• Tuberculosis and Respiratory Diseases
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• v.86 no.4
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• pp.245-250
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• 2023

The healing process of tracheobronchial tuberculosis (TB) results in tracheobronchial fibrosis causing airway stenosis in 11% to 42% of patients. In Korea, where pulmonary TB is still prevalent, post-TB tracheobronchial stenosis (PTTS) is one of the main causes of benign airway stenosis causing progressive dyspnea, hypoxemia, and often life-threatening respiratory insufficiency. The development of rigid bronchoscopy replaced surgical management 30 years ago, and nowadays PTTS is mainly managed by bronchoscopic intervention in Korea. Similar to pulmonary TB, tracheobronchial TB is treated with combination of anti-TB medications. The indication of rigid bronchoscopy is more than American Thoracic Society (ATS) grade 3 dyspnea in PTTS patients. First, the narrowed airway is dilated by multiple techniques including ballooning, laser resection, and bougienation under general anesthesia. Then, most of the patients need silicone stenting to maintain the patency of dilated airway; 1.5 to 2 years after indwelling, the stent could be removed, this has shown a 70% success rate. Acute complications without mortality develop in less than 10% of patients. Subgroup analysis showed successful removal of the stent was significantly associated with male sex, young age, good baseline lung function and absence of complete one lobe collapse. In conclusion, rigid bronchoscopy could be applied to PTTS patients with acceptable efficacy and tolerable safety.

• Tuberculosis and Respiratory Diseases
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• v.63 no.1
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• pp.83-87
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• 2007

Idiopathic pulmonary fibrosis (IPF) is strongly associated with lung cancer compared with the general population. However, other types of idiopathic interstitial pneumonia (IIP) are rarely associated with lung cancer. We describe a case of a primary lung cancer associated with IIP other than IPF, which was considered to be nonspecific interstitial pneumonia (NSIP), and NSIP disappeared spontaneously after treating the primary lung cancer.

• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.77-85
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• 2005

Background : According to the 2002 consensus report of the American Thoracic Society/European Respiratory Society (ATS/ERS), idiopathic pulmonary fibrosis (IPF) was classified as biopsy proven or probable IPF. Probable IPF is defined as those with distinctive features that allow for a confident diagnosis of IPF/usual interstitial pneumonia (UIP) within an appropriate clinical setting. The determination of the clinical course of probable IPF, as diagnosed by the ATS/ERS criteria, was studied. Methods : Between March 1995 and August 2002, 36 patients with probable IPF, from two tertiary referral hospitals, were enrolled in this study. The clinical characteristics, prognostic factors and treatment efficacy of these patients were retrospectively evaluated. Results : The mean age of the subjects was $65{\pm}6$ years. The one and 3 year survival rates were 82.4 and 50.3%, respectively, and a median survival period of 42.0 months. The total cell count of bronchoalveolar lavage was higher in the death than the survival group (p<0.05). No survival benefits were found in the cytoxan and steroid treatment groups compared with other treatment groups. Conclusion : These results suggest that the clinical course of probable IPF may be similar to that of biopsy-proven UIP. However, atypical patients must undergo an open lung biopsy for confirmation of the diagnosis.

• 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.39 no.5
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• pp.438-442
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• 1992

Actinomycosis is a chronic suppurative infection characterized by extensive necrosis, fibrosis and sinus formation without regard to normal tissue planes. The causative organism in human infection is Actinomyces israelii. Thoracic actinomycosis is diagnosed in the presence of poor oral hygiene, pulmonary infiltrate, empyema, sinus tract and osteomyelitis of ribs. However, in the absence of chest wall involvement, the diagnosis of pulmonary actinomycosis is difficult and its initial clinical manifestations may lead physicians to suspect tuberculosis or neoplasm. It could not be distinguished from tuberculosis or neoplasm radiologically. We report a case of pulmonary actinomycosis in a 64 year old woman with a review of the literature.

• Tuberculosis and Respiratory Diseases
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• v.57 no.6
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• pp.579-583
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• 2004

Actinomycosis is an indolent infectious disease characterized by pyogenic response and necrosis, followed by intense fibrosis. The main forms of human actinomycosis are cervicofacial, pulmonary, and abdominopelvic type. Pulmonary actinomycosis accounts for 15% to 20% of total cases and unfortunately, clinical manifestations and radiologic findings are nonspecific. Small pleural effusion or empyema may develop in advanced disease but massive empyema is infrequent and rarely reported. We report a case of huge empyema caused by pulmonary actinomycosis in a 55 year-old man, presented with one-month history of productive cough and fever. The CT scan revealed a huge cavity with air-fluid level occupying the left hemithorax. Empyema caused by actinomycosis was confirmed microscopically by demonstration of sulfur granules in empyema sac through thracotomy. Decortication and surgical resection of empyema sac and destructed lung was accomplished and followed by intravenous infusion of penicillin G.

• Tuberculosis and Respiratory Diseases
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• v.59 no.4
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• pp.413-417
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• 2005

Amiodarone is widely used to control fatal arrhythmia. However, amiodarone therapy is associated with a relatively high incidence of pulmonary toxicity, up to 5 to 10%. Typical symptoms are nonspecific and often manifest as nonproductive cough, dyspnea and interstitial infiltrates in patients with acute pneumonitis or chronic fibrosis. However, hemoptysis is a very rare symptom of amiodarone pulmonary toxicity. We report a case of amiodarone pulmonary toxicity, who presented with hemoptysis and was successfully treated with the cessation of amiodarone, with review of the relevant literature.

• Tuberculosis and Respiratory Diseases
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• v.61 no.1
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• pp.74-79
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• 2006

Idiopathic fibrosing mediastinitis is, an uncommon cause of pulmonary hypertension this is characterized by excessive fibrosis of the mediastinum with an unknown etiology. Steroid therapy has been suggested for individuals with progressive symptoms, bu there is littlet data demonstrating the efficacy of such therapy are lacking. We present a case of pulmonary hypertension secondary to a compression of a main pulmonary artery by fibrosing mediastinitis which was confirmed by a biopsy with a thoracotomy. The chest CT scan and 2D echocardiography performed before and after a trial of steroid therapy demonstrated improvement after steroid therapy.

• Molecular & Cellular Toxicology
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• v.3 no.4
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• pp.306-313
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• 2007

The welding fume has been implicated as a causal agent in respiratory disease such as pneumoconiosis. The molecular mechanism by which welding fume induces toxicity in the lung is still unknown, but studies have focused on histological structure and indirect approach measuring the pulmonary damage markers. In the present study, gene expression profiles were analyzed in the lung of rats exposed by manual metal-arc stainless-steel (MMA-SS) welding fume for 30 days using Affymetrix GeneChip$^{(R)}$. Totally, 379 genes were identified as being either up- or down-regulated over 2-fold changes (P<0.01) in the lung of low- or high-dose group and were analyzed by using hierarchical clustering. We focused on genes involved in immune/inflammation responses were differentially regulated during lung injury induced by welding fume exposure. The information of these deregulated genes may contribute in elucidation of the inflammation mechanism during lung injury such as lung fibrosis.

• Tuberculosis and Respiratory Diseases
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• v.47 no.5
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• pp.650-659
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• 1999

Background/Aims: It is well recognized that all aerobic cells have the protective mechanisms in order to minimize the tissue damage induced by various reactive oxygen species(ROS). Thioredoxin peroxidase(TPX) which has been recently identified and characterized functions to convert peroxide to water. The protein is also found in various subtypes(TPX-A & B, MER5, HS22 and HORF-06) and is known to be ubiquitous in most human cells. Especially, ischemic brain injuries, partial hepatectomy and radiation induced DNA damages. In treating lung cancer, radiation therapy has a major place in the local control and the relief of symptoms, but radiation induced free radical injury and resulting pulmonary fibrosis has been the major drawback of the therapy. However, little is known about the protective mechanisms and biologic modulations against radiation-induced tissue damages. Methods: Eighteen mice were divided into six groups, 3 in each group, and fifteen had received 900cGy of radiation. The mice were sacrificed according to the pre determined time schedule; immediate, 1, 2, 3 and 6 weeks after irradiation. Extracts were made from the lungs of each mice, Western blot analysis of various subtypes of TPX were done after SDS-P AGE. Examination of H & E stained slides from the same irradiated specimens and the control specimens were also performed. Results: No difference in the intensity of the immunoreactive bands in the irradiated lung samples of the mice compared to the unirradiated control was observed regardless of the time intervals, although H & E examination of the sample specimens demonstrated progressive fibrotic changes of the irradiated lung samples. Conclusion: In conclusion, according to our data, it is suggested that various thioredoxin peroxidase subtypes and catalase which are known to be increased in many repair processes may not be involved in the repair of the radiation injury to the lung and subsequent fibrosis.