Airflow Limitation Research Articles

Update of prognosis and characteristics of chronic obstructive pulmonary disease in a real-world setting: a 5-year follow-up analysis of a multi-institutional registry.

We conducted a prospective observational study to elucidate the long-term prognosis and management of chronic obstructive pulmonary disease (COPD) in clinical practice in Japan in the mid-2010s. This prospective cohort study included 29 facilities. Data from 427 patients clinically diagnosed with COPD, enrolled between September 2013 and April 2016, were analyzed. Interstitial pneumonia was excluded through a central multidisciplinary discussion. Follow-up data were collected for up to 5 years after patient registration. At the time of registration, 53 patients clinically diagnosed with COPD did not have airflow limitation (AFL). In the cohort with AFL (n = 374), 232 patients completed a 5-year follow-up, while 49 patients died during the 1576.6 person-years of observation. The mean age was 71.7 years with an overall 5-year survival rate of 85.4%. Stratified by % forced expiratory volume in one second (FEV1), survival rates were 93.6% in the mild and moderate AFL group, 82.5% in the severe AFL group, and 66.1% in the very severe AFL group. The prognosis of the subpopulation without AFL was poor with a 5-year survival of 81.6%. This subpopulation exhibited respiratory symptoms, low vital capacity and total lung capacity, and emphysematous changes. Our study presents the 5-year survival and real-world clinical practice scenario of a prospective cohort of patients clinically diagnosed with COPD in Japan in the mid-2010s. The survival rates of our cohort were numerically better than the Japanese cohort in the 1990s, regardless of the high median age of this cohort. Overall, 12.4% of the patients in this cohort with no AFL at registration exhibited respiratory symptoms and distinct spirometric patterns, and had a poor prognosis.

Persistent Airflow Limitation Prediction and Risk Factor Analysis Among Asthmatic Children: A Retrospective Cohort Study.

A minority of asthmatic children develop persistent airflow limitation (PAL), associated with an increased risk of chronic airflow obstruction and poor prognosis. This study aimed to identify risk factors for PAL and develop a prediction model to identify high-risk asthmatic children. This retrospective study included 2072 children (5-16 years) with asthma. After a 2-year follow-up, patients were categorized into non-PAL, reversible PAL (RPAL), and irreversible PAL (IPAL) groups. Logistic regression (LR) was used to identify independent risk factors for RPAL and IPAL. A prediction model based on multivariate LR was developed and validated to identify asthmatic children at high risk of developing PAL. A nomogram was created for visualization. Among the 2072 asthmatic patients, 14.72% (n = 305) developed PAL. Asthma exacerbation history (OR 1.80, 95% CI 1.03-3.01) and poor adherence (OR 1.83, 95% CI 1.26-2.65) were independent risk factors of RPAL. Independent risk factors for IPAL were BMI over 19.0 kg/m2 (OR: 1.81, 95% CI: 1.03-3.21) and a history of pneumonia (OR: 2.40, 95% CI: 1.30-4.26). The prediction model incorporated nine variables and showed good discriminatory ability, with AUC values of 0.79 (95% CI: 0.76-0.81) for the training set, 0.76 (95% CI: 0.76-0.77) for internal validation, and 0.73 (95% CI: 0.64-0.81) for temporal validation. Asthma exacerbation history and poor adherence were independent risk factors for developing RPAL. BMI over 19.0 kg/m2 and a history of pneumonia were risk factors for IPAL. Our prediction model effectively identified asthmatic children at high risk of developing PAL.

Associations of pulmonary microvascular blood volume with per cent emphysema and CT emphysema subtypes in the community: the MESA Lung study

BackgroundPulmonary microvasculature alterations are implicated in emphysema pathogenesis, but the association between pulmonary microvascular blood volume (PMBV) and emphysema has not been directly assessed at scale, and prior studies have...

Refractory phenotype of Aspergillus-sensitized asthma with bronchiectasis and allergic bronchopulmonary aspergillosis

BackgroundSensitization to Aspergillus, mucus plugs, and bacterial colonization may coexist and relate to a refractory phenotype during follow-up in asthma with bronchiectasis and allergic bronchopulmonary aspergillosis (ABPA). ObjectiveThis study aimed to clarify the features of Aspergillus-sensitized refractory asthma with bronchiectasis and determine the refractory phenotype in this population and ABPA. MethodsThis study included cases with the oldest available A. fumigatus-specific IgE data and chest computed tomography images from a nationwide survey of refractory asthma with bronchiectasis. The characteristics of the A. fumigatus-IgE positive (Af sIgE+) group were investigated and compared with its nonsensitized counterpart (Af sIgE−) and ABPA group. Cluster analysis was conducted to determine the refractory phenotype. ResultsThe Af sIgE+ group (n = 35) demonstrated type-2 inflammation levels intermediate between the ABPA (n = 42) and Af sIgE− (n = 38) groups while exhibiting higher blood monocyte counts than Af sIgE− group. Cluster analysis conducted in patients with ABPA and Af sIgE+ newly determined two clusters: one was characterized by a younger age of asthma onset with fungal detection in sputum and the other was characterized by mucus plugs, inflammation with eosinophil and monocyte, which was significantly related to mucus plugs, airflow limitation, and trend to show exacerbation. In the latter cluster, mucus plugs persisted and 30% yielded Pseudomonas aeruginosa in the sputum <5 years later. ConclusionThe refractory phenotype with persistent mucus plugs was identified in Aspergillus-sensitized refractory asthma with bronchiectasis and ABPA. Mucus plug prevention is warranted.

Brief Report: Alternative Pulmonary Function Measures of Emphysema in People With HIV.

People with HIV (PWH) have nearly twice the risk of emphysema than people without HIV. This risk, which has been associated with HIV-mediated changes in the lung immune environment and more extensive radiographic emphysema, may result in different patterns of airflow limitation on pulmonary function testing (PFT) than those traditionally used in people without HIV. In this prospective cohort of PWH in Atlanta, Georgia, we analyzed PFT and chest computed tomography data from July 2013 through June 2018. After comparing the prevalence of PFT measures of airflow limitation for those with and without radiographic emphysema, we used binary recursive partitioning to identify PFT measures that differentiated between PWH with and without radiographic emphysema. Among 167 PWH who had both PFT and computed tomography data during the study period, 89 (53%) had radiographic emphysema. Those with radiographic emphysema were more likely to have airflow limitations on PFTs. Recursive partitioning identified partitions at a forced expiratory volume in 1 second to forced vital capacity ratio (FEV1/FVC) of 0.78 and a residual volume of 116% predicted. These partitions enabled the identification of 84 (94%) PWH with radiographic emphysema, in contrast to the traditional diagnostic criteria of an FEV1/FVC ratio of 0.7, which only identified 49 (55%) of those with radiographic emphysema. Emphysema in PWH may have different patterns of airflow limitation on PFTs that are not adequately captured by traditional diagnostic criteria. Future studies can seek to validate these findings and determine optimal thresholds for diagnosing HIV-associated emphysema.

An underrecognized phenotype of pulmonary emphysema with marked pulmonary gas exchange but with mild or moderate airway obstruction

In patients with pulmonary emphysema and mild to moderate airflow limitation, one does not expect the features marked exertional dyspnea and hypoxemia as well as a profound decrease in diffusing capacity of the lung for carbon monoxide (DLCO). Here we describe this phenotype and its prognosis. From our database, we retrospectively selected cases associating emphysema, exertional breathlessness, O2 requirement at least upon exercise, forced expiratory volume in 1 sec (FEV1) ≥ 50% predicted, and DLCO ≤ 50% predicted, without associated combined pulmonary fibrosis and emphysema, right-to-left shunt, or severe pulmonary hypertension. Over a 12-year period, we identified 16 patients with emphysema and the above presentation. At the initial evaluation, the median age was 62 years (interquartile range 53.8–68.9). The median FEV1 and DLCO% predicted and mean pulmonary artery pressure were 86 (65–95)%, 38 (31–41)%, and 20 (17–25) mm Hg, respectively. On room air, the median arterial partial pressure of oxygen and partial pressure of carbon dioxide in arterial blood were 63.5 (55.8–69) mm Hg and 34.5 (31–36) mm Hg with increased median alveolar-arterial oxygen difference (46 [39–51] mm Hg). After the initial evaluation, the respiratory condition worsened in 13 of 14 (92.8%) patients with one or more re-evaluations (median follow-up 2.6 [0.9–5.8] years). In 12, lung transplantation was considered. Four patients died after 5.8, 5.7, 7.1, and 0.8 years of follow-up, respectively. We describe an underrecognized phenotype of pulmonary emphysema featuring a particular profile characterized by marked exertional dyspnea, impaired pulmonary gas exchange with low DLCO and marked oxygen desaturation at least on exercise but with mild or moderate airway obstruction.

Severe Respiratory Acidosis in Acute Exacerbation COPD, Is that Possible to Treat?

Introduction: Chronic obstructive pulmonary disease (COPD), currently the third leading cause of death worldwide, is a common condition characterized by progressive airflow limitation and tissue destruction. Patients with COPD may present to the Emergency Room (ER) with severe acute exacerbations (AECOPD), which can be associated with acute respiratory failure—a life-threatening condition with a mortality rate approaching 50% in Indonesia—requiring rapid intervention and ICU admission. In this report, we present a severe respiratory acidosis in AECOPD case with successful emergency followed by ICU management and the frequent pitfalls. Case Illustration: In this report we present a-67 years old male, pedicab driver and smoker came to the ER with acute onset shortness of breath and decrease of consciousness with history of shortness of breath in last 10 years. In primary survey we found clear wheezing sound, tachypnea, intercostal retraction, decrease of peripheral oxygen saturation, tachycardia and verbal respond of consciousness. Blood gas analysis result interpreted severe respiratory acidosis with pH 6.90 and pCO2 128.5 mmHg. Chest radiograph showed infiltrate that became the cause of exacerbation. Endotracheal intubation was performed due to decreased consciousness, persistent tachypnea and pCO2 over 100 mmHg. This patient was hospitalized for 12 days including 9 days in ICU followed by 3 days in regular ward. Conclusion: The goal for AECOPD management is to minimize and prevent the negative effects of the exacerbation.

A Study on the Correlation Between Sarcopenia and Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a disease that affects the entire body. Sarcopenia, one of the adverse manifestations of the whole body, can lead to a variety of adverse outcomes. The worldwide studies have shown that sarcopenia was associated with COPD. This article aims to further enrich this research direction by focusing on the relationship between sarcopenia and COPD in Chinese inpatients. The subjects of this study were patients hospitalized in the Department of Respiratory and Critical Care Medicine of Rongchang People&amp;apos;s Hospital of Chongqing from July 2022 to May 2024. After bioelectrical impedance analysis (BIA), test of 6 m walking speed, and tests for upper grip strength were accomplished, the sarcopenia can be diagnosed. According to the presence of chronic airflow limitation, which assessed by post-bronchodilator spirometry, we diagnosed COPD. COPD and sarcopenia as two variables, simple correlation analysis was adopted for them. The subjects were classified into sarcopenia group and non-sarcopenia group. And then, the correlation between sarcopenia and COPD was assessed with binary logistic regression analysis. Finally we get the results. Spearman&amp;apos;s correlation coefficient for sarcopenia and COPD was 0.166 (p&amp;lt;0.05). While, COPD was not an independent risk factor to sarcopenia in the binary logistic regression analysis. Therefore, this study draws conclusions that COPD and sarcopenia is associated, but not linked independently.

Psychiatric Disorders in Patients with Chronic Obstructive Pulmonary Disease: Clinical Significance and Treatment Strategies

Chronic obstructive pulmonary disease (COPD) is a debilitating lung disease characterized by chronic airflow limitation and persistent respiratory symptoms. It is a major cause of morbidity and mortality worldwide, significantly impacting healthcare systems with considerable socioeconomic consequences. The main risk factors include exposure to tobacco smoke, environmental pollutants, occupational dust, and genetic factors such as alpha-1 antitrypsin deficiency. COPD is often associated with extrapulmonary comorbidities, particularly psychiatric disorders like depression and anxiety, which worsen patients’ quality of life and prognosis. The prevalence of these disorders in patients with COPD varies significantly but is always higher than in healthy controls. Psychiatric disorders can negatively influence COPD management and vice versa, creating a complex bidirectional interaction. Depression and anxiety are the most common psychiatric comorbidities in patients with COPD, influenced by factors such as social isolation, physical limitations, and fear of exacerbations. Diagnosis of these psychiatric disorders is complicated by the overlap of symptoms with those of COPD. However, some screening tools can facilitate early detection. The treatment of psychiatric disorders in patients with COPD in a rehabilitation setting requires a multidisciplinary approach involving pulmonologists, neurologists and psychologists. Pharmacological therapy with antidepressants shows mixed results in terms of efficacy and safety, with some studies reporting benefits on quality of life and others suggesting an increased risk of exacerbations and pneumonia. An integrated approach that includes the assessment and intervention of mental disorders is essential to improve the overall management of COPD and the quality of life of patients. This narrative review provides an overview of the main psychiatric comorbidities in COPD patients, aiming to fill gaps in the literature and suggest areas for future research.

Peak Flow Feedback Intervention Improves Under-Perception of Airflow Limitation in Pediatric Asthma: A Randomized Clinical Trial.

Under-perception of asthma symptoms is associated with poor asthma outcomes. We assessed the effects of a behavioral intervention for improving perception of airflow limitation and asthma outcomes. A two-arm randomized controlled trial compared peak expiratory flow (PEF) feedback versus supportive counseling. Latino and Black adolescents with asthma ages 10-17 years old and caregivers were recruited from hospitals in the Bronx, NY. PEF feedback sessions reviewed accuracy of PEF guesses and medication adherence data, and targeted behavior change using motivational interviewing and problem-solving skills training. Supportive counseling received emotional support related to asthma. Both groups received 3 sessions across 6 weeks. All participants were blinded to PEF while guessing PEF during pre-intervention, 1, 6, and 12-month follow-up. Children in PEF feedback saw actual PEF after guesses were locked in during the 6-week intervention. Participants and assessors were blinded to group assignment. The primary outcome was under-perception of airflow limitation (divergence between actual PEF and guesses) on home spirometers. Secondary outcomes included daily PEF and forced expiratory volume in 1 second (FEV1), inhaled corticosteroid adherence measured by electronic monitors, Asthma Control Test, and emergency healthcare use for asthma. The sample comprised 354 children (M = 13.2±2.2 years; 62% Latino, 38% Black) and caregivers. PEF feedback (N = 153 analyzed) demonstrated greater improvements at 1-month follow-up on under-perception of airflow limitation (difference-in-differences, -12.64; 95% CI, -17.54 to -7.74), % personal best PEF (9.89; 95% CI, 7.13 to 12.65), % predicted FEV1 (4.93; 95% CI, 0.95 to 8.90) and ICS adherence (16.02; 95% CI, 7.15 to 24.89) compared with supportive counseling (N = 152 analyzed). At 12-month follow-up PEF feedback maintained improvements on under-perception of airflow limitation (-13.87; 95% CI, -19.03 to -8.71), higher PEF (14.23; 95% CI, 11.37 to 17.08) and %FEV1 (5.62; 95% CI, 1.56 to 9.67), and had smaller declines in ICS adherence (17.51; 95% CI, 7.12 to 27.89) versus pre-intervention than supportive counseling. No between-group differences existed for asthma control or healthcare use. The efficacy and sustainability of PEF feedback was established in improving children's perception of airflow limitation, pulmonary function, and medication adherence. Clinical trial registration available at www. gov, ID: NCT02702687.

Stability of severe asthma phenotypes

Introduction. Severe asthma (SA) is a heterogeneous disease with several phenotypes. There are lack of data about its stability.Aim. To assess stability of SA phenotypes in adult patients during 5 years follow-up.Materials and methods. Prospective study included 117 adult outpatients with allergic SA, 51 severe asthmatics with aspirin-induced disease, 59 patient with persistent airflow limitation (PAL) and 35 patients with SA and concomitant COPD, 65 steroid-dependent severe asthmatics and 89 patients with SA and frequent (≥2 per year) exacerbations. Spirometry and bronchodilator reversibility testing were carried out; fractional exhaled nitric oxide (FeNO) was measured; hypersensitivity to common inhalant allergens (skin prick and blood specific IgE testing) and peripheral blood eosinophil counts were estimated. Asthma control and asthma-related quality of life were assessed by using ACQ-5 and SGRQ questionnaire.Results. During 5-year prospective study stability of aspirin-induced SA and SA with COPD was 100%. Allergic phenotype was stable in 81% of SA cases and in patients with changed atopic status we revealed worsening of symptoms and accelerated lung function decline. Stability of SA phenotype with PAL without COPD was 86% and steroid-dependent SA was stable in 55% of cases. After 5 years of treatment frequent exacerbations remained in 28% of severe asthmatics.Conclusion. The most stable phenotypes of SA were aspirin-induced and asthma with concomitant COPD. Less stable were allergic SA, steroid-dependent SA and phenotype with persistent airflow limitation. The least stable was SA phenotype with frequent exacerbations.

Severe asthma phenotypes and endotypes

Introduction. Severe asthma is a heterogeneous disease with several phenotypes and endotypes. However, little is known about frequency of severe asthma phenotypes and endotypes in Russia.Aim. To assess frequency of severe asthma phenotypes and endotypes compared with mild/moderate asthma.Materials and methods. Cross-sectional single center study included 643 adult outpatients with mild/moderate asthma and 314 patients with severe asthma (SA) aged 18–90 years. Spirometry and bronchodilator reversibility testing were carried out. Fractional exhaled nitric oxide (FeNO) was measured by a chemiluminescent analyzer (logan 4100, UK). Hypersensitivity to common inhalant allergen was assessed by skin prick and blood specific IgE level. Peripheral blood eosinophil counts were measured by automatic analyzer. Asthma control and asthma-related quality of life were assessed by using ACQ-5 and SGRQ.Results. Allergic phenotype was more frequent in patients with mild/moderate asthma than in those with SA, but aspirin-induced asthma, steroid-dependent asthma, asthma with persistent airflow limitation and concomitant COPD, asthma with late onset and obesity were more frequent in SA. The majority of patients with SA had several phenotypes (mean 3 phenotypes) and at least one marker of T2-high endotype.Conclusion. The most frequent phenotypes of SA were allergic, with persistent airflow limitation, with concomitant obesity and COPD. Occurrence of asthma phenotypes differed between patients with SA and mild/moderate asthma. The majority of SA patients have T2-endotype.

Requirement for Fucosyltransferase 2 in Allergic Airway Hyperreactivity and Mucus Obstruction.

Mucus hypersecretion is an important pathological problem in respiratory diseases. Mucus accumulates in the airways of people with asthma, and it contributes to airflow limitation by forming plugs that occlude airways. Current treatments have minimal effects on mucus or its chief components, the polymeric mucin glycoproteins MUC5AC and MUC5B. This treatment gap reflects a poor molecular understanding of mucins that could be used to determine how they contribute to airway obstruction. Due to the prominence of glycosylation as a defining characteristic of mucins, we investigated characteristics of mucin glycans in asthma and in a mouse model of allergic asthma. Mucin fucosylation was observed in asthma, and in healthy mice it was induced as part of a mucous metaplastic response to allergic inflammation. In allergically inflamed mouse airways, mucin fucosylation was dependent on the enzyme fucosyltransferase 2 (Fut2). Fut2 gene deficient mice were protected from asthma-like airway hyperreactivity and mucus plugging. These findings provide mechanistic and translational links between observations in human asthma and a mouse model that may help improve therapeutic targeting of airway mucus.

Personalized COPD Care: The Future of Precision-Based Therapies

Chronic obstructive pulmonary disease (COPD) is a progressive respiratory illness characterized by long-standing respiratory symptoms and airflow limitation. It is a major contributor to respiratory disease-related deaths and currently ranked as the sixth leading cause of mortality in the United States. Approved pharmacological therapies for the stable disease primarily consist of inhaled short and long-acting bronchodilators, inhaled corticosteroids, azithromycin, and roflumilast. In recent years, significant progress has been made in the management of COPD through the identification of different COPD phenotypes and endotypes, which allows for a more personalized treatment approach. While earlier studies investigating targeted therapies were less promising, recent data on drugs targeting type 2 inflammatory pathways have shown promising results in carefully selected patients. In this article, we will review the available data on targeted therapies as well as the ongoing clinical studies of novel targeted therapies for COPD. Understanding and implementing these advancements hold promise for improving outcomes and quality of life for individuals living with COPD.

Intermittent Exercise and Cigarette Smoke Extract-Induced Pulmonary Tensegrity Dysfunction; Monitoring Elastin, Matrix Metalloproteinase-12, Transforming Growth Factor-beta 1

Background: Cigarette smoke causes inflammation of the alveoli, leading to airflow restriction and potentially irreversible changes in lung architecture, including pulmonary emphysema. This study investigates the effects of a six-week aerobic interval training regimen on elastin activity in a rat model of cigarette smoke-induced COPD (CS-COPD). Objectives: Specifically, we observe the variables matrix metalloproteinase-12 (MMP12) and transforming growth factor-beta (TGF-β1). Methods: Twenty male Wistar rats, aged eight weeks, were divided into four groups (n = 5 per group): Control, aerobic interval training (Exe), cigarette smoke extract (CSE), and CSE + Exe. The aerobic interval training (Exe) was performed for 49 min/day, five days per week for six weeks in interval form. The CSE group received an intraperitoneal (IP) injection of 150 µL of cigarette smoke extract, one day per week for six weeks. Results: The CSE and CSE + Exe groups showed a significant decrease in elastin gene expression in lung tissue compared to the healthy control group (P = 0.0002 and P = 0.0057, respectively) and the Exe group (P = 0.0002 and P = 0.0042, respectively). Additionally, the CSE group exhibited a significant increase in lung MMP12 gene expression compared to the healthy control and Exe groups (P = 0.0008 and P = 0.0013, respectively). Notably, the CSE + Exe group showed a significant decrease in MMP12 gene expression in lung tissue compared to the CSE group (P = 0.0015). Furthermore, the CSE and CSE + Exe groups demonstrated a significant increase in TGFB1 gene expression in lung tissue compared to the healthy control group (P &lt; 0.0001 and P = 0.0022, respectively) and the Exe group (P &lt; 0.0001 for both). Conclusions: Our findings indicate that the group exposed to cigarette smoke experienced a significant decrease in elastin levels, accompanied by an increase in MMP12 and TGF-β1 expression. Although aerobic interval training provided some protection against the detrimental effects of cigarette smoke exposure, it was not sufficient to fully reverse the harmful impacts of the disease.

A novel ventilation method: Experimental measurement and numerical simulation of vertical single-row inclined slit ventilation

Existing ventilation technologies often struggle to balance the limited airflow supply with the demands of indoor ventilation and air circulation in winter. This paper introduces a novel ventilation method, vertical single-row inclined slit ventilation (VSISV), which channels airflow through multiple inclined slits spaced at specific intervals along a vertical supply air duct. By ensuring continuity of the upstream and downstream slit jets, a continuous downward airflow is formed, enhancing both winter ventilation performance and indoor air circulation. The method was experimentally measured, with a focus on comparison to the IJV system. At the same airflow rate, it not only efficiently transports the supply air heat from the upper indoor area to the floor but also exhibits strong horizontal diffusion capability. The RNG turbulence model was selected for numerical simulation, focusing on indoor thermal comfort, air quality, and energy-saving potential. The results indicate that, at the same airflow rate, this method effectively maintains high indoor thermal comfort, directs airflow downward from the ceiling, reduces thermal stratification in the upper zone, achieves a more uniform and elevated indoor temperature, enhances indoor air quality, and demonstrates substantial energy-saving potential. This provides valuable insights for energy conservation, emission reduction, and the optimization in winter building ventilation systems.

Camel milk inhibits pulmonary oxidative stress and inflammation in a rat model of COPD induced by cigarette smoke exposure

BackgroundOne of the main causes of death in the world is chronic obstructive pulmonary disease (COPD) with partially reversible airflow limitation, which is defined as a preventable and treatable pathological condition. Anti-inflammatory and antioxidant properties of camel milk (CM) were indicated previously. The effect of CM in cigarette smoke induced-COPD in rats was evaluated in this study. MethodsFive groups of rats including a) control, b) chronic obstructive pulmonary diseases (COPD, cigarette smoke exposed), c) COPD group treated with dexamethasone, d) COPD group treated with low dose of camel milk (CM) and e) COPD group treated with high dose of CM by gavage during the cigarette smoke exposure period (n = 7) were studied. ResultsIn the COPD group, total and differential white blood cells (WBC) count in the bronchoalveolar fluid (BALF), tumor necrosis factor-alpha (TNF-α) level in the lung tissue and malondialdehyde (MDA) level in the BALF and lung tissue, lung pathological changes and tracheal responsiveness to methacholine were significantly increased, but catalase (CAT) and superoxide dismutase (SOD) activities and the level of thiol in the BALF and lung tissue were significantly decreased compared to the control group (all, p < 0.001). However, in the COPD groups treated with both doses of CM and dexamethasone, most variable did not achieved to the control levels and were significantly different with the control group (p < 0.05 to p < 0.001). In the COPD group treated with both doses of CM (dose dependently) and dexamethasone, almost all measured variables were significantly improved (p < 0.05 to p < 0.001). ConclusionThe potential effect of CM on lung inflammation and oxidative stress in a rat model of COPD comparable to dexamethasone was demonstrated.

Clinical significance of HIF-1α, ET-1, and NO as biomarkers in chronic obstructive pulmonary disease patients with pulmonary hypertension.

Pulmonary hypertension (PH) is a common complication of chronic obstructive pulmonary disease (COPD), with repeated infections and airflow limitation leading to endothelial dysfunction. The objective of this study was to retrospectively investigate the clinical significance of serum hypoxia-inducible factor 1-alpha (HIF-1α), plasma endothelin-1 (ET-1), and nitric oxide (NO) as non-invasive blood biomarkers for diagnosing patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). A total of 230 AECOPD patients were assessed for serum HIF-1α, plasma ET-1, and NO levels using Doppler echocardiography and blood tests. Clinical characteristics, including age, COPD duration, and comorbidities, were compared between patients with and without PH. The diagnostic value was determined through ROC analysis. Pearson correlation and multivariate logistic analyses explored the correlation of biomarkers in AECOPD with PH. Serum HIF-1α, plasma ET-1, and NO levels showed significant differences between COPD patients with and without PH. The combination model (0.027 * HIF-1α + 0.028 * ET-1 - 0.049 * NO) demonstrated an AUC of 0.89, indicating superior diagnostic value compared to individual biomarkers. Multivariate logistic analysis identified smoking, higher GOLD grade, hypertension, and elevated levels of HIF-1α, ET-1, and NO as independent risk factors for AECOPD. Positive correlations were observed between serum HIF-1α and plasma ET-1 levels with pulmonary artery systolic pressure (PASP), while NO demonstrated a negative correlation. Serum HIF-1α, plasma ET-1, and NO were associated with AECOPD and PH, and detecting individual or combined levels of these biomarkers in the blood can predict COPD-related PH.

Association of Nutritional Intake with Physical Activity and Handgrip Strength in Individuals with Airflow Limitation.

We investigated whether nutritional intake is associated with physical activity (PA) and handgrip strength (HGS) in individuals with airflow limitation. This study analyzed data from the 2014 to 2016 Korean National Health and Nutrition Examination Survey. We assessed total protein intake (g/day), caloric intake (kcal/day), and other nutritional intakes using a 24-hour dietary recall questionnaire. HGS was measured three times for each hand using a digital grip strength dynamometer, and PA was assessed as health-enhancing PA. Airflow limitation was defined as a forced expiratory volume/forced vital capacity ratio of 0.7 in individuals over 40 years of age. Participants were categorized into groups based on their PA levels and HGS measurements: active aerobic PA vs. non-active aerobic PA, and normal HGS vs. low HGS. Among the 622 individuals with airflow limitation, those involved in active aerobic PA and those with higher HGS had notably higher total food, calorie, water, protein, and lipid intake. The correlations between protein and caloric intake with HGS were strong (correlation coefficients = 0.344 and 0.346, respectively). The forest plots show that higher intakes of food, water, calories, protein, and lipids are positively associated with active aerobic PA, while higher intakes of these nutrients are inversely associated with low HGS. However, in the multivariate logistic regression analysis, no significant associations were observed between nutritional intake and active aerobic PA or HGS. Nutritional intake was not found to be an independent factor associated with PA and HGS. However, the observed correlations suggest potential indirect effects that warrant further investigation.

Radiomultiomics: quantitative CT clusters of severe asthma associated with multi-omics.

Lung quantitative computed tomographic (qCT) severe asthma clusters have been reported, but their replication and underlying disease mechanisms are unknown. We identified and replicated qCT clusters of severe asthma in two independent asthma cohorts and determined their association with molecular pathways. We used consensus clustering on qCT measurements of airway and lung CT scans, performed in 105 severe asthmatic adults from the U-BIOPRED cohort. The same qCT measurements were used to replicate qCT clusters in a subsample of the ATLANTIS asthma cohort (n=97). We performed integrated enrichment analysis using blood, sputum, bronchial biopsies, bronchial brushings and nasal brushings transcriptomics and blood and sputum proteomics to characterize radiomultiomic-associated clusters (RACs). qCT clusters and clinical features in U-BIOPRED were replicated in the matched ATLANTIS cohort. In the U-BIOPRED cohort, RAC1 (n=30) was predominantly female with elevated BMI, mild airflow limitation, normal qCT parameters and upregulation of the complement pathway. RAC2 (n=34) subjects had a lower degree of airflow limitation, airway wall thickness and dilatation, with upregulation of proliferative pathways, including neurotrophic receptor tyrosine kinase 2/tyrosine kinase receptor B (NTRK2/TRKB), and down-regulation of semaphorin pathways. RAC3 (n=41) showed increased lung attenuation area and air trapping, severe airflow limitation, hyperinflation, and upregulation of cytokine signaling and signaling by interleukin pathways, and matrix metallopeptidase 1, 2 and 9. U-BIOPRED severe asthma qCT clusters were replicated in a matched independent asthmatic cohort and associated with specific molecular pathways. Radiomultiomics might represent anovel strategy to identify new molecular pathways in asthma pathobiology.