• Tuberculosis and Respiratory Diseases
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• v.44 no.4
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• pp.871-888
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• 1997

Background : It is now thought that the earliest manifestation of idiopathic pulmonary fibrosis is alveolitis, that is, an accumulation of inflammatory and immune effector cells within alveolar walls and spaces. Inflammatory cells including alveolar macrophages and resident normal pulmonary tissue cells participate through the release of many variable mediators such as inflammatory growth factors and cytokines, which contribute to tissue damage and finally cause chronic pulmonary inflammation and fibrosis. This study was performed to investigate the source and distribution pattern of transforming growth factor-${\beta}_1$(TGF-${\beta}_1$), platelet derived growth factor(PDGF), basic fibroblast growth factor(bFGF), interleukin 1(IL-1), interleukin 6(IL-6), tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and the role of these mediators on bleomycin(BLM)-induced pulmonary injury and fibrosis in rats. Method : Wistar rats were divided into three groups(control group, BLM treated group, BLM and vitamine E treated group). Animals were sacrificed periodically at 1, 2, 3, 4, 5, 7, 14, 21, 28 days after saline or BLM administration. The effects were compared to the results of bronchoalveolar lavage fluid analysis, light microscopic findings, immunohistochemical stains for six different mediators(TGF-${\beta}_1$, PDGF, bFGF, IL-1, IL-6 and TNF-$\alpha$) and mRNA in situ hybridization for TGF-${\beta}_1$. Results : IL-1 and IL-6 are maximally expressed at postbleomycin 1~7th day which are mainly produced by neutrophils and bronchiolar epithelium. It is thought that they induce recruitment of inflammatory cells at the injury site. The expression of IL-1 and IL-6 at the bronchiolar epithelium within 7th day is an indirect evidence of contribution of bronchiolar epithelial cells to promote and maintain the inflammatory and immune responses adjacent to the airways. TNF-$\alpha$ is mainly produced by neutrophils and bronchiolar epithelial cells during 1~5th day, alveolar macrophages during 7~28th day. At the earlier period, TNF-$\alpha$ causes recruitment of inflammatory cells at the injury site and later stimulates pulmonary fibrosis. The main secreting cells of TGF-${\beta}_1$ are alveolar macrophages and bronchiolar epithelium and the target is pulmonary fibroblasts and extracellular matrix. TGF-${\beta}_1$ and PDGF stimulate proliferation of pulmonary fibroblasts and TGF-${\beta}_1$ and bFGF incite the fibroblasts to produce extracellular matrix. The vitamine E and BLM treated group shows few positive cells(p<0.05). Conclusion : After endothelial and epithelial injury, the neutrophils and bronchiolar epithelium secrete IL-1, IL-6, TNF-$\alpha$ which induce infiltration of many neutrophils. It is thought that variable enzymes and $O_2$ radicals released by these neutrophils cause destruction of normal lung architecture and progression of pulmonary fibrosis. At the 7~28th day, TGF-${\beta}_1$, PDGF, bFGF, TNF-$\alpha$ secreted by alveolar macrophages sting pulmonary fibroblasts into proliferating with increased production of extracellular matrix and finally, they make progression of pulmonary fibrosis. TNF-$\alpha$ compares quite important with TGF-${\beta}_1$ to cause pulmonary fibrosis. Vitamine E seems to decrease the extent of BLM induced pulmonary fibrosis.

• Tuberculosis and Respiratory Diseases
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• v.63 no.6
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• pp.511-514
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• 2007

Mycoplasma pneumoniae is a common pathogen of community-acquired pneumonia. Mycoplasma pneumonia causes upper and lower respiratory tract symptoms in all age groups, with the highest attack rates in subjects 5 to 20 years old. In patients with mycoplasma pneumonia, the most common radiographic findings may be reticulonodular or interstitial infiltration, which have a predilection for the lower lobes. Findings that show lung collapse on a chest X-ray are very rare. We report a case of mycoplasma pneumonia that showed right upper lobe collapse.

• Journal of the Korean Society of Radiology
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• v.82 no.4
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• pp.826-837
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• 2021

Immunoglobulin G4-related disease (IgG4-RD) is a chronic inflammatory condition involving multiple organs, including the salivary or lacrimal glands, orbit, pancreas, bile duct, liver, kidney, retroperitoneum, aorta, lung, and lymph nodes. It is histologically characterized by tissue infiltration with lymphocytes and IgG4-secreting plasma cells, storiform fibrosis, and obliterative phlebitis. In the thoracic involvement of IgG4-RD, mediastinal lymphadenopathy and perilymphangitic interstitial thickening of the lung are the most common findings. Peribronchovascular and septal thickening and paravertebral band-like soft tissue are characteristic findings of IgG4-RD. Other findings include pulmonary nodules or masses, ground-glass opacity, alveolar interstitial thickening, pleural effusion or thickening, mass in the chest wall or mediastinum, and arteritis involving the aorta and coronary artery. Radiologic differential diagnosis of various malignancies, infections, and inflammatory conditions is needed. In this review, we describe the imaging findings of IgG4-RD and the radiologic differential diagnoses in the thorax.

• Journal of Life Science
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• v.25 no.12
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• pp.1439-1444
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• 2015

Steroid receptor coactivators (SRC) are transcriptional coactivators. Among SRCs, SRC-3 is the most studied in relation to different types of tumors. However, the role of SRC-3 in early lung development and lung cancer has not been well studied. The expression profiles of SRC-3 showed that SRC-3 contributed to bronchial and alveolar development in embryonic lung development. SRC-3 was strongly expressed in Clara cells and type II alveolar cells during fetal lung development (E17.5- E18.5), and SRC-3 was expressed in both cell types in the adult lung. TTF-1 was expressed in the lungs of heterozygote SRC-3 mice and Clara cell-specific-CCSP-TAg tumor mice, along with SRC-3 expression. The expression of TTF-1 was localized at transformed Clara cells and multifocal adenocarcinomas in lung cancer mice. However, SRC-3 was not expressed in the multifocal adenocarcinomas, suggesting that SRC-3 might not be involved in the invasiveness of lung cancer. Cotransfection of TTF-1 in Clara cell-specific mtCC cell lines resulted in significant activation of CCSP expression. However, cotransfection of SRC-3 had no significant effects on transient transfection. These in vivo and in vitro results suggest that SRC-3 does not play a significant role in lung tumor progression. In conclusion, SRC-3 is involved in bronchial and alveolar development in fetal and adult lungs, but it does not play an important role in the progression of Clara cell-derived lung cancer.

• Tuberculosis and Respiratory Diseases
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• v.62 no.2
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• pp.105-112
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• 2007

Background: Oxidative stress may play an important role in the pathogenesis of endotoxin-induced acute lung injury (ALI). This study evaluated the therapeutic effect of ${\alpha}$-lipoic acid, a nonenzymatic antioxidant, in a rat model of lipopolysaccharide (LPS) induced ALI. Materials and Methods: ALI was induced in Sprague-Dawley rats by instilling LPS (E.coli, 3mg/Kg) into the trachea. The rats were classified into the control, control+${\alpha}$-lipoic acid, LPS, and LPS+${\alpha}$-lipoic acid groups.The lung lavage neutrophil count, cytokine-induced neutrophil chemoattractant (CINC), lung myeloperoxidase (MPO), and cytokine concentrations (TNF-${\alpha}$, IL-$1{\beta}$, IL-6 and IL-10) were measured at 2 h and 6 h after LPS administration. Results: The total cell and neutrophil counts of the LPS+${\alpha}$-lipoic acid groups were significantly lower than the LPS groups. The protein concentration in the BAL fluid was similar in the LPS groups and LPS+${\alpha}$-lipoic acid groups. The TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 concentrations in the BAL fluid were not decreased by the ${\alpha}$-lipoic acid treatment in the LPS treated rats. Conclusions: Although ${\alpha}$-lipoic acid decreased the level of LPS-induced neutrophil infiltration into the lung, it could not attenuate the LPS-induced ALI at the dose administered in this study.

• Journal of Life Science
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• v.16 no.5
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• pp.780-787
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• 2006

Asthma is a chronic inflammatory disorder of the airways, which characterized by bronchial hyperresponsiveness, reversible airflow limitation and respiratory symptoms. Internationally, the prevalence of asthma has been increased over last 3 decades. Recently, several studies of asthma have been reported with gradually increasing importance. To tesify the hypothesis that interleukin (IL)-4 and IL-10 may be an important determinant of the severity of airway inflammation, their expression was studied in mouse model of asthma. BALB/c mouse, IL-4 Knockout (KO) mouse and IL-10 KO mouse were sensitized with intraperitoneal injection of ovalbumin adsorbed to aluminum potassium sulfate, followed by challenges with intranasal ovalbumin on 3 consecutive days. The severity of pulmonary inflammation was assessed by eosinophilia in BAL fluid, number of total BAL cells, histopathological changes in lung tissues, and immunohistochemical staining against IL-4 and IL-10. In BAL fluid, the number of total cells was significantly increased in asthma induced mouse compare to the control. In asthma induced mouse, eosinophil was increased to 56% and neutrophil was 0.2%. In H &E stains, eosinophilic infiltration and epithelium hyperplasia were clearly noticed in asthma induced mouse. In immunohistochemical staining for IL-4 and IL-10, there was no positive reaction in control group. However, very strong reactions were appeared in asthma induced group. In this research, IL-4 and IL-10, which seem to play a central role in allergic asthma, KO mouse was utilized to test the causative relationship between airway inflammation and role of specific cytokine. Asthma induced IL-4 and IL-10 KO mice showed much decreased inflammatory reactions in the number of total BAL cells, in eosinophilic infiltration, and in immunohistochemical stains against diverse inflammatory proteins. These results suggest that IL-4 and IL-10 increase the asthmatic reactions in vivo mice model.

• Journal of Chest Surgery
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• v.32 no.3
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• pp.281-286
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• 1999

Background: The purpose of this study is to analyze the types of complications, the incidences of complications, and preoperative and postoperative risk factors affecting the incidence of the complication. Material and Method: Between August 1990 and August 1997 in Asan Medical Center, 42 patients(24 men and 18 women) underwent surgical resection for pulmonary aspergilloma. The mean age was 46.6${\pm}$11.5 years(range 29 to 69 years). Hemoptysis(90%) was the most common presentation. Pulmonary tuberculosis was the most common predisposing cause(81%). The associated diseases were bronchiectasis(n=11), active puolmonary tuberculosis(n=9), diabetes mellitus(n=8), lung carcinoid(n=1), and acute myeloblastic leukemia(n=1). Lobectomy was done in 32 cases(76%), segmentectomy or wedge resection in 4, pneumonectomy in 2, and lobectomy combined with segmentectomy in 4. Result: Operative mortality was 2%. The most common postoperative complication was persistent air leakage(n=6). The variables such as age, sex, pulmonary function test, amount and duration of hemoptysis, associated diseases(diabetes mellitus, active pulmonary tuberculosis), mode of preoperative management(steroid, antifungal agent, bronchial arterial embolization), and modes of operative procedures were statistically insignificant. The radiologic extent of infiltration to normal lung parenchyme was statistically significant(p=0.04). Conclusion: We conclude that the extent of the infiltration to normal lung parenchyme in preoperative radiologic studies should be carefully evaluated to reduce the postoperative complications in surgery for pulmonary aspergilloma.

• Tuberculosis and Respiratory Diseases
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• v.56 no.6
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• pp.683-686
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• 2004

Pulmonary alveolar proteinosis is a rare disorder in which lipoproteinaceous material accumulates within the alveoli. We report a case of pulmonary alveolar proteinosis in a 41 year old female patient. She complained of a dry cough in the preceding 6 months. She presented symptoms of mild hypoxemia and diffuse infiltration at both lower lung fields. A milky fluid was obtained by bronchoalveolar lavage. We confirmed by light microscopic examinations of the lung tissues obtained by transbronchial lung biopsy. Through several follow-ups, the patients symptoms were mild.

• Journal of Chest Surgery
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• v.28 no.2
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• pp.162-165
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• 1995

To evaluate the impact of open lung biopsy on diagnosis and treatment of diffuse infiltrative lung disease, we conducted a retrospective review of 28 patients who underwent this procedure at the Kyoungpook National University Hospital from 1986 to 1993. There were 19 men and 9 women; average age was 50.9 years. During open lung biopsy, The region of the lobe was radiographically and grossly identified and was examined by a biopsy. The biopsy yielded a specific diagnosis in 27 [96.4 % patients and changes in therapy in 24[85.7% patients. Complications developed in three[10.8% patients, directly related to the biopsy procedure in 2. One patient died[3.6% due to underlying disease. We conclude that open lung biopsy can be accomplished safely in the patient with diffuse infiltrative lung disease and it is an important tool in decision-making process and therapy.

• Tuberculosis and Respiratory Diseases
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• v.50 no.2
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• pp.258-264
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• 2001

A 26-year-old man with a one-year history of asthma and sinusitis presented with bilateral pleural effusions, patch basilar infiltrates on a chest x-ray and a pericardial effusion on an echocardiogram. The peripheral blood showed marked eosinophilia. An obstructive pattern was also observed during the pulmonary fuction test, which was responsive to bronchodilator inhalation. Nerve conduction studies showed right sural neuropathy. Thoracentesis yielded an acidotic exudative effusion with low glucose, low $C_3$ and eosinophilia. An open lung biopsy revealed an eosinophilic interstitial pneumonitis associated with a necrotizing eosinophilic vasculitis, and granulomatous inflammation foci. In the literature, pleural effusions were reported in 29 percent of Churg-Strauss patients, but the number of effusions was low and their characteristics have not been well described. This report describes the characteristic findings of pleural fluid and its histologic features in a case of classical Churg-Strauss syndrome.