• Tuberculosis and Respiratory Diseases
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• v.85 no.3
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• pp.221-226
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• 2022

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation due to chronic airway inflammation and destruction of the alveolar structure from persistent exposure to oxidative stress. The body has various antioxidant mechanisms for efficiently coping with such oxidative stress. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) is a representative system. Dysregulation of the Nrf2-ARE pathway is responsible for the development and promotion of COPD. Furthermore, COPD severity is also closely related to this pathway. There has been a clinical impetus to use Nrf2 for diagnostic and therapeutic purposes. Therefore, in this work, we systematically reviewed the clinical significance of Nrf2 in COPD patients, and discuss the value of Nrf2 as a potential COPD biomarker.

• CELLMED
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• v.14 no.2
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• pp.6.1-6.6
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• 2024

The prevalence of respiratory diseases is increasing due to social and environmental factors such as increased environmental pollution and air pollution, and among them, chronic obstructive pulmonary disease (COPD) in particular has a high mortality and morbidity rate worldwide. As a result, medical expenses are rapidly increasing, creating a social and economic burden. In response to this, there is a need to discuss ways to reduce the risk from diseases and manage them appropriately, and the most basic starting point in this process is how these chronic lung disease patients are treated in actual clinical settings and how to improve the quality of treatment. There is a need to look into whether there are effective drugs. Western treatment for chronic obstructive pulmonary disease is basically a disease in which the airway narrows, so bronchodilators are used to widen the bronchi, and corticosteroids and antibiotics are mainly used to relieve the inflammatory response in the lungs. However, since the mainly used Western medicine does not serve as a fundamental therapeutic drug and contains many side effects, there is a need for drugs that improve the quality of life of patients and are more effective in managing symptoms as symptomatic prescriptions. Therefore, Western and Oriental medicine treatments are needed. The purpose is to suggest better treatments through comparative analysis.

• Journal of Yeungnam Medical Science
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• v.26 no.1
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• pp.38-43
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• 2009

Kimura's disease is an idiopathic chronic condition, associated with a high-titer of IgE and peripheral eosinophilia. It frequently presents as a solitary or multiple lesions in the head and neck area. During the perioperative period, anesthesiologists should understand the anatomical structures of the patient who has Kimura's disease involvement of the head and neck, especially the airway. It is important to pay attention to the occurrence of signs and symptoms of acute allergic reactions related to a high-titer of IgE and eosinophilia. We report our experience with anesthetic management in an 18-year-old patient with multiple neck masses due to Kimura's disease.

• IMMUNE NETWORK
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• v.22 no.6
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• pp.45.1-45.15
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• 2022

Asthma is a chronic airway inflammatory disease characterized by reversible airway obstruction and airway hyperreactivity to various environmental stimuli, leading to recurrent cough, dyspnea, and wheezing episodes. Regarding inflammatory mechanisms, type 2/eosinophilic inflammation along with activated mast cells is the major one; however, diverse mechanisms, including structural cells-derived and non-type 2/neutrophilic inflammations are involved, presenting heterogenous phenotypes. Although most asthmatic patients could be properly controlled by the guided treatment, patients with severe asthma (SA; classified as a treatment-refractory group) suffer from uncontrolled symptoms with frequent asthma exacerbations even on regular anti-inflammatory medications, raising needs for additional controllers, including biologics that target specific molecules found in asthmatic airway, and achieving the precision medicine for asthma. This review summarizes the immunologic basis of airway inflammatory mechanisms and current biologics for SA in order to address unmet needs for future targets.

• Tuberculosis and Respiratory Diseases
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• v.79 no.2
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• pp.91-97
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• 2016

Background: Chronic obstructive pulmonary disease (COPD) is sometimes complicated with pneumonia, but little is known about the risk factors that promote the development of pneumonia in COPD. These risk factors were evaluated in the present study. Methods: The data of 324 patients with COPD from a prospective multi-center observational cohort with obstructive lung disease were evaluated retrospectively. To identify risk factors for the development of pneumonia in COPD, the clinical and radiological data at enrollment and the time to the first episode of pneumonia were analyzed by Cox proportional hazard analysis. Results: The median follow-up time was 1,099 days and 28 patients (8.6%) developed pneumonia. The Cox analysis showed that post-bronchodilator forced expiratory volume in one second ($FEV_1$, % of predicted) and the computed tomography (CT) emphysema extent (inspiratory V950) were independent risk factors for the development of pneumonia (post-bronchodilator $FEV_1$: hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.94-1.00; p=0.048 and inspiratory V950: HR, 1.04; 95% CI, 1.01-1.07; p=0.01). Conclusion: Emphysema severity measured by CT and post-bronchodilator $FEV_1$ are important risk factors for the development of pneumonia in COPD.

• IMMUNE NETWORK
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• v.10 no.4
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• pp.109-114
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• 2010

The molecular mechanisms involved in the pathogenesis of chronic obstructive pulmonary disease (COPD) are poorly defined. Accumulating evidences indicate that chronic inflammatory responses and adaptive immunity play important roles in the development and progression of the disease. Recently, it has been shown that IL-17 producing CD4 T cells, named Th17 cells, which have been implicated in the pathogenesis of several inflammatory and autoimmune diseases, are involved in airway inflammation and COPD. In addition, we and others suggest that autoimmunity may play a critical role in the pathogenesis of COPD. Here, we will review the current understanding of roles of Th17 cells and autoimmune responses in COPD.

• Tuberculosis and Respiratory Diseases
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• v.83 no.3
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• pp.185-194
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• 2020

Blood eosinophil counts have emerged as a chronic obstructive pulmonary disease (COPD) biomarker that predict the effects of inhaled corticosteroids (ICS) in clinical practice. Post-hoc and prospective analysis of randomized control trials have shown that higher blood eosinophil counts at the start of the study predict a greater response to ICS. COPD patients with frequent exacerbations (2 or more moderate exacerbations/yr) or a history of hospitalization have a greater response to ICS. Ex-smokers also appear to have a greater ICS response. Blood eosinophil counts can be combined with clinical information such as exacerbation history and smoking status to enable a precision medicine approach to the use of ICS. Higher blood eosinophil counts are associated with increased eosinophilic lung inflammation, and other biological features that may contribute to the increased ICS response observed. Emerging data indicates that lower blood eosinophil counts are associated with an increased risk of bacterial infection, suggesting complex relationships between eosinophils, ICS response, and the airway microbiome.

• Tuberculosis and Respiratory Diseases
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• v.72 no.1
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• pp.8-14
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• 2012

Background: Although airway obstruction in chronic obstructive pulmonary disease (COPD) is due to pathologic processes in both the airways and the lung parenchyma, the contribution of these processes, as well as other factors, have not yet been evaluated quantitatively. We therefore quantitatively evaluated the factors contributing to airflow limitation in patients with COPD. Methods: The 213 COPD patients were aged >45 years, had smoked >10 pack-years of cigarettes, and had a post-bronchodilator forced expiratory volume in one second ($FEV_1$)/forced vital capacity (FVC) <0.7. All patients were evaluated by medical interviews, physical examination, spirometry, bronchodilator reversibility tests, lung volume, and 6-minute walk tests. In addition, volumetric computed tomography (CT) was performed to evaluate airway wall thickness, emphysema severity, and mean lung density ratio at full expiration and inspiration. Multiple linear regression analysis was performed to identify the variables independently associated with $FEV_1$ - the index of the severity of airflow limitation. Results: Multiple linear regression analysis showed that CT measurements of mean lung density ratio (standardized coefficient ${\beta}$=-0.46; p<0.001), emphysema severity (volume fraction of the lung less than -950 HU at full inspiration; ${\beta}$=-0.24; p<0.001), and airway wall thickness (mean wall area %; ${\beta}$=-0.19, p=0.001), as well as current smoking status (${\beta}$=-0.14; p=0.009) were independent contributors to $FEV_1$. Conclusion: Mean lung density ratio, emphysema severity, and airway wall thickness evaluated by volumetric CT and smoking status could independently contribute to the severity of airflow limitation in patients with COPD.

• Advances in Traditional Medicine
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• v.8 no.1
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• pp.1-16
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• 2008

Immunity is responsible for the defense mechanism of the body but in case of autoimmune diseases, its role gets diverted. Like so many other diseases, asthma is also considered as one of the most common autoimmune diseases to be occurring in community. Asthma is defined as a chronic inflammatory airway disease that is characterized by airway hyper reactivity and mucus hypersecretion that result in intermittent airway obstruction. The incidence of allergic asthma has almost doubled in the past two decades. Although, precise causative mechanism of asthma is unknown, but several mechanisms have been proposed that is immunological, pharmacological and genetic mechanisms, and airway and neurogenic inflammation. The inflammatory process observed in the asthmatic patients is the final result of a complex network of interactions between various immunological cell lineages, its mediators and secreted substances. Thus, among the mechanisms proposed, the immunological one plays a key role. Through this article, we have tried to provide some insight into immunological mechanisms in pathogenesis of asthma.

• Sleep Medicine and Psychophysiology
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• v.6 no.1
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• pp.19-25
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• 1999

Sleep alters both breathing pattern and the ventilatory responses to external stimuli. These changes during sleep permit the development or aggravation of sleep-related hypoxemia in patients with respiratory disease and contribute to the pathogenesis of apneas in patients with the sleep apnea syndrome. Fundamental effects of sleep on the ventilatory control system are 1) removal of wakefulness input to the upper airway leading to the increase in upper airway resistance, 2) loss of wakefulness drive to the respiratory pump, 3) compromise of protective respiratory reflexes, and 4) additional sleep-induced compromise of ventilatory control initiated by reduced functional residual capacity on supine position assumed in sleep, decreased $CO_2$ production during sleep, and increased cerebral blood flow in especially rapid eye movement(REM) sleep. These effects resulted in periodic breathing during unsteady non-rapid eye movement(NREM) sleep even in normal subjects, regular but low ventilation during steady NREM sleep, and irregular breathing during REM sleep. Sleep-induced breathing instabilities are divided due primarily to transient increase in upper airway resistance and those that involve overshoots and undershoots in neural feedback mechanisms regulating the timing and/or amplitude of respiratory output. Following ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include 1) hypocapnia, 2) inhibitory effect from lung stretch, 3) baroreceptor stimulation, 4) upper airway mechanoreceptor reflexes, 5) central depression by hypoxia, and 6) central system inertia. While the respiratory control system functions well during wakefulness, the control of breathing is commonly disrupted during sleep. These changes in respiratory control resulting in breathing instability during sleep are related with the pathophysiologic mechanisms of obstructive and/or central apnea, and have the therapeutic implications for nocturnal hypoventilation in patients with chronic obstructive pulmonary disease or alveolar hypoventilation syndrome.