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Outcomes of <i>Mycobacterium avium</i> complex lung disease based on clinical phenotype
Koh, Won-Jung,Moon, Seong Mi,Kim, Su-Young,Woo, Min-Ah,Kim, Seonwoo,Jhun, Byung Woo,Park, Hye Yun,Jeon, Kyeongman,Huh, Hee ,Jae,Ki, Chang-Seok,Lee, Nam Yong,Chung, Myung Jin,Lee, Kyung ,Soo,Sh ERS Journals Ltd 2017 The European respiratory journal Vol.50 No.3
<P>Treatment outcomes and redevelopment of NTM lung disease after treatment completion differed by clinical phenotype of MAC lung disease.</P>
Moon, Seong Mi,Jhun, Byung Woo,Daley, Charles L.,Koh, Won-Jung ERS Journals Ltd 2019 The European respiratory journal Vol.53 No.5
<P>The incidence and prevalence of nontuberculous mycobacterial pulmonary disease (NTM-PD) is increasing worldwide [1, 2]. NTM-PD treatment is challenging due to long-term, multiple antibiotic therapy and poor treatment outcomes [3, 4]. Standardised treatment outcome definitions for NTM-PD were recently reported in the Nontuberculous Mycobacteria Network European Trials Group (NTM-NET) consensus statement [5], and are an important development for patient management and clinical research [5].</P>
Kim, Cheon Tae,Kim, Tae-Ok,Shin, Hong-Joon,Ko, Young Chun,Hun ,Choe, Yeong,Kim, Hak-Ryul,Kwon, Yong-Soo ERS Journals Ltd 2018 The European respiratory journal Vol.51 No.3
<P>Bedaquiline and delamanid were effective and safe for treating MDR-TB, with initial evidence of sequential administration of these two drugs as a viable treatment strategy for patients when an adequate treatment regimen cannot be constructed.</P>
Acute exacerbation of idiopathic pulmonary fibrosis associated with air pollution exposure
Johannson, Kerri A.,Vittinghoff, Eric,Lee, Kiyoung,Balmes, John R.,Ji, Wonjun,Kaplan, Gilaad G.,Kim, Dong Soon,Collard, Harold R. ERS Journals Ltd 2014 The European respiratory journal Vol.43 No.4
<P>Acute exacerbations of idiopathic pulmonary fibrosis are associated with high mortality and are of unknown cause. The effect of air pollution on exacerbations of interstitial lung disease is unknown. This study aims to define the association of air pollution exposure with acute exacerbation of idiopathic pulmonary fibrosis.</P><P>Patients with idiopathic pulmonary fibrosis and corresponding air pollution data were identified from a longitudinal cohort. Air pollution exposures were assigned to each patient for ozone, nitrogen dioxide, particulate matter, sulfur dioxide and carbon monoxide based on geo-coded residential addresses. Cox proportional hazards models were used to estimate the association of air pollution exposures and acute exacerbations.</P><P>Acute exacerbation was significantly associated with antecedent 6-week increases in mean level, maximum level and number of exceedances above accepted standards of ozone (hazard ratio (HR) 1.57, 95% CI 1.09–2.24; HR 1.42, 95% CI 1.11–1.82; and HR 1.51, 95% CI 1.17–1.94, respectively) and nitrogen dioxide (HR 1.41, 95% CI 1.04–1.91; HR 1.27, 95% CI 1.01–1.59; and HR 1.20, 95% CI 1.10–1.31, respectively).</P><P>Increased ozone and nitrogen dioxide exposure over the preceding 6 weeks was associated with an increased risk of acute exacerbation of idiopathic pulmonary fibrosis, suggesting that air pollution may contribute to the development of this clinically meaningful event.</P>
Identification of asthma clusters in two independent Korean adult asthma cohorts
Kim, Tae-Bum,Jang, An-Soo,Kwon, Hyouk-Soo,Park, Jong-Sook,Chang, Yoon-Seok,Cho, Sang-Heon,Choi, Byoung Whui,Park, Jung-Won,Nam, Dong-Ho,Yoon, Ho-Joo,Cho, Young-Joo,Moon, Hee-Bom,Cho, You Sook,Park, Ch ERS Journals Ltd 2013 The European respiratory journal Vol.41 No.6
<P>Asthma is a heterogeneous airway disease with various clinical phenotypes. It is crucial to clearly identify clinical phenotypes to achieve better asthma management.</P><P>We used cluster analysis to classify the clinical groups of 724 asthmatic patients from the Cohort for Reality and Evolution of Adult Asthma in Korea (COREA), and in 1843 subjects from another independent Korean asthma cohort of Soonchunhyang University Asthma Genome Research Centre (SCH) (Bucheon, Republic of Korea). Hierarchical cluster analysis was performed by Ward's method, followed by κ-means cluster analysis.</P><P>Cluster analysis of the COREA cohort indicated four asthma subtypes: 1) smoking asthma; 2) severe obstructive asthma; 3) early-onset atopic asthma; and 4) late-onset mild asthma. An independent cluster analysis of the SCH cohort also indicated four clusters that were similar to the COREA clusters.</P><P>Our results indicate that adult Korean asthma patients can be classified into four distinct clusters.</P>
Lee, Sang-Nam,Lee, Da-Hyung,Sohn, Myung Hyun,Yoon, Joo-Heon ERS Journals Ltd 2013 The European respiratory journal Vol.42 No.5
<P>The proprotein convertases (PCs) are serine proteases responsible for the proteolytic maturation of many precursor proteins involved in upper airway remodelling during nasal polyposis. We have previously found that PC1/3 is expressed in human nasal mucosa. However, whether PC1/3 is related to nasal polyp formation has not been investigated. To gain insight into the functional role of PC1/3 in nasal polyps, we determined PC1/3 expression in nasal polyps by immunostaining, Western blotting and enzyme assays and generated stable cells expressing PC1/3 using airway epithelial cell line NCI-H292. Nasal polyps exhibit increased PC1/3 expression compared to normal nasal mucosa. PC1/3 was expressed in neuroendocrine cells in normal nasal mucosa and it was also expressed in goblet and ciliated cells in nasal polyps. NCI-H292 cells stably expressing PC1/3 displayed morphological changes, enhanced cell proliferation and migration, downregulation of E-cadherin and cytokeratins and upregulation of N-cadherin, vimentin, matrix metalloproteinase-2, collagen-I, snail and twist. Importantly, PC1/3 expression was positively correlated with epithelial-mesenchymal transition in cultured human nasal epithelial cells and in nasal polyps. Taken together, our data suggest that PC1/3 overexpression induces morphological and phenotypic epithelial-mesenchymal transition changes of airway epithelial cells and these changes may contribute to the pathogenesis of nasal polyps.</P>
Lee, Chang Seok,Yi, Eun Hee,Lee, Jin-Ku,Won, Cheolhee,Lee, Young Ju,Shin, Min Kyung,Yang, Young Mok,Chung, Myung-Hee,Lee, Jung Weon,Sung, Sang-Hyun,Ye, Sang-Kyu ERS Journals Ltd 2013 The European respiratory journal Vol.41 No.5
<P>Recently, statins have been shown to have anti-inflammatory effects on lung inflammatory diseases. However, the mechanisms of action of simvastatin in viral pneumonia have yet to be elucidated, although viral infection remains a considerable health threat. In this study, we hypothesised that simvastatin inhibits polyinosinic–polycytidylic acid (poly I:C)-induced airway inflammation, such as RANTES (regulated on activation, normal T-cell expressed and secreted) expression and inflammatory cell recruitment.</P><P>In bronchial cells, the effect of simvastatin on poly I:C-induced RANTES expression and signal transducer and activator of transcription (STAT)3-mediated signal transduction was determined using an ELISA and short hairpin (sh)RNA system. In a poly I:C-induced pneumonia mouse model, immunological changes in the lungs after simvastatin inhalation, such as inflammatory cell recruitment and cytokine/chemokine release, were examined.</P><P>In poly I:C-stimulated bronchial cells, RANTES secretion was increased by STAT3 activation, and simvastatin suppressed poly I:C-induced STAT3 activation, resulting in inhibition of RANTES expression. In BALB/c mice stimulated with inhaled poly I:C, RANTES expression and neutrophil infiltration into the airway were elevated. However, simvastatin treatment attenuated STAT3 activation, RANTES release and subsequent neutrophilia in the lungs.</P><P>These findings suggest that simvastatin inhibits airway inflammation, but there are other mechanisms that need to be fully elucidated.</P>