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Background There is a large gap in the treatments for patients with COPD according to the Global Initiative for COPD (GOLD) recommendations. Determining the situation of therapies in the real world is necessary. This study aimed to characterize the real-world practical therapies of COPD and prognosis of patients after treatment for 1 year. Methods This study was a multicenter prospective observational study performed using a database set up by the Second Xiangya Hospital of Center South University. Detailed usage information for pharmacotherapies and nonpharmacotherapies for patients was collected, as well as the consistency of recommendations and patient adherence. Moreover, the effect of therapies after 1 year was calculated by comparing lung function and symptoms. Results Ultimately, 4,796 patients with COPD from 12 hospitals in China were eligible. LAMA (39.1%), LAMA + LABA/ICS (39.0%) and LABA/ICS (14.4%) were the top three inhalants. We found that 42.7% of Group A patients, 61.6% of Group B patients and 30% of Group C patients were following inappropriate therapy, especially overuse of ICS. Only 3.9% (95% CI 2.4, 5.4) of patients used oxygen therapy, and 1.8% (95% CI 1.5, 2.3) used noninvasive positive pressure ventilation at home. Among these patients, 33.2% had poor adherence. A total of 452 patients completed 1 year of follow-up. After 1 year of treatment, the lung function of FEV1/FVC decreased (P=0.001) and the mMRC score increased (P 0.05). Conclusion This study highlights a significant discrepancy between recommendations for managing patients with COPD in GOLD report, and in real-world clinical practice in China. Over-prescription of ICS and under-prescription of nonpharmacologic therapy were common. The adherence to treatment of patients was poor, and the real-life treatment effectiveness was unsatisfactory. More attention should be paid to the implementation of recommendations and standardized administration of therapies.

Background and Objectives Long non-coding RNAs (lncRNAs) play an important role in the pathogenesis of many diseases, including cancer, pulmonary fibrosis and chronic obstructive pulmonary disease (COPD). In this study, we intended to identify the differentially expressed lncRNAs and the role of HOXA cluster antisense RNA 2 (HOXA-AS2) in patients with COPD. Methods We analyzed lncRNA profiles of three non-COPD and seven COPD patients' lungs via microarray and then validated the expression of the top differentially expressed lncRNAs by using real-time polymerase chain reaction (PCR). To identify the mechanism of HOXA-AS2 during COPD pathogenesis and endothelial cell proliferation, we knocked down and overexpressed HOXA-AS2 with siRNA and lentivirus transfection approach in human pulmonary microvascular endothelial cells (HPMECs). Results Among 29,150 distinct lncRNA transcripts, 353 lncRNAs were significantly (≥2-fold change and P

Background Fractional exhaled nitric oxide (FENO) has been shown to be a marker of airway inflammation in various pulmonary diseases, including chronic obstructive pulmonary disease (COPD). In this study, we assessed the FENO level in patients with acute exacerbations of COPD (AECOPD) and analyzed the predictive value of the FENO level for treatment response. Methods Demographic data were collected at admission. FENO, lung function, blood gases, COPD Assessment Test (CAT), and modified Medical Research Council (mMRC) scores were measured at admission and on day 7. At the second visit, the patients were asked to report their health status; scores ranged from 1 to 5, representing "much better", "slightly better", "no change", "slightly worse", and "much worse", respectively. The treatment response was evaluated based on the patient's reported health status (responders were those who reported much better and slightly better) and lung function (responders were those who presented an increase in FEV1 over 200 mL). Results A total of 182 patients were recruited into the analysis. The FENO level positively correlated with an increase in FEV1 and FEV1% (r = 0.291, p < 0.001 and r = 0.205, p = 0.005, respectively), but negatively correlated with a decrease in the COPD Assessment Test (CAT) score (r = -0.197, p = 0.008) and patient-reported health status (rho = -0.408, p

Purpose Chronic obstructive pulmonary disease (COPD), usually caused by tobacco smoking, is increased in China. Smoking cessation is the first step in COPD management. Data on predictors of smoking cessation are sparse in COPD patients in China. We aim to find the differences in the clinical characteristics between ex-smokers and current smokers with COPD to determine the factors related to smoking cessation. Patients and methods From outpatient departments of 12 hospitals in Hunan and Guangxi provinces, a total of 4331 patients were included. Information on demographic and sociological data, lung function, and modified Medical Research Council (mMRC) dyspnea scale scores were recorded. Patients were divided into an ex-smokers group and a current smokers group based on whether they gave up smoking. A logistic regression analysis was performed to analyze the factors associated with smoking cessation. Results Of the total, the mean age was 62.9±8.5 years, and 47.3% were ex-smokers. Compared with the current smokers, the ex-smokers were older, and had heavier dyspnea, more severe airflow limitation, fewer pack-years, shorter smoking duration, and a higher proportion of Global Initiative for Chronic Obstructive Lung Disease (GOLD) groups C and D. The logistic regression model showed that smoking cessation was negatively correlated with widowhood, years of smoking, and forced expiratory volume in 1 second (FEV1), but was positively correlated with age, education level, amount smoked, mMRC score, GOLD grades, and GOLD groups. Conclusion Among patients with COPD, more than half still smoked. In the group of patients who quit smoking, many of them quit rather late in age after they had significant symptoms. Several predictors of smoking cessation were identified, indicating that ex-smokers differ substantially from continuing smokers. This should be taken into account in smoking-cessation interventions.

The purposes of this study were to: (1) study the prevalence of pain in patients with mild-to-very severe chronic obstructive pulmonary disease (COPD) in China; (2) compare the differences in pain characteristics between stable COPD and acute exacerbation of COPD (AECOPD); (3) explore the clinical associations with pain in those with COPD. This cross-sectional study was conducted in China from October 24, 2017, to January 11, 2019. A face-to-face interview was conducted to collect data. The Chinese version of the brief pain inventory (BPI-C) was applied to investigate the pain characteristics in patients with COPD. Of the 901 patients in this study, 226 (25.1%) patients reported pain problems. The prevalence of pain in patients with mild to very severe COPD was 32.9%, 23.9%, 25.2%, and 23.5%, respectively (

Yating Peng,1– 3 Jiaxi Duan,1– 3 Xin Li,4 Yuqin Zeng,1– 3 Zijing Zhou,1– 3 Minghua Deng,1– 3,5 Ruoyun Ouyang,1– 3 Yan Chen,1– 3 Shan Cai,1– 3 Ping Chen1– 3 1Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People’s Republic of China; 2Research Unit of Respiratory Disease, Central South University, Changsha, Hunan, People’s Republic of China; 3Hunan Centre for Evidence-Based Medicine, Changsha, Hunan, People’s Republic of China; 4Division of Occupational Lung Disease, Hunan Prevention and Treatment Institute for Occupational Diseases, Changsha, Hunan, People’s Republic of China; 5Department of Respiratory, PLA Rocket Force Characteristic Medical Center, Beijing, People’s Republic of ChinaCorrespondence: Ping Chen Email pingchen0731@csu.edu.cnBackground: Pneumoconiosis has high prevalence of chronic obstructive pulmonary disease (COPD), respiratory morbidity, and mortality.Objective: The aim of the present study was to examine patient characteristics and adherence to inhaled therapy among pneumoconiosis with COPD in a real-world clinical setting.Methods: A cohort of pneumoconiosis patients with COPD prescript with at least one type of long-acting inhaled drug was followed for adherence for 2 years. Demographic and COPD-related characteristics were collected in baseline.Results: In baseline, after adjusting for age, dust exposure duration positively correlated with number of acute exacerbation (AE) frequency in the last year. There were close associations among COPD Assessment Tool (CAT) score, modified Medical Research Council Dyspnea Scale (mMRC) grade, number of AE, and pre-FEV1 value. Of 296 participants originally recruited, 213 participants finished the 2-year follow-up for adherence. 122 (57.28%) were non-adherent to inhaled therapy. The most common reason for non-adherence was “relief of symptoms after short-term controller medication use” (53.28%). Patients who were non-adherent reported higher body mass index (BMI), less AE events in the last year, higher pre-FEV1 value, higher post-FEV1 value and low CAT, mMRC scores compared to adherent in baseline. High pre-FEV1 value (OR = 1.04, CI = 1.018– 1.064) and low mMRC scores (OR = 0.406, CI = 0.214– 0.771) were risk factors found associated with non-adherence.Conclusion: A majority of pneumoconiosis patients complicated with COPD have suboptimal inhaled therapy adherence. Evidence-based, adherence-enhancing interventions should be targeted on less severe subjects.Keywords: adherence, inhaled therapy, pneumoconiosis, COPD

Purpose: This real-world study evaluated the effectiveness of different inhalation therapies in patients with symptomatic chronic obstructive pulmonary disease (COPD) in China and also explored the relevant factors that influence the effectiveness of inhalation therapy.Patients and Methods: We conducted a multicenter prospective longitudinal study that was carried out in 12 hospitals in China from December 2016 to June 2021. A face-to-face interview was conducted to collect data. Baseline data were collected at the first visit. Minimum clinically important difference (MCID) was defined as attaining a COPD assessment test (CAT) decrease ≥2. We mainly assessed the MCID and the incidence of exacerbations at the 6 months follow-up.Results: In 695 patients, the mean age was 62.5 ± 8.2 years, with a mean CAT score of 15.1 ± 6.0. Overall, 341 (49.1%) patients attained the MCID of CAT and the incidence of exacerbation during follow-up was 22.3%. Females were significantly more likely to attain MCID than male in COPD patients (adjusted odd ratio (aOR) = 1.93, adjusted 95% confidence interval (a95%CI) = 1.09–3.42, p = 0.024). Patients treated with LABA/LAMA or ICS/LABA/LAMA (ICS, inhaled corticosteroid; LABA, long-acting β2-agonist; LAMA, long-acting muscarinic antagonist) were more likely to attain MCID than patients treated with LAMA (aOR = 3.97, a95%CI = 2.48–6.35, p < 0.001; aOR = 3.17, a95%CI = 2.09–4.80, p < 0.001, respectively). Patients treated with LABA/LAMA had a higher incidence of severe exacerbation than patients treated with ICS/LABA/LAMA (aOR = 1.95, a95%CI = 1.04–3.66, p = 0.038).Conclusion: The incidence of MCID in symptomatic COPD patients treated with inhalation therapy was nearly 50%. Patients treated with LABA/LAMA or ICS/LABA/LAMA were more likely to attain MCID than patients treated with LAMA. Patients treated with LABA/LAMA had a higher incidence of severe exacerbations than with ICS/LABA/LAMA.

Among many of the autoimmune diseases observed in patients with myasthenia gravis (MG), myocarditis is one of the most critical. The goal of this review is to systematically describe and investigate the characteristics of MG complicated with myocarditis. We identified 183 records in PubMed (MEDLINE), Web of Science, and EMBASE from 1948 to September 10, 2020. Studies were included if they presented clinical data on MG complicated with myocarditis. Of the 35 patients from 28 studies in this review, 57.14% (20/35) were males, with a mean age of 59.11 ± 15.87. Dyspnea was the most common cardiac symptom accounting for over 60% in the study. Among the 35 patients, 13 cases of myocarditis occurred concomitantly with MG and the longest interval between MG and myocarditis was 7 years. Forty percent of patients developed myocarditis caused by immune checkpoint inhibitors (ICI). Among the patients with myocarditis, over half of the patients were diagnosed by myocardial biopsy. After active immune regulation and symptomatic treatment, only 15 of 35 patients with MG complicated with myocarditis improved, 18 patients died during hospitalization, one patient died due to tumor progression and 1patient died 5 years later. The prognosis of patients with MG complicated with myocarditis is poor, and myocardial enzymes and other indexes need to be monitored for patients taking ICI drugs. Patients with dyspnea who are still not ideally treated by mechanical ventilation should be vigilant against the occurrence of MG complicated with myocarditis.

Jia-xi Duan,1,2 Wei Cheng,1,2 Yu-qin Zeng,1,2 Yan Chen,1,2 Shan Cai,1,2 Xin Li,3 Ying-qun Zhu,4 Ming Chen,5 Mei-ling Zhou,6 Li-bing Ma,7 Qi-mi Liu,8 Ping Chen1,2 1Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, People’s Republic of China; 2Research Unit of Respiratory Disease, Central South University, Changsha, Hunan 410011, People’s Republic of China; 3Division 4 of Occupational Diseases, Hunan Prevention and Treatment Institute for Occupational Diseases, Changsha, Hunan 410000, People’s Republic of China; 4Department of Respiratory Medicine, The Third Hospital of Changsha, Changsha, Hunan 410011, People’s Republic of China; 5Department of Respiratory Medicine, The No.1 Traditional Chinese Medicine Hospital in Changde, Changde, Hunan 415000, People’s Republic of China; 6Department of Respiratory Medicine, The First People’s Hospital of Huaihua, Huaihua, Hunan 418000, People’s Republic of China; 7Department of Respiratory Medicine, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541000, People’s Republic of China; 8Department of Respiratory and Critical Care Medicine, The Second People’s Hospital of Guilin, Guilin, Guangxi 541000, People’s Republic of ChinaCorrespondence: Ping ChenDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, 139 Renmin Middle Road, Changsha, Hunan 410011, People’s Republic of ChinaTel +86 731 8529 5248Email pingchen0731@csu.edu.cnPurpose: Tobacco smoking, biomass smoke, and occupational exposure are the main risk factors for chronic obstructive pulmonary disease (COPD). The present study analyzes data on exposure to these factors in a cohort of patients with COPD and assesses their differences in demographic and clinical characteristics.Patients and Methods: The cross-sectional observational study was conducted from November 2016 to December 2019. Inclusion criteria were patients aged over 40 years old with post-bronchodilator forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) < 0.7. At baseline, demographic features and exposure history were recorded. Moreover, respiratory symptoms were assessed by the COPD Assessment Test (CAT) and modified Medical Research Council scale (mMRC). A generalized linear mixed model was used to adjust for potential confounders.Results: A total of 5183 patients with COPD were included in the final analysis. The results demonstrate that exposure to tobacco combined with other risk factors resulted in significantly higher CAT scores (16.0 ± 6.7 vs 15.3 ± 6.3, P = 0.003) and more severe dyspnea (patients with mMRC ≥ 2, 71.5% vs 61.6%, P < 0.001) than exposure to tobacco alone. In addition, COPD patients with biomass smoke exposure alone had higher CAT scores than patients with only tobacco or occupational exposure (17.5 ± 6.3 vs 15.3 ± 6.3, and 15.2 ± 6.3, respectively, P < 0.05 for each comparison) and were more likely to be female and older. In addition, COPD patients who suffered from occupational exposure developed more severe dyspnea than those exposed to tobacco alone (70.8% vs 61.6%, P < 0.05), as did those exposed to biomass smoke alone (74.2% vs 61.6%, P < 0.05). This difference remained strong even after adjustment for potential confounders.Conclusion: There are significant demographic and clinical differences among COPD patients with tobacco smoking, biomass smoke, and occupational exposures.Keywords: chronic obstructive pulmonary disease, tobacco, biomass smoke, occupational exposure

Arachidonic acid can be metabolized to prostaglandins and epoxyeicosatrienoic acids (EETs) by cyclooxygenase-2 (COX-2) and cytochrome P450 (CYP), respectively. While protective EETs are degraded by soluble epoxide hydrolase (sEH) very fast. We have reported that dual inhibition of COX-2 and sEH with specific inhibitor PTUPB shows anti-pulmonary fibrosis and renal protection. However, the effect of PTUPB on cecal ligation and puncture (CLP)-induced sepsis remains unclear. The current study aimed to investigate the protective effects of PTUPB against CLP-induced sepsis in mice and the underlying mechanisms. We found that COX-2 expressions were increased, while CYPs expressions were decreased in the liver, lung, and kidney of mice undergone CLP. PTUPB treatment significantly improved the survival rate, reduced the clinical scores and systemic inflammatory response, alleviated liver and kidney dysfunction, and ameliorated the multiple-organ injury of the mice with sepsis. Besides, PTUPB treatment reduced the expression of hypoxia-inducible factor-1α in the liver, lung, and kidney of septic mice. Importantly, we found that PTUPB treatment suppressed the activation of NLRP3 inflammasome in the liver and lung of septic mice. Meanwhile, we found that PTUPB attenuated the oxidative stress, which contributed to the activation of NLRP3 inflammasome. Altogether, our data, for the first time, demonstrate that dual inhibition of COX-2 and sEH with PTUPB ameliorates the multiple organ dysfunction in septic mice.

Zijing Zhou,1–3 Aiyuan Zhou,1–3 Yiyang Zhao,1–3 Jiaxi Duan,1–3 Ping Chen1–3 1Department of Respiratory Medicine, The Second Xiangya Hospital, Central South University, Changsha, China; 2Research Unit of Respiratory Disease, Central South University, Changsha, China; 3Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, China Background: Both the COPD Assessment Test (CAT) and the Clinical COPD Questionnaire (CCQ) were recommended as comprehensive symptom measures by the Global Initiative for Chronic Obstructive Lung disease. The main objective of this work was to compare the evalua­tion of symptom severity with the CAT and the CCQ and find a cutoff value of the CCQ for the Chinese clinical population. Methods: Patients diagnosed with stable COPD in the outpatient department who completed the CAT and CCQ were enrolled from November 2015 to December 2016. Scores of 0–10, 11–20, 21–30, and 31–40 represent low, medium, high, and very high impact level, respectively, by CAT. Scores of the CCQ can be considered as acceptable (CCQ

Vasoactive intestinal peptide (VIP) is an intrapulmonary neuropeptide with multi-function, including anti-fibrosis. However, the exact role of VIP in pulmonary fibrosis has not been documented. Here, we investigated the protective effect of VIP against pulmonary fibrosis in a murine model induced by bleomycin (BLM). We found that the overexpression of VIP mediated by the adenoviral vector significantly attenuated the lung tissue destruction, reduced the deposition of the extracellular matrix, and inhibited the expression of alpha-smooth muscle actin (α-SMA) in the lungs of mice received BLM. Mechanismly, we found that VIP significantly suppressed the transforming growth factor-beta 1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) and inhibited the matrix-producing ability of alveolar epithelial cells in vitro. Furthermore, we found that TGF-β1 depressed the autophagy and an autophagy inductor partly reversed the TGF-β1-induced EMT in alveolar epithelial cells. The impaired autophagy was also observed in the lungs of BLM-treated mice, which was restored by VIP treatment. And VIP treatment enhanced autophagy in TGF-β1-stimulated alveolar epithelial cells, contributing to its anti-EMT effect. In summary, our data, for the first time, show that VIP attenuates BLM-induced pulmonary fibrosis in mice with anti-EMT effect through restoring autophagy in alveolar epithelial cells. This study provides a possibility that inhaled long-acting VIP may be an anti-fibrotic drug in the treatment of pulmonary fibrosis.

Non-alcoholic fatty liver disease (NAFLD) affects 25% of the global adult population, and no effective pharmacological treatment has been found. Products of arachidonic acid metabolism have been developed into a novel therapy for metabolic syndrome and diabetes. It has been demonstrated that protective actions of a novel dual cyclooxygenase-2 (COX-2) and soluble epoxide hydrolase (sEH) inhibitor, PTUPB, on the metabolic abnormalities. Here, we investigated the effects of PTUPB on hepatic steatosis in high-fat diet (HFD)-induced obese mice, as well as in hepatocytes in vitro. We found that PTUPB treatment reduced body weight, liver weight, liver triglyceride and cholesterol content, and the expression of lipolytic/lipogenic and lipid uptake related genes (Acc, Cd36, and Cidec) in HFD mice. In addition, PTUPB treatment arrested fibrotic progression with a decrease of collagen deposition and expression of Col1a1, Col1a3, and α-SMA. In vitro, PTUPB decreased palmitic acid-induced lipid deposition and downregulation of lipolytic/lipogenic genes (Acc and Cd36) in hepatocytes. Additionally, we found that PTUPB reduced the production of pro-inflammatory cytokines and suppressed the NLRP3 inflammasome activation in HFD mice and hepatocytes. In conclusion, dual inhibition of COX-2/sEH attenuates hepatic steatosis by inhibiting the NLRP3 inflammasome activation. PTUPB might be a promising potential therapy for liver steatosis associated with obesity.

Background: There is currently no recognized discharge criteria for patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). In clinical work, pulmonologists determine whether a patient can be discharged considering the patient self-reported health status and some measurements which are related to the health status of AECOPD patients. Various measurements have been used to evaluate health status in patients with AECOPD, including lung function, fractional exhaled nitric oxide (FENO), blood gas analysis, COPD Assessment Test (CAT) and modified Medical Research Council test (mMRC). However, which one is most closely related to the patient self-reported health status remains unknown. Methods: Patients with AECOPD were assessed at two visits: on admission and on day 7. The above measurements were tested at each visit. At the second visit, the patients were asked to report the health status according to a five-point Likert scale ranging from 1 to 5, representing ‘much better’, ‘slightly better’, ‘no change’, ‘slightly worse’ and ‘much worse’. Based on patients self-reported outcome, we defined the responders as those patients who reported “much better,” or “slightly better”, non-responders were those who reported ‘no change,’ ‘slightly worse’ or ‘much worse’. Results: 55 patients were recruited into analysis. FENO and CAT could change sensitively based on different health status, except failing to differentiate the patients between those who reported ‘slightly better’ and ‘no changes’. The changes in predicted percentage of forced expiratory volume in 1 s (FEV1%) didn’t change significantly between ‘no change’ group and ‘slightly better or much better’ group, it could only identify the ‘slightly worse’ patients. Although mMRC and blood gas analysis (PaO2, PaCO2) changed significantly after treatment, they didn’t reflect sensitively the evolution of health status. Among these measurements, the changes in CAT was best correlated with the evolution of health status (Rho=0.81), followed by FENO and FEV1%, the rho was 0.59 and -0.42, respectively. Conclusion: It’s reasonable to monitor CAT and FENO during exacerbation stage, the use of lung function and mMRC to evaluate the evolution of patients’ reported health status of patients with AECOPD is limited. Registry number: ChiCTR-ROC-16009087 (http://www.chictr.org.cn/).

Objective. Allergic asthma is a chronic inflammatory disease, which seriously affects the life quality of patients, especially children. Alanylglutamine is a nutritional supplement with potential protective and anti-inflammatory effects, but its function in allergic asthma remains elusive. In this study, we focused on the investigations of the roles and functional mechanism of Alanylglutamine in asthma. Methods. Ovalbumin (OVA) induction was utilized to establish a mouse asthma model. 16S rDNA sequencing was performed to compare the diversity of intestinal microorganisms under different treatments. Gas chromatography was utilized to screen the intestinal microbe-short-chain fatty acids in the stool. The lung tissue was extracted to determine signaling pathways, including AMPK, NF-κB, mTOR, STAT3, IKKβ, TGF-β, and IL-1β through Western blot or RT-qPCR. Results. It was observed that Alanylglutamine reduced the cytokine in OVA-induced allergic asthma mice. H&E staining showed obvious pneumonia symptoms in the asthma group, while Alanylglutamine alleviated the inflammatory infiltration. Alanylglutamine reversed gut microbiota compositions in OVA-induced allergic asthma mice and enhanced the butyric acid level. The protective role of Alanylglutamine may be associated with the gut microbiota-butyric acid-GPR43 pathway in asthma mice. In contrast to the OVA group, Alanylglutamine activated the protein expression of P-AMPK/AMPK and inhibited the protein expression of P-mTOR/mTOR, P-P65/P65, P-STAT3/STAT3, P-IKKβ/IKKβ, TGF-β, and IL-1β, with similar effects from butyric acid. Conclusion. The results indicated that Alanylglutamine might be beneficial for asthma, and its effect was achieved through the regulation on microbiota and the derived metabolites. The therapeutic effects might be associated with AMPK, NF-κB, mTOR, and STAT3 signaling pathways. These findings will help identify effective therapeutic direction to alleviate allergic inflammation of the lungs and airways.

Background: The Clinical COPD Questionnaire (CCQ) has been suggested by the Global Initiative of Chronic Obstructive Lung Disease (GOLD) as a comprehensive symptom measurement tool, which helps to classify patients in order to direct pharmacological treatment. Therefore, it is essential to understand its determinants. Objectives: To identify the determinants of the overall CCQ score and scores of its 3 subdomains among chronic obstructive pulmonary disease (COPD) patients from China. Methods: A total of 1,241 COPD patients in the outpatient department of the Second Xiangya Hospital in China were recruited. Basic information and clinical data were collected. Differences in the GOLD categories based on Modified Medical Research Council Dyspnea Scale (mMRC), COPD Assessment Test (CAT), and CCQ were compared. Multiple linear regression analyses were performed to evaluate determinant factors of the total CCQ and subdomain scores. Results: The total CCQ and/or separate domain scores significantly differed with sex, age, BMI, smoking status, biomass fuel exposure, exacerbation frequency, mMRC, CAT, and GOLD grades and groups. Subjects with asthma-COPD overlap (ACO) had worse health status based on CCQ than those with COPD alone. As for the 16 subgroups based on GOLD 2017, statistical differences in the total CCQ and functional domain scores were found among subgroups 1A–4A, 1B–4B, and 1D–4D. The mMRC classified much more patients into more symptom groups than CAT and CCQ. No significant difference was observed in the GOLD categories between the CAT and CCQ (cut point = 1.5). Multiple linear regression analysis showed that smoking status, underweight, ACO, post-bronchodilator FEV1% predicted Conclusions: The classification of COPD produced by mMRC, CAT, and CCQ was not identical. Smoking status, underweight, ACO, post-bronchodilator FEV1% predicted

Aiyuan Zhou,1–3 Zijing Zhou,1–3 Yating Peng,1–3 Yiyang Zhao,1–3 Jiaxi Duan,1–3 Ping Chen1–3 1Department of Respiratory Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; 2Research Unit of Respiratory Disease, Central South University, Changsha, Hunan 410011, China; 3Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, Hunan 410011, China Background: The chronic obstructive pulmonary disease (COPD) Assessment Test (CAT) questionnaire is a short patient-completed questionnaire, which is used to assess the health status of patients with stable COPD. However, whether it is a good tool to evaluate the response to treatment in acute exacerbation of COPD (AECOPD) has been less studied.Methods: The patients were assessed at two visits, at admission and on the seventh day. Anthropometric variables were collected at admission. CAT and lung function were measured twice at the above time points. At the second visit, the health status of the patients were divided into five groups based on a 5-point Likert scale, ranging from 1 to 5, which represents “much better,” “slightly better,” “no change,” “slightly worse,” and “much worse.” Responders were those who reported “much better” or “slightly better,” and nonresponders were those who claimed “no change,” “worse,” or “much worse.”Results: In total, 225 patients were recruited. The average CAT score at admission was 24.82±7.41, which declined to 17.41±7.35 on the seventh day. There were 81.33% responders, whose improvement in CAT score (9.37±5.24) was much higher than that of the nonresponders (−1.36±4.35). A moderate correlation was observed between the changes in CAT score and improvement in FEV1, FEV1%, and the length of hospital stay. There was a strong correlation between the changes in CAT score and health status. A 3.5-unit improvement in the CAT score, with highest area under the curve, was the cutoff to differentiate responders from nonresponders.Conclusion: The evolution of CAT scores during exacerbation can provide useful information to assess the health status of patients with AECOPD. A 3.5-unit improvement in CAT score is the best cutoff to differentiate between patients who have a response or no response to treatment, which offers a convenient and easy way for clinicians to monitor the health status of patients with an AECOPD. Keywords: COPD, acute exacerbation, CAT, curative effect

Epoxyeicosatrienoic acids (EETs), the metabolites of arachidonic acid derived from the cytochrome P450 (CYP450) epoxygenases, are mainly metabolized by soluble epoxide hydrolase (sEH) to their corresponding diols. EETs but not their diols, have anti-inflammatory properties and inhibition of sEH might provide protective effects against inflammatory fibrosis. We test the effects of a selected sEH inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), on bleomycin-induced pulmonary fibrosis (PF) in mice. A mouse model of PF was established by intratracheal injection of bleomycin and TPPU was administered for 21days after bleomycin injection. We found TPPU treatment improved the body weight loss and survival rate of bleomycin-stimulated mice. Histological examination showed that TPPU treatment alleviated bleomycin-induced inflammation and maintained the alveolar structure of the pulmonary tissues. TPPU also decreased the bleomycin-induced deposition of collagen and the expression of procollagen I mRNA in lung tissues of mice. TPPU decreased the transforming growth factor-β1 (TGF-β1), interleukin-1β (IL-1β) and IL-6 levels in the serum of bleomycin-stimulated mice. Furthermore, TPPU inhibited the proliferation and collagen synthesis of mouse fibroblasts and partially reversed TGF-β1-induced α-smooth muscle actin expression. Our results indicate that the inhibition of sEH attenuates bleomycin-induced inflammation and collagen deposition and therefore prevents bleomycin-induced PF in a mouse model.

BACKGROUND:Pneumoconiosis may play an important role in the development of chronic obstructive pulmonary disease (COPD), and the complication of COPD may impose a heavy burden of illness. METHODS:The study was conducted in Hunan Province in China from December 1, 2015, to December 1, 2016. Consecutive underground male pneumoconiosis patients employed for at least 1year were recruited from the Hunan Occupational Disease Prevention Institute. Patient information, respiratory symptoms and clinical data were collected using a structured questionnaire. The diagnosis of COPD were assessed using the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria. Logistic regression analyses were conducted to examine the clinical and demographic risk factors of COPD among pneumoconiosis patients. RESULTS:The prevalence of COPD in our sample of pneumoconiosis patients was 18.65% (119/638). In pneumoconiosis patients with and without smoking history, the prevalence of COPD was 19.32 and 16.77%. Compared with non-COPD patients, those with COPD are older in age, have longer exposure time, have lower body mass index (BMI), have a higher smoking index and have worse pulmonary function (all p

Pulmonary fibrosis is a life-threatening disease characterized by progressive dyspnea and worsening of pulmonary function. No effective therapeutic strategy for pulmonary fibrosis has been established. Aucubin is a natural constituent with a monoterpene cyclic ring system. The potency of aucubin in protecting cellular components against inflammation, oxidative stress, and proliferation effects is well documented. In this study, we investigated the protective effect of aucubin against pulmonary fibrosis in mice. A mouse model of pulmonary fibrosis was established by intratracheal injection of bleomycin (BLM), and aucubin was administered for 21 days after BLM injection. We found that aucubin decreased the breathing frequency and increased the lung dynamic compliance of BLM-stimulated mice detected by Buxco pulmonary function testing system. Histological examination showed that aucubin alleviated BLM-induced lung parenchymal fibrotic changes. Aucubin also reduced the intrapulmonary collagen disposition and inflammatory injury induced by BLM. In addition, aucubin reduced the expression of pro-fibrotic protein transforming growth factor (TGF)-β1 and α-smooth muscle actin (α-SMA) of pulmonary fibrosis mice induced by BLM. Furthermore, the effect of aucubin on the proliferation and differentiation of fibroblast was investigated in vitro. Aucubin inhibited the mRNA and protein expression of Ki67 and proliferating cell nuclear antigen (PCNA) induced by TGF-β1 and reduced the cell proliferation in a murine fibroblast cell NIH3T3. Aucubin also reduced the collagen syntheses and α-SMA expression induced by TGF-β1 in fibroblast. Our results indicate that aucubin inhibits inflammation, fibroblast proliferation, and differentiation, exerting protective effects against BLM-induced pulmonary fibrosis in a mouse model. This study provides an evidence that aucubin may be a novel drug for pulmonary fibrosis.

Background and aims: Various prediction indices based on the single time point observation have been proposed in chronic obstructive pulmonary disease (COPD), but little was known about disease trajectory as a predictor of future exacerbations. Our study explored the association between disease trajectory and future exacerbations, and validated the predictive value of the modified and simplified short-term clinically important deterioration (CID). Methods: This study was a multicenter, prospective observational study. Patients with COPD were recruited into our study and followed up for 18 months. The modified CID (CID-C) was defined as a decrease of 100 mL in forced expiratory volume in 1 second (FEV1), or suffering exacerbations, or increase of 2 units in COPD Assessment Test (CAT) during the first 6 months follow-up. Simplified CID was defined when excluding CAT from the CID-C model. Results: A total of 127 patients were enrolled in our final analysis. Compared with patients without exacerbations during the period of the 6th to the 18th month, patients with exacerbations were more likely to have frequent short-term exacerbations in the first 6 months (2.14 versus 0.21, p Conclusion: Disease trajectory, including both the CID-C and the Simplified CID had significant predictive value for future exacerbations. The reviews of this paper are available via the supplemental material section.