB.B tail skin. Unexpectedly, longitudinal bioluminescence imaging and flow cytometric analyses revealed that H60-specific CD8 T cells were not always subdominant to H4-specific cells but instead showed a brief dominance before the H4 response became predominant. H60-specific CD8 T cells could expand in the draining lymph node and migrate to the BALB.B allografts, indicating their active participation in the anti-BALB.B allo-response. Enhancing the frequencies of H60-reactive CD8 T cells prior to skin transplantation reversed the immune hierarchy between H60 and H4. Additionally, H60 became predominant when antigen presentation was limited to the direct pathway. However, when antigen presentation was restricted to the indirect pathway, the expansion of H60-specific CD8 T cells was limited, whereas H4-specific CD8 T cells expanded significantly, suggesting that the temporary immunodominance and eventual subdominance of H60 could be due to their reliance on the direct antigen presentation pathway. These results enhance our understanding of the immunodominance phenomenon following allogeneic tissue transplantation.
    Experimental and Molecular Medicine 02/2015; 47(2). DOI:10.1038/emm.2014.107 · 3.45 Impact Factor
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    ABSTRACT: To investigate the relationship between changes of corneal epithelium and subbasal nerves in non-Sjögren dry eye using in vivo confocal microscope (IVCM) and self-reported clinical symptoms.
    Journal of the Korean Ophthalmological Society 01/2015; 56(5):680. DOI:10.3341/jkos.2015.56.5.680
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    ABSTRACT: Background Individuals with panic disorder (PD) exhibit a hypersensitivity to inhaled carbon dioxide (CO2), possibly reflecting a lowered threshold for sensing signals of suffocation. Animal studies have shown that CO2-mediated fear behavior depends on chemosensing of acidosis in the amygdala via the acid sensing ion channel ASIC1a. We examined whether the human ortholog of the ASIC1a gene, ACCN2, is associated with the presence of PD and with amygdala structure and function. Methods We conducted a case-control analysis (N=414 PD cases, 846 healthy controls) of ACCN2single nucleotide polymorphisms (SNPs) and PD. We then tested whether variants showing significant association with PD are also associated with amygdala volume (n=1,048) and/or task-evoked reactivity to emotional stimuli (n=103) in healthy individuals. Results Two SNPs at the ACCN2 locus showed evidence of association with PD: rs685012 (OR=1.32, gene-wise corrected p=0.011) and rs10875995 (OR=1.26, gene-wise corrected p=0.046). The association appeared to be stronger when early-onset (age ≤ 20) PD cases and when cases with prominent respiratory symptoms were compared to controls. The PD risk allele at rs10875995 was associated with increased amygdala volume (p=0.035), as well as task-evoked amygdala reactivity to fearful and angry faces (p=0.0048). Conclusions Genetic variation at ACCN2 appears to be associated with PD and with amygdala phenotypes that have been linked to anxiety proneness. These results support the possibility that modulation of acid-sensing ion channels may have therapeutic potential for PD.
    Biological psychiatry 12/2014; 76(11). DOI:10.1016/j.biopsych.2013.12.018 · 10.26 Impact Factor
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    ABSTRACT: Indoleamine 2,3-dioxygenases (IDOs) are tryptophan-catabolizing enzymes with immunomodulatory functions. However, the biological role of IDO2 and its relationship with IDO1 are unknown. To assess the relationship between IDO2 and IDO1, we investigated the effects of co-expression of human (h) IDO2 on hIDO1 activity. Cells co-expressing hIDO1 and hIDO2 showed reduced tryptophan metabolic activity compared with those expressing hIDO1 only. In a proteomic analysis, hIDO1-expressing cells exhibited enhanced expression of proteins related to the cell cycle and amino acid metabolism, and decreased expression of proteins related to cell survival. However, cells co-expressing hIDO1 and hIDO2 showed enhanced expression of negative regulators of cell apoptosis compared with those expressing hIDO1 only. Co-expression of hIDO1 and hIDO2 rescued the cell death induced by tryptophan-depletion through hIDO1 activity. Cells expressing only hIDO2 exhibited no marked differences in proteome profiles or cell growth compared with mock-transfectants. Cellular tryptophan metabolic activity and cell death were restored by co-expressing the hIDO2 mutant substituting the histidine 360 residue for alanine. These results demonstrate that hIDO2 plays a novel role as a negative regulator of hIDO1 by competing for heme-binding with hIDO1, and provide information useful for development of therapeutic strategies to control cancer and immunological disorders that target IDO molecules.
    Experimental and Molecular Medicine 11/2014; 46(11):e121. DOI:10.1038/emm.2014.69 · 3.45 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):2084-2084. DOI:10.1158/1538-7445.AM2014-2084 · 9.33 Impact Factor
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    Young Joo Cho · Eun Young Choi · Hyoung Jun Koh · Sung Chul Lee · Min Kim
    Korean Journal of Ophthalmology 10/2014; 28(5):424-426. DOI:10.3341/kjo.2014.28.5.424
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    ABSTRACT: Indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme in tryptophan catabolism that plays an important role in the induction of immune tolerance. Its role in graft-versus-tumor effect (GVT) after allogeneic stem cell transplantation (allo-SCT) remains unclear. Using a murine GVT model of reduced-intensity allo-HSCT followed by donor leukocyte infusion (DLI), we examined the role of IDO inhibition. Two stereoisomers of 1-methyl tryptophan (1-MT), a small-molecule inhibitor of IDO, reduced the growth of inoculated tumor in the mice that received DLI and had higher expression of IDO1 and IFNγ. However, L-1MT, but not D-1MT, mitigated tumor growth in mice that did not receive DLI and did not express IDO1 and IFNγ. Accordingly, both stereoisomers reduced plasma kynurenine concentrations early after DLI and enhanced in vitro cytotoxic lymphocyte function after allogeneic mixed lymphocyte reaction. Furthermore, L-1MT was more efficient in causing direct cytotoxic effects than D-1MT. Our results suggest that IDO inhibition can benefit in the setting of reduced-intensity allo-SCT using DLI.
    Experimental Hematology 10/2014; 42(10). DOI:10.1016/j.exphem.2014.06.006 · 2.48 Impact Factor

Publication Stats

3k Citations
694.16 Total Impact Points


  • 2015
    • University of Wisconsin–Madison
      Madison, Wisconsin, United States
    • Chosun College Of Science and Technology
      Gwangju, Gwangju, South Korea
  • 2013–2015
    • Hanyang University Medical Center
      Sŏul, Seoul, South Korea
    • Ewha Womans University
      • Department of Physics
      Sŏul, Seoul, South Korea
    • Asan Medical Center
      Sŏul, Seoul, South Korea
  • 2011–2015
    • Ajou University
      Sŏul, Seoul, South Korea
    • Yonsei University
      • College of Dentistry
      Sŏul, Seoul, South Korea
    • National Cancer Center Korea
      • Specific Organs Cancer Branch
      QYK, Gyeonggi-do, South Korea
    • Kwandong University
      Gangneung, Gangwon, South Korea
    • Gangneung-Wonju National University
      • Department of Nursing
      Gangneung, Gangwon-do, South Korea
    • Korea Institute of Science and Technology
      Sŏul, Seoul, South Korea
  • 2003–2015
    • Yonsei University Hospital
      • Department of Internal Medicine
      Sŏul, Seoul, South Korea
    • Wonkwang University School of Medicine and Hospital
      Riri, North Jeolla, South Korea
    • The Jackson Laboratory
      Bar Harbor, Maine, United States
    • Blood Systems Research Institute
      San Francisco, California, United States
  • 2014
    • Kyung Hee University
      Sŏul, Seoul, South Korea
  • 2013–2014
    • Seoul National University Bundang Hospital
      • Department of Pediatrics
      Sŏul, Seoul, South Korea
  • 2012–2014
    • Harvard University
      • Department of Psychology
      Cambridge, Massachusetts, United States
    • Korea Internet & Security Agency
      Sŏul, Seoul, South Korea
    • Dankook University
      Eidō, North Chungcheong, South Korea
  • 2009–2014
    • Kyungpook National University
      • • College of Ecology and Environmental Science
      • • Applied Biology
      • • School of Life Science
      Daikyū, Daegu, South Korea
    • National Institutes of Health
      • Branch of Experimental Immunology
      Maryland, United States
    • National Health Insurance Corporation Ilsan Hospital
      Sŏul, Seoul, South Korea
    • Northern Inyo Hospital
      BIH, California, United States
  • 2004–2014
    • Yeungnam University
      • • Division of Internal Medicine
      • • College of Medicine
      Gyeongsan, Gyeongsangbuk-do, South Korea
  • 1997–2014
    • Seoul National University Hospital
      • • Department of Internal Medicine
      • • Department of Thoracic and Cardiovascular Surgery
      • • Department of Nuclear Medicine
      • • Department of Pathology
      Sŏul, Seoul, South Korea
  • 1996–2014
    • Seoul National University
      • • Department of Biomedical Sciences
      • • Department of Pediatrics
      • • College of Medicine
      • • Department of Pathology
      • • College of Pharmacy
      Sŏul, Seoul, South Korea
    • Chungbuk National University
      Chinsen, Chungcheongbuk-do, South Korea
  • 2012–2013
    • Ulsan University Hospital
      Urusan, Ulsan, South Korea
  • 2010–2013
    • Sejong General Hospital
      Bucheon, Gyeonggi-do, South Korea
  • 2011–2012
    • University of Ulsan
      • Graduate School
      Ulsan, Ulsan, South Korea
  • 2010–2012
    • Hongik University
      • Department of Chemical Engineering
      Sŏul, Seoul, South Korea
  • 2010–2011
    • Seegene Institute of Life Sciences
      Sŏul, Seoul, South Korea
  • 2008–2011
    • National Cancer Institute (USA)
      • Experimental Immunology Branch
      Maryland, United States
  • 2000–2011
    • Pusan National University
      • • Division of Materials Science and Engineering
      • • Department of Chemistry
      Busan, Busan, South Korea
  • 2007–2009
    • NCI-Frederick
      Фредерик, Maryland, United States
  • 2006–2007
    • Korea University
      • Department of Life Sciences
      Sŏul, Seoul, South Korea
    • Dankook University Hospital
      Anjŏ, Gyeonggi Province, South Korea
  • 2005–2006
    • Inha University
      • College of Medicine
      Sŏul, Seoul, South Korea
  • 2004–2005
    • Sungkyunkwan University
      • • Department of Chemistry
      • • Institute of Basic Science
      Sŏul, Seoul, South Korea
  • 1999
    • Inje University Paik Hospital
      Sŏul, Seoul, South Korea