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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, C.‐,F.,Bae, J.‐,S.,Park, B.‐,L.,Cheong, H. S.,Kim, J.‐,H.,Park, T.‐,J.,Lee, J.‐,S.,Kim, Y.,Park, C.‐,S.,Kim, B.‐,J.,Cha, B.,Kim, J. W.,Choi, W. Blackwell Publishing Ltd 2011 Genes, brain, and behavior Vol.10 No.8
<P><B>Located on chromosome 10q22‐q23, the human <I>neuregulin3</I> (<I>NRG3</I>) is considered to be a strong positional and functional candidate gene for schizophrenia pathogenesis. Several case–control studies examining the association of polymorphisms in <I>NRG3</I> with schizophrenia and/or related traits such as delusion have been reported recently in cohorts of Han Chinese, Ashkenazi Jews, Australians and white Americans of Western European ancestry. Thus, this study aimed to comprehensively investigate the association of <I>NRG3</I> genetic variations with the risk of schizophrenia and smooth pursuit eye movement (SPEM) abnormality in a Korean population. Using TaqMan assay, six single‐nucleotide polymorphisms (SNPs) in the intronic region of <I>NRG3</I> were genotyped and two major haplotypes were identified in 435 patients with schizophrenia as cases and 393 unrelated healthy individuals as controls. A total of 113 schizophrenia patients underwent an eye tracking task, and degree of SPEM abnormality was measured using the logarithmic values of the signal/noise (Ln <I>S</I>/<I>N</I>) ratio. Differences in frequency distributions were analyzed using logistic and regression models following various modes of genetic inheritance and controlling for age and sex as covariates. Subsequent analysis revealed that the frequency distributions of <I>NRG3</I> polymorphisms and haplotypes were similar between schizophrenia patients and healthy controls of Korean ethnicity. Furthermore, no significant differences were observed between the genetic variants tested for SPEM abnormality. By elucidating a lack of association in a Korean population, findings from this study may contribute to the understanding of the genetic etiology focusing on the role of <I>NRG3</I> in schizophrenia pathogenesis.</B></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>
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.
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.