http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
( 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.
( 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.
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.
Baek Ae-Rin,Choo Eun Ju,Kim Ji-Yeon,Ha Tae Sun,Park Sung Woo,Shin Hee Bong,Shin Hee Bong,Park Joo Hyun,Kim Tark 대한감염학회 2022 Infection and Chemotherapy Vol.54 No.3
A 65-year-old male patient with an end-stage renal disease was diagnosed with coronavirus disease 2019 (COVID-19) by reverse transcription polymerase chain reaction. The patient complained of cough, sputum, and respiratory distress that worsened three days ago. The patient required mechanical ventilation and extracorporeal mentrane oxygenation. On day 9, convalescent plasma collected from a 34-year old man who recovered from COVID-19 45 days ago was administered. The patient showed immediate clinical improvement. However, on day 14, the patient’s clinical course worsened again. On day 19 and day 24, vancomycin-resistant Enterococcus faecium bacteremia and methicillin-resistant Staphylococcus aureus pneumonia were found. After long-term supportive care, he slowly recovered. He was discharged on day 91 without any oxygen requirement. This case report suggests that convalescent plasma therapy might just provide a short-term relief and that persistent effort for critical care is necessary to save patients from severe COVID-19.
Baek Moon Seong,Baek Ae-Rin,Hong Sang-Bum,Bae Soohyun,Park Hye Kyeong,Kim Changhwan,Lee Hyun-Kyung,Cho Woo Hyun,Kim Jin Hyoung,Chang Youjin,Lee Heung Bum,Gil Hyun-Il,Shin Beomsu,Yoo Kwang Ha,Moon Jae 대한의학회 2023 Journal of Korean medical science Vol.38 No.41
Background: There is insufficient data on the benefits of empiric antibiotic combinations for hospital-acquired pneumonia (HAP). We aimed to investigate whether empiric antipseudomonal combination therapy with fluoroquinolones decreases mortality in patients with HAP. Methods: This multicenter, retrospective cohort study included adult patients admitted to 16 tertiary and general hospitals in Korea between January 1 and December 31, 2019. Patients with risk factors for combination therapy were divided into anti-pseudomonal non-carbapenem β-lactam monotherapy and fluoroquinolone combination therapy groups. Primary outcome was 30-day mortality. Propensity score matching (PSM) was used to reduce selection bias. Results: In total, 631 patients with HAP were enrolled. Monotherapy was prescribed in 54.7% (n = 345) of the patients, and combination therapy was prescribed in 45.3% (n = 286). There was no significant difference in 30-day mortality between the two groups (16.8% vs. 18.2%, P = 0.729) or even after the PSM (17.5% vs. 18.2%, P = 0.913). After the PSM, adjusted hazard ratio for 30-day mortality from the combination therapy was 1.646 (95% confidence interval, 0.782–3.461; P = 0.189) in the Cox proportional hazards model. Moreover, there was no significant difference in the appropriateness of initial empiric antibiotics between the two groups (55.0% vs. 56.8%, P = 0.898). The proportion of multidrug-resistant (MDR) pathogens was high in both groups. Conclusion: Empiric anti-pseudomonal fluoroquinolone combination therapy showed no survival benefit compared to β-lactam monotherapy in patients with HAP. Caution is needed regarding the routine combination of fluoroquinolones in the empiric treatment of HAP patients with a high risk of MDR.
IL-37 Attenuates Lung Fibrosis by Inducing Autophagy and Regulating TGF-β1 Production in Mice
Kim, Mi So,Baek, Ae Rin,Lee, June Hyuk,Jang, An Soo,Kim, Do Jin,Chin, Su Sie,Park, Sung Woo American Association of Immunologists 2019 Journal of Immunology Vol. No.
<P><B>Key Points</B></P><P><OL><LI>IL-37 is expressed in alveolar epithelial cells and macrophages.</LI><LI>IL-37 levels are decreased in lung and blood obtained from IPF patients.</LI><LI>IL-37 attenuates lung fibrosis by inducing autophagy and inhibiting TGF-β1 signaling.</LI></OL></P><P>Idiopathic pulmonary fibrosis (IPF) is a progressive and destructive lung disease with a poor prognosis resulting in a high mortality rate. IL-37 is an anti-inflammatory cytokine that inhibits innate and adaptive immunity by downregulating proinflammatory mediators and pathways. However, the exact role of IL-37 in lung fibrosis is unclear. In this study, we found that the IL-37 protein was expressed in alveolar epithelial cells (AECs) and alveolar macrophages in healthy controls but significantly reduced in patients with IPF. IL-37 significantly inhibited oxidative stress–induced primary mouse AEC death in a dose-dependent manner, and knockdown of IL-37 significantly potentiated human lung cancer–derived AEC (A549 cells) death. IL-37 attenuated constitutive mRNA and protein expression of fibronectin and collagen I in primary human lung fibroblasts. IL-37 inhibited TGF-β1–induced lung fibroblast proliferation and downregulated the TGF-β1 signaling pathway. Moreover, IL-37 enhanced beclin-1–dependent autophagy and autophagy modulators in IPF fibroblasts. IL-37 significantly decreased inflammation and collagen deposition in bleomycin-exposed mouse lungs, which was reversed by treatment with the autophagy inhibitor 3-methyladenine. Our findings suggested that a decrease in IL-37 may be involved in the progression of IPF and that IL-37 inhibited TGF-β1 signaling and enhancement of autophagy in IPF fibroblasts. Given its antifibrotic activity, IL-37 could be a therapeutic target in fibrotic lung diseases, including IPF.</P>
( Jin Hyoung Kim ),( Ae-rin Baek ),( Song-i Lee ),( Won-young Kim ),( Yong Sub Na ),( Bo Young Lee ),( Gil Myeong Seong ),( Moon Seong Baek ) 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.0
Background ROX index after high-flow nasal cannula (HFNC) initiation can be helpful to identify low-risk patients of HFNC failure in patients with acute hypoxemic respiratory failure. However, it remains unknown which variables are useful for predicting HFNC failure in coronavirus disease 2019 (COVID-19) receiving HFNC. This study aims to determine the discrimination ability of the ROX index and SpO2/FiO2 ratio in COVID-19 patients after HFNC initiation. Methods This multicenter study was conducted at seven university-affiliated hospitals in Korea. We retrospectively reviewed the hospitalized patients diagnosed with COVID-19 between February 10, 2020 and February 28, 2021. The ROX index and SpO2/ FiO2 ratio were calculated at 1 hour and 4 hours after HFNC initiation. The primary outcome was HFNC failure, defined as the subsequent use of mechanical ventilation despite using HFNC. Discrimination of prediction for HFNC failure was evaluated by receiver operating characteristic (ROC) curve analysis. Results During the study period, 1,565 patients with COVID-19 were hospitalized and eligible 133 patients who received HFNC were analyzed. Among them, 63 (47.4%) were successfully weaned from HFNC, and 70 (52.6%) were intubated. SpO2/FiO2 ratio at 1 hour after HFNC initiation was a more accurate predictor of HFNC failure compared to ROX index (AUC 0.762; 95% CI: 0.679- 0.846 vs. 0.733; 95% CI: 0.640-0.826) (Figure 1). In the multivariable analysis, patients older than 70 years old had 3.4 times of HFNC failure compared to younger patients (AUC 3.367 [95% CI: 1.358-8.349], p=0.009), and SpO2/FiO2 at 1 hour (AUC 0.983 [95% CI: 0.972-0.994], p=0.003) were associated with HFNC failure. Conclusions SpO2/FiO2 ratio at 1 hour after HFNC initiation demonstrated a useful predictive ability for HFNC failure. SpO2/FiO2 could be a bedside tool to identify the need for mechanical ventilation in COVID-19 patients receiving HFNC.
( Yong Sub Na ),( Ae-rin Baek ),( Moon Seong Baek ),( Won-young Kim ),( Jin Hyoung Kim ),( Bo Young Lee ),( Gil Myeong Seong ),( Song-i Lee ) 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.-
Background and objective Secondary infection with the influenza virus occurs in critically ill patients and is associated with substantial morbidity and mortality; however, information remains limited about it in patients with severe COVID-19. Thus, we investigated the clinical outcomes and risk factors of secondary infections in patients with severe COVID-19. Methods This multicentre retrospective cohort study included patients with severe COVID-19 who were admitted to seven tertiary or referral hospitals in South Korea from February 2, 2020, to February 28, 2021. Multivariate logistic regression analyses were performed to assess factors associated with the risk of secondary infections. Results Of the 348 included patients, 120 (34.5%) had at least one infection and 228 (65.5%) had no infection. The most common pathogens of hospital-acquired or ventilator-associated pneumonia were Acinetobacter baumannii (24/92, 26.1%), and of bloodstream infections or central line-associated bloodstream infections were coagulase-negative staphylococci (9/36, 25.0%), and of catheter-associated urinary tract infections were Escherichia coli (9/17, 52.9%) (Figure 1). The time of diagnosis of infection was 16.0 ± 13.7 days from symptom onset and 10.6 ± 12.9 days from hospital admission. There was no statistically significant difference in the 28-day mortality (Table 1). However, in-hospital mortality was higher in the infected group. The risk factors for secondary infection were APACHE II, frailty scale, and corticosteroid use (Table 2). Conclusions In patients with severe COVID-19 and secondary infections, in-hospital mortality was more than doubled. A higher APACHE II score, frailty scale, and use of steroids were risk factors for secondary infection.