• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.2
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• pp.292-304
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• 2006

The Atrophy of lung among chronic asthenia disease is a kind of tuberculosis. It is divided in two types. One is the Atrophy of lung with consumptive fever, the other is the Atrophy of lung with consumptive cold. Four prescriptions can be used treat this disease. Pulmonary abscess(肺癰) is infected by poisonous fatcors of wind and heat. It's symptoms like coughing, chest pain, fever and phlegm with pus after coughing are appeared generally, in case of serious condition, pyemia after coughing can be appeared. This disease is applicable to lung abscess, bronchiectasis, lung gangrene. Six prescriptions can be used to treat this disease. Coughing and congestion of the head(咳嗽上氣) is called Lung-distension(肺腸). Its symptom is dyspnea caused by more expiration rather than inspiration. This disease is divided into two types like chronic asthenia type and inflammatory type. Seven prescriptions can be used to treat this disease.

• Genomics & Informatics
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• v.17 no.1
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• pp.2.1-2.12
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• 2019

Chronic obstructive pulmonary disease (COPD) is a type of progressive lung disease, featured by airflow obstruction. Recently, a comprehensive analysis of the transcriptome in lung tissue of COPD patients was performed, but the heterogeneity of the sample was not seriously considered in characterizing the mechanistic dysregulation of COPD. Here, we established a new transcriptome analysis pipeline using a deconvolution process to reduce the heterogeneity and clearly identified that these transcriptome data originated from the mild or moderate stage of COPD patients. Differentially expressed or co-expressed genes in the protein interaction subnetworks were linked with mitochondrial dysfunction and the immune response, as expected. Computational protein localization prediction revealed that 19 proteins showing changes in subcellular localization were mostly related to mitochondria, suggesting that mislocalization of mitochondria-targeting proteins plays an important role in COPD pathology. Our extensive evaluation of COPD transcriptome data could provide guidelines for analyzing heterogeneous gene expression profiles and classifying potential candidate genes that are responsible for the pathogenesis of COPD.

• The Journal of Korean Medicine
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• v.42 no.3
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• pp.56-71
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• 2021

Objectives: This study is aimed to evaluate the protective effects of GGX on lung injury of Chronic Obstructive Lung Disease (COPD) mice model. Materials and Methods: C57BL/6 mice were challenged with lipopolysaccharide (LPS) and cigarette smoke extract (CSE) and then treated with vehicle only (Control group), dexamethasone 3 mg/kg (Dexa group), gam-gil-tang 200 mg/kg (GGT group), GGX 100, 200, and 400 mg/kg (GGX group). After sacrifice, its bronchoalveolar lavage fluid (BALF) or lung tissue was analyzed with cytospin, Enzyme-Linked Immunosorbent Assay (ELISA), real-time polymerase chain reaction (PCR) and hematoxylin & eosin (H&E), and Masson's trichrome staining. Results: In the COPD model, GGX significantly inhibited the increase of neutrophils, TNF-𝛼, IL-17A, CXCL-1, MIP2 in BALF and TNF-𝛼, IL-1𝛽, IL-10 mRNA expression in lung tissue. It also decreased the severity of histological lung injury. Conclusion: This study suggests the usability of GGX for COPD patients by controlling lung tissue injury.

• Tuberculosis and Respiratory Diseases
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• v.78 no.1
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• pp.8-17
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• 2015

Background: AMP-activated protein kinase (AMPK) not only functions as an intracellular energy sensor and regulator, but is also a general sensor of oxidative stress. Furthermore, there is recent evidence that it participates in limiting acute inflammatory reactions, apoptosis and cellular senescence. Thus, it may oppose the development of chronic obstructive pulmonary disease. Methods: To investigate the role of AMPK in cigarette smoke-induced lung inflammation and emphysema we first compared cigarette smoking and polyinosinic-polycytidylic acid [poly(I:C)]-induced lung inflammation and emphysema in $AMPK{\alpha}1$-deficient ($AMPK{\alpha}1$-HT) mice and wild-type mice of the same genetic background. We then investigated the role of AMPK in the induction of interleukin-8 (IL-8) by cigarette smoke extract (CSE) in A549 cells. Results: Cigarette smoking and poly(I:C)-induced lung inflammation and emphysema were elevated in $AMPK{\alpha}1$-HT compared to wild-type mice. CSE increased AMPK activation in a CSE concentration- and time-dependent manner. 5-Aminoimidazole-4-carboxamide-1-${\beta}$-4-ribofuranoside (AICAR), an AMPK activator, decreased CSE-induced IL-8 production while Compound C, an AMPK inhibitor, increased it, as did pretreatment with an $AMPK{\alpha}1$-specific small interfering RNA. Conclusion: $AMPK{\alpha}1$-deficient mice have increased susceptibility to lung inflammation and emphysema when exposed to cigarette smoke, and AMPK appears to reduce lung inflammation and emphysema by lowering IL-8 production.

• Tuberculosis and Respiratory Diseases
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• v.86 no.2
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• pp.120-132
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• 2023

Background: To systematically review studies on inhaled corticosteroids (ICS) and lung cancer incidence in chronic airway disease patients. Methods: We conducted electronic bibliographic searches on OVID-MEDLINE, EMBASE, and the Cochrane Database before May 2020 to identify relevant studies. Detailed data on the study population, exposure, and outcome domains were reviewed. Results: Of 4,058 screened publications, 13 eligible studies in adults with chronic obstructive pulmonary disease (COPD) or asthma evaluated lung cancer incidence after ICS exposure. Pooled hazard ratio and odds ratio for developing lung cancer in ICS exposure were 0.81 (95% confidence interval, 0.64 to 1.02; I²=95.7%) from 10 studies and 1.02 (95% confidence interval 0.50 to 2.07; I²=94.7%) from three studies. Meta-regression failed to explain the substantial heterogeneity of pooled estimates. COPD and asthma were variously defined without spirometry in 11 studies. Regarding exposure assessment, three and 10 studies regarded ICS exposure as a time-dependent and fixed variable, respectively. Some studies assessed ICS use for the entire study period, whereas others assessed ICS use for 6 months to 2 years within or before study entry. Smoking was adjusted in four studies, and only four studies introduced 1 to 2 latency years in their main or subgroup analysis. Conclusion: Studies published to date on ICS and lung cancer incidence had heterogeneous study populations, exposures, and outcome assessments, limiting the generation of a pooled conclusion. The beneficial effect of ICS on lung cancer incidence has not yet been established, and understanding the heterogeneities will help future researchers to establish robust evidence on ICS and lung cancer incidence.

• Tuberculosis and Respiratory Diseases
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• v.59 no.1
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• pp.5-13
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• 2005

Chronic obstructive pulmonary disease (COPD) is a chronic progressive disease, characterized by irreversible airflow limitation, with a partially reversible component. The pathological abnormalities of COPD are associated with lung inflammation, imbalances of proteinase and antiproteinase, and oxidative stress, which are induced by noxious particles and gases in susceptible individuals. The physiological changes of COPD are mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, cor pulmonale and systemic effects. The airflow limitation principally results from an increase in the resistance of the small conducting airways and a decrease in pulmonary elastic recoil due to emphysematous lung destruction. This article provides a general overview of the pathophysiology of COPD.

• Journal of Chest Surgery
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• v.8 no.2
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• pp.153-158
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• 1975

Actinomycosis is a chronic suppurative granulomatous disease due to Actinomyces israelii characterized by multiple abscess and sinus tract formation with dense fibrous scarring. This disease, especially thoracic infection, is very rare in Korea so we are not famiIliar with to make diagnosis and treatment. Otherwise the unspecificity of the clinical symptoms and the lack of adequate examination recedure (as anaerobic fungus culture) are the causes of misdiagnosis. Thoracic actinomycosis is very similar to chronic infectious disease of the lung and chest or thoracic neoplasm. Recently we experienced a case of thoracic actinomycosis (bronchopulmonary) which had been confused with chronic lung abscess and pathologically confirmed as broncho-pulmonary actinomycosis. The purpose of this report is to review our experience more thorouly to enhance consideration of Artinomycosis.

• BMB Reports
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• v.50 no.2
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• pp.79-84
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• 2017

Emphysema, a pathologic component of the chronic obstructive pulmonary disease, causes irreversible destruction of lung. Many researchers have reported that mesenchymal stem cells can regenerate lung tissue after emphysema. We evaluated if spheroid human adipose-derived mesenchymal stem cells (ASCs) showed greater regenerative effects than dissociated ASCs in mice with elastase-induced emphysema. ASCs were administered via an intrapleural route. Mice injected with spheroid ASCs showed improved regeneration of lung tissues, increased expression of growth factors such as fibroblast growth factor-2 (FGF2) and hepatocyte growth factor (HGF), and a reduction in proteases with an induction of protease inhibitors when compared with mice injected with dissociated ASCs. Our findings indicate that spheroid ASCs show better regeneration of lung tissues than dissociated ACSs in mice with elastase-induced emphysema.

• Tuberculosis and Respiratory Diseases
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• v.40 no.6
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• pp.646-652
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• 1993

Background: Lung cancer and chronic obstructive lung disease often coexist in the same person who are elderly and cigarette smoking. There are several reports that the presence of chronic obstructive pulmonary disease constitutes an independent risk factor for the development of lung cancer. Moreover, the association between mucus hypersecrtion and lung cacer has been reported. Method: In 72 cases with primary lung cancer which were confirmed histopathologically at Chonbuk University Hospital from August 1986 to July 1991, We evaluated the relationship between spirometry and lung cancer characteristics. Results: Six cases(8.3%) showed normal lung function, 16(22.2%) cases showed pure restrictive lung disease, 46(63.9%) cases showed moderated obstructive lung disease and 4(5.6%) cases showed severe obstructive lung disease. $FEV_1$(%) was lower in central type than in peripheral type, lower in advanced non-small cell cancer and lower in subjects with phlegm. $FEV_1$/FVC(%) was higher in small cell cancer than in squamous cell cancer and higher in patients without previous pulmonary disease than with previous pulmonary disease. But there was no statistically significant difference in lung function according to histologic types and smoking history. Lung cancers with $FEV_1$/FVC less than 75% consisted of 35 cases of squamous cell cancer, 7 of small cell cancer(14%), 5 of adenocarcinoma(10%), 2 of large-cell carcinoma and 1 of unclassified carcinoma. Squamous cell carcinoma occured more in patients with $FEV_1$/FVC<75% than with $FEV_1$/FVC$\geq$75%(p<0.05). Conclusion: It was suggest that low $FEV_1$/FVC, as reflection of obstructive lung disease, may be at greater risk for squamous cell carcinoma in cigarette smoker.

• Tuberculosis and Respiratory Diseases
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• v.77 no.4
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• pp.155-160
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• 2014

Chronic obstructive pulmonary disease (COPD) is characterized by a diverse array of pulmonary and nonpulmonary manifestations, but our understanding of COPD pathogenesis and the factors that influence its heterogeneity in disease presentation is poor. Despite this heterogeneity, treatment algorithms are primarily driven by a single measurement, forced expiratory volume in 1 second ($FEV_1$) as a percentage of its predicted value ($FEV_1%$). In 2011, a major shift in Global Initiative for Chronic Obstructive Lung Disease (GOLD) treatment recommendations was proposed that stratifies patients with COPD on the basis of symptoms and exacerbation history. This article reviews the work reported in 2013 that enlightens our understanding of COPD with respect to COPD classification systems, phenotype, biomarker, exacerbation, and management for patients with COPD.