• Journal of Chest Surgery
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• v.9 no.1
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• pp.78-82
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• 1976

Bullous emphysema is usually associated with extensive chronic obliterative pulmonary disease. It is the disease of old age but rare in children or infancy. The bulla in this disease is acquired one. In general the symptoms are due to not the mere presence of the bulla but the extent of underlying lung pathology as emphysema or bronchitis. Occassionally giant bulla of great size may cause symptoms and in this occassion it should be differentiated from other diseases. Especially in children or infancy pneumothorax, congenital pulmonary cyst of lobar obstructive-emphysema should be excluded. Recently we experienced 2 cases of bullous emphysema in infancy with severe respiratory symptoms because of bullae of great size. We felt difficulties in differentiating with other conditions. The purpose of this report is to review our cases thoroughly and enhance considerations of this disease.

• The Journal of Internal Korean Medicine
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• v.40 no.4
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• pp.567-581
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• 2019

Objective: This study aimed to evaluate the inhibitory effects of SGX01 on the lung injuries of COPD mice model. Materials and Methods: This study was carried out in two ways: in vitro and in vivo. In vitro, L929 cells were challenged with LPS, and then treated with six concentrations of SGX01 (10, 30, 50, 100, 300, and $500{\mu}g/ml$) and analyzed by ELISA. In vivo, C57BL/6 mice were challenged with LPS and cigarette smoking solution (CSS), and then treated with a vehicle only (control group), dexamethasone 3 mg/kg (dexa group), or a SGX01 200 mg/kg (SGX01 group). After sacrifice, the BALF or lung tissue was analyzed with Cytospin, FACS, ELISA, real-time PCR and H&E, and Masson's trichrome staining. Results: SGX01 significantly decreased NO, $TNF-{\alpha}$, and IL-6 on L929 cells challenged with LPS. In the COPD model, SGX01 significantly inhibited the increase of neutrophils, $TNF-{\alpha}$, IL-17A, CXCL-1, MIP2, CD8+ cells in BALF, and $TNF-{\alpha}$, $IL-1{\beta}$ mRNA expression in lung tissue. It also decreased the severity of the histological lung injury. Conclusion: This study suggests the usability of SGX01 for COPD patients by controlling lung tissue injury.

• Tuberculosis and Respiratory Diseases
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• v.63 no.1
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• pp.94-99
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• 2007

The spontaneous regression (SR) of cancer is defined as the complete disappearance of a malignant disease without adequate treatment. SR is a very rare biological event, particularly in a pulmonary sarcoma. We report the first documented case of an endobronchial sarcoma that regressed spontaneously in Korea. We encountered a rare case of a 72-year-old woman with an undiagnosed intrapelvic cystic mass, who presented with a smooth surfaced endobronchial tumor obstructing the orifice of the right lower lobe bronchus on a bronchoscopic examination. She had a prior history cervical cancer and adenocarcinoma in the right middle lobe lateral segment of her lung for which she had undergone radiation therapy. The tumor was diagnosed as an endobronchial sarcoma by the histopathology findings and immunohistochemistry. It was unclear if the tumor was a primary sarcoma of the lung or a metastatic lesion of an intrapelvic cystic mass because she refused a diagnostic exploratory laparotomy. Two months later, obstructive pneumonia of the right lower lobe with parapneumonic effusion developed with fever above 38.5degrees C for 10 days. After recovering from pneumonia, she was followed up regularly in the outpatient clinic without any specific treatment. One year later after treating the obstructive pneumonia, the follow-up bronchoscopy revealed complete SR of endobronchial sarcoma. It is believed that the obstructive pneumonia accompanied by fever above 38.5degrees C for 10 days might have played a role in this SR.

• Tuberculosis and Respiratory Diseases
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• v.42 no.2
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• pp.149-155
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• 1995

Background: Cytokeratin 19 is 40KD acidic molecule whose distribution is restricted to simple or pseudo-stratified epithelia, such as the epithelial layer of the bronchial tree. Immunohistochemical study have shown that cytokeratin 19 is overexpressed in lung carcinoma tissue. An immunoradiometric assay, CYFRA 21-1 has been developed using two monoclonal antibody, BM 19-21 and KS 19-1, reactive to different epitopes on cytokeratin 19. We studied the diagnostic value of CYFRA 21-1 in lung cancer. Method: The serum CYFRA 21-1 level using immunoradiometric kit(ELSA-CYFRA 21-1) was measured in 54 patients who admit to Yeungnam University Hospital from April, 1993 to August, 1994. Lung cancer group was 39 primary lung cancer patients(19 patients with squamous cell carcinoma, 11 patients with adenocarcinoma and 9 patients with small cell carcinoma). Control group was 15 patients with non malignant lung diseases(8 patients with pulmonary tuberculosis, 3 patients with chronic obstructive pulmonary disease, 2 patients with pneumonia and 2 patients with chronic obstructive pulmonary disease combined with pulmonary tuberculosis). Results: The mean serum value of CYFRA 21-1 was $20.2{\pm}4.7ng/ml$ in squamous cell carcinoma, $7.2{\pm}1.6ng/ml$ in adenocarcinoma and $15.5{\pm}4.7ng/ml$ in non-small cell lung cancer. The serum value of CYFRA 21-1 in control group was $1.7{\pm}0.5ng/ml$. All of the serum values of 3 histologic types were significantly higher than that of control group(p<0.01). The serum value of CYFRA 21-1 of squamous cell carcinoma was significantly higher than that of adenocarcinoma(p <0.05). Serum value of CYFRA 21-1 in small cell lung cancer was $2.9{\pm}0.9ng/ml$ and not significantly different compared with control group. Using cut off value of 3.3ng/ml, sensitivity and specificity was 11.1%, 65.2% in small cell lung cancer, 70.0%, 62.5% in non-small cell lung cancer, 73.7%, 75% in squamous cell carcinoma and 63.6%, 78.9% in adenocarcinoma, respectively. Conclusion: The serum levels of CYFRA 21-1 may be useful in diagnosis of non-small cell lung carcinoma, especially in squamous cell carcinoma with its high specificity.

• Laboraroty Animal Research
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• v.33 no.1
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• pp.40-47
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• 2017

HemoHIM, herbal preparation has designed for immune system recovery. We investigated the anti-inflammatory effect of HemoHIM on cigarette smoke (CS) and lipopolysaccharide (LPS) induced chronic obstructive pulmonary disease (COPD) mouse model. To induce COPD, C57BL/6 mice were exposed to CS for 1 h per day (eight cigarettes per day) for 4 weeks and intranasally received LPS on day 26. HemoHIM was administrated to mice at a dose of 50 or 100 mg/kg 1h before CS exposure. HemoHIM reduced the inflammatory cell count and levels of tumor necrosis factor receptor (TNF)-${\alpha}$, interleukin (IL)-6 and IL-$1{\beta}$ in the broncho-alveolar lavage fluid (BALF) induced by CS+LPS exposure. HemoHIM decreased the inflammatory cell infiltration in the airway and inhibited the expression of iNOS and MMP-9 and phosphorylation of Erk in lung tissue exposed to CS+LPS. In summary, our results indicate that HemoHIM inhibited a reduction in the lung inflammatory response on CS and LPS induced lung inflammation via the Erk pathway. Therefore, we suggest that HemoHIM has the potential to treat pulmonary inflammatory disease such as COPD.

• Tuberculosis and Respiratory Diseases
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• v.80 no.3
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• pp.247-254
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• 2017

Background: Airway epithelial cells are the first line of defense, against pathogens and environmental pollutants, in the lungs. Cellular stress by cadmium (Cd), resulting in airway inflammation, is assumed to be directly involved in tissue injury, linked to the development of lung cancer, and chronic obstructive pulmonary disease (COPD). We had earlier shown that ACN9 (chromosome 7q21), is a potential candidate gene for COPD, and identified significant interaction with smoking, based on genetic studies. However, the role of ACN9 in the inflammatory response, in the airway cells, has not yet been reported. Methods: We first checked the anatomical distribution of ACN9 in lung tissues, using mRNA in situ hybridization, and immunohistochemistry. Gene expression profiling in bronchial epithelial cells (BEAS-2B), was performed, after silencing ACN9. We further tested the roles of ACN9, in the intracellular mechanism, leading to Cd-induced production, of proinflammatory cytokines in BEAS-2B. Results: ACN9 was localized in lymphoid, and epithelial cells, of human lung tissues. ACN9 silencing, led to differential expression of 216 genes. Pathways of sensory perception to chemical stimuli, and cell surface receptor-linked signal transduction, were significantly enriched. ACN9 silencing, further increased the expression of proinflammatory cytokines, in BEAS-2B after Cd exposure. Conclusion: Our findings suggest, that ACN9 may have a role, in the inflammatory response in the airway.

• IMMUNE NETWORK
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• v.24 no.2
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• pp.3.1-3.23
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• 2024

Cigarette smoke extract (CSE)-treated mouse airway epithelial cells (MAECs)-derived exosomes accelerate the progression of chronic obstructive pulmonary disease (COPD) by upregulating triggering receptor expressed on myeloid cells 1 (TREM-1); however, the specific mechanism remains unclear. We aimed to explore the potential mechanisms of CSE-treated MAECs-derived exosomes on M1 macrophage polarization and pyroptosis in COPD. In vitro, exosomes were extracted from CSE-treated MAECs, followed by co-culture with macrophages. In vivo, mice exposed to cigarette smoke (CS) to induce COPD, followed by injection or/and intranasal instillation with oe-TREM-1 lentivirus. Lung function and pathological changes were evaluated. CD68⁺ cell number and the levels of iNOS, TNF-α, IL-1β (M1 macrophage marker), and pyroptosis-related proteins (NOD-like receptor family pyrin domain containing 3, apoptosis-associated speck-like protein containing a caspase-1 recruitment domain, caspase-1, cleaved-caspase-1, gasdermin D [GSDMD], and GSDMD-N) were examined. The expression of maternally expressed gene 3 (MEG3), spleen focus forming virus proviral integration oncogene (SPI1), methyltransferase 3 (METTL3), and TREM-1 was detected and the binding relationships among them were verified. MEG3 increased N6-methyladenosine methylation of TREM-1 by recruiting SPI1 to activate METTL3. Overexpression of TREM-1 or METTL3 negated the alleviative effects of MEG3 inhibition on M1 polarization and pyroptosis. In mice exposed to CS, EXO^-CSE further aggravated lung injury, M1 polarization, and pyroptosis, which were reversed by MEG3 inhibition. TREM-1 overexpression negated the palliative effects of MEG3 inhibition on COPD mouse lung injury. Collectively, CSE-treated MAECs-derived exosomal long non-coding RNA MEG3 may expedite M1 macrophage polarization and pyroptosis in COPD via the SPI1/METTL3/TREM-1 axis.

• Tuberculosis and Respiratory Diseases
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• v.80 no.3
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• pp.277-283
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• 2017

Background: Smoking cessation is the most powerful intervention to modify progress of chronic obstructive pulmonary disease (COPD), and nicotine dependence is one of the most important determinants of success or failure in smoking cessation. We evaluated nicotine dependence status and investigated factors associated with moderate to high nicotine dependence in patients with COPD. Methods: We included 53 current smokers with COPD in the Korean Obstructive Lung Disease II cohort enrolled between January 2014 and March 2016. Nicotine dependence was measured by using Fagerstrom test for nicotine dependence (FTND). Cognitive function was assessed by Korean version of Montreal Cognitive Assessment. Results: The median FTND score was 3, and 32 patients (60%) had moderate to high nicotine dependence. The median smoking amount was 44 pack-years, which was not related to nicotine dependence. Multiple logistic regression analysis revealed that high education status (odds ratio, 1.286; 95% confidence interval, 1.036-1.596; p=0.023), age <70 (odds ratio, 6.407; 95% confidence interval, 1.376-29.830; p=0.018), and mild to moderate airflow obstruction (odds ratio, 6.969; 95% confidence interval, 1.388-34.998; p=0.018) were related to moderate to high nicotine dependence. Conclusion: Nicotine dependence does not correlate with smoking amount, but with education level, age, and severity of airflow obstruction. Physicians should provide different strategies of smoking cessation intervention for current smokers with COPD according to their education levels, age, and severity of airflow obstruction.

• Journal of Chest Surgery
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• v.30 no.9
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• pp.941-944
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• 1997

Pulmonary infarction is rarely diagnosed with certainty except at postmortem examination. Part of this uncertainty is because of the inability to distinguish between hemorrhage, congestive a electasis, and necrosis clinically and radiographically. The pathogenesis of pulmonary infarction is poorly understood. It is dif%cult to induce pulmonary infarction in animals by ligation of the arterial supply to the lung. Many factors seem to be important in its pathogenesis, in addition to congestive heart failure, malignant tumor, thrombophlebitis, chronic obstructive lung disease, nephrotic syndrome, and postopeiative state. However, pulmonary infarction have not been reported in association with chest trauma. We report a case of pulmonary infarction associated with fractures of right clavicle and multiple ribs. A 45-year-old male had admitted due to right chest pain and dyspnea, which developed after right chest trauma occurred at about 3 weeks ago. He was treated at local clinics under the diagnosis of fractures of right clavicle and ribs until the admission. Chest CT disclosed a huge mass with central low density in right upper lobe, and small masses were also seen on both l ng fields. Open lung biopsy resulted in negativity for the malignancy. Clinical symptoms and radiological findings were not improved by conservative treatment. Right upper lobectomy was done eventually. The final diagnosis was pulmonary infarction. And, the patient has been well after operation.

• Tuberculosis and Respiratory Diseases
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• v.60 no.5
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• pp.571-575
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• 2006

Mycobacterium avium has been traditionally described as an opportunistic organism that causes disseminated disease in human immunodeficiency virus-positive patients and acts as a pulmonary pathogen in patients with underlying lung diseases such as chronic obstructive pulmonary disease or previously treated tuberculosis. Infections caused by M. avium in immunocompetent hosts usually manifest as 2 distinct subtypes, the upper lobe cavitary form and the nodular bronchiectatic form. However endobronchial lesions due to M. avium infections in immunocompetent host are reasonably rare, and there are no reports of this condition in Korea. We report here a case of endobronchial lesions involved in an M. avium infection in an immunocompetent 21 year-old female patient with no preexisting lung disease.