• Journal of Ginseng Research
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• v.44 no.2
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• pp.179-193
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• 2020

Ginseng products on the market show high variability in their composition and overall quality. This becomes a challenge for both consumers and health-care professionals who are in search of high-quality, reliable ginseng products that have a proven safety and efficacy profile. The botanical extract standardization is of crucial importance in this context as it determines the reproducibility of the quality of the product that is essential for the evaluation of effectiveness and safety. This review focuses on the well-characterized and standardized ginseng extract, G115, which represents an excellent example of an herbal drug preparation with constant safety and efficacy within the herbal medicinal products. Over the many decades, extensive preclinical and clinical research has been conducted to evaluate the efficacy and safety of G115. In vitro and in vivo studies of G115 have shown pharmacological effects on physical performance, cognitive function, metabolism, and the immune system. Furthermore, a significant number of G115 clinical studies, most of them double-blind placebo-controlled, have reinforced the findings of preclinical evidence and proved the efficacy of this extract on blood glucose and lipid regulation, chronic obstructive pulmonary disease, energy, physical performance, and immune and cognitive functions. Clinical trials and 50 years of presence on the market are proof of a good safety profile of G115.

• BMB Reports
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• v.54 no.10
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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.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.34 no.1
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• pp.57-66
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• 2024

Objective: Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow obstruction that is only partly reversible, inflammation in the airways, and systemic effects. This study aimed to investigate the association between low peripheral oxygen saturation levels (SpO₂), and composite indices predicting death in male patients with (COPD). Method: A total of 140 participants with post-bronchodilator FEV₁/FVC ratio less than 0.7 were included. Three composite indices (ADO, DOSE, BODEx) were calculated using six variables such as age (A), airflow obstruction (O), body mass index (B), dyspnea (D), exacerbation history (E or Ex), and smoking status (S). Severity of airflow limitation was classified according to Global Initiative for Obstructive Lung Disease (GOLD) guidelines. SpO₂ was measured by pulse oximetry, and anemia and iron deficiency were assessed based on blood hemoglobin levels and serum markers such as ferritin, transferrin saturation, or soluble transferrin receptor. Results: Participants with low SpO₂ (<95%) showed significantly lower levels of %FEV₁ predicted (p=0.020) and %FEV₁/FVC ratio (p=0.002) compared to those with normal SpO₂ levels. The mMRC dyspnea scale (p<0.001) and GOLD grade (p=0.002) showed a significant increase in the low SpO₂ group. Receiver Operating Characteristic analysis revealed higher area under the curve for %FEV₁ (p=0.020), %FEV₁/FVC(p=0.002), mMRC dyspnea scale (p=0.001), GOLD grade (p=0.010), ADO (p=0.004), DOSE (p=0.002), and BODEx (p=0.011) in the low SpO₂ group. Conclusion: These results suggest that low SpO₂ levels are related to increased airflow limitation and the composite indices of COPD.

• The Korean journal of internal medicine
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• v.39 no.1
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• pp.7-24
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• 2024

Post-tuberculosis lung disease (PTLD) is emerging as a significant area of global interest. As the number of patients surviving tuberculosis (TB) increases, the subsequent long-term repercussions have drawn increased attention due to their profound clinical and socioeconomic impacts. A primary obstacle to its comprehensive study has been its marked heterogeneity. The disease presents a spectrum of clinical manifestations which encompass tracheobronchial stenosis, bronchiectasis, granulomas with fibrosis, cavitation with associated aspergillosis, chronic pleural diseases, and small airway diseases-all persistent consequences of PTLD. The spectrum of symptoms a patient may experience varies based on the severity of the initial infection and the efficacy of the treatment received. As a result, the long-term management of PTLD necessitates a detailed and specific approach, addressing each manifestation individually-a tailored strategy. In the immediate aftermath (0-12 months after anti-TB chemotherapy), there should be an emphasis on monitoring for relapse, tracheobronchial stenosis, and smoking cessation. Subsequent management should focus on addressing hemoptysis, managing infection including aspergillosis, and TB-associated chronic obstructive pulmonary disease or restrictive lung function. There remains a vast expanse of knowledge to be discovered in PTLD. This review emphasizes the pressing need for comprehensive, consolidated guidelines for management of patients with PTLD.

• Journal of Hospice and Palliative Care
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• v.20 no.2
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• pp.81-92
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• 2017

Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation that is usually progressive. It is a major cause of morbidity and mortality worldwide, leading to substantial and increasing economic and social burden. Palliative care for COPD patients aims to reduce symptoms and exacerbations and improve exercise tolerance and quality of life. It is difficult to make a prognosis for COPD patients due to the variable illness trajectory and advanced care of patients. However, severity of breathlessness, assessment of lung function impairment, and frequency of exacerbations can help to identify palliative care needs and determine effective methods to mitigate symptoms, which is discussed in this paper. In these patients, it is recommended to provide individualized palliative care along with curative/restorative care at the onset of COPD symptoms. Before launching a palliative care system in Korea, it is necessary to prepare pulmonary rehabilitation resources, patient-centered communication, timely palliative responsiveness, and a program for effective advanced care planning. A multidisciplinary approach involving collaboration with not only the respiratory and palliative care teams but also primary care offers a new model of care for these patients and should be considered with a priority.

• BMB Reports
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• v.36 no.1
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• pp.95-109
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• 2003

Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance. The sources of the increased oxidative stress in patients with chronic inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and various structural cells of the airways. Increased levels of ROS produced in the airways is reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with lung diseases. ROS, either directly or via the formation of lipid peroxidation products such as 4-hydroxy-2-nonenal may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38) and redox sensitive transcription factors such as NF-${\kappa}B$ and AP-1. Recent evidences have indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Understanding of the mechanisms of redox signaling, NF-${\kappa}B$/AP-1 regulation, the balance between histone acetylation and deacetylation and the release and expression of pro- and anti-inflammatory mediators may lead to the development of novel therapies based on the pharmacological manipulation of antioxidants in lung inflammation and injury. Antioxidants that have effective wide spectrum activity and good bioavailability, thiols or molecules which have dual antioxidant and anti-inflammatory activity, may be potential therapeutic agents which not only protect against the direct injurious effects of oxidants, but may fundamentally alter the underlying inflammatory processes which play an important role in the pathogenesis of chronic inflammatory lung diseases.

• Journal of the Korean Data and Information Science Society
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• v.27 no.5
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• pp.1349-1360
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• 2016

The purpose of this study was to identify the degree of quality of life (QoL) and its related factors in patients with Korean Chronic Obstructive Pulmonary Disease (COPD). With data collected by Korea National Health and Nutrition Survey in 2013, general and disease-related variables, pulmonary function test, and EuroQol-5Dimension (EQ-5D) were analyzed. The mean of EQ-5D index was 0.916 in patients with COPD and 0.941 in non-COPD. The EQ-5D index and its sub dimensions (mobility, self-care, usual activity, pain/discomfort, anxiety/depression) of COPD patients were significantly lower than that of non-COPD. However, difference in COPD patients' airway limitation was significant only for self-care of EQ-5D (${\chi}^2=9.50$, p=.013). The related factors of QoL in COPD patients were age, gender, level of education, quartile of household income, smoking status, and number of comorbid diseases. Based on the results, it is important to pay close attention to COPD patients' QoL as well as comprehensive interventions which possibly improve their QoL.

• Tuberculosis and Respiratory Diseases
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• v.77 no.3
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• pp.116-123
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• 2014

Background: Mesenchymal stem cells (MSCs) obtained from bone marrow or adipose tissue can successfully repair emphysematous animal lungs, which is a characteristic of chronic obstructive pulmonary disease. Here, we describe the cellular distribution of MSCs that were intravenously injected into mice with elastase-induced emphysema. The distributions were also compared to the distributions in control mice without emphysema. Methods: We used fluorescence optical imaging with quantum dots (QDs) to track intravenously injected MSCs. In addition, we used a human Alu sequence-based real-time polymerase chain reaction method to assess the lungs, liver, kidney, and spleen in mice with elastase-induced emphysema and control mice at 1, 4, 24, 72, and 168 hours after MSCs injection. Results: The injected MSCs were detected with QD fluorescence at 1- and 4-hour postinjection, and the human Alu sequence was detected at 1-, 4- and 24-hour postinjection in control mice (lungs only). Injected MSCs remained more in mice with elastase-induced emphysema at 1, 4, and 24 hours after MSCs injection than the control lungs without emphysema. Conclusion: In conclusion, our results show that injected MSCs were observed at 1 and 4 hours post injection and more MSCs remain in lungs with emphysema.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.29 no.1
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• pp.42-49
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• 2019

Objective: Chronic obstructive pulmonary disease(COPD) is characterized by persistent airflow limitations associated with chronic inflammatory response due to noxious particles or gases in the lung. Iron deficiency is associated with chronic inflammation, such as COPD. The aim of this study was to evaluate the relationship among iron deficiency, iron homeostasis, and inflammation in retired miners with COPD. Methods: The serum levels of ferritin, soluble transferrin receptor(sTfR), and transferrin saturation(TSat) as biomarkers for iron deficiency and high-sensitivity C-reactive protein(hsCRP) as a biomarker for inflammation and hepcidin as a biomarker for iron homeostasis were measured in 93 male subjects. Iron deficiency was defined as any one or more of (1) sTfR>28.1 nmol/L, (2) TSat<16%, and (3) ferritin< $12{\mu}g/L$. Results: Iron deficiency was found 28% of the study subjects. Median levels of serum hsCRP was significantly increased related to airflow limitation of COPD(GOLD 1, $0.09{\mu}g/dL$ vs. GOLD 2, $0.17{\mu}g/dL$ vs. GOLD $3{\leq}$, $0.30{\mu}g/dL$, p=0.010), and was positively correlated with hepcidin(p=0.009). Mean level of serum hepcidin was lower in COPD subjects with iron deficiency(p=0.004) and serum levels of hepcidin was negatively correlated with %$FEV_1$ predicted(p=0.030). Conclusions: These results suggest that high serum levels of hepcidin are related to severe airflow limitation or inflammation and can decrease iron availability, regardless of iron status.

• Tuberculosis and Respiratory Diseases
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• v.85 no.3
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• pp.205-220
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• 2022

This study aimed to describe the prevalence of comorbidities associated with chronic obstructive pulmonary disease (COPD) and their relation with relevant outcomes. A systematic review based on the PRISMA methodology was performed from January 2020 until July 2021. The MEDLINE, Lilacs, and Scielo databases were searched to identify studies related to COPD and its comorbidities. Observational studies on the prevalence of comorbidities in COPD patients and costs with health estimates, reduced quality of life, and mortality were included. Studies that were restricted to one or more COPD pain assessments and only specific comorbidities such as osteoporosis, bronchitis, and asthma were excluded. The initial search identified 1,409 studies and after applying the inclusion and exclusion criteria, 20 studies were finally selected for analysis (comprising data from 447,459 COPD subjects). The most frequent COPD comorbidities were: hypertension (range, 17%-64.7%), coronary artery disease (19.9%-47.8%), diabetes (10.2%-45%), osteoarthritis (18%-43.8%), psychiatric conditions (12.1%-33%), and asthma (14.7%-32.5%). Several comorbidities had an impact on the frequency and severity of COPD exacerbations, quality of life, and mortality risk, in particular malignancies, coronary artery disease, chronic heart failure, and cardiac arrhythmias. Comorbidities, especially cardiovascular diseases and diabetes, are frequent in COPD patients, and some of them are associated with higher mortality.