• 동의생리병리학회지
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• 제38권1호
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• pp.16-21
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• 2024

Haepyoijin-tang and its main components have been used for phlegm, cough and dyspnea. Using a respiratory inflammation model, we intend to reveal the anti-inflammatory effect and pharmacological mechanism of Haepyoijin-tang. We induced the respiratory inflammation model by Aspergillus oryzae protease and ovalbumin administration. Female Balb/c mice (8 weeks old) were classified into four groups as follows: saline control group, aspergillus oryzae protease and ovalbumin induced respiratory inflammation group (vehicle), inflammation with Haepyoijin-tang (200 mg/kg) administration group, inflammation with dexamethasone (5 mg/kg) administration group (n=7). To identify the anti-inflammatory effects of Haepyoijin-tang water extracts, we measured the inflammatory cell number in bronchoalveolar lavage fluid (BALF) and total live lung cell number. In addition, we checked eosinophil ratio and number in BALF. And Interleukin (IL)-5 level was also measured in lung cell culture supernatant. To confirm the mechanism of anti-inflammatory effects, we analyzed the activated helper T cell (CD4⁺CD25⁺ cell) and Th2 cell (CD4⁺GATA3⁺ cell) ratio and number in lung by using flow cytometry. Finally, we attempted to confirm the immune mechanism by measuring the ratio and number of regulatory T cells (CD4⁺Foxp3⁺ cell). Haepyoijin-tang extracts treatment diminished inflammatory cell, especially, eosinophil number in BALF and total live lung cell number. Moreover, IL-5 level was reduced in Haepyoijin-tang treated group. Surprisingly, Haepyoijin-tang extracts administration not only decreased the activated helper T cell but also Th2 cell population in lung. Additionally, regulatory T cell population was increased in Haepyoijin-tang administration group. Our findings proved that Haepyoijin-tang extract have anti-inflammatory efficacy by suppressing Th2 cell activation and promoting regulatory T cell population.

• 한국대기환경학회지
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• 제22권5호
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• pp.564-573
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• 2006

This study was performed to examine the effect of particulate matter less than 10 ${\mu}m$ in diameter($PM_{10}$) on respiratory-related admission in Seoul, 1999. Daily counts of respiratory-related admission were analyzed by generalized additive model with adjustment for effects of air temperature, humidity, and day of the week as confounders in a nonparametric approach. The results follow associations between $PM_{10}$ and asthma, acute upper respiratory disease, acute lower respiratory disease, pneumonia, and chronic respiratory disease. The relative risks were 1.30(95% CI=1.14$\sim$1.50) for pneumonia, 1.18(95% CI=1.01$\sim$1.37) for acute lower respiratory disease in less than 15 years, respectively. The relative risks were 1.85(95% CI=1.22$\sim$2.81) for acute lower respiratory disease, 1.28(95% CI=1.04$\sim$1.57) for asthma, 1.25(95% CI=1.01$\sim$1.54) for pneumonia and 1.19(95% CI=1.01$\sim$1.41) for acute upper respiratory disease in 15 to 64 years, respectively The relative risks were 1.54(95% CI=1.15$\sim$2.08) for asthma, 1.38(95% CI=1.06$\sim$l.80) for chronic respiratory disease in more than 65 years, respectively. The study showed that $PM_{10}$ was considerably affects daily counts of respiratory-related admission in Seoul, 1999 Statistically significant associations were mostly found in the adult group like If to 64 years. The highly relative risks come out in the elderly.

• 한국대기환경학회지
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• 제23권5호
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• pp.563-574
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• 2007

There seems to be a consensus among most people that visibility impairment is the most obvious indicator of air pollution. While considerable evidence on the association between air pollution and health outcomes including death and disease have been established, based on industrial complex areas or huge urban cities, time-series, case-crossover and cohort studies, scarce literature exists on the direct evidence for the association between visibility and adverse health outcomes. Our study is assessed the effect of air pollution measured by visibility impairment on respiratory mortality over a period of six years. Relative risks in respiratory deaths were estimated by a Poisson regression model of daily deaths between $1999{\sim}2004$. Daily counts of respiratory deaths as dependent variable was modelled with daily 24-hr mean visibility measurements (kilometers) as independent variable by means of Poisson regression. This model is controlled for confounding factors such as day of weeks, weather variables, seasonal variables and $PM_{10}$. The results in this study is observed the statistically significant association between an inverse health effect and visibility during the study period for respiratory mortality (percentage change in the relative risk for all aged -0.57%, 95% Cl, $-1.01%{\sim}-0.12%$; for $0{\sim}15$ aged -7.12%, 95% Cl, $-13.29%{\sim}-0.51%$; for 65+ aged -0.43%, 95% Cl, $-0.93%{\sim}-0.06%$ per 1 km increased in visibility). The effect size was much reduced during warm season. Visibility impairment resulting from air pollution is strongly associated with respiratory mortality, especially for children may be spent at outdoor. Our result provides a quick and useful indicator for eliciting the contribution of air pollution to the excess risk of respiratory mortality in Seoul, Korea.

• Clinical and Experimental Pediatrics
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• 제54권11호
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• pp.456-462
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• 2011

Purpose: Synthesis of regulated on activation, normal T-cells expressed and secreted (RANTES) in the airway has previously been shown to be elevated after respiratory syncytial virus (RSV) infection. However, since few studies have examined whether RSV-infected asthma patients express a higher level of RANTES than do normal individuals, we used a murine model of asthma to address this question. Methods: We prepared Dermatophagoides farinae-sensitized mice as an asthma model, and then infected them with RSV and analyzed the changes in airway responsiveness and the cell populations and cytokine levels of bronchoalveolar lavage fluid. Results: RANTES synthesis increased in response to RSV infection in both control mice and in asthma model (D. farinae) mice. However, there was no significant difference in the amount of RANTES produced following RSV infection between control and D. farinae mice. RSV infection affected neither interferon-${\gamma}$ synthesis nor airway responsiveness in either control or D. farinae mice. Conclusion: RSV infection did not induce more RANTES in a murine model of asthma than in control mice.

• 보건행정학회지
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• 제32권2호
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• pp.164-172
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• 2022

Background: The purpose of this study was to the impact of the coronavirus disease 2019 (COVID-19) outbreak on emergency departments (EDs) in patients under the age of 18 years with respiratory disease. Also, we analyzed similarities and differences in patients including revisit before and after the COVID-19 outbreak. Methods: This study population was respiratory patients under the age of 18 years who visited all 403 EDs in Korea between January 1st, 2019 and December 31st, 2020, using the National Emergency Department Information System Database. The primary outcome was the number of respiratory patients according to age, sex, the type of EDs, season, Korean Triage and Acuity Scale (KTAS) levels, the result of ED, and length of stay. The secondary outcome was the number of revisit respiratory patients within 72 hours. We calculated the risk-adjusted revisit rates according to the KTAS level using a multiple logistic regression model. Results: The number of ED visits decreased from 274,526 in 2019 to 79,007 in 2020; this number was 71.2% lower than that before COVID-19. In spring 2020, this number was 90.1% lower than during the same period in 2019. For the revisit rate in the study population, the adjusted odds ratio (95% confidence interval) was 1.22 (1.05-1.41) in 2019 and 1.39 (1.07-1.81) in 2020. Conclusion: Implementing appropriate emergency care policies in severe respiratory patients would have contributed to improving the safety of reducing in revisit rate.

• Journal of the Korean Data and Information Science Society
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• 제28권2호
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• pp.297-307
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• 2017

질병 확산 모형은 질병의 확산 과정을 모형화 함으로써 질병이 발생하고 퍼지는 시간 내에서 통제하기 위하여 활용하고자 하는 모형이다. 본 연구에서는 질병 확산 모형의 가장 대표적인 SIR 모형에 기본적인 확장 접근을 하여 접촉군 (exposed)이라는 단계를 추가한 SEIR 모형을 이용하여 모형 구축을 하였다. 이 모형은 감염 대상군 (susceptible)의 사람들이 질병에 노출 된 잠복기를 거쳐 일정 시간이 경과한 후 감염되어 감염군 (infected)으로 이동한 후 다시 회복군 (removed)으로 이동하는 모형이다. 이와 같이 질병에 감염된 후 감염력이 생기는 잠복기가 있는 경우에 연구에 활용될 수 있다. 본 연구에서는 2015년 국내에서 발생한 메르스 코로나바이러스 (Middle East respiratory syndrome coronavirus; MERS CoV)에 의한 호흡기 감염증 자료를 수집하였다. 질병의 확산 과정이 결정적이 아닌 확률적인 흐름을 따른다고 가정하여 포아송 확률과정을 따른다고 보고 확률적 화학반응 모형을 이용하여 모형을 구축하였다. 모형을 구현하기 위해서 SEIR 모형의 세 모수인 질병에 노출된 정도를 나타내는 접촉률 (exposed rate), 질병의 감염 정도를 나타내는 감염률 (transmission rate), 질병의 회복정도를 나타내는 회복률 (recovery rate)를 추정함으로써, SEIR 모형에 적합하고 전염병 확산에 대한 예측을 수행하였다. 또한 접촉군이 정확하게 관찰되지 않을 부분을 보완하기 위하여 접촉군을 생성하는 과정을 전체 모형 구축 과정에 추가하였다.

• Tuberculosis and Respiratory Diseases
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• 제79권3호
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• pp.143-152
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• 2016

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.

• 대한한방내과학회지
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• 제32권2호
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• pp.217-231
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• 2011

Objectives : This study aimed to evaluate the effects of Saengmaekcheongpye-eum (SCE) on a LPS-induced COPD (chronic obstructive pulmonary disease) model. Materials and Methods : The extract of SCE was treated to A549 cells and and LPS-induced COPD mouse model. Then, various parameters such as cell-based cyto-protective activity and histopathological finding were analyzed. Results : SCE showed a protective effect on LPS-induced cytotoxicity in A549 cells. This effect was correlated with analysis for caspase 3 levels, elastin contents, protein levels of cyclin B1, Cdc2, and phospho-Erk1/2, and gene expression of TNF-${\alpha}$ and IL-$1{\beta}$ in A549 cells. SCE treatment also revealed a protective effect on LPS-induced lung injury in COPD mouse model. This effect was evidenced via histopathological findings including immunofluorescence stains against elastin and caspase 3, and protein levels of cyclin B1, Cdc2, and Erk1/2 in lung tissue. Conclusions : These data suggest that SCE has pharmaceutical properties on lung injury. This study thus provides scientific evidence for the efficacy of SCE for clinical application to patients with COPD.

• 대한한방내과학회지
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• 제36권4호
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• pp.547-561
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• 2015

Objectives In this study, we divided Korean asthma patients into excess syndrome or deficiency syndrome groups according to clinical phenotype. Genetic analysis was conducted to investigate the association of exonic SNPs in the CD46 gene polymorphism with the clinical phenotype based on the differentiation syndrome of the bronchial asthma patients.Methods There were 95 healthy patients (control group) and 53 asthma patients. (The deficiency syndrome group included 24 and the excess syndrome group 29). We searched the exonic areas of the CD46 gene in the NCBI website SNPs with <0.01 minor allele frequency (MAF) and <0.01 heterozygosity. We finally selected two SNPs: rs138843816, Ser13Phe and rs7144, 3’-UTR. Hardy-Weinberg equilibrium was calculated using SNPStats.Results There were significant differences in the codominant 1 model and the dominant model between the healthy group and the asthma group. There were significant differences between deficiency syndrome group and the excess syndrome group in the genotype frequencies and in the codominant 1 model, the dominant model, and the log-additive model. The allele frequency of rs7144C showed a significant difference between the deficiency syndrome group and the excess syndrome group. Two-SNP haplotype analysis showed a significant difference in frequency in the deficiency syndrome group and in the excess syndrome group. There were significant differences between the healthy group and the excess syndrome group in the codominant 1 model, the dominant model, and the log-additive model. The frequency of the rs7144 C allele exhibited a significant difference in the demonstration. SNP haplotype analysis between the healthy group and the excess syndrome group showed a significant difference in the frequency of the CT haplotype and the CC haplotype.Conclusions The results indicate that two CD46 SNPs (rs138843816, Ser13Phe and rs7144, 3′–UTR) might be associated with the symptomatic excess syndrome in Korean asthma patients.

• 한국대기환경학회지
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• 제22권5호
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• pp.554-563
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• 2006

Numerous epidemiological studies have shown stronger associations between $PM_{2.5}$ and both mortality and morbidity than $PM_{10}$. The association of $PM_{2.5}$ with respiratory mortality was examined in Seoul, during the period of $1996{\sim}2002$. Because $PM_{2.5}$ data were available for only 10% of this time period, a prediction regression model was developed to estimate $PM_{2.5}$ concentration. Death count due to respiratory-related diseases(total respiratory mortality; ICD-10, J00-J98) and death counts(cause-specific mortality) due to pneumonia(ICD-10, J12-J18), COPD(ICD-10, J40-J44) and asthma(ICD-10, J45-J46) were considered in this study. Averaged daily mortality was 5.6 for total respiratory mortality and 1.1 to 1.6 for cause-specific mortality. Generalized additive Poisson models controlling for confounders were used to evaluate the acute effects of particle exposures on total respiratory mortality and cause-specific mortality. An IQR increase in 5-day moving average of $PM_{2.5}(22.6{\mu}g/m^3)$ was associated with an 8.2%(95% CI: 4.5 to 12.1%) increase in total respiratory mortality The association of $PM_{2.5}$ was stronger for the elderly ($\geq$65 years old, 10.1%, 95% CI: 5.8 to 14.5%) and for males(8.9%, 95% CI: 2.1 to 11.3%). A $10{\mu}g/m^3$ increase in 5-day moving average of $PM_{2.5}$ was strongly associated with total respiratory mortality in winter(9.5%, 95% CI: 6.6 to 12.4%), followed by spring(3.1%, 95% CI: -1.2 to 7.5%), which was a different pattern with the finding in North American cities. However, our results are generally consistent with those observed in recent epidemiological studies, and suggest that $PM_{2.5}$ has a stronger effect on respiratory mortality in Seoul.