Byoung Whui Choi

Seoul National University, Seoul, Seoul, South Korea

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Publications (76)170.46 Total impact

  • [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
  • The International Journal of Tuberculosis and Lung Disease 02/2014; 18(2):251-2. · 2.76 Impact Factor
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    ABSTRACT: Though insurance claims data are useful for researching asthma, they have important limitations, such as a diagnostic inaccuracy and a lack of clinical information. To overcome these drawbacks, we used the novel method by merging the clinical data from our asthma cohort with the National Health Insurance (NHI) claims data.
    PLoS ONE 01/2014; 9(11):e112844. · 3.53 Impact Factor
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    ABSTRACT: The therapeutic potential of human multipotent mesenchymal stromal cells, especially human adipose tissue-derived stem cells (hASC), is promising. However, there are concerns about the safety of infusion of hASC in human. Recently, we have experienced pulmonary embolism and infarct among family members who have taken multiple infusions of intravenous autologous hASC therapy. A 41-year-old man presented with chest pain for one month. Chest CT showed multiple pulmonary artery embolism and infarct at right lung. Serum D-dimer was 0.8 μg/mL (normal; 0-0.5 μg/mL). He had received intravenous autologous adipose tissue-derived stem cell therapy for cervical herniated intervertebral disc three times (one, two, and three months prior to the visit). His parents also received the same therapy five times and their chest CT also showed multiple pulmonary embolism. These cases represent artificial pulmonary embolisms and infarct after IV injection of hASC. Follow-up chest CT showed spontaneous resolution of lesions in all three patients.
    Yonsei medical journal 09/2013; 54(5):1293-6. · 0.77 Impact Factor
  • Journal of the American Geriatrics Society 09/2013; 61(9):1631-2. · 4.22 Impact Factor
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    ABSTRACT: Benign schwannoma is the most common neurogenic tumor in the mediastinum. Mediastinal benign schwannomas are most often asymptomatic and rarely accompanied by bloody pleural effusion. In the clinical analysis of 7 cases of pulmonary schwannomas, pleural effusion, and blood invasion were evident in 3 patients with malignant schwannoma. Herein, we report a rare case of giant, benign schwannoma presented with total collapse of right lung by massive, bloody pleural effusion.
    Tuberculosis and Respiratory Diseases 08/2013; 75(2):71-4.
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    ABSTRACT: A 69-year-old female patient visited the emergency room with fever (38.3℃) and dyspnea. She had been taking prednisolone (5 mg once per day) and methotrexate (2.5 mg once per week) for rheumatoid arthritis for 2 years. Chest computed tomography (CT) showed bilateral, multifocal ground glass opacity with interlobular septal thickening. Peripheral blood leukocyte count was 6,520/mm(3) (neutrophils, 77.4%; eosinophils, 12.1%). During the night, mechanical ventilation was initiated due to the development of severe hypoxemia. Bronchoalveolar lavage fluid showed a high proportion of eosinophils (49%). Her symptoms improved dramatically after commencement of intravenous methylprednisolone therapy. This is the first report of idiopathic acute eosinophilic pneumonia developing in a current user of systemic corticosteroids.
    Allergy, asthma & immunology research 07/2013; 5(4):242-4. · 2.65 Impact Factor
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    ABSTRACT: BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is characterized by progressive dyspnea and worsening lung function. ACE is increased in the bronchoalveolar lavage fluid from patients with IPF, suggesting the role of ACE in the pathogenesis of IPF. We evaluated the role of single-nucleotide polymorphisms (SNPs) in the development risk of IPF. METHODS: Two-hundred twenty patients with IPF and 456 healthy subjects were included in this study. Eleven polymorphisms were selected among those reported previously. Genotype was performed by single base extension. RESULTS: Although absolute LD (|D'| = 1 and r (2 )= 1) was not present, 11 SNPs showed tight LDs. The logistic analysis of the all of 11 SNPs on the ACE genes between patients with IPF and healthy subjects were found to be related with the risk of IPF in recessive type. However, in patients with IPF diagnosed by surgical lung biopsy, only two SNP of -5538T>C and +21288_insdel SNPs were related with the risk of IPF in co-dominant type, and there were no SNPs related with the risk of IPF in dominant type. In patients with IPF diagnosed by clinical criteria or surgical lung biopsy, four SNPs on promoter (-5538T>C, -5508A>C, -3927T>C, -115T>C), one on intron (+15276A>G), one on exon (+21181G>A), and one in three prime region (+21288_insdel) were related with the risk of IPF. CONCLUSIONS: This study showed a newly discovered SNP of ACE associated with the risk of development of IPF. ACE -5538T>C and -5508A>C significantly associated with risk of IPF in Korea.
    Beiträge zur Klinik der Tuberkulose 05/2013; · 2.06 Impact Factor
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    ABSTRACT: BACKGROUND: In this study, the association of asthma with CD53, a member of the tetraspanin family, was assessed for the first time in a mechanism-based study. METHODS: Genetic polymorphisms of CD53 were analyzed in 591 subjects and confirmed in a replication study of 1,001 subjects. CD53 mRNA and protein levels were measured in peripheral blood leukocytes, and the effects of the promoter polymorphisms on nuclear factor binding were examined by electrophoretic mobility shift assay. Cellular functional studies were conducted by siRNA transfections. RESULTS: Among tagging SNPs of CD53, the -1560 C>T in the promoter region was significantly associated with asthma risk. Compared with the CC genotype, the CT and TT genotypes were associated with a higher asthma risk, with odd ratios of 1.74 (P=0.009) and 2.03 (P=0.004), respectively. These findings were confirmed in the replication study with odd ratios of 1.355 (P=0.047) and 1.495 (P=0.039), respectively. The -1560C>T promoter SNP had functional effects on nuclear protein binding as well as mRNA and protein expression levels in peripheral blood leukocytes. When CD53 was knocked down by siRNA in THP-1 human monocytic cells stimulated with house dust mite, the production of inflammatory cytokines as well as NFκB activity was significantly over-activated, suggesting that CD53 suppresses over-activation of inflammatory responses. CONCLUSIONS: The -1560 C>T SNP is a functional promoter polymorphism that is significantly associated with population asthma risk, and is thought to act by directly modulating nuclear protein binding, thereby altering the expression of CD53, a suppressor of inflammatory cytokine production.
    Biochimica et Biophysica Acta 01/2013; · 4.66 Impact Factor
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    ABSTRACT: Immunoglobulin E (IgE) is one of the central players in asthma and allergic diseases. Although the serum IgE level, a useful endophenotype, is generally increased in patients with asthma, genetic factors influencing IgE regulation in asthma are still not fully understood. To identify the genetic variations associated with total serum and mite-specific IgEs in asthmatics, a genome-wide association study (GWAS) of 657,366 single nucleotide polymorphisms (SNPs) was performed in 877 Korean asthmatics. This study found that several new genes might be associated with total IgE in asthmatics, such as CRIM1 (rs848512, P = 1.18×10(-6); rs711254, P = 6.73×10(-6)), ZNF71 (rs10404342, P = 7.60×10(-6)), TLN1 (rs4879926, P = 7.74×10(-6)), and SYNPO2 (rs1472066, P = 8.36×10(-6); rs1038770, P = 8.66×10(-6)). Regarding the association of specific IgE to house dust mites, it was observed that intergenic SNPs nearby to OPRK1 and LOC730217 might be associated with Dermatophagoides pteronyssinus (D.p.) and Dermatophagoides farinae (D.f.) in asthmatics, respectively. In further pathway analysis, the phosphatidylinositol signaling system and adherens junction pathways were estimated to play a role in the regulation of total IgE levels in asthma. Although functional evaluations and replications of these results in other populations are needed, this GWAS of serum IgE in asthmatics could facilitate improved understanding of the role of the newly identified genetic variants in asthma and its related phenotypes.
    PLoS ONE 01/2013; 8(8):e71958. · 3.53 Impact Factor
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    ABSTRACT: Aspirin exacerbated respiratory disease (AERD) results in a severe asthma attack after aspirin ingestion in asthmatics. The filamin A interacting protein 1 (FILIP1) may play a crucial role in AERD pathogenesis by mediating T cell activation and membrane rearrangement. We investigated the association of FILIP1 variations with AERD and the fall rate of forced expiratory volume in one second (FEV1). A total of 34 common FILIP1 single nucleotide polymorphisms (SNPs) were genotyped in 592 Korean asthmatic subjects that included 163 AERD patients and 429 aspirin-tolerant asthma (ATA) controls. This study found that 5 SNPs (P=0.006-0.01) and 2 haplotypes (P=0.01-0.03) of FILIP1 showed nominal signals; however, corrections for the multiple testing revealed no significant associations with the development of AERD (P(corr)>0.05). In addition, association analysis of the genetic variants with the fall rate of FEV1, an important diagnostic marker of AERD, revealed no significant evidence (P(corr)>0.05). Although further replications and functional evaluations are needed, our preliminary findings suggest that genetic variants of FILIP1 might be not associated with the onset of AERD.
    Allergy, asthma & immunology research 01/2013; 5(1):34-41. · 2.65 Impact Factor
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    ABSTRACT: AIM: To investigate the association of single nucleotide polymorphisms (SNP) on IL17RA gene with Aspirin Exacerbated Respiratory Disease (AERD) and the functional effect of these variants on expression of IL17RA gene products. MATERIAL & METHODS: 15 SNPs of IL17RA gene were analyzed in 825 normal controls and 143 subjects with AERD and 411 with aspirin-tolerant asthma (ATA) and functionally characterized using measurement of protein and m-RNA expression. Result: Minor alleles frequencies of the three SNPs (-1075 A>G, -947 A>G, -50 C>T) and one haplotype (BL1_ht1) were significantly lower in AERD compared to those in ATA (p(corr) = 0.002-0.03). IL17RA protein expression and mRNA amount in CD14(+) peripheral blood monocytes and mononuclear cells were significantly increased in subjects carrying the common alleles homozygote compared with those carrying the minor alleles. CONCLUSIONS: The minor alleles of the three SNPs may decrease the risk of AERD via attenuation of IL17RA gene expression.
    Human immunology 12/2012; · 2.55 Impact Factor
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    ABSTRACT: Aspirin-exacerbated respiratory disease (AERD) is a nonallergic clinical syndrome characterized by a severe decline in forced expiratory volume in one second (FEV1) following the ingestion of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin. The effects of genetic variants have not fully explained all of the observed individual differences to an aspirin challenge despite previous attempts to identify AERD-related genes. In the present study, we performed genome-wide association study (GWAS) and targeted association study in Korean asthmatics to identify new genetic factors associated with AERD. A total of 685 asthmatic patients without AERD and 117 subjects with AERD were used for the GWAS of the first stage, and 996 asthmatics without AERD and 142 subjects with AERD were used for a follow-up study. A total of 702 SNPs were genotyped using the GoldenGate assay with the VeraCode microbead. GWAS revealed the top-ranked variants in 3' regions of the HLA-DPB1 gene. To investigate the detailed genetic effects of an associated region with the risk of AERD, a follow-up targeted association study with the 702 single nucleotide polymorphisms (SNPs) of 14 genes was performed on 802 Korean subjects. In a case-control analysis, HLA-DPB1 rs1042151 (Met105Val) shows the most significant association with the susceptibility of AERD (p = 5.11 × 10(-7); OR = 2.40). Moreover, rs1042151 also shows a gene dose for the percent decline of FEV1 after an aspirin challenge (p = 2.82 × 10(-7)). Our findings show that the HLA-DPB1 gene polymorphism may be the most susceptible genetic factor for the risk of AERD in Korean asthmatics and confirm the importance of HLA-DPB1 in the genetic etiology of AERD.
    Human Genetics 11/2012; · 4.63 Impact Factor
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    ABSTRACT: Asthma is a heterogeneous airway disease with various clinical phenotypes. It is crucial to clearly identify clinical phenotypes to achieve better asthma management.We used cluster analysis to classify the clinical groups of 724 asthmatic patients from the Korean Cohort for Reality and Evolution of adult Asthma (COREA), and in 1843 subjects from another independent Korean asthma cohort of Soonchunhyang University Hospitals (SCH cohort). Hierarchical cluster analysis was performed by Ward's method, followed by k-means cluster analysis.Cluster analysis of the COREA cohort indicated four asthma subtypes: (i) smoking asthma, (ii) severe obstructive asthma, (iii) early-onset atopic asthma, and (iv) late-onset mild asthma. An independent cluster analysis of the SCH cohort also indicated four clusters that were similar to the COREA clusters.Our results indicate that adult Korean asthma patients can be classified into four distinct clusters.
    European Respiratory Journal 10/2012; · 6.36 Impact Factor
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    ABSTRACT: The aim of the present study was to develop a diagnostic set of single-nucleotide polymorphisms (SNPs) for discriminating aspirin-exacerbated respiratory disease (AERD) from aspirin-tolerant asthma (ATA) using the genome-wide association study (GWAS) data; the GWAS data were filtered according to p-values and odds ratios (ORs) using PLINK software, and the 10 candidate SNPs most closely associated with AERD were selected, based on 100 AERD and 100 ATA subjects. Using multiple logistic regression and receiver-operating characteristic (ROC) curve analysis, eight SNPs were chosen as the best model for distinguishing between AERD and ATA. The relative risk for AERD in each subject was calculated based on the relative risk of each of the eight SNPs. Ten of the original 109,365 SNPs highly associated (filtered with p<0.001 and ORs) with the risk for AERD were selected. A combination model of the eight SNPs among the 10 SNPs showed the highest area under the ROC curve of 0.9. The overall relative risk for AERD based on the eight SNPs was significantly different between the AERD and ATA groups (p=2.802E-21), and the sensitivity and specificity were 78% and 88%, respectively. The candidate set of eight SNPs may be useful in predicting the risk for AERD.
    DNA and cell biology 09/2012; 31(11):1604-9. · 2.28 Impact Factor
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    ABSTRACT: Background: Obesity is a risk factor for asthma in the general population, but the effect of obesity on airway hyperresponsiveness (AFHR) or airway inflammation in asthma is not clear. This study evaluated the relationship between obesity and asthma, assessing aspects of symptoms, AHR, and severity. Methods: In total, 852 patients with asthma diagnosed by asthma specialists based on AHR as confirmed by a methacholine bronchial provocation test, were enrolled from the Cohort for Reality and Evolution of Adult Asthma in Korea (COREA) adult asthma cohort. The intensity of AHR was assessed by the concentration of methacholine needed to cause a 20% decrease in FEV(1) (PC(20)). Patients were classified into four categories based on body mass index (BMI): underweight (<18.5), normal weight (18.5-24.9), overweight (25.0-29.9), and obese (≥30). Results: BMI was negatively correlated with FEV(1) (l), FVC (l), and FEV(1)/FVC (%) in lung function tests. The prevalence of wheezing increased with higher BMI after adjustment for age, sex, smoking, medication history, and PC(20) (p < 0.0001). logPC(20) was lower in the normal weight group compared with the overweight group (p = 0.003). The risk of moderate or severe AHR (PC(20) ≤ 4 mg/ml) decreased with increased BMI after adjustment for age, sex, smoking, and medication history (p = 0.035). Conclusions: Obesity is a risk factor for asthma in the general population, but obesity in asthmatic patients is negatively correlated with the intensity of AHR and is not related to asthma severity. Obesity is positively related with the prevalence of wheezing but negatively related to AHR in asthmatic patients.
    International Archives of Allergy and Immunology 06/2012; 159(2):187-93. · 2.25 Impact Factor
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    ABSTRACT: The effects of β-catenin promoter haplotypes on its mRNA expression levels and asthma risks were investigated in Korean subjects. The genotype analyses were conducted by a Taqman method for 684 Korean subjects, 400 controls and 284 with asthma. Measurement of mRNA expression levels in peripheral blood nucleated cells were conducted on subjects whose buffy coat fractions were available (n=185). Logistic regression analyses were conducted to test the associations of the β-catenin promoter haplotypes with asthma risks. Four SNPs, -10,288C>T (rs7630377), -6,426C>G (rs9859392), -4,361G>C (rs9870255), and -765G>A (rs3864004), were identified in the promoter region of the β-catenin gene, and three common haplotypes were constructed from them. Haplotype ht1[CCGG] was associated with decreased β-catenin mRNA expression levels and a lower asthma risk with an odds ratio of 0.53, while ht2[TGCA] was associated with increased mRNA expression levels and a higher asthma risk with an odds ratio of 2.34. Ht3[TCGG] had no significant effects on both. Our findings show that β-catenin promoter polymorphism affects its mRNA expression levels, and also is significantly associated with the asthma risk of Korean subjects.
    Clinical biochemistry 05/2012; 45(15):1187-91. · 2.02 Impact Factor
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    ABSTRACT: Carbapenem-resistance is rapidly evolving among the pathogenic microbes in intensive care units (ICUs). This study aimed to determine annual trend of carbapenem-resistance in the ICU for 4 years, since the opening of a university-affiliated hospital in South Korea. From 2005 to 2008, microbial samples from consecutive 6,772 patients were screened in the ICU. Three hundred and ninety-seven patients (5.9%) and their first isolates of carbapenem-resistant pathogens were analyzed. The percentage of patients infected with carbapenem-resistant organisms increased constantly during the initial three years (2.3% in 2005, 6.2% in 2006, 7.8% in 2007), then it declined to 6.5% in 2008. Acute Physiology and Chronic Health Evaluation (APACHE) III score at admission was 58.0±23.5, the median length of the ICU stay was 37 days, and the mortality rate was 37.5%. The sampling sites were endotracheal suction (67%), catheterized urine (17%), wound (6%) and others (10%). Bacteria with carbapenem-resistance were Pseudomonas aeruginosa (247 isolates, 62%), Acinetobacter baumannii (117 isolates, 30%), Enterobacteriaceae (12 isolates, 3%), and others (21, 5%). Of note, peak isolation of carbapenem-resistant microorganisms in medical ICU was followed by the same epidemic at surgical ICU. Taken together, carbapenem-resistant pathogens are of growing concern in the ICU.
    Tuberculosis and Respiratory Diseases 04/2012; 72(4):360-6.
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    ABSTRACT: The discoidin domain receptor tyrosine kinase 1 (DDR1) is positioned within the major histocompatibility complex (MHC) region which plays an important role in the immune system. In addition, DDR1 has been elucidated to be downregulated during the epithelial-mesenchymal transition of bronchial epithelium. To investigate the potential genetic associations between DDR1 and aspirin-exacerbated respiratory disease (AERD), this study conducted association studies of DDR1 single nucleotide polymorphisms (SNPs) with AERD and the obstructive symptom of forced expiratory volume in 1 s (FEV(1)) decline after aspirin provocation. Nine common SNPs were genotyped in 93 AERD patients and 96 aspirin-tolerant asthma (ATA) controls. The genotype distributions of all loci were in Hardy-Weinberg equilibrium (HWE; p > .05). Results. In the results of logistic analyses using age, sex, smoking status, and atopy as covariates, DDR1 rs1264320 in the intronic region showed a potent association signal with FEV(1) decline by aspirin provocation in asthmatics of this study even after corrections for multiple testing (p = .003 and corrected p = .01). However, the variants of DDR1 were not significantly associated with the AERD development (corrected p > .05). On further comparison of FEV(1) decline by aspirin provocation between AERD and ATA, the variant rs1264320 was found to be associated with the FEV(1) decline of ATA rather than AERD. Despite the need for further functional evaluations and replications, we conclude that DDR1 polymorphisms are not likely to contribute to predispositions of AERD, but may be potentially associated with FEV(1) decline by aspirin provocation in asthmatics.
    Journal of Asthma 03/2012; 49(3):237-42. · 1.85 Impact Factor
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    ABSTRACT: Bee stings can cause severe adverse reactions, leading to anaphylaxis, cardiovascular collapse, and death. In some cases, bee venom also induces disseminated intravascular coagulation (DIC). However, to our knowledge, there has been no fatal case of intravascular coagulation accompanied by anaphylaxis caused by bee sting acupuncture. Here, we report a fatal case of a 65-year-old woman with DIC, following anaphylactic shock after bee sting acupuncture. This case emphasizes that practitioners should consider anaphylaxis followed by coagulation abnormalities when a patient's vital signs are unstable after bee sting acupuncture.
    Allergy, asthma & immunology research 03/2012; 4(2):107-9. · 2.65 Impact Factor

Publication Stats

441 Citations
170.46 Total Impact Points

Institutions

  • 2013
    • Seoul National University
      • Department of Internal Medicine
      Seoul, Seoul, South Korea
  • 2010–2013
    • Sogang University
      • Department of Life Science
      Seoul, Seoul, South Korea
    • Hanyang University
      Sŏul, Seoul, South Korea
  • 2007–2013
    • Chung-Ang University Hospital
      Sŏul, Seoul, South Korea
  • 2010–2012
    • Seoul National University Hospital
      • Department of Internal Medicine
      Seoul, Seoul, South Korea
  • 2003–2012
    • Soonchunhyang University
      • College of Medicine
      Onyang, South Chungcheong, South Korea
    • Wonkwang University School of Medicine and Hospital
      Riri, North Jeolla, South Korea
    • Ulsan University Hospital
      Urusan, Ulsan, South Korea
  • 2004–2010
    • Chung-Ang University
      • College of Medicine
      Seoul, Seoul, South Korea