http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
( Hye Yun Park ),( Hyun Lee ),( Danbee Kang ),( Chin Kook Rhee ),( Juhee Cho ),( Kwang Ha Yoo ) 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.-
Background: COPD is characterized by persistent respiratory symptoms and airflow limitation but, the clinical presentations of COPD appear to be substantially different by ethnicity. This study aims to characterize profiles of COPD patients with smoking history in different ethnic group. Methods: COPD patients aged 45 or older with at least 10 pack-year smoking history from The Korean COPD Subtype Study (KOCOSS) (n=1,772) and The Genetic Epidemiology of COPD (COPDGene) Study (3,461 non-Hispanic whites (NHW) and 1,016 African Americans (AA)) were analyzed to compare the clinical characteristics by race. Results: Koreans were older (69.6 years) than NHW and AA (64.3 and 58.6 years, respectively) and had higher prevalence of males (97.2%) than NHW and AA (56.3% and 54.6%, p <0.01). The prevalence of current-smokers was highest among AA (65.6%), followed by NHW (36.9%), and Koreans (27.9%, p <0.01). The average body mass index (BMI) of NHW and AA was similar (27.9 kg/m2 for both), but Koreans had significantly lower BMI (22.4 kg/m2, p < 0.01). The proportion of subjects with cough and phlegm >3 months in the previous year were higher in NHW (42.9% and 39.4%, respectively) than AA (36.2% and 36%, respectively) and Koreans (21.4% and 30.8%, respectively, p <0.01 for both). The mean St. George’s Respiratory Questionnaire (SGRQ) total score was highest among AA (40.1±24.2), followed by NHW (35.9±22.4), and Koreans (35.3±21.0, p <0.01). Conclusions: Clinical profiles varied significantly by race among COPD patients with smoking history. Different strategies may be required for the optimal management of COPD in different race.
COPD and lung cancer incidence in never smokers: A cohort study
( Sun Hye Shin ),( Hye Yun Park ),( Danbee Kang ),( Kwang Ha Yoo ),( Chin Kook Rhee ),( Gee Young Suh ),( Hojoong Kim ),( Young Mog Shim ),( Juhee Cho ),( O Jung Kwon ) 대한결핵 및 호흡기학회 2019 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.127 No.-
There has been limited evidence for the association between COPD and incidence of lung cancer among never smokers. We aimed to estimate the risk of lung cancer incidence in never smokers with COPD, and to compare it with the risk associated with smoking. Cohort study of 338,548 subjects 40 to 84 years of age with no history of lung cancer at baseline enrolled in the National Health Insurance Service National Sample Cohort. During 2,355,005 personyears of follow-up (median follow-up 7.0 years), 1,834 participants developed lung cancer. Compared to never smokers without COPD, the fully-adjusted hazard ratios for lung cancer in never smokers with COPD, ever smokers without COPD, and ever smokers with COPD were 2.67, 1.97, and 6.19, respectively. In this large national cohort study, COPD was also a strong independent risk factor for lung cancer incidence in never smokers, implying that COPD patients are at high risk of lung cancer, irrespective smoking status.
Glatiramer acetate 투여에 의한 자가면역성 뇌척수염 마우스의 중추신경계에서의 NFκB 활성 억제
황인선,하단비,김대승,주해진,지영흔,Hwang, Insun,Ha, Danbee,Kim, Dae Seung,Joo, Haejin,Jee, Youngheun 대한수의학회 2011 大韓獸醫學會誌 Vol.51 No.3
Glatiramer acetate (GA; Copaxone) has been shown to be effective in preventing and suppressing experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). It has been recently shown that GA-reactive T cells migrate through the blood-brain barrier, accumulate in the central nervous system (CNS), secrete antiinflammatory cytokines and suppress production of proinflammatory cytokines of EAE and MS. Development of EAE requires coordinated expression of a number of genes involved in the activation and effector functions of inflammatory cells. Activation of inflammatory cells is regulated at the transcriptional level by several families of transcription factors. One of these is the nuclear factor kappa B ($NF{\kappa}B$) family which is present in a variety of cell types and involved in the activation of immune-relative genes during inflammatory process. Since it is highly activated at site of inflammation, $NF{\kappa}B$ activation is also implicated in the pathogenesis of EAE. In this study, we examined whether the inhibition of $NF{\kappa}B$ activation induced by GA can have suppressive therapeutic effects in EAE mice. We observed the expression of $NF{\kappa}B$ and phospho-$I{\kappa}B$ proteins increased in GA-treated EAE mice compared to EAE control groups. The immunoreactivity in inflammatory cells and glial cells of $NF{\kappa}B$ and phospho-$I{\kappa}B$ significantly decreased at the GA-treated EAE mice. These results suggest that treatment of GA in EAE inhibits the activation of $NF{\kappa}B$ and phophorylation of $I{\kappa}B$ in the CNS. Subsequently, the inhibition of $NF{\kappa}B$ activation and $I{\kappa}B$ phosphorylation leads to the anti-inflammatory effects thereby to reduce the progression and severity of EAE.
C57BL/6 마우스에서 Retroviral 벡터를 이용한 Foxp3 유전자의 도입에 의한 Foxp3 단백의 발현 양상
황인선,하단비,빙소진,전경익,안긴내,김대승,조진희,임재학,임신혁,황규계,지영흔,Hwang, Insun,Ha, Danbee,Bing, So Jin,Jeon, Kyong-Leek,Ahn, Ginnae,Kim, Dae Seung,Cho, Jinhee,Lim, Jaehak,Im, Sin-Hyeog,Hwang, Kyu-Kye,Jee, Youngheun 대한수의학회 2012 大韓獸醫學會誌 Vol.52 No.3
The maintenance of peripheral immune tolerance and prevention of chronic inflammation and autoimmune disease require $CD4^{+}CD25^{+}$ T cells (regulatory T cells). The transcription factor Foxp3 is essential for the development of functional, regulatory T cells, which plays a prominent role in self-tolerance. Retroviral vectors can confer high level of gene transfer and transgene expression in a variety of cell types. Here we observed that following retroviral vector-mediated gene transfer of Foxp3, transductional Foxp3 expression was increased in the liver, lung, brain, heart, muscle, spinal cord, kidney and spleen. One day after vector administration, high levels of transgene and gene expression were observed in liver and lung. At 2 days after injection, transductional Foxp3 expression level was increased in brain, heart, muscle and spinal cord, but kidney and spleen exhibited a consistent low level. This finding was inconsistent with the increase in both $CD4^{+}CD25^{+}$ T cell and $CD4^{+}Foxp3^{+}$ T cell frequencies observed in peripheral immune cells by fluorescence-activated cell-sorting (FACS) analysis. Retroviral vector-mediated gene transfer of Foxp3 did not lead to increased numbers of $CD4^{+}CD25^{+}$ T cell and $CD4^{+}Foxp3^{+}$ T cell. These results demonstrate the level and duration of transductional Foxp3 gene expression in various tissues. A better understanding of Foxp3 regulation can be useful in dissecting the cause of regulatory T cells dysfunction in several autoimmune diseases and raise the possibility of enhancing suppressive functions of regulatory T cells for therapeutic purposes.