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( Ae Rin Baek ),( Ji Min Lee ),( Hyun Jung Seo ),( Jong Sook Park ),( June Hyuk Lee ),( Sung Woo Park ),( An Soo Jang ),( Do Jin Kim ),( Eun Suk Koh ),( Soo Taek Uh ),( Yong Hoon Kim ),( Choon Sik Par 대한결핵 및 호흡기학회 2016 Tuberculosis and Respiratory Diseases Vol.79 No.3
Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor β1 (TGF-β1).induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/ myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-β1.induced EMT in experimental lung fibrosis and clarify its mechanism of action. Methods: The A549 alveolar epithelial cell line was treated with TGF-β1 with or without ApoA1. Morphological changes and expression of EMT-related markers, including E-cadherin, N-cadherin, and α-smooth muscle actin were evaluated. Expressions of Smad and non-Smad mediators and TGF-β1 receptor type 1 (TβRI) and type 2 (TβRII) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. Results: TGF-β1.treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-β1.induced change of the EMT phenotype. ApoA1 inhibited the TGF-β1.induced increase in the phosphorylation of Smad2 and 3 as well as that of ERK and p38 mitogenactivated protein kinase mediators. In addition, ApoA1 reduced the TGF-β1.induced increase in TβRI and TβRII expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. Conclusion: Our data demonstrate that ApoA1 inhibits TGF-β1.induced EMT in experimental lung fibrosis.
Disability-Adjusted Life Years for Communicable Disease in the Korean Burden of Disease Study 2012
Lee, Ye-Rin,Moon, Kanghee,Kim, Young Ae,Park, So-Youn,Oh, Chang-Mo,Lee, Kyung-Suk,Oh, In-Hwan The Korean Academy of Medical Sciences 2016 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.31 No.suppl2
<P>Globally, the incidence of communicable diseases has decreased compared to non-communicable diseases. However, chronic communicable diseases such as HIV/AIDS and tuberculosis persist worldwide. Furthermore, emerging new infections such as H1N1 influenza pose a new threat to public health. However, most studies have focused on non-communicable diseases because of their increasing incidence, with fewer studies investigating communicable diseases. Therefore, we estimated the burden of communicable diseases in Korea using national representative 2012 data. To estimate the disability-adjusted life years (DALY), we used cause of death data from the Statistics Korea to estimate the years of life lost (YLL), applied the Korean garbage code algorithm, and used national claims data from the National Health Insurance Service (NHIS) to estimate years lived with disability (YLD). In 2012, the total DALYs of communicable disease were 445 per 100,000, with 129 YLLs per 100,000 and 316 YLDs per 100,000. The total DALYs in men were 468 per 100,000, greater than the 422 per 100,000 DALYs seen in women. The DALYs of lower respiratory infections were the highest value among communicable diseases at 143/100,000 DALYs followed by tuberculosis and upper respiratory infections. The 40-49 years old age group had the largest number of total DALYs. In contrast, the over 80 years old age group had the largest number of total DALYs per 100,000 followed by the 70-79 and 0-9 years old age groups. These results enable the prioritization of interventions related to communicable diseases and can be used for evidence-based public health policies.</P>
( Ae-rin Baek ),( Gil Myeong Seong ),( Song-i Lee ),( Won-young Kim ),( Yong Sub Na ),( Jin Hyoung Kim ),( Bo Young Lee ),( Moon Seong Baek ) 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.0
Purpose High-flow nasal cannula (HFNC) is a useful tool in patients with hypoxic respiratory failure. However, there is a concern for the association between HFNC and delayed intubation or increased mortality. This study aims to investigate that late failure of HFNC is associated with mortality in patients with coronavirus disease 2019 (COVID-19). Method A retrospective multicenter study was conducted at seven university-affiliated hospitals in Korea. We collected the data of hospitalized patients with COVID-19 between February 10, 2020, and February 28, 2021. Failure of HFNC was defined as the need for mechanical ventilation despite HFNC application. According to the time of intubation, HFNC failure was divided into early failure (within 48 hours) and late failure (after 48 hours). The primary outcome was in-hospital mortality. Result During the study period, 157 patients received HFNC, and 133 were eligible. Among them, 70 received mechanical ventilation. Median time from HFNC initiation to intubation of early failure group was 4.1 hours (interquartile range [IQR]: 1.1-13.5 hours), and those of late failure group was 70.9 hours (IQR: 54.4-145.4 hours). Although the ROX index within 24 hours of HFNC initiation had a low tendency in the early failure group than the late failure group, the ROX index before two hours of intubation was significantly lower in the late failure group (5.74 [IQR: 4.58-6.98] vs. 4.80 [IQR: 3.67-5.97], p=0.040, Fig 1). In the multivariable logistic regression analysis, higher CCI (OR 5.38 [95% CI: 1.18-24.56]), higher SOFA score (OR 5.04 [95% CI: 1.34- 18.90]), and late HFNC failure (OR 4.76 [95% CI: 1.12-20.24]) were independent risk factors for in-hospital mortality. Conclusion Late failure of HFNC may be associated with higher mortality in COVID-19 patients with acute respiratory failures.
Baek, Ae Rin,Lee, Ji Min,Seo, Hyun Jung,Park, Jong Sook,Lee, June Hyuk,Park, Sung Woo,Jang, An Soo,Kim, Do Jin,Koh, Eun Suk,Uh, Soo Taek,Kim, Yong Hoon,Park, Choon Sik The Korean Academy of Tuberculosis and Respiratory 2016 Tuberculosis and Respiratory Diseases Vol.79 No.3
Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor ${\beta}1$ (TGF-${\beta}1$)-induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-${\beta}1$-induced EMT in experimental lung fibrosis and clarify its mechanism of action. Methods: The A549 alveolar epithelial cell line was treated with TGF-${\beta}1$ with or without ApoA1. Morphological changes and expression of EMT-related markers, including E-cadherin, N-cadherin, and ${\alpha}$-smooth muscle actin were evaluated. Expressions of Smad and non-Smad mediators and TGF-${\beta}1$ receptor type 1 ($T{\beta}RI$) and type 2 ($T{\beta}RII$) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. Results: TGF-${\beta}1$-treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-${\beta}1$-induced change of the EMT phenotype. ApoA1 inhibited the TGF-${\beta}1$-induced increase in the phosphorylation of Smad2 and 3 as well as that of ERK and p38 mitogen-activated protein kinase mediators. In addition, ApoA1 reduced the TGF-${\beta}1$-induced increase in $T{\beta}RI$ and $T{\beta}RII$ expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. Conclusion: Our data demonstrate that ApoA1 inhibits TGF-${\beta}1$-induced EMT in experimental lung fibrosis.
Lee, Ye-Rin,Kim, Young Ae,Park, So-Youn,Oh, Chang-Mo,Kim, Young-eun,Oh, In-Hwan The Korean Academy of Medical Sciences 2016 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.31 No.suppl2
<P>Years of life lost (YLLs) are estimated based on mortality and cause of death (CoD); therefore, it is necessary to accurately calculate CoD to estimate the burden of disease. The garbage code algorithm was developed by the Global Burden of Disease (GBD) Study to redistribute inaccurate CoD and enhance the validity of CoD estimation. This study aimed to estimate cause-specific mortality rates and YLLs in Korea by applying a modified garbage code algorithm. CoD data for 2010–2012 were used to calculate the number of deaths. The garbage code algorithm was then applied to calculate target cause (i.e., valid CoD) and adjusted CoD using the garbage code redistribution. The results showed that garbage code deaths accounted for approximately 25% of all CoD during 2010–2012. In 2012, lung cancer contributed the most to cause-specific death according to the Statistics Korea. However, when CoD was adjusted using the garbage code redistribution, ischemic heart disease was the most common CoD. Furthermore, before garbage code redistribution, self-harm contributed the most YLLs followed by lung cancer and liver cancer; however, after application of the garbage code redistribution, though self-harm was the most common leading cause of YLL, it is followed by ischemic heart disease and lung cancer. Our results showed that garbage code deaths accounted for a substantial amount of mortality and YLLs. The results may enhance our knowledge of burden of disease and help prioritize intervention settings by changing the relative importance of burden of disease.</P>
이하린,이미애,강형철,함정희 梨花女子大學校 醫科大學 醫科學硏究所 1994 EMJ (Ewha medical journal) Vol.17 No.4
Xeroderma pigmentosrm is rare autosomal recessive with cognitive impairment, referred to as depressive pseudodementia, may be mistaken for a progressive degenerative dementia. Recognition of primary depression is clinically important because of its treatability. To differentiate depression from degenerative dementia, author rsed brain Tc 99m-HMPAO SPECT. By the result the regionar cerebral blood flew(rCBF) in elderly depressed patient was decreased in the left temporoparietal cortex. The pattern of rCBF was different from that of dementia which shows decreased rCBF in bilateral cortex. By using brain SPECT in depressed elderly patient with cognitive impairment, the discrimination from dementia will be more effective and accurate.