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Association of PTGER gene family polymorphisms with aspirin intolerant asthma in Korean asthmatics
( Byung Lae Park ),( Se Min Park ),( Jong Sook Park ),( Soo Taek Uh ),( Jae Sung Choi ),( Yong Hoon Kim ),( Mi Kyeong Kim ),( Inseon S. Choi ),( Byoung Whui Choi ),( Sang Heon Cho ),( Chein Soo Hong ) 생화학분자생물학회 (구 한국생화학분자생물학회) 2010 BMB Reports Vol.43 No.6
Aspirin-intolerant asthma (AIA) is characterized by severe asthmatic attack after ingestion of aspirin and/or non-steroidal anti-inflammatory drugs. In this study, we investigated the relationship between Prostaglandin E2 receptor (PTGER) gene family polymorphisms and AIA in 243 AIA patients and 919 aspirin- tolerant asthma (ATA) controls of Korean ethnicity in two separate study cohorts. After genotyping 120 SNPs of the PTGER gene family for the 1st cohort study, four SNPs in PTGER1, ten in PTGER3, six in PTGER3, and a haplotype of PTGER2 showed association signals with decreased or increased risk of AIA. Among the positively associated SNPs, one in PTGER1 and four in PTGER3 were analyzed in the 2nd cohort study. The results show that rs7543182 and rs959 in PTGER3 retained their effect, although no statistical significance was retained in the 2nd cohort study. Our findings provide further evidence that polymorphisms in PTGER3 might play a significant role in aspirin hypersensitivity among Korean asthmatics. [BMB reports 2010; 43(6): 445-449]
기관지 천식 환자에서 혈청 IL - 6 , ICAM - 1 , RANTES 농도 측정의 임상적 의의
최재선(Jae Sun Choi),이병훈(Byung Hoon Lee),안창혁(Chang Hyuk Ahn),유지훈(Ji Hoon Yoo),나문준(Moon Jun Na),김재열(Jae Yeol Kim),박인원(In Won Park),최병휘(Byung Whui Choi),허성호(Sung Ho Hue) 대한내과학회 1998 대한내과학회지 Vol.55 No.5
N/A Bronchial asthma is a chronic airway inflammation disorder involving lymphocyte activation and various cytokines secretion by lymphocyte. The inflammatory response results from a complex network of interactions between inflammatory cells (mast cells, eosinophils, macrophages) and resident cells belonging to the lung structure itself like EC, fibroblasts, or bronchial epithelial cells. IL-6 which is known to up-regulate the endothelial cell expression of adhesion molecules participating in the development of the inflammatory reaction in bronchial asthma is produced by alveolar macrophage. ICAM-1 is produced by bronchial epithelial cell and expression by endothelial cell, which is known to enhance of the influx of various cells, RANTES which is known to a potent chemoattractant for eosinophils, lymphocytes, and monocytes, a member of the CC chemokine family, is expressed by bronchial epithelial cell. To evaluate whether markers of lymphocyte activation are useful markers of disease activity in bronchial asthma, we measured slL-6, sICAM- 1, sRANTES in 42 patients with mild to moderate bronchial asthma and in 26 normal controls and con the result with other disease activity markers in asthma(pulmonary function, blood eosinophil counts). The mean level of sIL-6 was higher than that of normal control and correlated significantly with sICAM-1, FEV1% to predicted value. The mean level of sICAM-1 was higher than that of normal control and correlated significantly with FEV1%, FEV1% to predicted value. The mean level of sRANTES showed the tendency to be higher than that of normal control, but not significant statistically, and did not correlated with sIL-6, sICAM-1, FEV1%, FEV1% to predicted value, blood eosinophil counts. It appeared that sIL-6 and sICAM-1 could be a disease marker in bronchial asthma. But, clinical application of the measurement of these markers needs to be studied further.
Association of the G134A and G184C Polymorphisms in the CYP1A1 Gene with Lung Cancer Incidence
Doug-Young Ryu,Mingai Huang,Changbo Park,Soo Im Chang,Ruth Im,Seong-Jin Choi,Na-Young Kim,In Won Park,Byoung Whui Choi,Jae Yeol Kim,Jong Wook Shin,Jae Chul Choi,Byung-Sun Choi,Jung-Duck Park 한국독성학회 2008 Toxicological Research Vol.24 No.2
The G184C and G134A single nucleotide polymorphisms (SNPs) of the CYP1A1 gene result in Ala62Pro and Gly45Asp substitutions, respectively. Here, we tested whether these SNPs are associated with an alteration in lung cancer incidence. We examined 80 Korean subjects with lung cancer and 240 age- and sex-matched controls. For each subject, the CYP1A1 gene was PCR amplified and sequenced. We observed that the odds ratio (OR) for lung cancer was 3.37 higher in subjects with the G184C polymorphism than in controls (95% confidence interval (CI), 0.89~12.73, P = 0.07). In contrast, the OR for lung cancer was 1.23 in subjects with the G134A polymorphism compared to controls (95% CI, 0.68~2.20, P = 0.49). The G184C polymorphism exacerbated the effects of smoking on lung cancer development. Gene-smoking interaction analyses revealed that past or present smokers with the G184C polymorphism had a higher incidence of lung cancer (OR, 24.72; 95% CI, 4.48~136.31; P < 0.01) than control smokers (OR, 6.65; 95% CI, 2.72~16.28; P < 0.01). However, there was only a slight difference in the ORs for lung cancer between control smokers and smokers with the G134A polymorphism. These findings suggest that the G184C polymorphism, but not the G134A polymorphism, is associated with an increased risk of lung cancer.
Association of the G134A and G184C Polymorphisms in the CYP1A1 Gene with Lung Cancer Incidence
Ryu, Doug-Young,Huang, Ming-Ai,Park, Chang-Bo,Chang, Soo-Im,Im, Ruth,Choi, Seong-Jin,Kim, Na-Young,Park, In-Won,Choi, Byoung-Whui,Kim, Jae-Yeol,Shin, Jong-Wook,Choi, Jae-Chul,Choi, Byung-Sun,Park, Jun Korean Society of ToxicologyKorea Environmental Mu 2008 Toxicological Research Vol.25 No.3
The G184C and G134A single nucleotide polymorphisms(SNPs) of the CYP1A1 gene result in Ala62Pro and Gly45Asp substitutions, respectively. Here, we tested whether these SNPs are associated with an alteration in lung cancer incidence. We examined 80 Korean subjects with lung cancer and 240 age- and sex-matched controls. For each subject, the CYP1A1 gene was PCR amplified and sequenced. We observed that the odds ratio(OR) for lung cancer was 3.37 higher in subjects with the G184C polymorphism than in controls(95% confidence interval(CI), $0.89{\sim}12.73$, P=0.07). In contrast, the OR for lung cancer was 1.23 in subjects with the G134A polymorphism compared to controls(95% CI, $0.68{\sim}2.20$, P=0.49). The G184C polymorphism exacerbated the effects of smoking on lung cancer development. Gene-smoking interaction analyses revealed that past or present smokers with the G184C polymorphism had a higher incidence of lung cancer(OR, 24.72; 95% CI, $4.48{\sim}136.31$; P<0.01) than control smokers(OR, 6.65; 95% CI, $2.72{\sim}16.28$; P<0.01). However, there was only a slight difference in the ORs for lung cancer between control smokers and smokers with the G134A polymorphism. These findings suggest that the G184C polymorphism, but not the G134A polymorphism, is associated with an increased risk of lung cancer.
A case of pulmonary cryptococcosis mimicking pulmonary tuberculosis in a healthy young man
( Byung Ook Lee ),( Sun Young Cho ),( In Won Park ),( Jae Chol Choi ),( Byoung Whui Choi ),( Jae Yeol Kim ),( Jong Wook Shin ) 대한내과학회 2011 대한내과학회 추계학술대회 Vol.2011 No.1
Cryptococcosis is a common opportunistic infection in patients with acquired immunodeficiency syndrome and other causes of reduced immunity. Majority of pulmonary cryptococcosis patients exhibiting non specific clinical manifestations. So diagnosis of pulmonary cryptococcosis in patients without underlying diseases is generally difficult. Especially in an area with a high prevalence of pulmonary tuberculosis and when it shows cavitary lesion, pulmonary cryptococcosis is likely to be misdiagnosed as a pulmonary tuberculosis. We present here a case of pulmonary cryptococcosis that mimicked pulmonary tuberculosis in an immunocompetent patient. A 29 -year- old man presented with a 4 -day history of productive cough, low grade fever and left pleuritic chest pain. The serum anti-HIV antibody was negative. A chest X-ray showed patchy infiltration on the left upper lung field. Computed tomography (CT) showed segmental consolidation in the anterior segment of the left upper. The examination of the sputum for acid-fast bacilli with gram staining and culture did not reveal any organisms. Four days later the patient respiratory symptoms was aggravated. A follow-up chest CT demonstrated progression of the segmental consolidation with cavitation and necrosis. We conducted bronchoalveolar lavage and fluid culture was negative and there were neither acid-fast bacilli nor any pathogens. To get a tissue specimen, we conducted ultrasonography guided percutaneous needle aspiration. The specimen exhibited multiple areas of granulomatous inflammation and round, yeast-like bodies. Mucicarmine stain for the capsular material was incompletely positive and the Fontana-Masson silver stain was negative. The tissue fungal culture did not grow Cryptococcus. The result of the serum cryptococcal antigen test was positive, with a titer of 1:256. The result of the histology and the high titer of SCA strongly suggested pulmonary cryptoccosis, so we conducted polymerase chain reaction (PCR) for the tissue and the PCR from the tissue specimen was positive for cryptoccosis. Treatment with 400 mg/d of oral fluconazole for 9-month course was initiated. At the end of treatment, pulmonary lesions were improved on the follow-up CT.
호산구성 폐렴과 기관지염을 동반한 과호산구 증후군 (Hypereosinophilic syndrome) 1 례
최재선,김미경,박인원,김재열,이병훈,유지훈,지현석,최병휘,안창혁,신종욱,임성룡 대한알레르기학회 2001 천식 및 알레르기 Vol.21 No.4
Idiopathic hypereosinophilic syndrome is characterized by multiorgan involvement without any cause, and peripheral eosinophilia(1,500/μl) for more than 6 months. Clinically, many organs can be involved, but the heart is the most commonly involved organ. Although lung involvement is usual(20-30%)1) in hypereosinophilic syndrome, there are few reports of eosinophilic pneumonia proven by biopsy confirmation in Korea. We experienced a case of hypereosinophilic syndrome with eosinophilic pneumonia and bron- chitis confirmed by biopsy, and we report it here with a review of the literature.
( Byung Lae Park ),( Lyoung Hyo Kim ),( Yoo Hyun Choi ),( Hyun Sub Cheong ),( Hae Sim Park ),( Soo Jong Hong ),( Byoung Whui Choi ),( June Hyuk Lee ),( Soo Taek Uh ),( Choon Sik Park ),( Hyoung Doo Sh 생화학분자생물학회 2005 BMB Reports Vol.38 No.1
The monocyte chemotactic protein-3 (MCP3), on chromosome 17q11.2-q12, is a secreted chemokine, which attracts macrophages during inflammation and metastasis. In an effort to discover additional polymorphism(s) in genes whose variant(s) have been implicated in asthma, we scrutinized the genetic polymorphisms in MCP3 to evaluate it as a potential candidate gene for asthma host genetic study. By direct DNA sequencing in twenty-four individuals, we identified four sequence variants within the 3 kb full genome including 1,000bp promoter region of MCP3; one in promoter region (-420T>C), three in intron (+136C>G, +563C>T, +984G>A) respectively. The frequencies of those four SNPs were 0.020 (-420T>C), 0.038 (+I36C>G), 0.080 (+563C>T), 0.035 (+984G>A), respectively, in Korean population (n = 598). Haplotypes, their frequencies and linkage disequilibrium coefficients (ID^(7)I) between SNP pairs were estimated. The associations with the risk of asthma, skin-test reactivity and total serum IgE levels were analyzed. Using statistical analyses for association of MCP3 polymorphisms with asthma development and asthma-related phenotypes, no significant signals were detected. In conclusion, we identified four genetic polymorphisms in the important MCP3 gene, but no significant associations of MCP3 variants with asthma phenotypes were detected. MCP3 variation/haplotype information identified in this study will provide valuable information for future association studies of other allergic diseases.
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>
Park, Byung-Lae,Kim, Lyoung-Hyo,Choi, Yoo-Hyun,Cheong, Hyun-Sub,Park, Hae-Sim,Hong, Soo-Jong,Choi, Byoung-Whui,Lee, June-Hyuk,Uh, Soo-Taek,Park, Choon-Sik,Shin, Hyoung-Doo Korean Society for Biochemistry and Molecular Biol 2005 Journal of biochemistry and molecular biology Vol.38 No.1
The monocyte chemotactic protein-3 (MCP3), on chromosome 17q11.2-q12, is a secreted chemokine, which attracts macrophages during inflammation and metastasis. In an effort to discover additional polymorphism(s) in genes whose variant(s) have been implicated in asthma, we scrutinized the genetic polymorphisms in MCP3 to evaluate it as a potential candidate gene for asthma host genetic study. By direct DNA sequencing in twenty-four individuals, we identified four sequence variants within the 3 kb full genome including 1,000bp promoter region of MCP3; one in promoter region (-420T>C), three in intron (+136C>G, +563C>T, +984G>A) respectively. The frequencies of those four SNPs were 0.020 (-420T>C), 0.038 (+136C>G), 0.080 (+563C>T), 0.035 (+984G>A), respectively, in Korean population (n = 598). Haplotypes, their frequencies and linkage disequilibrium coefficients (|D'|) between SNP pairs were estimated. The associations with the risk of asthma, skin-test reactivity and total serum IgE levels were analyzed. Using statistical analyses for association of MCP3 polymorphisms with asthma development and asthma-related phenotypes, no significant signals were detected. In conclusion, we identified four genetic polymorphisms in the important MCP3 gene, but no significant associations of MCP3 variants with asthma phenotypes were detected. MCP3 variation/haplotype information identified in this study will provide valuable information for future association studies of other allergic diseases.