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Kim, Jin-Moo,Park, Byung-Lae,Park, Se-Min,Lee, Shin-Hwa,Kim, Myung-Ok,Jung, Seok,Lee, Eun Hee,Uh, Soo-Taek,Park, Jong Sook,Choi, Jae-Sung,Kim, Yong-Hoon,Kim, Mi-Kyeong,Choi, Inseon S,Cho, Sang Heon,Ch Ashley Publications 2010 Pharmacogenomics Vol.11 No.7
<P>AIMS: Cysteinyl leukotrienes are inactivated by acetyl coenzyme A-dependent N-acetyltransferase (NAT). Thus, functional alterations of the NAT gene may contribute to the risk of aspirin-intolerant asthma. MATERIALS & METHODS: Asthmatics (n = 438) were categorized into aspirin-intolerant asthma (15% or greater decrease in the forced expiratory volume in 1 s or cutaneous reactions, n = 170) or aspirin-tolerant asthma (n = 268) groups. In total, 14 polymorphisms of the NAT2 gene were genotyped by a single-base extension method. RESULTS: The distributions of all loci of the 14 SNPs were in Hardy-Weinberg equilibrium (p > 0.05). Among the 14 SNPs, six common SNPs (minor allele frequency >5%) in a Korean population were used for haplotype construction and further statistical analysis. The logistic regression analysis demonstrated that NAT2 -9246G>C and haplotype 2 (TCACGG) were significantly associated with the risk of aspirin-intolerant asthma. The rare allele frequencies of the SNP and Ht2 were significantly higher in the aspirin-intolerant asthma group than in the aspirin-tolerant asthma group (p(corr) = 0.03 and p(corr) = 0.02 in codominant model). CONCLUSION: In a large genetic epidemiology study of aspirin-intolerant asthma in a Korean population, genetic polymorphisms of NAT2 were found to be related to a risk of aspirin hypersensitivity among asthmatics.</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>
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>
( Sung Soo Kim ),( Inseon S. Choi ),( Yeon Joo Kim ),( Chang Seong Kim ),( Eui Ryoung Han ),( Dong Jin Park ),( Dae Eun Kim ) 대한내과학회 2010 The Korean Journal of Internal Medicine Vol.25 No.3
Background/Aims: Many patients with aspirin-induced asthma have severe methacholine airway hyperresponsiveness (AHR), suggesting a relationship between aspirin and methacholine in airway response. This study was performed to determine whether methacholine AHR affects the response of asthmatics to inhaled aspirin. Methods: The clinical records of 207 asthmatic patients who underwent inhalation challenges with both aspirin and methacholine were reviewed retrospectively. An oral aspirin challenge was performed in patients with a negative inhalation response. The bronchial reactivity index (BRindex) was calculated from the percent decrease in lung function divided by the last dose of the stimulus. Results: Forty-one (20.9%) and 14 (7.1%) patients showed a positive response to aspirin following an inhalation and oral challenge, respectively. Only 24.3 and 14.3% of the responders had a history of aspirin intolerance, respectively. The methacholine BRindex was significantly higher in the inhalation responders (1.46±0.02) than in the oral responders (1.36±0.03, p<0.01) and in non-responders (n=141, 1.37±0.01, p<0.001). The aspirin BRindex was significantly correlated with the methacholine BRindex (r=0.270, p<0.001). Three of four patients who received the oral challenge, despite a positive inhalation test, showed negative responses to the oral challenge. Two of these patients had severe AHR. Conclusions: A considerable number of asthmatic patients with no history of aspirin intolerance responded to the inhalation aspirin challenge. The airway response to aspirin was significantly correlated with methacholine-AHR, and a false-positive response to aspirin inhalation test seemed to occur primarily in patients with severe AHR. (Korean J Intern Med 2010;25:309-316)
( Tae Woong Kong ),( In Tae Kim ),( Tridib Kumar Sinha ),( Junho Moon ),( Dong Ho Kim ),( Inseon Kim ),( Kwangyong Na ),( Min-woo Kim ),( Hye-lin Kim ),( Taegyeong Hyeong ),( Jeong Seok Oh ) 한국고무학회 2020 엘라스토머 및 콤포지트 Vol.55 No.4
Stearic acid (SA), polyethylene glycol (PEG), and malic acid (MA) have been used to modify the surface of waste gypsum to develop corresponding poly (butylene adipate-co-terephthalate) (PBAT) composites. According to the mechanical properties, MA-treated gypsum (MA-gypsum) showed the best performance, whereas SA-gypsum showed the worst performance. In contrast to SA and PEG (having -COOH and -OH as polar functional groups, respectively), the presence of both -OH and -COOH in MA is responsible for the superior surface treatment of gypsum and its better dispersion in the polymer matrix (as revealed by FE-SEM analyses). The presence of long aliphatic chain in SA is supposed to inhibit the dispersion of SA-gypsum. Further, the performance of MA-gypsum/PBAT was enhanced by adding polylactic acid (PLA). The maximum optimized contents of MA-gypsum and PLA are 20 and 7.5 wt% for developing a high-performance PBAT composite.
Kim, Hee-Jeong,Cho, Sung-Hwan,Park, Jong-Sook,Lee, Tae-Hyeong,Lee, Eun-Ju,Kim, Yong-Hoon,Uh, Soo-Taek,Chung, Il Yup,Kim, Mi-Kyeong,Choi, Inseon S,Park, Byung-Lae,Shin, Hyoung-Doo,Park, Choon-Sik Springer-Verlag 2012 Journal of human genetics Vol.57 No.4
<P>Aspirin-exacerbated respiratory diseases (AERD) are associated with the metabolism of arachidonic acid. FPR2 (formyl peptide receptor2) is a high-affinity ligand receptor for potent anti-inflammatory lipid metabolites: lipoxins. Thus, functional alterations of the FPR2 may contribute to AERD. We investigated the relationship between single-nucleotide polymorphisms (SNPs) in the FPR2 and AERD. Asthmatics were categorized into AERD <15% decreases in forced expiratory volume in one second (FEV(1)), and/or naso-ocular reactions after oral aspirin challenge (n=170) and aspirin-tolerant asthma (ATA, n=268). In all, 11 SNPs were genotyped. FPR2 protein expressions on CD14-positive monocytes in peripheral blood were measured using flow cytometric analysis. We performed RT-PCR of the FPR2 mRNA expressed by peripheral blood mononuclear cells. Logistic regression analysis showed that the minor allele frequency of FPR2 -4209T>G (rs1769490) in intron 2 was significantly lower in the AERD group (n=170) than in the ATA group (n=268) (P=0.006, P(corr)=0.04, recessive model). The decline of FEV(1) after aspirin challenge was significantly lower in the subjects with GG homozygotes of FPR2 -4209T>G than those with the other genotypes (P=0.0002). Asthmatic homozygotes for FPR2 -4209T>G minor allele exhibited significantly higher FPR2 protein expression in CD14-positive monocytes than did those with the common allele of FPR2 -4209T>G allele (P=0.01). There was no difference in the expression of the wild form and the exon 2 deleted variant form of FPR2 gene according to the genotypes of FPR2 -4209T>G. The minor allele at FPR2 -4209T>G may have a protective role against the development of AERD, via increase of FPR2 protein expression in inflammatory cells.</P>
Association of FANCC polymorphisms with FEV1 decline in aspirin exacerbated respiratory disease
Kim, Jeong-Hyun,Park, Byung-Lae,Pasaje, Charisse Flerida A.,Bae, Joon Seol,Park, Jong Sook,Park, Sung Woo,Uh, Soo-Taek,Choi, Jae-Sung,Kim, Yong-Hoon,Kim, Mi-Kyeong,Choi, Inseon S.,Cho, Sang Heon,Choi, Springer-Verlag 2012 MOLECULAR BIOLOGY REPORTS Vol.39 No.3