• Food Science and Industry
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• v.48 no.1
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• pp.10-16
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• 2015

• Tuberculosis and Respiratory Diseases
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• v.77 no.5
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• pp.209-214
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• 2014

Background: Bronchiectasis and asthma are different in many respects, but some patients have both conditions. Studies assessing the effect of bronchiectasis on asthma exacerbation are rare. The aim of this study is to investigate the effect of bronchiectasis on asthma exacerbation. Methods: We enrolled 2,270 asthma patients who were followed up in our hospital. Fifty patients had bronchiectasis and asthma. We selected fifty age- and sex-matched controls from the 2,220 asthma patients without bronchiectasis, and assessed asthma exacerbation and its severity based on the annual incidence of total asthma exacerbation, annual prevalence of steroid use, and frequency of emergency room visits and hospitalizations due to asthma exacerbation in each group. Results: Fifty patients (2.2%) had bronchiectasis and asthma. The annual incidence of asthma exacerbation was higher in patients with asthma and bronchiectasis than in patients with asthma alone ($1.08{\pm}1.68$ vs. $0.35{\pm}0.42$, p=0.004). The annual prevalence of steroid use ($0.9{\pm}1.54$ vs. $0.26{\pm}0.36$, p=0.006) and the frequency of emergency room visits ($0.46{\pm}0.84$ vs. $0.02{\pm}0.13$, p=0.001) due to asthma exacerbation were also higher in patients with asthma and bronchiectasis than in patients with asthma alone. Conclusion: Bronchiectasis is associated with difficult asthma control.

• Journal of Microbiology and Biotechnology
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• v.15 no.2
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• pp.265-268
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• 2005

To study the effect of bifidobacteria on preventing allergy response, levels of IFN-$\gamma$, IgG2a, IL-4, and IgG1 were investigated in splenocytes isolated from ovalbumin (OVA)­sensitized allergic mice and BGN4-administered allergy­suppressed mice in the presence of various bifidobacterial strains. Most of the bifidobacteria, except 2A, increased production of Th I-associated immune markers, IFN -$\gamma$ and IgG2a. In addition, most of the bifidobacteria, except 2A and 19A, decreased production of IL-4, whereas the differences in the production of IgG1 were less pronounced. These results suggest that some strains of bifidobacteria may have the potential to prevent the occurrence of allergy by switching Th1/Th2-type antibodies and/or related cytokines.

• Tuberculosis and Respiratory Diseases
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• v.79 no.4
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• pp.289-294
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• 2016

Background: The aim of our study was to evaluate the prognostic value of Charlson's weighted index of comorbidities (WIC) in patients with prolonged acute mechanical ventilation (PAMV, ventilator care ${\geq}96$ hours). Methods: We retrospectively enrolled 299 Korean PAMV patients who were admitted in a medical intensive care unit (ICU) of a university-affiliated tertiary care hospital between 2008 and 2013. Survivors were defined as patients who survived for 60 days after ICU admission. Results: The patients' mean age was $65.1{\pm}14.1$ years and 70.6% were male. The mean ICU and hospital length of stay was $21.9{\pm}19.7$ and $39.4{\pm}39.1$ days, respectively. In addition, the 60-day mortality rate after ICU admission was 35.5%. The mean WIC was $2.3{\pm}1.8$, with significant differences between nonsurvivors and survivors ($2.7{\pm}2.1$ vs. $2.1{\pm}1.7$, p<0.05). The area under the curve of receiver-operating-characteristics curve for WIC was 0.593 (95% confidence interval [CI], 0.523-0.661; p<0.05). Based on Kaplan-Meier curves of 60-day survival, WIC ${\geq}5$ had statistically lower survival than WIC <5 (logrank test, p<0.05). In a multivariate Cox proportional hazard model, WIC ${\geq}5$ was associated with poor prognosis (hazard ratio, 1.901; 95% CI, 1.140-3.171; p<0.05). The mortality rate of patients with WIC ${\geq}5$ was 54.2%. Conclusion: Our study showed a WIC score ${\geq}5$ might be helpful in predicting 60-day mortality in PAMV patients.

• Journal of Microbiology and Biotechnology
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• v.16 no.7
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• pp.1010-1016
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• 2006

The effects of the cell viability and integrity of Bifidobacterium on suppression of allergy were investigated. C3H/HeJ mice were sensitized on weeks 3, 4, 6, and 8 with ovalbumin and choleratoxin to induce an allergic reaction. Mice fed 0.2% of live, disrupted, or heat-killed Bifidobacterium bifidum BGN4 in the pellets of their diet for 8 weeks starting 2 weeks before initial sensitization differentially suppressed the allergy response in terms of levels of IgE and IgG1 in their sera, and symptoms on their tails. Viable Bifidobacterium was more effective than disrupted or heat-killed cells in suppressing the allergy. Growth inhibition, which occurred in the sham group at week 4, did not occur in the treated groups. These results show that Bifidobacterium has a suppressive effect on the allergic response of mice, and that the viability and integrity of the Bifidobacterium is required for effective suppression in our experimental model.

• Tuberculosis and Respiratory Diseases
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• v.79 no.3
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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.

• Tuberculosis and Respiratory Diseases
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• v.80 no.4
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• pp.392-400
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• 2017

Background: Most patients with influenza recover spontaneously or following treatment with an anti-viral agent, but some patients experience pneumonia requiring hospitalization. We conducted a retrospective review to determine the incidence and risk factors of pneumonia in hospitalized patients with influenza A or B. Methods: A total of 213 patients aged 18 years or older and hospitalized with influenza between January 2012 and January 2015 were included in this study. A reverse-transcriptase polymerase chain reaction assay was used to detect the influenza A or B virus in the patients' sputum samples. We collected demographic and laboratory data, combined coexisting diseases, and radiologic findings. Results: The incidence of pneumonia was higher in patients in the influenza A group compared to those in the influenza B group (68.6% vs. 56.9%), but this difference was not statistically significant. The presence of underlying respiratory disease was significantly associated with pneumonia in the influenza A group (adjusted odds ratio [OR], 3.975; 95% confidence interval [CI], 1.312-12.043; p=0.015). In the influenza B group, the white blood cell count (adjusted OR, 1.413; 95% CI, 1.053-1.896; p=0.021), platelet count (adjusted OR, 0.988; 95% CI, 0.978-0.999; p=0.027), and existence of an underlying medical disease (adjusted OR, 15.858; 95% CI, 1.757-143.088; p=0.014) were all significantly associated with pneumonia in multivariate analyses. Conclusion: The incidence of pneumonia was 65.7% in hospitalized patients with influenza A or B. The risk factors of pneumonia differed in hospitalized patients with influenza A or B.

• The Journal of Internal Korean Medicine
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• v.37 no.3
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• pp.484-494
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• 2016

Objective: This study was designed to analyze the treatment effects of Chungsangboha-tang through retrospective chart reviews.Methods: Fifty-one outpatients who had visited the Allergy, Immune & Respiratory System Division at the Kyung Hee Korean Medicine Hospital and who had taken Chungsangboha-tang from February 1, 2006, to February 1, 2016, had their basic medical records and examinationsretrospectively reviewed with respect to IgE, eosinophil, AST, and ALT. The PFT results of 11 patients were also investigated with respect to FEV1, FVC, and FEV1/FVC.Results: The percentage of males and females was 49.02% and 50.98%, respectively. The past histories of patients included asthma (66.67%), unspecified cough (21.57%), COPD (9.80%), allergic rhinitis (7.84%), and others. The subjective symptoms included cough (82.35%), sputum (39.22%), dyspnea (37.25%), and others. The most numerous pattern identification was wheezing dyspnea. IgE was significantly reduced, and eosinophil had a reduced tendency after 116.76±160.40 days of taking Chungsangboha-tang. PFT results also significantly increased after 213.09±266.62 days, while AST and ALT results showed a reduced tendency. In the asthmatic group, IgE also showed a reduced tendency. In particular, IgE was significantly reduced in patient groups taking medicine for more than 12 weeks.Conclusions: The conditions of patients with chronic pulmonary disease such as asthma and COPD significantly improved with Chungsangboha-tang after more than 12 weeks.

• Tuberculosis and Respiratory Diseases
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• v.62 no.1
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• pp.62-66
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• 2007

A bronchial artery aneurysm is a rare condition, which needs optimal treatment due to the possibility of a life-threatening hemorrhage by rupture. The surgical removal of the aneurysm is the standard treatment. However, there are a few reports of coil embolization with a transcatheter. A 69 year-old man was referred for a further evaluation of a mass in the right hilum on chest radiography. He denied any respiratory symptoms. A chest CT scan showed a $3{\times}3{\times}4.5cm$ sized vascular mass with strong contrast enhancement on the right hilar area that originated from the bronchial artery. On the angiogram, the bronchial artery originated from the descending thoracic aorta at the T8 level. A bronchial artery aneurysm was catheterized selectively. and embolized successfully with a coil. After coil embolization, the selective bronchial arteriography confirmed complete occlusion. We report this case of bronchial aneurysm that was treated successfully with coil embolization.

• Tuberculosis and Respiratory Diseases
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• v.69 no.1
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• pp.48-51
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• 2010

Sarcoidosis is a multi-systemic granulomatous disorder of unknown etiology. The characteristic pathological finding is the presence of non-caseating granulomas. The lungs are primarily affected, however other organs may be involved causing various symptoms and ambiguous laboratory findings can be present. There are a few reported cases of sarcoidosis with elevated tumor markers. We describe a 68-year-old woman presenting with sarcoidosis showing elevated serum carcinoembryonic antigen (CEA). The possibility of cancer arising from serum CEA such as gastrointestinal cancer, breast cancer and lung cancer was excluded. A transbronchial lung biopsy demonstrated a non-caseating granuloma without necrosis. As a result prescribed 30 mg prednisolone daily to the patient and serum CEA was decreased after 1 month of treatment. We report a case of pulmonary sarcoidosis with elevated serum CEA.