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Ye An Kim,Ji Won Yoon,Young Lee,최혁진,Jae Won Yun,Eunsin Bae,Seung-Hyun Kwon,So Eun Ahn,Ah-Ra Do,Heejin Jin,Sungho Won,Do Joon Park,Chan Soo Shin,서제현 대한내분비학회 2021 Endocrinology and metabolism Vol.36 No.6
Background: Epidemiological data have shown that vitamin D deficiency is highly prevalent in Korea. Genetic factors influencing vitamin D deficiency in humans have been studied in Europe but are less known in East Asian countries, including Korea. We aimed to investigate the genetic factors related to vitamin D levels in Korean people using a genome-wide association study (GWAS). Methods: We included 12,642 subjects from three different genetic cohorts consisting of Korean participants. The GWAS was performed on 7,590 individuals using linear or logistic regression meta- and mega-analyses. After identifying significant single nucleotide polymorphisms (SNPs), we calculated heritability and performed replication and rare variant analyses. In addition, expression quantitative trait locus (eQTL) analysis for significant SNPs was performed. Results: rs12803256, in the actin epsilon 1, pseudogene (ACTE1P) gene, was identified as a novel polymorphism associated with vitamin D deficiency. SNPs, such as rs11723621 and rs7041, in the group-specific component gene (GC) and rs11023332 in the phosphodiesterase 3B (PDE3B) gene were significantly associated with vitamin D deficiency in both meta- and mega-analyses. The SNP heritability of the vitamin D concentration was estimated to be 7.23%. eQTL analysis for rs12803256 for the genes related to vitamin D metabolism, including glutamine-dependent NAD(+) synthetase (NADSYN1) and 7-dehydrocholesterol reductase (DHCR7), showed significantly different expression according to alleles. Conclusion: The genetic factors underlying vitamin D deficiency in Korea included polymorphisms in the GC, PDE3B, NADSYN1, and ACTE1P genes. The biological mechanism of a non-coding SNP (rs12803256) for DHCR7/NADSYN1 on vitamin D concentrations is unclear, warranting further investigations.
Novel pendrin inhibitor attenuates lipopolysaccharide-induced acute lung injury in mice
( Eun Hye Lee ),( Jae Young Choi ),( Mi Hwa Shin ),( Wan Namkung ),( Ji Soo Choi ),( Su Hwan Lee ),( Ah Young Leem ),( Sang Hoon Lee ),( Kyung Soo Chung ),( Song Yee Kim ),( Ji Ye Jung ),( Young Ae Ka 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.0
Background: Pendrin is encoded by SLC26A4 and its mutation leads to congenital hearing loss. Additionally, pendrin is up-regulated in inflammatory airway diseases such as chronic obstructive pulmonary disease, allergic rhinitis, and asthma. In this study, the effects of a novel pendrin inhibitor, YS-01, were investigated in an LPS-induced acute lung injury (ALI) mice model, and the mechanism underlying the effect of YS-01 was examined. Methods: LPS (10 mg/kg) was intranasally instilled in wild type (WT) and pendrin-null mice. Lung injury parameters were assessed in the lung tissue and bronchoalveolar lavage fluid (BALF). Pendrin levels in the BALF of 41 pneumonia/ARDS patients and 25 control (solitary pulmonary nodule) patients were also measured. Results: LPS instillation induced lung injury in WT mice but not in pendrin-null mice. YS-01 treatment dramatically attenuated lung injury and reduced BALF cell counts and protein concentration after LPS instillation in WT mice. Proinflammatory cytokines and NF-κB activation were suppressed by YS-01 treatment in LPS-induced ALI mice. However, the protective effects of pendrin inhibitor lost after SCN- instillation. Furthermore, pendrin expression was upregulated in pneumonia/ARDS patient compared to that in control patient BALF (mean, 24.86 vs. 6.83 ng/mL, p < 0.001). Conclusions: A novel Pendrin inhibitor, YS-01, suppressed lung injury in LPS-induced ALI mice and our data provide a new strategy for the treatment of inflammatory airway diseases including sepsis-induced ALI.
( Eun Kyong Goag ),( Ah Young Leem ),( Song Yee Kim ),( Joo Han Song ),( Kyung Soo Chung ),( Ji Ye Jung ),( Moo Suk Park ),( Young Sam Kim ),( Se Kyu Kim ),( Joon Chang ),( Eun Young Kim ) 대한결핵 및 호흡기학회 2016 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.121 No.-
Background: The EGFR mutation T790M is reported in approximately 50% of NSCLC patients with acquired resistance to EGFR-TKI. Recently, its assessment become more important because the 3rd generation EGFR-TKIs targeting T790M mutant NSCLC are developed and become available in the real world. We aim to investigate the feasibility of bronchoscopy as rebiopsy tool and prevalence of T790M mutations after failure of EGFR-TKI. Methods: We investigated 139 patients who had undergone rebiopsy by flexible bronchoscopy (endobronchial biopsy and transbronchial biopsy) and EBUS-TBNA between Sep 2014 and Jul 2016. Results: Of 139 patients, 102(73.4%) were pathologically diagnosed successfully by bronchoscopic rebiopsy. The most common method used for rebiopsy was transbronchial biopsy(41.5%). The EBUS-TBNA and endobronchial biopsy were used in 26.8% and 19.5%. Among them, we selected a total of 41 EGFR-mutant lung adenocarcinoma patients, who had a history of acquired resistance to EGFR-TKI and available tumor tissue for reassessment of EGFR mutations at rebiopsy. Median duration of EGFR-TKI treatment was 10.0 months. Initial EGFR mutation was E19 del(56.1%), L858R or L861Q(34.1%), and others. The T790M mutation was identified in 18(43.9%) patients. The E19 del was most significant factors for T790M development( p=0.002). There was no significant difference in the incidence of T790M according to the type of EGFR-TKI. Conclusion: Bronchoscopic biopsy is feasible for rebiopsy after failure of EGFR-TKI. The T790M mutation is more frequently induced with E19 deletion than L858R and others.
( Eun Hye Lee ),( Eun Young Kim ),( Yun Ho Roh ),( Ah Young Leem ),( Joo Han Song ),( Song Yee Kim ),( Kyung Soo Chung ),( Ji Ye Jung ),( Young Ae Kang ),( Young Sam Kim ),( Joon Chang ),( Moo Suk Par 대한결핵 및 호흡기학회 2017 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.124 No.0
Background: Solid malignancies are associated with the development of Pneumocystis jirovecii pneumonia (PJP). This study aimed to evaluate the risk factors for PJP among patients with lung cancer. Methods: This retrospective case-control study compared patients who had lung cancer with PJP (n = 112) or without PJP (n = 336) at Severance Hospital between January 2013 and December 2016. The patients were matched according to age, sex, histopathology, and stage. PJP was considered present when the patient had (i) positive PCR or direct immunofluorescence results for pneumocystis, (ii) clinical symptoms and radiological abnormalities that were consistent with a pneumonic process, and (iii) received targeted PJP treatment. Results: The development of PJP was associated with radiotherapy (RTx), concurrent chemoradiotherapy (CCRTx), lymphopenia, and prolonged high-dose steroid therapy (20 mg of prednisolone equivalent per day for ≥3 weeks). Multivariate analysis revealed independent associations with prolonged high-dose steroid therapy (odds ratio [OR]: 2.02, 95% confidence interval [CI]: 1.07-3.80; p=0.029) and CCRTx (OR: 1.77, 95% CI: 0.99-3.16; p=0.054). Steroid use was frequently related to RTx pneumonitis or esophagitis (29 patients, 43.3%) and cancer infiltration symptoms (24 patients, 35.8%). Sixty-nine of the 112 patients with PJP (61.6%) died during their PJP treatment. Conclusion: Prolonged high-dose steroid therapy and CCRTx were risk factors for PJP development among patients with lung cancer. Clinicians should consider PJP prophylaxis for those high-risk patients.
Eun Jung Thak,Dong-Jik Lee,Hyunah Kim,Ye Ji Son,Jung Ho Kim,Su-Bin Lee,Yong-Sun Bahn,Hyun Ah Kang 한국당과학회 2021 한국당과학회 학술대회 Vol.2021 No.01
The human fungal pathogen Cryptococcus neoformans assembles N-/O-linked glycans on its proteins in two types with and without xylose (1, 2). In this study, the CAP6 gene, encoding an α1,3-mannosyltransferase responsible for the second mannose addition to the minor O-glycans with xylose, was identified and functionally analyzed. The CAP6 deletion in the ktr3Δ strain, in which the α1,2-mannose addition to the major O-glycans is defected, resulted in almost complete blockage of O-glycan extension. Notably, the putative two cell surface sensor proteins, Wml (Wsc/Mid2-Like)1p and Wml2p, were shown to be subjected to minor and major O-mannosylation by Cap6 and Ktr3, respectively. The proteins levels of Wml1 and Wml2 were remarkably decreased in the ktr3Δ cap6Δ mutant, indicating that proper O-mannosylation is essential for their stability. The phosphorylation of Mpk1, induced by tunicamycin, was greatly decreased in the ktr3Δcap6Δ and the wml1Δwml2Δ, supporting an essential role of O-glycans on cell surface sensors in cell wall integrity signaling. As reflecting its defective growth under several stress conditions, the ktr3Δcap6Δ strain showed fully attenuated virulence in a mouse model of cryptococcosis. The delineation of the roles of protein glycosylation in fungal pathogenesis will not only provide a deep insight into the glycan-based fungal infection mechanism but also aid in the development of novel antifungal agents.
( Eun Hye Lee ),( Mi Hwa Shin ),( Jong-min Park ),( Sang-guk Lee ),( Nam Su Ku ),( Ah Young Leem ),( Sang Hoon Lee ),( Joo Han Song ),( Song Yee Kim ),( Kyung Soo Chung ),( Ji Ye Jung ),( Young Ae Kan 대한결핵 및 호흡기학회 2018 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.126 No.-
Purpose: Sepsis remains a critical problem worldwide and one of the main causes of death in intensive care units (ICU). We investigated plasma lysophosphatidylcholine (LPC) 16:0 level using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) in ICU sepsis patients. Methods: Patients admitted medical ICU were prospectively enrolled from March 2017 through June 2018 at Severance Hospital. The inclusion criteria for the study were a fulfillment of at least 2 criteria of systemic inflammatory response syndrome (SIRS) or presence of sepsis. The definition of sepsis followed the revised sepsis 3-definition. Results: Of the 120 enrolled patients, 15 patients were non-infectious SIRS, 37 patients were classified as sepsis and 68 were septic shock. Of these 105 patients who meet the sepsis diagnostic criteria, 70 patients survived and 35 patients were dead at 28-day. Mean plasma LPC concentration (μmol/L) of septic shock patients was significantly lower than those of non-infectious SIRS (26.55 vs. 70.65, p<0.001) and sepsis patients (26.55 vs. 48.50, p<0.01). The area under the curve (AUC) predicting 28-day mortality of ΔLPC16:0 (D7-D0) was 0.792 that was higher than APACHE II score (AUC;0.694) and SOFA score (AUC;0.678). In the multivariate analysis, LPC16:0 change less than cut-off value (Δ LPC16:0 (D7-D0) ≤14.859; HR, 5.467) were associated with increased 28-day mortality. Conclusion: Our results indicate that Δ LPC16:0 in sepsis patients using MALDI-TOF MS could help to better predict prognosis and mortality of sepsis patients in ICU.
The change of serum inflammatory markers and cytokines following anti-tuberculosis drug therapy.
( Eun Hye Lee ),( Ah Young Leem ),( Joo Han Song ),( Song Yee Kim ),( Kyung Soo Chung ),( Eun Young Kim ),( Ji Ye Jung ),( Moo Suk Park ),( Young Sam Kim ),( Se Kyu Kim ),( Joon Chang ),( Young Ae Kan 대한내과학회 2015 대한내과학회 추계학술대회 Vol.2015 No.1
Introduction: Active pulmonary tuberculosis (TB) is associated with cell-mediated immunity. Multiple cytokines and inflammatory markers are known to have roles in control TB infection. In this study, we aimed to investigate the change of multiple cytokines and inflammatory markers in active TB patients following anti-TB drug therapy. Methods: Patients with active TB were prospectively recruited between December 2010 and February 2013 at Severance Hospital, in Seoul, South Korea. Treatment was based on the standard regimen of rifampicin (10 mg/kg body weight [BW]/day), isoniazid( 5 mg/kg BW/day), ethambutol (15-25 mg/kg BW/day),and pyrazinamide (15-30 mg/kg BW/day). Blood samples were collected from active TB patients (total n=18) at before (T0), after 2 months (T2), and after 6 months (T6) of anti-TB treatment. We measured the levels of IFN-γ, IL-2, IL-12, IL-10, IL-13, and TNF-αin the supernatant from the QuantiFERON-TB Gold In-Tube assay (QFT-GIT) and WBC count, neutrophil count, lymphocyte count, platelet count, red cell distribution width (RDW), mean platelet volume(MPV), neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR). Results: Compared to baseline levels, IL-10, TNF-α in the supernatant from QFT-GIT, WBC count, neutrophil count, platelet count were produced in significantly lower amounts in response to the treatment. As for IFN-γ, IL-2, IL-12, IL-13 responses, the decrease of median values were not statistically significant. Also the results showed that the IL-10/ IFN-γ ratio of supernatant of QFT-GIT and neutrophil to lymphocyte ratio (NLR)after treatment significantly decreased compared to the baseline, whereas the IL-2/ IFN-γ ratio of supernatant of QFT-GIT increased after treatment. Conclusions: In conclusion, IL-10, TNF-αin the supernatant from QFT-GIT, WBC count, neutrophil count, platelet count decreased following anti-TB drug therapy. And also the IL-2/IFN-γ ratio, IL-10/IFN-γ ratio of supernatant of QFT-GIT, neutrophil to lymphocyte ratio (NLR) may be used as biomarkers to evaluate the effectiveness of drug therapy in active TB patients.