Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of disability and death worldwide. Early identification remains challenging, as existing prediction models largely rely on clinic-based assessments and self-report measures that are resource-intensive and prone to bias. This study aimed to determine whether real-world mobility metrics could predict incident COPD.

This prospective cohort study included 28,251 UK Biobank participants aged 60-78 years who wore wrist-worn accelerometers. Digital gait biomarkers were derived using signal-processing and machine-learning algorithms. Incident COPD was identified via linked electronic health records. Associations between digital gait biomarkers and incident COPD were examined using Cox proportional hazards models with internal validation adjusted for age, sex, body mass index, smoking pack-years, air pollution exposure, and asthma history. Model discrimination was evaluated using Harrell's concordance index.

Among 28,251 participants, 639 (2.26%) developed COPD over a mean follow-up period of 8.5 (SD=1.3) years. Lower running duration, slower maximal walking speed, shorter walking bout duration, and a lower proportion of walks longer than 8 seconds were independently associated with incident COPD. A model incorporating these four digital gait biomarkers, and four easily collectable self-report measures, age, sex, smoking pack-years, and asthma history, achieved a Harrell's concordance index of 0.80; comparable to existing models that require clinic-based tests and extensive self-report items.

Real-world mobility metrics are early indicators of incident COPD, providing an accessible and automatic approach for early risk identification in older people and enabling early intervention to delay disease progression and preserve quality of life.

Inhaled therapies are essential for chronic obstructive pulmonary disease (COPD) management but also contribute to healthcare-related carbon emissions. Real-world evidence linking inhaler-related carbon burden to clinical outcomes remains limited. This study evaluated the relationship between inhaler-related CO₂ emissions and clinical effectiveness of different treatment regimens.

This retrospective single-center observational study included patients with COPD. Patients were categorized into four groups based on the inhaled therapy: long-acting muscarinic antagonists (LAMA) monotherapy, LAMA/long-acting β2-agonists (LABA), LABA/inhaled corticosteroids (ICS), and triple therapy (LAMA/LABA/ICS). Clinical outcomes, including pulmonary function test (PFT) parameters and health-related quality of life (HRQL), were assessed over one year. Total inhaler-related CO₂ emissions were calculated using published conversion factors. Emission-adjusted outcomes were derived to evaluate the clinical benefits per unit of CO₂ emission.

Clinical improvements in HRQL and PFT were comparable across groups, with no significant differences in ΔFEV1, ΔFVC, or ΔCAT. However, CO₂ emissions differed significantly, being the lowest in the LAMA monotherapy group and the highest in the LABA/ICS and triple therapy groups (p < 0.001). Emission-adjusted analysis demonstrated that lower-intensity regimens, particularly LAMA monotherapy, were associated with more favorable CO₂-adjusted treatment efficiency, particularly in ΔmMRC/CO₂ (p = 0.001) and ΔFEV1 (%)/CO₂ (p = 0.026), indicating higher clinical benefit per unit carbon emission. After adjustment for baseline severity-related variables, including age, sex, smoking status, baseline FEV1, baseline CAT score, and baseline mMRC score, higher-intensity regimens remained associated with lower CO₂-adjusted pulmonary function improvement compared with LAMA monotherapy.

High-intensity regimens were associated with substantially increased inhaler-related CO₂ emissions. Although major clinical outcomes were generally comparable across groups, lower-emission regimens showed relatively more favorable CO₂-adjusted outcomes in this cohort. These findings highlight the importance of balancing clinical effectiveness with environmental considerations while maintaining guideline-based, individualized COPD management according to disease severity and clinical needs.

Considerable heterogeneity exists in patients experiencing acute exacerbation of chronic obstructive pulmonary disease (AECOPD) concerning etiology, clinical manifestations, phenotypic features, comorbidities, and treatment responsiveness. The concept of "treatable traits" is adapted to evaluate the clinical features of patients with chronic airway diseases from multiple dimensions and ultimately guiding precision treatment strategies. This prospective randomized controlled study mainly aims to evaluate the impact of accurate identification and intervention strategies guided by "treatable traits" on the prognosis of AECOPD patients.

This prospective randomized controlled study will be performed in 6 centers in China, with a planned enrollment of 314 AECOPD participants. 314 participants will be randomly assigned to either the precision intervention group or the control group with a ratio of 1:1. During admission, participants in the precision intervention group will receive accurate identification and intervention based on "treatable traits", while patients in the control group receive conventional medical treatment as usual. Patients will be followed up at 6 and 12 months after discharge. Primary outcomes of the study include the incidence of total acute exacerbations and hospitalizations due to acute exacerbations during follow-up. Secondary outcomes involve changes in CAT scores and mMRC classification, and the occurrence of death during follow-up.

By employing standardized, multi-dimensional baseline and follow-up assessments, the study seeks to develop a comprehensive framework of treatable traits encompassing pulmonary, extrapulmonary, and socio-behavioral domains for AECOPD. It will further evaluate the prognostic impact of precision interventions tailored to these treatable traits in AECOPD patients for the first time.

Chronic obstructive pulmonary disease (COPD) is a long-term respiratory condition with high rates of morbidity and mortality. Its pathophysiology is complex, and currently, there are no effective clinical treatments that can fully reverse or halt the disease's progression. Animal models play a significant role in elucidating the pathogenesis of COPD, dynamic pathological processes, and evaluating potential therapeutic strategies, serving as a key to advancing in-depth research on this disease. However, existing modeling methods still face many limitations in accurately simulating the clinical symptoms, pathophysiological features, and progression of human disease, and there is a lack of standardized guidelines and industry consensus. This paper systematically reviews methods for constructing COPD animal models reported in the literature by reviewing 5,071 relevant articles from CNKI, PubMed, and Wanfang Database published in the past decade. The main models include cigarette smoke exposure, protease-induced, genetically modified, harmful substance exposure, and various combined factor models. A comprehensive review and comparison of their construction principles, procedures, pathological features, advantages, and limitations are provided. This review aims to serve as a valuable reference for COPD researchers and clinicians in the construction of animal models of COPD.

Allergic sensitization and respiratory infections are common in childhood. The "two-hit" hypothesis suggests these interact in early-life to increase risk of subsequent asthma. The "two-hit" effect on lung function, however, remains unknown.

We assessed for interactions between food allergic sensitization and respiratory infection in infancy and associations with lung function in childhood.

In a longitudinal community-based cohort, sensitization was assessed at age 1 year by skin prick testing to common food allergens. Respiratory infection was assessed via parental reports of doctor diagnosed bronchiolitis or antibiotics for lower respiratory infection in the first year of life. Regression models were fitted with interactions between these exposures to assess for associations with lung function at ages 6 and 10 years, controlling for potential confounders.

No interaction was observed between food sensitization and lower respiratory infection in infancy on lung function at either age 6 or 10 years. Respiratory infection was associated with modest reductions in lung function at age 10 years for post-bronchodilator FEV₁ in both sensitized (-0.25, 95% CI: -0.55 to 0.05 z-score units, p = .108, n = 285) and non-sensitized (-0.12, 95% CI: -0.26 to 0.02 z-score units, p = .081, n = 1179) children. Similar patterns were observed for FEV₁/FVC, FVC, and FEF_25-75. Associations were weaker and less consistent at age 6 years.

A two-hit interaction between food sensitization and respiratory infection during infancy on subsequent lung function was not confirmed. Early-life lower respiratory infection was however associated with modest reductions in lung function at age 10 years, regardless of sensitization status.

Asthma exacerbations in children represent a significant contributor to disease burden, with the risk of occurrence depending on the type of allergic sensitization. Identification of clinical and biological factors may improve risk stratification and support therapeutic management. The aim of this study was to assess the relationships between exacerbation frequency, lung function, inflammatory biomarkers, and the severity of sinonasal symptoms in children with asthma.

In a retrospective observational study, 80 children with allergic rhinitis and asthma were enrolled. Patients were stratified according to exacerbation frequency (<2 vs. ≥2 over 12 months) and sensitization to house dust mites (HDM). Assessments included spirometry (FEV₁, FEV₁/FVC), fractional exhaled nitric oxide (FeNO), peripheral blood eosinophil count, and serum soluble receptor for advanced glycation end products (sRAGE). Asthma control was evaluated using the Childhood Asthma Control Test (c-ACT), while sinonasal symptoms were assessed using the Sino-Nasal 5 (SN-5) questionnaire. Advanced glycation end products were assessed using skin autofluorescence.

In children without sensitization to HDM, more frequent exacerbations correlated with higher sRAGE concentrations (p = 0.0259) and greater activity limitation due to sinonasal symptoms (p = 0.0309). In HDM-sensitized children, frequent exacerbations were associated with lower FEV₁ (p = 0.0089), reduced FEV₁/FVC (p = 0.0186), and poorer asthma control (p = 0.0117). Greater severity of sinonasal symptoms was observed in children with poorer asthma control (p = 0.012).

Exacerbation risk in asthma is associated with distinct profiles depending on sensitization status. Elevated sRAGE concentrations and increased sinonasal inflammation may characterize phenotypes not associated with HDM. In contrast, impaired lung function and poor asthma control predominate in HDM-associated asthma. Int J Occup Med Environ Health. 2026;39(3):270-9.

Drug-Induced Sleep Endoscopy (DISE) is increasingly used to evaluate upper airway dynamics in obstructive sleep apnea patients (OSA). It enables real-time visualization of collapse and may support treatment selection; however, its true clinical impact and limitations remain controversial. This study aims to summarize the current evidence regarding the real role of DISE in OSA management.

A structured literature review of the literature was conducted, focusing on key aspects of DISE, including its diagnostic utility, comparison with awake endoscopy, pharmacological agents used, effects on sleep architecture and muscle tone, the role of bispectral index, indications and contraindications, relevance in hypoglossal nerve stimulation selection, and its impact on surgical outcomes.

DISE provides dynamic assessment of upper airway collapse, facilitating anatomical diagnosis and treatment personalization. It is useful in complex cases, treatment failures, and candidate selection for HNS. Commonly used agents -propofol, midazolam, and dexmedetomidine- differ in their effects on sleep architecture and muscle tone, none fully reproducing natural sleep. Importantly, current evidence shows no consistent improvement in surgical outcomes when DISE is used compared with awake evaluation alone. Additionally, variability in protocols and interpretation limits reproducibility.

DISE is a valuable complementary tool for anatomical localization of upper airway collapse and treatment planning in OSA. However, it cannot replace polysomnography as the diagnostic gold standard and should be interpreted within a comprehensive clinical context. Further standardization and high-quality studies are needed to better define its role and optimize its clinical utility.

Pulmonary alveolar proteinosis (PAP) is a rare pulmonary syndrome characterized by impaired surfactant clearance, driven by dysfunctional cholesterol efflux in alveolar macrophages (AMs). However, the molecular determinants governing AM cholesterol homeostasis remain incompletely defined. Here, through a genome-wide CRISPR screen in foamy macrophages and bulk RNA sequencing of AMs from PAP patients, we identify DTX4 as a pivotal regulator of cholesterol efflux in AMs. In mice, AAV-mediated silencing of DTX4 led to excessive AM lipid accumulation, exacerbated proteinosis, increased lung opacities, and deteriorated pulmonary function. Similarly, DTX4 depletion in primary AMs impaired cholesterol efflux and promoted intracellular lipid deposition. Conversely, AM-specific overexpression of DTX4 in the Csf2ra-/- PAP model markedly alleviated lipid accumulation, mitigated alveolar proteinosis, restored lung densities, and rescued pulmonary function. Mechanistically, DTX4 stabilizes the GM-CSF receptor via an E3-independent interaction to sustain JAK2/STAT5 signaling, which reciprocally maintains DTX4 transcription. This positive-feedback loop drives PPARγ expression, and its disruption in PAP impairs cholesterol efflux, a defect partially reversible by ectopic PPARγ expression. Collectively, our findings identify DTX4 as a central orchestrator of AM cholesterol efflux and surfactant homeostasis, positioning it as a promising therapeutic target for PAP.

Bronchoalveolar lavage fluid (BALF) analysis is a key diagnostic tool in veterinary respiratory medicine. The IDEXX ProCyte Dx analyzer was developed for blood formulation and cellular counting in various fluids, but its applicability for BALF analysis remains unexplored.

To assess the agreement between manual counting and automated counting using the IDEXX ProCyte Dx analyzer for total cell count (TCC) and differential cell count (DCC) in BALF samples from healthy and diseased dogs, under two pretreatment conditions: mucolytic treatment with dithiothreitol (DTT) or filtration.

BALF from 10 healthy beagles and 14 diseased dogs were analyzed to compare TCC and DCC between manual and automated methods across pretreatment conditions.

In healthy dogs, Bland-Altman analysis on log-transformed data demonstrated a mean ratio close to 1 and acceptable 95% limits of agreement between manual and automated methods and between pretreatment conditions. In diseased dogs, good agreement was observed between manual and automated methods for filtered samples only; the other comparisons showed poor agreement. In both healthy and diseased dogs, Passing-Bablok regression analysis did not detect systematic or proportional bias between methods. Automated DCC was inconsistent compared with manual methods in both healthy and diseased dogs.

The IDEXX ProCyte Dx analyzer can be used for TCC measurement of pre-treated BALF samples in healthy dogs. In diseased dogs, filtration is preferred over DTT-treatment for automated counting, and results should be interpreted with caution due to the unpredictable influence of pretreatment on cellular counts. For DCC, automated methods are unreliable.

to analyze healthcare workers' health and well-being, as well as the environmental conditions of hospital settings during the COVID-19 pandemic, considering the challenge of meeting goal three of the Sustainable Development Goals.

a descriptive, exploratory, and qualitative study was conducted with 32 healthcare workers employed in a public hospital in Macapá/AP, who contracted COVID-19 and answered interviews using Google Forms® between October and November 2022. Data were organized using IRaMuTeQ® and analyzed using content analysis.

regarding health and well-being, work overload, absenteeism, presenteeism, fear, anxiety, exposure to death, and suffering were reported. Concerning environmental conditions, physical and structural limitations, improvised work environments, and lack of personal protective equipment were reported.

the need to promote workers' physical and mental health, improve hospital settings, and reorient work dynamics, especially during times of crisis, minimizing impacts on workers' health and well-being, was evident.