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Pasaje, Charisse Flerida A.,Bae, Joon Seol,Park, Byung-Lae,Cheong, Hyun Sub,Jang, An-Soo,Uh, Soo-Taek,Kim, Mi-Kyeong,Kim, Jeong-Hyun,Park, Tae-Joon,Lee, Jin-Sol,Kim, Yongha,Park, Choon-Sik,Shin, Hyoun Informa Healthcare 2011 The Journal of asthma Vol.48 No.6
<P><I>Background</I>. Exacerbation of asthma symptoms due to aspirin ingestion may lead to life-threatening lung failure. The adhesion molecule <I>CD58</I> gene may play a crucial role in aspirin-exacerbated respiratory disease (AERD) pathogenesis by mediating the biological functions of asthma-inducing mechanisms including T helper cells, proinflammatory cytokines, and natural killer T cells. <I>Objective</I>. This study aimed to investigate the association of <I>CD58</I> variations with aspirin-induced bronchospasm in Korean asthma patients. <I>Methods</I>. Seven single-nucleotide polymorphisms were selected for genotyping based on previously reported polymorphisms in the International HapMap database. Genotyping was carried out using TaqMan assay and 2 major haplotypes were obtained in 163 AERD cases and 429 aspirin-tolerant asthma controls. Frequency distributions of <I>CD58</I> variations were analyzed using logistic and regression models. <I>Results</I>. Results showed that none of the analyzed <I>CD58</I> single-nucleotide polymorphisms and haplotypes was significantly associated with AERD development and fall rate of FEV<SUB>1</SUB> by aspirin provocation, an important diagnostic marker of aspirin hypersensitivity. <I>Conclusions</I>. This preliminary study suggests that <I>CD58</I> does not affect AERD susceptibility in a Korean population, and may provide a new direction for future disease etiology.</P>
Pasaje, Charisse Flerida A.,Kim, Jeong-Hyun,Park, Byung-Lae,Cheong, Hyun Sub,Chun, Ji-Yong,Park, Tae-Joon,Lee, Jin-Sol,Kim, Yongha,Bae, Joon Seol,Park, Jong Sook,Yoon, Sang-Hyuk,Uh, Soo-Taek,Choi, Jae Wiley (Blackwell Publishing) 2010 Annals of human genetics Vol.74 No.4
<P>Aspirin-intolerant asthma (AIA) occurs from asthma exacerbation after exposure to aspirin. However, the underlying mechanisms of AIA occurrence are still unclear. The critical role of the solute carrier family 6 (neurotransmitter transporter, betaine/GABA) member 12 (SLC6A12) gene in GABAergic transmission, which is associated with mucus production in asthma, makes it a candidate gene for AIA association study. Eight single nucleotide polymorphisms (SNPs) in SLC6A12 were genotyped in 163 aspirin-intolerant asthma (AIA) and 429 aspirin-tolerant asthma (ATA) patients of Korean ethnicity. Associations between polymorphisms of SLC6A12 and AIA were analysed using multivariate logistic analysis. Results showed that two polymorphisms and a haplotype in SLC6A12, rs499368 (P= 0.005; P(corr)= 0.03), rs557881 (non-synonymous C10R, P= 0.007; P(corr)= 0.04), and SLC6A12_BL1_ht1 (P= 0.009; P(corr)= 0.05) respectively, were significantly associated with AIA after multiple testing corrections. In addition, SNPs of SLC6A12 were significantly associated with the fall rate of FEV(1) by aspirin provocation suggesting that SLC6A12 could affect reversibility of lung function abnormalities in AIA patients. Although these results are preliminary and future replications are needed to confirm these findings, this study showed evidence of association between variants in SLC6A12 and AIA occurrence among asthmatics in a Korean population.</P>
WDR46 is a Genetic Risk Factor for Aspirin-Exacerbated Respiratory Disease in a Korean Population
Charisse Flerida A. Pasaje,배준설,Byung-Lae Park,정현섭,Jeong-Hyun Kim,어수택,박춘식,신형두 대한천식알레르기학회 2012 Allergy, Asthma & Immunology Research Vol.4 No.4
Purpose: The human WD repeat-containing protein 46 (WDR46; also known as C6orf11), located at the disease-relevant centromere side of the class II major histocompatibility complex region, is hypothesized to be associated with risk of aspirin-exacerbated respiratory disease (AERD) as well as a decline in forced expiratory volume in the first second (FEV1), an important diagnostic marker of asthma. Methods: To investigate the association between WDR46 and AERD, five single-nucleotide polymorphisms (SNPs) were genotyped in 93 AERD cases and 96 aspirin-tolerant asthma controls of Korean ethnicity. Three major haplotypes were inferred from pairwise comparison of the SNPs, and one was included in the association analysis. Differences in the frequency distribution of WDR46 SNPs and haplotype were analyzed using logistic and regression models via various modes of genetic inheritance. Results: Depending on the genetic model, the logistic and regression analyses revealed significant associations between rs463260, rs446735, rs455567, rs469064, and WDR46_ht2 and the risk of AERD (P=0.007-0.04, Pcorr =0.01-0.04) and FEV1 decline after aspirin provocation (P=0.006-0.03, Pcorr =0.01-0.03). Furthermore, functional analysis in silico showed that the G>A allele of rs463260 located in the 5’untranslated region potentially matched a nucleotide sequence within an upstream open reading frame of WDR46. Conclusions: These findings show for the first time that WDR46 is an important genetic marker of aspirin-induced airway inflammation and may be useful for formulating new disease-management strategies.
DCBLD2 gene variations correlate with nasal polyposis in Korean asthma patients.
Pasaje, Charisse Flerida A,Bae, Joon Seol,Park, Byung-Lae,Cheong, Hyun Sub,Kim, Jeong-Hyun,Jang, An-Soo,Uh, Soo-Taek,Park, Choon-Sik,Shin, Hyoung Doo Springer International 2012 Lung Vol.190 No.2
<P>Nasal polyps are abnormal lesions that cause airway obstruction and can occur along with other respiratory diseases. On account of its association with aspirin exacerbated respiratory disease (AERD), the human discoidin, CUB and LCCL domain containing 2 (DCBLD2) is hypothesized to be a candidate gene for the development of nasal polyps in asthma patients.</P>
A possible association of EMID2 polymorphisms with aspirin hypersensitivity in asthma
Pasaje, Charisse Flerida A.,Kim, Jeong-Hyun,Park, Byung-Lae,Cheong, Hyun Sub,Kim, Mi-Kyeong,Choi, Inseon S.,Cho, Sang Heon,Hong, Chein-Soo,Lee, Yong Won,Lee, Jae-Young,Koh, In Song,Park, Tae-Joon,Lee, Springer-Verlag 2011 Immunogenetics Vol.63 No.1
Genetic analysis between FGD6 and aspirin exacerbated respiratory disease in a Korean population
Charisse Flerida A. Pasaje,배준설,박병래,정현섭,장안수,어수택,김미경,김정현,박태준,이진솔,Yongha Kim,박춘식,신형두 한국유전학회 2011 Genes & Genomics Vol.33 No.5
The human FYVE, RhoGEF and PH domain containing 6(FGD6) gene regulates mechanisms that are implicated in airway bronchospasm, and therefore, may be a risk factor for aspirin exacerbated respiratory disease (AERD). This study aims to investigate the association between FGD6 variations and AERD in a Korean asthma cohort. A total of 34 single nucleotide polymorphisms (SNPs) were selected for genotyping based on previously reported polymorphisms in the HapMap database. Genotyping was carried out using TaqMan assay and nine major haplotypes from two haplotype blocks were obtained in 163 AERD cases and 429 aspirin-tolerant asthma (ATA) controls. Genotype frequency distributions ofFGD6 polymorphisms and haplotypes were analyzed using logistic and regression models. Findings from logistic and regression analyses revealed a lack of association of FGD6genetic variations with AERD and fall rate of FEV_1 (P >0.05 in co-dominant, dominant and recessive models). This preliminary report provides evidences that variations in the FGD6 gene do not influence the risk of AERD and its relevant phenotype in a Korean population. This report may contribute to the etiology of aspirin hypersensitivity in Korean asthma patients.
Putative Association of ITGB1 Haplotype with the Clearance of HBV Infection
박태준,천지용,배준설,이진솔,Charisse Flerida Pasaje,박병래,정현섭,이효석,김윤준,신형두,Jason Y. Kim 한국유전체학회 2010 Genomics & informatics Vol.8 No.1
Integrins are transmembrane receptor proteins that mediate cell-cell adhesion and cell-extracellular matrix (ECM) adhesion. The deregulation of cell-ECM adhesion and the abnormal expression of beta1 (β1) integrins (ITGB1s) are involved in tumor development and metastasis. In the liver, the expression of integrins and ECM proteins can be a cause of hepatocellular carcinoma (HCC) development. We performed direct DNA sequencing of 24 individuals, and identified 23 sequence variants of ITGB1 polymorphisms. Among these 23 variants, 7 common variants were selected based on frequencies and linkage disequilibrium, and then genotyped in a larger-scale group of subjects (n=1,103). The genetic associations of ITGB1 polymorphisms with the clearance of HBV and HCC outcome of HBV patients were analyzed using logistic regression models and Cox relative hazard models. Although there was no significant association observed between the polymorphisms and the HCC outcome of HBV patients, the second most common haplotype (ITGB1 haplotype-2 [C-C-C-C-T-C-T ]) was putatively associated with HBV clearance (OR=0.75, p=0.008 and Pcorr=0.05). The minor allele frequency (MAF) of ITGB1 haplotype -2 of the spontaneously recovered (SR) group was significantly higher than that of the chronic carrier group (CC) (freq. = 0.248 vs. 0.199). The information derived from this study could be valuable for understanding the genetic factors involved in the clearance of HBV.
Genetic association analysis of CIITA variations with nasal polyp pathogenesis in asthmatic patients
BAE, JOON SEOL,PASAJE, CHARISSE FLERIDA A.,PARK, BYUNG LAE,CHEONG, HYUN SUB,KIM, JEONG-HYUN,UH, SOO-TAEK,PARK, CHOON-SIK,SHIN, HYOUNG DOO Spandidos Publications 2013 MOLECULAR MEDICINE REPORTS Vol.7 No.3
<P>Nasal polyps are abnormal lesions arising mainly from the nasal mucosa and paranasal sinuses. Since the human class?II, major histocompatibility complex, transactivator (CIITA) is a positive regulator of class?II, major histocompatibility complex gene transcription, the CIITA gene is thought to be involved in the presence of nasal polyps in asthma and aspirin hypersensitive patients. To investigate the association between CIITA and nasal polyposis, 18?single nucleotide polymorphisms (SNPs) were genotyped in 467?asthmatics who were classified into 158?aspirin-exacerbated respiratory disease (AERD) and 309?aspirin-tolerant asthma (ATA) subgroups. Differences in the frequency distribution of CIITA variations between polyp-positive cases and polyp-negative controls were determined using logistic analyses. Initially, a total of 9?CIITA variants were significantly associated with the presence of nasal polyps in the overall asthma, AERD and ATA groups [P=0.001-0.05, odds ratio (OR)=0.53-2.35 in the overall asthma group; P=0.01-0.02, OR=2.45-2.66 in the AERD group; P=0.001?0.05, OR=0.45-2.61 in the ATA group using various modes of genetic inheritance]. One the variations (rs12932187) retained this association after multiple testing corrections (Pcorr=0.01) in the overall asthma group. In addition, two variations (rs12932187 and rs11074938) were associated with the presence of nasal polyps following multiple testing corrections (Pcorr=0.02?and?0.04, respectively) in the ATA group. These novel findings suggest that rs12932187 and rs11074938 may constitute susceptibility markers of inflammation of the nasal passages in asthma patients.</P>