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Cheongju, South Korea

Lee Y.,Yonsei University | Kim C.-K.,Korean Institute of Tuberculosis | Lee H.,Catholic Kwandong University | Jeong S.H.,Yonsei University | And 2 more authors.
Antimicrobial Agents and Chemotherapy | Year: 2011

We investigated an outbreak caused by carbapenem-resistant Acinetobacter baumannii carrying the blaOXA-23 gene. A novel insertion sequence (IS), named ISAba10, was found to be inserted into the ISAba1 element preceding the blaOXA-23 gene in a group of isolates showing higher carbapenem MICs. The presence of ISAba10 was associated with increased OXA-23 expression, likely by providing additional promoter sequences. ISAba10 was also inserted into the carO outer membrane protein gene in most of these isolates. Copyright © 2011 American Society for Microbiology. All Rights Reserved. Source

Lee S.W.,Armed Forces Capital Hospital | Lee S.W.,University of Ulsan | Lee S.H.,Korean Institute of Tuberculosis | Yim J.-J.,Seoul National University
Infection | Year: 2012

Purpose: Interferon-gamma release assay (IGRA) results have been suggested as a surrogate marker of treatment response in latent tuberculosis infection (LTBI). However, data have not been consistent, and most previous studies focused on participants taking isoniazid prophylaxis. The aim of this study was to elucidate the changes in the IGRA results in patients who underwent chemoprophylaxis with isoniazid and rifampicin daily for 3 months. Methods: In a TB outbreak cohort, 26 asymptomatic close contacts with normal chest radiographs and positive QuantiFERON-TB Gold In-Tube assay (QFT-GIT) results were recruited. These patients were treated with isoniazid and rifampicin daily for 3 months. The QFT-GIT was repeated at 3 and 6 months following treatment initiation. Results: Compared with the initial QFT-GIT results (3.59 ± 3.39 IU/mL), the interferon-gamma (IFN-γ) levels had decreased significantly at 6 months (0.84 ± 1.14 IU/mL; P = 0.005), but not at 3 months (3.58 ± 3.64 IU/mL; P = 0.98). Reversions occurred in seven (26.9 %) patients at 3 months and in an additional two participants at 6 months; a total of nine participants (34.6 %) had reversions. Recent conversion was associated with reversion of the test results (odds ratio 26.3, 95 % confidence interval 3.04-226.6). Conclusion Chemoprophylaxis with isoniazid and rifam-picin generally decreased IFN-y levels among tuberculosis contacts. However, only a small portion of participants achieved reversion. © Springer-Verlag 2012. Source

Song Y.,Sungkyunkwan University | Seol J.-H.,Sungkyunkwan University | Yang J.-H.,Sungkyunkwan University | Kim H.-J.,Korean Institute of Tuberculosis | And 3 more authors.
Nucleic Acids Research | Year: 2013

The mammalian genome encodes multiple variants of histone H3 including H3.1/H3.2 and H3.3. In contrast to H3.1/H3.2, H3.3 is enriched in the actively transcribed euchromatin and the telomeric heterochromatins. However, the mechanism for H3.3 to incorporate into the different domains of chromatin is not known. Here, taking the advantage of well-defined transcription analysis system of yeast, we attempted to understand the molecular mechanism of selective deposition of human H3.3 into actively transcribed genes. We show that there are systemic H3 substrate-selection mechanisms operating even in yeasts, which encode a single type of H3. Yeast HIR complex mediated H3-specific recognition specificity for deposition of H3.3 in the transcribed genes. A critical component of this process was the H3 A-IG code composed of amino acids 87, 89 and 90. The preference toward H3.3 was completely lost when HIR subunits were absent and partially suppressed by human HIRA. Asf1 allows the influx of H3, regardless of H3 type. We propose that H3.3 is introduced into the active euchromatin by targeting the recycling pathway that is mediated by HIRA (or HIR), and this H3-selection mechanism is highly conserved through the evolution. These results also uncover an unexpected role of RI chaperones in evolution of variant H3s. © 2013 The Author(s) 2013. Source

Lee S.W.,Armed Forces Capital Hospital | Jang Y.S.,Three Armed Forces | Park C.M.,Seoul National University | Kang H.Y.,Korean Institute of Tuberculosis | And 3 more authors.
Chest | Year: 2010

Background: In TB outbreaks, detecting active cases is the key step in stopping transmission of the disease. The aim of this study was to evaluate the role of high-resolution CT (HRCT) scanning of the chest in the investigation of a TB outbreak that developed in a cohort of 92 soldiers in the South Korean army. Methods: Outbreak investigation, including tuberculin skin test (TST), QuantiFERON TB Gold In-Tube (QFT) test, and simple chest radiograph (CXR), was performed. For participants with any abnormal findings in these tests, HRCT scanning was done. Active pulmonary TB was diagnosed based on sputum studies or HRCT scan findings. In addition, participants with positive results in both TST and QFT were treated as having a latent TB infection (LTBI). TST and QFT were repeated in participants with a positive result in one of these tests. CXR was repeated in all participants at 3 and 6 months of follow-up. Results: Eighty-seven participants completed the study protocol. Among them, 18 active TB cases were diagnosed. Nine of these had normal CXR, but had lesions that were suggestive of active TB on HRCT scan. Twenty-two participants with normal HRCT scans and positive results with TST and QFT at initial investigation were treated as LTBI. Among 13 participants with normal CXR and positive results in either TST or QFT, nine completed a 3-month investigation. All but one of nine participants revealed positive results in both tests. Conclusion: Inclusion of HRCT scanning in the outbreak investigation of TB may be helpful in differentiating active TB from LTBI more reliably. Trial registration: clinicaltrials.gov; Identifier: NCT00889759. © 2010 American College of Chest Physicians. Source

Jnawali H.N.,Korean Institute of Tuberculosis | Hwang S.C.,Ajou University | Park Y.K.,Korean Institute of Tuberculosis | Kim H.,Korean Institute of Tuberculosis | And 4 more authors.
Diagnostic Microbiology and Infectious Disease | Year: 2013

In order to characterize molecular mechanisms of first- and second-line drug resistance in Mycobacterium tuberculosis and to evaluate the use of molecular markers of resistance, we analyzed 62 multidrug-resistant, 100 extensively drug-resistant, and 30 pan-susceptible isolates from Korean tuberculosis patients. Twelve genome regions associated with drug resistance, including katG, ahpC, and inhA promoter for isoniazid (INH); embB for ethambutol (EMB), rpoB for rifampin (RIF), pncA for pyrazinamide (PZA), gyrA for fluoroquinolones; rpsL, gidB, and rrs for streptomycin; rrs and eis for kanamycin (KM); rrs and tylA for capreomycin (CAP); and rrs for amikacin (AMK) were amplified simultaneously by polymerase chain reaction, and the DNA sequences were determined. We found mutations in 140 of 160 INH-resistant isolates (87.5%), 159 of 162 RIF-resistant isolates (98.15%), 127 of 143 EMB-resistant isolates (88.8%), 108 of 123 ofloxacin-resistant isolates (87.8%), and 107 of 122 PZA-resistant isolates (87.7%); 43 of 51 STM-resistant isolates (84.3%), 15 of 17 KM-resistant isolates (88.2%), and 14 of 15 (AMK and CAP)-resistant isolates (93.3%) had mutations related to specific drug resistance. In addition, the sequence analyses of the study revealed many novel mutations involving these loci. This result suggests that mutations in the rpoB531, katGSer315Thr, and C-15T in the inhA promoter region, and gyrA94, embB306, pncA159, rpsL43, and A1401G in the rrs gene could serve as useful markers for rapid detection of resistance profile in the clinical isolates of M. tuberculosis in Korea, with potentials for the new therapeutic benefits in actual clinical practice. © 2013 Elsevier Inc. Source

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