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HLA-DRA Polymorphisms associated with Risk of Nasal Polyposis in Asthmatic Patients
Kim, Jeong-Hyun,Park, Byung-Lae,Cheong, Hyun Sub,Pasaje, Charisse Flerida A.,Bae, Joon Seol,Park, Jong Sook,Uh, Soo-Taek,Kim, Yong-Hoon,Kim, Mi-Kyeong,Choi, Inseon S.,Choi, Byoung Whui,Park, Choon-Sik SAGE Publications 2012 American journal of rhinology & allergy Vol.26 No.1
<P>Nasal polyps, part of the aspirin triad symptoms, are edematous protrusions arising from the mucosa of the nasal sinuses. Although the causative factors and pathogenesis of the polyps are unknown, the significant effect of human leukocyte antigen-DR (HLA-DR) expression in nasal polyps and genetic associations of the major histocompatibility complex class II, DR alpha (HLA-DRA) with immune-mediated diseases have been revealed.</P>
Kim, Jeong-Hyun,Park, Byung-Lae,Pasaje, Charisse Flerida A,Bae, Joon Seol,Park, Jong Sook,Park, Sung Woo,Uh, Soo-Taek,Kim, Mi-Kyeong,Choi, Inseon S,Cho, Sang Heon,Choi, Byoung Whui,Park, Choon-Sik,Shi Springer-Verlag 2011 Journal of human genetics Vol.56 No.9
<P>Aspirin exacerbated respiratory disease (AERD) induces bronchoconstriction in asthmatic patients characterized with a clinical condition of severe decline in forced expiratory volume in one second (FEV1) after ingestion of aspirin. Two genes consisting a heterodimer, transporter 1 and 2, ATP-binding cassette, sub-family B (MDR/TAP) (TAP1 and TAP2) within the major histocompatibility complex (MHC) region, have been implicated in immunodeficiency and bronchiectasis development. To investigate the associations of TAP1 and TAP2 genetic polymorphisms with AERD and phenotypic FEV1 decline, a total of 43 common single-nucleotide polymorphisms (SNPs) including 12 SNPs of TAP1 and 31 SNPs of TAP2 were genotyped in 93 AERD patients and 96 aspirin-tolerant asthma controls. Interestingly, regression analysis revealed that polymorphisms and haplotypes of TAP2 were associated with FEV1 decline by aspirin provocation (P=0.002-0.04), with about twofold decline rate of FEV1 in most of minor homozygotes compared with major homozygotes. In addition, nominal evidences of association between TAP2 and AERD development were observed (P=0.02-0.04). However, TAP1 polymorphisms showed no relations to both AERD and FEV1 decline after aspirin challenge (P>0.05). Although further functional evaluations and replications are required, our preliminary findings provide supporting information that variants of TAP2 might be predisposing factors for FEV1 decline-related symptoms.</P>
Easy Diagnosis of Asthma: Computer-Assisted, Symptom-Based Diagnosis
Choi, Byoung Whui,Yoo, Kwang-Ha,Jeong, Jae-Won,Yoon, Ho Joo,Kim, Sang-Heon,Park, Yong-Mean,Kim, Wo-Kyung,Oh, Jae-Won,Rha, Yeong-Ho,Pyun, Bok-Yang,Chang, Suk-Il,Moon, Hee-Bom,Kim, You-Young,Cho, Sang-H KOREAN ACADEMY OF MEDICAL SCIENCE 2007 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.22 No.5
<P>Diagnosis of asthma is often challenging in primary-care physicians due to lack of tools measuring airway obstruction and variability. Symptom-based diagnosis of asthma utilizing objective diagnostic parameters and appropriate software would be useful in clinical practice. A total of 302 adult patients with respiratory symptoms responded to a questionnaire regarding asthma symptoms and provoking factors. Questions were asked and recorded by physicians into a computer program. A definite diagnosis of asthma was made based on a positive response to methacholine bronchial provocation or bronchodilator response (BDR) testing. Multivariate logistic regression analysis was used to evaluate the significance of questionnaire responses in terms of discriminating asthmatics. Asthmatic patients showed higher total symptom scores than non-asthmatics (mean 5.93 vs. 4.93; <I>p</I><0.01). Multivariate logistic regression analysis identified that response to questions concerning the following significantly discriminated asthmatics; wheezing with dyspnea, which is aggravated at night, and by exercise, cold air, and upper respiratory infection. Moreover, the presence of these symptoms was found to agree significantly with definite diagnosis of asthma (by kappa statistics). Receiver-operating characteristic curve analysis revealed that the diagnostic accuracy of symptom-based diagnosis was high with an area under the curve of 0.647±0.033. Using a computer-assisted symptom-based diagnosis program, it is possible to increase the accuracy of diagnosing asthma in general practice, when the facilities required to evaluate airway hyperresponsiveness or BDR are unavailable.</P>
연구보고 : 기관지천식환자에 있어서 고해상도 전산화단층촬영술을 이용한 기관지유발에 대한 기도의 반응
최병휘 ( Byoung Whui Choi ),강윤정 ( Yoon Jeong Kang ),고형기 ( Hyung Ki Ko ),박인원 ( In Won Park ),허성호 ( Sung Ho Hue ),김양수 ( Yang Soo Kim ),김영구 ( Young Goo Kim ),김건상 ( Kun Sang Kim ),김종효 ( Jong Hyo Kim ) 대한결핵 및 호흡기학회 1995 Tuberculosis and Respiratory Diseases Vol.42 No.6
자연기흉에 있어서 8 French 도관과 흉관의 삽입 치료 효과
강윤정 ( Yoon Jeong Kang ),고형기 ( Hyoung Gee Koh ),신종욱 ( Jong Wook Shin ),임성룡 ( Seong Yong Lim ),최재선 ( Jae Sun Choi ),유지훈 ( Ji Hoon Yu ),박인원 ( In Won Park ),최병휘 ( Byoung Whui Choi ),허성호 ( Sung Ho Hue ),서승 대한결핵 및 호흡기학회 1996 Tuberculosis and Respiratory Diseases Vol.43 No.3
Putative association of <i>SMAPIL</i> polymorphisms with risk of aspirin intolerance in asthmatics
Yongha Kim, Jason,Kim, Jeong-Hyun,Park, Byng-Lae,Sub Cheong, Hyun,Sook Park, Jong,Soo Jang, An,Uh, Soo-Taek,Choi, Jae-Sung,Kim, Yong-Hoon,Kim, Mi-Kyeong,Choi, Inseon S.,Heon Cho, Sang,Whui Choi, Byoun Informa Healthcare 2010 The Journal of asthma Vol.47 No.9
<P><I>Background.</I> Aspirin-intolerant asthma (AIA), as a clinical syndrome caused by aspirin, is characterized by lung inflammation and reversible bronchoconstriction. Recently, the altered trafficking and diminished airway reactivity have been implicated in allergic airway remodeling. The stromal membrane-associated protein 1-like (SMAP1L) exerts common and distinct functions in vesicle trafficking including endocytosis. The disturbance of pulmonary surfactant synthesis has been elucidated to be associated with asthma experimentally. Moreover, in alveolar type II (ATII) cells that synthesize pulmonary surfactant, alterations of clathrin-dependent endocytosis cause disturbance at the surfactant function, suggesting that SMAP1L, which directly interacts with clathrin, could be associated with asthma and related phenotypes. <I>Objective.</I> To verify our hypothesis that <I>SMAP1L</I> could play a role in the development of AIA, this study investigated associations between single-nucleotide polymorphisms (SNPs) of the <I>SMAP1L</I> gene and AIA. <I>Methods.</I> We conducted an association study between 19 SNPs of the <I>SMAP1L</I> gene and AIA in a total of 592 Korean subjects including 163 AIA and 429 aspirin-tolerant asthma (ATA) patients. Associations between polymorphisms of <I>SMAP1L</I> and AIA were analyzed with sex, smoking status, atopy, and body mass index as covariates. <I>Results.</I> Logistic analyses revealed that three common polymorphisms, <I>rs2982510</I>, <I>rs2294752</I>, and <I>rs446738</I>, were putatively associated with the increased susceptibility to AIA (<I>p</I> = .003, <I>p</I><SUP>corr</SUP> = .004, OR = 0.24, 95% CI = 0.09-0.62 for <I>rs2982510</I> and <I>rs2294752</I>; <I>p</I> = .008, <I>p</I><SUP>corr</SUP> = .03, OR = 0.44, 95% CI = 0.24-0.80 for <I>rs446738</I>, in the recessive model). In addition, <I>rs2982510</I> and <I>rs2294752</I> were significantly associated with the fall of forced expiratory volume in 1 s (FEV<SUB>1</SUB>) by aspirin provocation (<I>p</I> = .001, <I>p</I><SUP>corr</SUP> = .04 in the recessive model for both SNPs). <I>Conclusions.</I> Our findings suggest that <I>SMAP1L</I> might be a susceptible gene to AIA, providing a new strategy for the control of aspirin intolerance.</P>
Kim, Jason Yongha,Kim, Jeong-Hyun,Park, Byung-Lae,Pasaje, Charisse Flerida A.,Bae, Joon Seol,Uh, Soo-Taek,Kim, Yong-Hoon,Kim, Mi-Kyeong,Choi, Inseon S.,Cho, Sang Heon,Choi, Byoung Whui,Park, Jong Sook Informa Healthcare 2012 The Journal of asthma Vol.49 No.3
<P><I>Background.</I> The <I>discoidin domain receptor tyrosine kinase 1</I> (<I>DDR1</I>) 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. <I>Objective.</I> To investigate the potential genetic associations between <I>DDR1</I> and aspirin-exacerbated respiratory disease (AERD), this study conducted association studies of <I>DDR1</I> single nucleotide polymorphisms (SNPs) with AERD and the obstructive symptom of forced expiratory volume in 1 s (FEV<SUB>1</SUB>) decline after aspirin provocation. <I>Methods.</I> 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; <I>p</I> > .05). <I>Results.</I> In the results of logistic analyses using age, sex, smoking status, and atopy as covariates, <I>DDR1 rs1264320</I> in the intronic region showed a potent association signal with FEV<SUB>1</SUB> decline by aspirin provocation in asthmatics of this study even after corrections for multiple testing (<I>p</I> == .003 and corrected <I>p</I> == .01). However, the variants of <I>DDR1</I> were not significantly associated with the AERD development (corrected <I>p</I> > .05). On further comparison of FEV<SUB>1</SUB> decline by aspirin provocation between AERD and ATA, the variant <I>rs1264320</I> was found to be associated with the FEV<SUB>1</SUB> decline of ATA rather than AERD. <I>Conclusion.</I> Despite the need for further functional evaluations and replications, we conclude that <I>DDR1</I> polymorphisms are not likely to contribute to predispositions of AERD, but may be potentially associated with FEV<SUB>1</SUB> decline by aspirin provocation in asthmatics.</P>
Genome-wide association study of aspirin-exacerbated respiratory disease in a Korean population.
Park, Byung Lae,Kim, Tae-Hoon,Kim, Jeong-Hyun,Bae, Joon Seol,Pasaje, Charisse Flerida A,Cheong, Hyun Sub,Kim, Lyoung Hyo,Park, Jong-Sook,Lee, Ho Sung,Kim, Myung-Sin,Choi, Inseon S,Choi, Byoung Whui,Ki Springer-Verlag 2013 HUMAN GENETICS Vol.132 No.3
<P>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 x 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 x 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.</P>