Choon-Sik Park

Soonchunhyang University, Onyang, South Chungcheong, South Korea

Are you Choon-Sik Park?

Claim your profile

Publications (199)689.61 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Previously, we used a proteomic approach to demonstrate that the protein level of fatty acid-binding protein 1 (FABP1) is increased in nasal polyps in patients with aspirin-exacerbated respiratory disease (AERD). To reveal the genetic effect of FABP1 variants, we evaluated the association of FABP1 polymorphisms with the risk of AERD in 207 asthmatics with AERD and 1019 aspirin-tolerant asthmatics (ATA). Seven polymorphisms of FABP1 were selected from the National Center for Biotechnology Information (build 36) using minor allele frequency and linkage disequilibrium criteria. The genotype and haplotype distributions were not significantly different between the AERD and ATA groups in all of the genetic models. The percent decline of forced expiratory volume in 1 second (FEV1) after the oral aspirin challenge (OAC) test did not differ according to single-nucleotide polymorphism (SNP) genotypes. In haplotype analysis, asthmatic patients who were BL2ht2 homozygotes showed a greater decline in FEV1 after the OAC test than subjects who possessed 1 or no copy of BL2ht2 (P = 0.035). However, these observations were not significant after correction for multiple comparisons (corrected P value = 1.00). Neither genotype nor haplotype was associated with the presence of nasal polyposis in the study subjects. Although we did not find a significant association between the FABP1 polymorphisms and AERD, our data suggest that the 7 SNPs are not associated with the increased expression of FABP1 in asthmatic patients with AERD. Further studies of epigenetic factors that may contribute to the increased expression of FABP1 in AERD should be performed.
    Experimental Lung Research 10/2014; · 1.47 Impact Factor
  • Tae-Hyeong Lee, Hyun Ji Song, Choon-Sik Park
    [Show abstract] [Hide abstract]
    ABSTRACT: Human airways contact with pathogen-associated molecular patterns and danger-associated molecular patterns present in many environments. Asthmatic's airways may be more susceptible to these patterns and lead to inflammasome activation; however, the participation of inflammasome in the development and exacerbation of asthma is not fully understood and remains controversial. Asthma is a heterogeneous group composed of different airway inflammation patterns with different underlying immune mechanisms. One mechanism is neutrophilic airway inflammation based on the axis of inflammasome activation, interleukin (IL) 1β/IL-18 production, T helper 17 activation, IL-8/IL-6 overproduction, and neutrophilic inflammation. The role of inflammasome activation has been highlighted in experimental asthma models and some evidence of inflammasome activation has been recently demonstrated in human neutrophilic asthmatic airways. In addition to caspase-1 activation, proteinase 3 and other protease from activated neutrophils directly cleave pro-IL-1β and pro-IL-18 to IL-1β and IL-18, which contribute to the phenotype of subsequent adaptive immune responses without inflammasome activation. Data suggests that neutrophilics in asthmatic airways may have an additional effect in initiating inflammasome activation and amplifying immune responses. Among the mediators from neutrophils, S100A9 seems to be one candidate mediator to explain the action of neutrophils in amplifying the airway inflammation in concert with inflammasome.
    Asia Pacific allergy. 10/2014; 4(4):187-96.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Angiopoietin-1 (Ang-1) is an essential mediator of angiogenesis that establishes vascular integrity, and angiopoietin-2 (Ang-2) acts as its natural inhibitor. We considered that angiopoietin might be important in bronchial asthma.
    BMC Pulmonary Medicine 09/2014; 14(1):143. · 2.76 Impact Factor
  • The Journal of allergy and clinical immunology. 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: To better understand the respiratory lipid phenotypes of asthma, a novel method for lipid profiling of bronchoalveolar lavage fluid (BALF) was developed using HPLC-QTOF-MS with an internal spectral library and high-throughput lipid identifying software. The method was applied to BALF from 38 asthmatic patients (18 patients with non-steroid treated bronchial asthma [NSBA] and 20 patients with steroid treated bronchial asthma [SBA]) and 13 healthy subjects (NC). We identified 69 lipids, which were categorized into one of six lipid classes: lysophosphatidylcholine (LPC), phosphatidylcholine (PC), phosphatidylglycerol (PG), phosphatidylserine (PS), sphingomyelin (SM) and triglyceride (TG). Compared to the NC group, the individual quantity levels of the six classes of lipids were significantly higher in the NSBA subjects; in the SBA subjects, the PC, PG, PS, SM and TG levels were similar with the levels observed in the NC group. Using differentially expressed lipid species (p-value < 0.05, FDR < 0.1 and VIP score of PLS-DA > 1), 34 lipid biomarker candidates with high prediction performance between asthmatics and controls were identified (AUROC > 0.9). These novel findings revealed specific characteristics of lipid phenotypes in asthmatic patients and suggested the importance of future research on the relationship between lipid levels and asthma.
    Journal of Proteome Research 07/2014; · 5.06 Impact Factor
  • Source
    June-Hyuk Lee, Choon-Sik Park
    [Show abstract] [Hide abstract]
    ABSTRACT: Monocyte chemoattractant proteins (MCPs) are important cytokines that involved in cellular activation and releasing of inflammatoy mediators by basophils and eosinophils in allergic disease. Some MCP gene variants implicate in asthma and monoclonal antibody for MCP-3 blocks allergic inflammations in the patients with asthma. Detection of interactions between gene and environment or between genes for complex disease such as asthma is important. We searched for an evidence of genetic effect of single nucleotide polymorphisms (SNPs) of MCP genes as well as gene - gene interactions involved in asthma.
    Allergy, asthma & immunology research 07/2014; 6(4):333-40. · 2.65 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The tyrosine-protein kinase Tec (TEC) is a member of non-receptor tyrosine kinases and has critical roles in cell signaling transmission, calcium mobilization, gene expression, and transformation. TEC is also involved in various immune responses, such as mast cell activation. Therefore, we hypothesized that TEC polymorphisms might be involved in aspirin-exacerbated respiratory disease (AERD) pathogenesis. We genotyped 38 TEC single nucleotide polymorphisms in a total of 592 subjects, which comprised 163 AERD cases and 429 aspirin-tolerant asthma controls. Logistic regression analysis was performed to examine the associations between TEC polymorphisms and the risk of AERD in a Korean population. The results revealed that TEC polymorphisms and major haplotypes were not associated with the risk of AERD. In another regression analysis for the fall rate of forced expiratory volume in 1 second (FEV1) by aspirin provocation, two variations (rs7664091 and rs12500534) and one haplotype (TEC_BL2_ht4) showed nominal associations with FEV1 decline (p = 0.03-0.04). However, the association signals were not retained after performing corrections for multiple testing. Despite TEC playing an important role in immune responses, the results from the present study suggest that TEC polymorphisms do not affect AERD susceptibility. Findings from the present study might contribute to the genetic etiology of AERD pathogenesis.
    Genomics & informatics. 06/2014; 12(2):58-63.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Asthma can be suppressed by inhaled corticosteroids (ICS). However, response to ICS shows marked inter-individual variability. This study is aimed to identify the genetic variants associated with the change in the percentage of forced expiratory volume in 1 second (%ΔFEV1) following ICS treatment. A genome-wide association study was performed in a Korean asthmatic cohort. To further investigate these genetic associations, 11 additional single nucleotide polymorphisms (SNPs) on the allantoicase (ALLC) gene were selected from the HapMap database and genotyped in the same asthmatic patients in the follow-up study. In a genome-wide study, we identified the lowest P-value in ALLC, but none of the SNPs met the genome-wide association criteria (P <1.0 × 10-8). However, among 25 SNPs on ALLC in the follow-up study, six variants showed significant associations with the mean %ΔFEV1 in the study subjects (P < 3.73 × 10-6). Although the associated signals could not overcome the genome-wide multiple correction due to small sample size (n = 189), our results suggest that associated SNPs of ALLC might be genetic predictors of response to ICS, at least with respect to ΔFEV1 in Korean asthmatics.
    Clinica chimica acta; international journal of clinical chemistry 04/2014; · 2.54 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is characterized by progressive dyspnea and worsening lung function due to remodeling of the lung, including epithelial mesenchymal transition. ADAM33 is a disintegrin and metalloprotease domain-containing protein, which may be related to lung fibrosis by exerting angiogenesis and remodeling of the lung. Thus, we evaluated the association of single-nucleotide polymorphisms (SNPs) of ADAM33 with the risk of IPF. A total of 237 patients with IPF and 183 healthy subjects participated in the present study. Nine polymorphisms were selected. Genotyping was performed by single-base extension. Polymorphisms and haplotypes were analyzed for associations with the risk of IPF using multiple logistic regression models controlling for age, gender, and smoking status as covariates. All SNPs were in Hardy-Weinberg equilibrium. The minor allele frequency (MAF) of rs628977G>A in intron 21 was significantly lower in subjects with surgical IPF than in normal controls in the recessive model [33.2 vs. 38.0 %, p = 0.02, OR = 0.40 (0.19-0.84)]. When the subjects with clinical IPF were included, the difference in MAF persisted with a p value of 0.03 [OR = 0.50 (0.27-0.94)]. ADAM33 rs628977G>A was marginally associated with a decreased risk of IPF in a recessive model.
    Beiträge zur Klinik der Tuberkulose 04/2014; · 2.06 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The well-known genetic polymorphisms in ADH1B(His47Arg) and ALDH2(Glu487Lys) have dramatic effects on the rate of metabolizing alcohol and acetaldehyde. We investigated possible involvement of these functional polymorphisms in other common complex-trait diseases. The genetic effects of these two polymorphisms on hepatitis, asthma, type-2 diabetes mellitus (T2DM), and tuberculosis (TB) were examined in a Korean population. We demonstrated that the well-known functional polymorphism of a primary alcohol-metabolizing enzyme (ALDH2 Glu487Lys) has a strong genetic association with the risk of TB. The frequency of the minor allele (ALDH2*487Lys) was found to be much lower in TB patients (freq. = 0.099/n = 477) than among controls (freq. = 0.162/n = 796) (P = 0.00001, OR (95% confidential interval) = 0.57 (0.45-0.74)). Our data may indicate that TB was once an endemic disease, which exerted selection pressure for higher frequencies of ALDH2*487Lys in Asian populations. In addition, the calculated attributable fraction (AF) indicates that 39.5% of TB patients can attribute their disease to the detrimental effects of ALDH2Glu487Glu. Our results suggest that this polymorphism is one of the genetic components of TB, at least in the Korean population.
    BMC Medical Genetics 04/2014; 15(1):40. · 2.54 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Endoplasmic reticulum (ER) stress has recently been observed to activate NF-kappaB and induce inflammatory responses such as asthma. Activating transcription factor 6β (ATF6B) is known to regulate ATFα-mediated ER stress response. The aim of this study is to investigate the associations of ATF6B genetic variants with aspirin-exacerbated respiratory disease (AERD) and its major phenotype, % decline of FEV1 by aspirin provocation. Four common single nucleotide polymorphisms (SNPs) of ATF6B were genotyped and statistically analyzed in 93 AERD patients and 96 aspirin-tolerant asthma (ATA) as controls. Logistic analysis revealed that 2 SNPs (rs2228628 and rs8111, P=0.008; corrected P=0.03) and 1 haplotype (ATF6B-ht4, P=0.005; corrected P=0.02) were significantly associated with % decline of FEV1 by aspirin provocation, whereas ATF6B polymorphisms and haplotypes were not associated with the risk of AERD. Although further functional and replication studies are needed, our preliminary findings suggest that ATF6B may be related to obstructive phenotypes in response to aspirin exposure in adult asthmatics.
    Allergy, asthma & immunology research 03/2014; 6(2):142-8. · 2.65 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Member RAS oncogene family (RAB1A), a member of the RAS oncogene family, cycles between inactive GDP-bound and active GTP-bound forms regulating vesicle transport in exocytosis. Thus, functional alterations of the RAB1A gene may contribute to aspirin intolerance in asthmatic sufferers. To investigate the relationship between single-nucleotide polymorphisms (SNPs) in the RAB1A gene and aspirin-exacerbated respiratory disease (AERD), asthmatics (n=1197) were categorized into AERD and aspirin-tolerant asthma (ATA). All subjects were diagnosed as asthma on the basis of the Global Initiative for Asthma (GINA) guidelines. AERD was defined as asthmatics showing 15% or greater decreases in forced expiratory volume in one second (FEV1) or naso-ocular reactions by the oral acetyl salicylic acid (ASA) challenge (OAC) test. In total, eight SNPs were genotyped. Logistic regression analysis identified that the minor allele frequency of +14444 T>G and +41170 C>G was significantly higher in the AERD group (n=181) than in the ATA group (n=1016) (p=0.0003-0.03). Linear regression analysis revealed a strong association between the SNPs and the aspirin-induced decrease in FEV1 (p=0.0004-0.004). The RAB1A gene may play a role in the development of AERD in asthmatics and the genetic polymorphisms of the gene have the potential to be used as an indicator of this disease.
    DNA and cell biology 02/2014; · 2.28 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The Publisher regrets that this article is an accidental duplication of an article that has already been published in J Allergy Clin Immunol, 133 (2014) AB67, http://dx.doi.org/10.1111/j.1365-2222.2011.03801.x. The duplicate article has therefore been withdrawn.
    The Journal of allergy and clinical immunology 02/2014; 133(2 Suppl):AB67. · 12.05 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To evaluate airway changes in ovalbumin-induced asthmatic mice in terms of postmortem micro-CT images and pathological findings. Asthma was induced in mice by intraperitoneal injection and nasal instillation of ovalbumin aluminium hydroxide into mice (experimental group, n=6), and another group of mice received intraperitoneal injection and nasal instillation of distilled phosphate-buffered saline (control group, n=6). Bronchial lumen area was measured in the main bronchial lumen of the distal third bronchial branch level (6 parts per each mouse) on axial scans of Micro-CT, using a Lucion's smart pen (semi-automated) and a curve pen (manual). Bronchial wall thickness was obtained in 4 sections (2 levels on either side) after the third bronchial branch by measuring the diameter which was perpendicular to the longitudinal axis of the main bronchus on curved Multi-planar reconstruction (MPR) images. Histologic slides were obtained from the lesion that was matched with its CT images, and bronchial wall thicknesses were determined. The mean bronchial lumen area was 0.196±0.072 mm(2) in the experimental group and 0.243±0.116 mm(2) in the control group; the difference was significant. Bronchial wall thickness on micro-CT images (mean, 0.119±0.01 vs. 0.108±0.013 mm) and in pathological specimens (mean, 0.066±0.011 vs. 0.041±0.009 mm) were thicker in the experimental group than in the control group; bronchial wall thickness on micro-CT images correlated well with pathological thickness (for the experimental group, r=0.712; for the control group, r=0.46). The thick bronchial wall in the experimental group demonstrated submucosal hypertrophy along with goblet cell hyperplasia and smooth muscle hyperplasia. The results of this study suggest that asthma may induce thickening of bronchial wall and narrowing of the lumen area on micro-CT images and that these results may significantly correlate with pathological findings.
    Allergy, asthma & immunology research 01/2014; 6(1):75-82. · 2.65 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objectives Asthma can be suppressed by inhaled corticosteroids (ICS). However, response to ICS shows marked inter-individual variability. This study is aimed to identify the genetic variants associated with the change in the percentage of forced expiratory volume in 1 second (%ΔFEV1) following ICS treatment. Methods A genome-wide association study was performed in a Korean asthmatic cohort. To further investigate these genetic associations, 11 additional single-nucleotide polymorphisms (SNPs) on the allantoicase (ALLC) gene were selected from the HapMap database and genotyped in the same asthmatic patients in the follow-up study. Results In a genome-wide study, we identified the lowest P-value in ALLC, but none of the SNPs met the genome-wide association criteria (P < 1.0 × 10− 8). However, among 25 SNPs on ALLC in the follow-up study, 6 variants showed significant associations with the mean %ΔFEV1 in the study subjects (P < 3.73 × 10− 6). Conclusions Although the associated signals could not overcome the genome-wide multiple correction due to small sample size (n = 189), our results suggest that associated SNPs of ALLC might be genetic predictors of response to ICS, at least with respect to ΔFEV1 in Korean asthmatics.
    Clinica Chimica Acta. 01/2014; 436:20–26.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Eosinophils function as an effector cell in the development of asthma and allergic disease. Eotaxins are cytokines that promote pulmonary eosinophilia via the receptor CCR3. Single-nucleotide polymorphisms (SNPs) in CCR3 and eotaxin genes are associated with asthma. In this study, genetic interactions among SNPs of several eotaxin genes and CCR3 were assessed and their relationship with blood eosinophilia in asthma was examined. A total of 533 asthmatics were enrolled in this study. Asthmatics with eosinophilia (>0.5×10(9)/L) were compared with those without eosinophilia (≤0.5×10(9)/L). Chi-square tests were used to compare SNP frequencies. Two different models were used to evaluate gene-gene interactions: logistic regression and generalized multifactor dimensionality reduction (GMDR). EOT2+304C>A (29L>I) was significantly associated with 3 of the 4 CCR3 SNPs among asthmatics with eosinophilia (P=0.037-0.009). EOT2+304C>A (29L>I) and the CCR3 SNPs were also significantly associated with blood eosinophilia in an interaction model constructed by logistic regression (P=0.0087). GMDR analysis showed that the combination of EOT2+304C>A (29L>I) and CCR3-174C>T was the best model (accuracy=0.536, P=0.005, CVC 9/10). The epistatic influence of CCR3 on eotaxin gene variants indicates that these variants may be candidate markers for eosinophilia in asthma.
    Allergy, asthma & immunology research 01/2014; 6(1):55-60. · 2.65 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aspirin-exacerbated respiratory disease (AERD) is one phenotype of asthma, often occurring in the form of a severe and sudden attack. Due to the time-consuming nature and difficulty of oral aspirin challenge (OAC) for AERD diagnosis, non-invasive biomarkers have been sought. The aim of this study was to identify AERD-associated exonic SNPs and examine the diagnostic potential of a combination of these candidate SNPs to predict AERD. DNA from 165 AERD patients, 397 subjects with aspirin-tolerant asthma (ATA), and 398 normal controls were subjected to an Exome BeadChip assay containing 240K SNPs. 1,023 models (210-1) were generated from combinations of the top 10 SNPs, selected by the p-values in association with AERD. The area under the curve (AUC) of the receiver operating characteristic (ROC) curves was calculated for each model. SNP Function Portal and PolyPhen-2 were used to validate the functional significance of candidate SNPs. An exonic SNP, exm537513 in HLA-DPB1, showed the lowest p-value (p = 3.40×10-8) in its association with AERD risk. From the top 10 SNPs, a combination model of 7 SNPs (exm537513, exm83523, exm1884673, exm538564, exm2264237, exm396794, and exm791954) showed the best AUC of 0.75 (asymptotic p-value of 7.94×10-21), with 34% sensitivity and 93% specificity to discriminate AERD from ATA. Amino acid changes due to exm83523 in CHIA were predicted to be "probably damaging" to the structure and function of the protein, with a high score of '1'. A combination model of seven SNPs may provide a useful, non-invasive genetic marker combination for predicting AERD.
    PLoS ONE 01/2014; 9(11):e111887. · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Air pollutants and obesity are important factors that contribute to asthma. The aim of this study was to assess the airway responsiveness and inflammation in Otsuka-Long Evans Tokushima Fatty (OLETF) obese rats and Long Evans Tokushima-Otsuka (LETO) nonobese rats exposed to diesel exhaust particles (DEPs). Otsuka Long Evans Tokushima fatty rats and LETO rats were exposed intranasally to DEP and then challenged with aerosolized DEP on days 6 to 8. Body plethysmography, bronchoalveolar lavage (BAL), and histology were performed. Enhanced pause (Penh) was measured as an indicator of airway resistance on day 9 and samples were collected on day 10. After exposure to DEP, the OLETF group exhibited a greater increase in Penh compared to that in the LETO group. Moreover, the BAL fluid in mice showed an increase in the total and differential cell counts in the DEP-exposed OLETF group compared to that in the DEP-exposed LETO group. Histological assessment of lung tissue from each group revealed that the DEP-exposed OLETF group tended to have increased inflammatory cell infiltrations in the prebronchial area. Increased peroxisome proliferator-activated receptor γ, coactivator 1β messenger RNA was observed in the lungs of obese rats compared to that in nonobese rats following DEP exposure. These data indicate that the DEP-exposed OLETF group had increased airway responses and inflammation compared to the DEP-exposed LETO group, indicating that diesel particulates and obesity may be co-contributors to asthma.
    International Journal of Toxicology 01/2014; 33(1):21-8. · 1.35 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and objective Chronic obstructive pulmonary disease (COPD) is a complex disease in which multiple genes and their interaction with environmental factors contribute to disease development. Recent genome-wide association studies in COPD revealed the chromosome 4 region near hedgehog interacting protein (HHIP). However, these studies were mostly performed in Caucasians, and additional studies in multiple ethnic groups are needed. We investigated genetic associations of HHIP in Korean COPD and control subjects. Methods Two separate case–control studies were performed. Firstly, 139 subjects with COPD and 199 control subjects were selected from the Soonchunhyang University Bucheon Hospital Biobank. Secondly, 219 individuals with COPD were recruited from the Korean Obstructive Lung Disease (KOLD) cohort. The control subjects consisted of 305 smokers or ex-smokers with normal lung function who were registered in the Korean Genome Epidemiology Study. Associations between COPD susceptibility and single-nucleotide polymorphism (SNP) genotypes were tested by logistic regression. Associations between lung function and SNP genotypes were tested by linear regression. Results In the first study, the mean forced expiratory volume in 1 s (FEV1) of these COPD subjects was 1.32 L. None of 15 SNP was significantly associated with COPD susceptibility. However, four SNP associated significantly with FEV1 in subjects with COPD. In the KOLD cohort study, two SNPs (rs11938704 and rs10013495) near HHIP were significantly associated with FEV1 (P = 0.0001 and 0.001, respectively) in subjects with COPD. Conclusions Genetic variants in HHIP are associated with lung function in subjects with COPD.
    Respirology 11/2013; 18(8). · 2.78 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aspirin-exacerbated respiratory disease (AERD) has attracted a great deal of attention because of its association with increased asthma severity. To identify plasma biomarkers for the prediction of AERD, the six most abundant plasma proteins (albumin, IgG, antitrypsin, IgA, transferrin, and haptoglobin) in pooled plasma samples were removed using a multiple affinity removal system column. Two-dimensional gel electrophoresis (2DE) was used for differential display proteomic analysis of the pooled plasma. Proteins were identified by matrix assisted laser desorption ionization time-of-flight (MALDI-TOF)/TOF. Enzyme-linked immunosorbent assay (ELISA) was performed to identify and quantify apolipoprotein H (ApoH) in plasma from subjects with AERD and aspirin-tolerant asthma (ATA). Eight protein spots showed differences in relative intensity between pooled plasma from subjects with AERD (n = 8) and those with ATA (n = 8). MALDI-TOF/TOF analysis showed decreases in the levels of alpha-fibrinogen precursor, Apo H, fibrin beta, and proapolipoprotein in AERD as compared with ATA, and increases in chain A human complement component C3, 90-kDa heat shock protein, complement component C4a, and kininogen-1 isoform 2. ApoH concentrations were significantly increased in plasma from subjects with ATA than those with AERD and normal controls, as measured by ELISA (P < 0.01). AERD is characterized by changes in the levels of proteins involved in the coagulation and complement pathways. In addition, Apo H is up-regulated in ATA compared to AERD and normal controls, suggesting that Apo H may be involved in different pathogenesis of ATA from AERD.
    Pulmonary Pharmacology &amp Therapeutics 10/2013; · 2.54 Impact Factor

Publication Stats

2k Citations
689.61 Total Impact Points

Institutions

  • 2003–2014
    • Soonchunhyang University
      • College of Medicine
      Onyang, South Chungcheong, South Korea
  • 2010–2013
    • Sogang University
      • Department of Life Science
      Seoul, Seoul, South Korea
  • 2003–2013
    • Hanyang University
      • • Department of Molecular and Life Science
      • • Major in Biochemistry & Molecular Biology
      Seoul, Seoul, South Korea
  • 2003–2012
    • Ulsan University Hospital
      Urusan, Ulsan, South Korea
  • 2011
    • Korea University
      Sŏul, Seoul, South Korea
    • Chonnam National University
      • Department of Allergy
      Gwangju, Gwangju, South Korea
  • 2004–2010
    • Ajou University
      • Department of Allergy and Rheumatology
      Sŏul, Seoul, South Korea
  • 2009
    • Yonsei University Hospital
      • Department of Internal Medicine
      Seoul, Seoul, South Korea
    • Hallym University
      Sŏul, Seoul, South Korea
  • 2003–2006
    • Wonkwang University School of Medicine and Hospital
      Riri, North Jeolla, South Korea