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반대측 비기능성 선종을 동반한 기능성 부신 선종에 의한 쿠싱 증후군 1예
경선영,한혜숙,윤효중,황용하,서찬종,정연실,김홍규,박혜영,김형식,이정남,하승연,강문호 대한내분비학회 2002 Endocrinology and metabolism Vol.17 No.2
We report the case of a 43-year-old woman with Cushing‘s syndrome showing bilateral adrenococortical adenomas. We performed bilateral selective adrenal vein samplings. Hypersecretion of cortisol on the left sided adrenal tumor was observed, but no evidence of cortisol hypersecretion from the adrenal tumor on the right side was observed. The left adrenal tumor was resected selectively, but the right adrenal gland was reserved. The left adrenal tumor was histologically diagnosed as a adrenal adenoma without any evidence of nodular hyperplasia. Following the resection of the left adrenal gland, no cortisol hypersecretion from the remaining adrenal tumor on the right side was observed until now, suggesting that a selective adrenalectomy of functioning adenoma may be an acceptable treatment modality
P-123 Particulate matter deteriorates CSE-induced inflammation in bronchial epithelial cells
경선영,손은숙,홍정희,박정웅,정성환 대한결핵 및 호흡기학회 2017 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.124 No.-
Particulate matter (PM) is air pollution that induces adverse health effects in several organs, including the lungs. Epidemiologic evidence has shown an association between the concentration of PM and exacerbation of pulmonary diseases. We hypothesized that co-exposure to PM and cigarette smoke extract (CSE) may exacerbate the cellular toxicity and inflammation of bronchial epithelial cells. Human bronchial epithelial cells (BEAS-2B cells) cultured with or without 1-5% CSE for 7 days were exposed with or without each concentration of PM for 1 day. Inflammatory cytokines and mitogen-activated protein kinase (MAPK) pathways were evaluated by enzyme-linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction (RT-PCR) or Western blot assay in the control, CSE, and CSE/PM groups. The inflammatory cytokines interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, chemokine (C-X-C motif) ligand 1, cyclooxygenase-2 and inducible nitric oxide synthase showed increased levels in CSE/PM-exposed cells compared with those in control or CSE-exposed cells. MAPK pathway evaluation via Western blotting revealed that ERK and P38 showed increased phosphorylation in CSE/PM-exposed cells. The inflammatory upregulation induced by CSE/PM exposure was attenuated significantly when cells were pre-treated with chemical inhibitors of ERK or p38.These results suggest that PM exacerbates inflammation in CSE-exposed bronchial epithelial cells through MAPK activation, such as ERK and p38 phosphorylation, leading to the production of inflammatory cytokines.
경선영,손은숙,김세희,김유진,박정웅,정성환 대한결핵 및 호흡기학회 2018 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.126 No.-
Particulate matter (PM) is air pollution that induces adverse health effects including acute exacerbation of chronic obstructive pulmonary disease (COPD). In previous study, we confirmed that co-exposure to PM and cigarette smoke extract (CSE) may exacerbate the oxidative stress and inflammation of bronchial epithelial cells. The aim of this study is investigated whether or not the antioxidants such as sulforaphane (SFN) or sulforaphane N-acetyl-L-cysteine (SFNAC) has inhibitory effects on oxidative stress and inflammation in CSE/PM co-exposed human bronchial epithelial cells (Beas 2B). The results, SFN or SFNAC were showed to inhibit oxidative stress by the significant reduction of reactive oxygen species (ROS) generation. SFN or SFN inhibited the production of pro-inflammatory cytokines (IL-6 and IL-8) by downregulation the CSE/PM-induced inflammatory mediators. The Nrf2 transcriptional activity in the nucleus was significantly increased, but phosphorylated ERK and JNK MAPK were decreased by SFN or SFNAC treated. In conclusion, SFN or SFNAC attenuated CSE/PM-induced epithelial toxicity through inhibition of oxidative stress and inflammation via MAPK signaling, as well as suppression of intracellular ROS property via activating antioxidant enzyme and Nrf2 signaling. Treatment with antioxidants may be considered for potential therapeutic trials in exacerbation of pulmonary disease such as COPD caused by air pollution such as PM.
P-59 미세먼지로 인한 건강피해 최소화 중재방안: 만성폐쇄성폐질환 환자에서 N95마스크착용의 안전성 연구
경선영,황현중,김유진,강신명,박정웅,정성환 대한결핵 및 호흡기학회 2016 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.121 No.0
미세먼지 또는 황사가 발생하면 외출 시 마스크를 착용하도록 권고하고 있으나 호흡기능이 저하된 만성폐쇄성폐질환자들이 마스크를 착용하고 실외활동을 하는 것에 대한 안전성과 유효성이 입증되지 않았다. 이에 본 연구자들은 만성폐쇄성폐질환(COPD) 환자들을 대상으로 미세먼지 발생 시 건강피해 예방효과가 있는 N95 마스크를 착용한 후 안정 시 또는 운동 시 활력징후를 비롯한 호흡지표들을 조사하여 환자들이 미세먼지 발생 시 마스크를 착용하는 것이 안전한 지 확인하고자 하였다. 전향적 연구로 COPD로 진단받고 외래에서 치료 중이고, 주거주지가 인천시인 환자를 대상으로 하였으며, 호흡부전이 심하여 자력으로 외출 또는 거동이 불가능한 대상자는 제외하였다. 대상자들의 폐기능, 호흡곤란 증상 점수 (MMRC, CAT)를 조사하였고, 마스크 (3M 9210) 착용 전 후로 안정 시 및 6분도보검사 시 혈압, 맥박수, 호흡수, 산소포화도 (SaO2), 호기말 이산화탄소 분압 (ETCO2)을 측정하였다. 또한 마스크 착용 중 대상자들이 호소하는 주요 증상을 조사하였다. 총 97명의 환자가 연구에 참여하였으며, 90명은 마스크 착용 후 안정 시 또는 운동 시 유의한 문제가 없었으나 7명이 마스크 착용 후 호흡곤란 및 SaO2 저하 또는 ETCO2 상승이 있어 마스크를 벗어야 했다. 마스크 착용에 실패한 환자들은 성공한 환자들에 비해 유의하게 MMRC 점수와 CAT점수가 높았고, 기저 폐기능 (FEV1, FVC, FEV1/FVC)과 안정 시 산소포화도가 낮았다. 다변량로지스틱회귀분석 결과 MMRC 점수가 마스크 실패 위험도를 가장 잘 예측하는 위험인자로 나타났으며, MMRC 점수 1점씩 오를 때마다 마스크 착용 실패 위험도는 12.5배 높아졌다. MMRC 점수가 높은 (특히 3점 이상) COPD 환자들은 미세먼지 발생 시 N95 마스크를 착용하고 외출하는 것이 오히려 위험할 수 있으므로 착용 권고 시 신중해야할 것으로 생각된다.
경선영,김유진,손은숙,정성환,박정웅 대한결핵및호흡기학회 2018 Tuberculosis and Respiratory Diseases Vol.81 No.2
Background: Recent studies show that mitophagy, the autophagy-dependent turnover of mitochondria, mediates pulmonary epithelial cell death in response to cigarette smoke extract (CSE) exposure and contributes to the development of emphysema in vivo during chronic cigarette smoke (CS) exposure, although the underlying mechanisms remain unclear. Methods: In this study, we investigated the role of mitophagy in the regulation of CSE-exposed lung bronchial epithelial cell (Beas-2B) death. We also investigated the role of a phosphodiesterase 4 inhibitor, roflumilast, in CSE-induced mitophagy-dependent cell death. Results: Our results demonstrated that CSE induces mitophagy in Beas-2B cells through mitochondrial dysfunction and increased the expression levels of the mitophagy regulator protein, PTEN-induced putative kinase-1 (PINK1), and the mitochondrial fission protein, dynamin-1-like protein (DRP1). CSE-induced epithelial cell death was significantly increased in Beas-2B cells exposed to CSE but was decreased by small interfering RNA-dependent knockdown of DRP1. Treatment with roflumilast in Beas-2B cells inhibited CSE-induced mitochondrial dysfunction and mitophagy by inhibiting the expression of phospho-DRP1 and -PINK1. Roflumilast protected against cell death and increased cell viability, as determined by the lactate dehydrogenase release test and the MTT assay, respectively, in Beas-2B cells exposed to CSE. Conclusion: These findings suggest that roflumilast plays a protective role in CS-induced mitophagy-dependent cell death.