• 대한간호학회지
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• 제33권1호
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• pp.9-16
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• 2003

Purpose : The objective of this study was the development and validation of a scale to measure the self-care of patients with chronic obstructive pulmonary disease(COPD) in Korea. Method: Self-care scale was developed based on the self-care activities patients had to carry out in order to manage their COPD. The original scale contained 34 items rated along a five-point Likert scale and was reviewed by 18 professional nurses and 10 Korean patients with COPD for content validity. Subsequently, patients with COPD were asked to complete this 23-item scale and further tests were done with the 125 useable responses. Result: Factor analysis identified eight factors-'maintaining a clean air way', 'taking medication', 'support from family', 'preventing infection', 'managing symptoms', 'breathing exercising', and 'taking in nutrition'. The internal consistency of the total scale was Cronbach's α=0.7226. These eight factors explained 60.8% of total variance. There was correlation among Korean Self-Care Scale score, administration level, and knowledge level but there was no correlation to patients' satisfaction with medical services. Conclusion: The 23 item questionnaire positively identified 8 areas defined important for COPD patients. Further studies are required to see how these can be integrated into patient education.

• BMB Reports
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• 제54권10호
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• pp.522-527
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• 2021

Lysine-specific demethylase 1 (LSD1) is an epigenetic regulator that modulates the chromatin status, contributing to gene activation or repression. The post-translational modification of LSD1 is critical for the regulation of many of its biological processes. Phosphorylation of serine 112 of LSD1 by protein kinase C alpha (PKCα) is crucial for regulating inflammation, but its physiological significance is not fully understood. This study aimed to investigate the role of Lsd1-S112A, a phosphorylation defective mutant, in the cigarette smoke extract/LPS-induced chronic obstructive pulmonary disease (COPD) model using Lsd1^SA/SA mice and to explore the potential mechanism underpinning the development of COPD. We found that Lsd1^SA/SA mice exhibited increased susceptibility to CSE/LPS-induced COPD, including high inflammatory cell influx into the bronchoalveolar lavage fluid and airspace enlargement. Additionally, the high gene expression associated with the inflammatory response and oxidative stress was observed in cells and mice containing Lsd1-S112A. Similar results were obtained from the mouse embryonic fibroblasts exposed to a PKCα inhibitor, Go6976. Thus, the lack of LSD1 phosphorylation exacerbates CSE/LPS-induced COPD by elevating inflammation and oxidative stress.

• Tuberculosis and Respiratory Diseases
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• 제79권4호
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• pp.241-247
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• 2016

Bronchodilators are the cornerstone of symptomatic chronic obstructive pulmonary disease (COPD) treatment. They are routinely recommended for symptom reduction, with a preference of long-acting over short-acting drugs. Bronchodilators are classified into two classes based on distinct modes of action, i.e., long-acting antimuscarinics (LAMA, once-daily and twice-daily), and long-acting ${\beta}2$-agonists (LABA, once-daily and twice-daily). In contrast to asthma management, evidence supports the efficacy of both classes of long-acting bronchodilators as monotherapy in preventing COPD exacerbations, with greater efficacy of LAMA drugs versus LABAs. Several novel LAMA/LABA fixed dose combination inhalers are currently approved for COPD maintenance treatment. These agents show superior symptom control to monotherapies, and some of these combinations have also demonstrated superior efficacy in exacerbation prevention versus monotherapies, or combinations of inhaled corticosteroids plus LABA. This review summarizes the current data on clinical effectiveness of bronchodilators alone or in combination to prevent exacerbations of COPD.

• Tuberculosis and Respiratory Diseases
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• 제79권4호
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• pp.207-213
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• 2016

Chronic obstructive pulmonary disease (COPD) encompasses several clinical syndromes, most notably emphysema and chronic bronchitis. Most of the current treatments fail to attenuate severity and progression of the disease, thereby requiring better mechanistic understandings of pathogenesis to develop disease-modifying therapeutics. A number of theories on COPD pathogenesis have been promulgated wherein an increase in protease burden from chronic inflammation, exaggerated production of reactive oxygen species and the resulting oxidant injury, or superfluous cell death responses caused by enhanced cellular injury/damage were proposed as the culprit. These hypotheses are not mutually exclusive and together likely represent the multifaceted biological processes involved in COPD pathogenesis. Recent studies demonstrate that mitochondria are involved in innate immune signaling that plays important roles in cigarette smoke-induced inflammasome activation, pulmonary inflammation and tissue remodeling responses. These responses are reviewed herein and synthesized into a view of COPD pathogenesis whereby mitochondria play a central role.

• Tuberculosis and Respiratory Diseases
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• 제80권4호
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• pp.325-335
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• 2017

Chronic obstructive pulmonary disease (COPD) is associated with abnormal inflammatory response and airflow limitation. Acute exacerbation involves increased inflammatory burden leading to worsening respiratory symptoms, including dyspnea and sputum production. Some COPD patients have frequent exacerbations (two or more exacerbations per year). A substantial proportion of COPD patients may remain stable without exacerbation. Bacterial and viral infections are the most common causative factors that breach airway stability and lead to exacerbation. The increasing prevalence of exacerbation is associated with deteriorating lung function, hospitalization, and risk of death. In this review, we summarize the mechanisms of airway inflammation in COPD and discuss how bacterial or viral infection, temperature, air pollution, eosinophilic inflammation, and concomitant chronic diseases increase airway inflammation and the risk of exacerbation.

• Tuberculosis and Respiratory Diseases
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• 제85권2호
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• pp.101-110
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• 2022

There is a considerable number of individuals who exhibit features of both asthma and chronic obstructive pulmonary disease (COPD), defined as asthma-COPD overlap (ACO). Many studies have reported that these patients have a greater burden of symptoms, including cough and dyspnea, and experience more exacerbations and hospitalizations than those with non-ACO COPD or asthma. Although diagnostic criteria for ACO have not yet been clearly established, their clinical significance remains to be determined. As interest in ACO grows, related studies have been conducted in South Korea as well. The present review summarizes ACO-related studies in South Korea to better understand Korean ACO patients and guide further research. Several cohort studies of asthma and COPD and population-based studies for ACO were reviewed and the key results from demographics, clinical features, lung function, biomarkers, treatment, and prognosis were summarized.

• Tuberculosis and Respiratory Diseases
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• 제86권3호
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• pp.166-175
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• 2023

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. The lower airways contain a rich and diverse microbiome, which may play a significant regulatory role in both health and disease. In COPD, the microbiome becomes perturbed, causing dysbiosis. Increased representation of members in the Proteobacteria phylum and certain members in the Firmicutes phylum has been associated with increased risk of exacerbations and mortality. Therapies such as inhaled corticosteroids and azithromycin may modulate the airway microbiome or its metabolites in patients with COPD. This paper provides an up-to-date overview of the airway microbiome and its importance in the pathophysiology of COPD and as potential therapeutic target in the future.

• Tuberculosis and Respiratory Diseases
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• 제61권4호
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• pp.330-338
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• 2006

연구배경: 만성폐쇄성폐질환은 기도염증으로 인한 기도폐쇄를 특징으로 하는 질환이지만, 질병의 경과중에 체중감소나 근위축 같은 전신증상을 동반하게 된다. 만성 염증과 산화 스트레스가 만성폐쇄성폐질환의 병인에 중요한 역할을 하므로 신체질량지수의 감소와 관련이 있을 것으로 추측할 수 있다. 연구자 등은 안정된 만성폐쇄성폐질환 환자에서 신체질량지수와 관련된 인자를 알아보기 위해 다음과 같은 연구를 시행하였다. 방 법: 안정된 만성폐쇄성폐질환 환자 53명(남:여=49:4, 평균나이=$68.25{\pm}6.32$)과 정상 대조군 33명을 대상으로 폐기능 검사를 실시하고 전신염증인자로 혈청 IL-6, TNF-$\alpha$를 측정하고 산화 스트레스 인자로 혈청 8-iso-prostaglandin $F_2{\alpha}$와 carbonyl protein을 측정하여 비교하였다. 또한 만성폐쇄성폐질환 환자를 신체질량지수에 따라 다시 3군(<18.5, 18.5-25, >25)으로 나누어 각각의 수치들을 비교하였고 만성폐쇄성폐질환의 중증도에 따라 신체질량지수를 비교하였다. 결 과: 만성폐쇄성폐질환 환자와 정상 대조군의 혈청에서 IL-6, TNF-$\alpha$, carbonyl protein은 유의한 차이가 없었으며 8-iso-prostaglandin $F_2{\alpha}$은 각각 $456.08{\pm}574.12pg/ml$, $264.74{\pm}143.15pg/ml$로 만성폐쇄성폐질환 환자에서 유의하게 높았다(p<0.05). 만성폐쇄성폐질환에서 신체질량지수의 차이에 따라 혈청 IL-6, TNF-$\alpha$, carbonyl protein과 8-iso-prostaglandin $F_2{\alpha}$은 유의한 차이를 보이지 않았다. 신체질량지수에 따른 환자의 $FEV_1$은 각각 $0.93{\pm}0.25L$, $1.34{\pm}0.52L$, $1.72{\pm}0.41L$로 신체질량지수가 낮을수록 $FEV_1$ 값도 감소하는 경향을 보였고(p=0.002, r=0.42), 최중증 만성폐쇄성폐질환 환자의 신체질량지수는 $19.8{\pm}2.57$로 중등증의 환자의 $22.6{\pm}3.14$에 비해 유의하게 낮았다(p<0.05). 결 론: 본 연구에서 안정된 만성폐쇄성폐질환 환자의 신체질량지수는 전신염증인자와 산화 스트레스의 정도와는 관련을 보이지 않았으나 기도폐쇄의 정도와는 관련이 있을 것으로 사료된다. 만성폐쇄성폐질환 환자에서 신체질량지수의 감소와 관련된 인자에 대해서는 추가적인 연구가 필요할 것으로 사료된다.

• 월간산업보건
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• 통권354호
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• pp.39-51
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• 2017

• Tuberculosis and Respiratory Diseases
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• 제59권1호
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• pp.14-22
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• 2005