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Acute exacerbation (AE) of chronic obstructive pulmonary disease (COPD) compromises health status; it increases disease progression and the risk of future exacerbations. We aimed to develop a model to predict COPD exacerbation. We merged the Korean COPD subgroup study (KOCOSS) dataset with nationwide medical claims data, information regarding weather, air pollution, and epidemic respiratory virus data. The Korean National Health and Nutrition Examination Survey (KNHANES) dataset was used for validation. Several machine learning methods were employed to increase the predictive power. The development dataset consisted of 590 COPD patients enrolled in the KOCOSS cohort; these were randomly divided into training and internal validation subsets on the basis of the individual claims data. We selected demographic and spirometry data, medications for COPD and hospital visit for AE, air pollution data and meteorological data, and influenza virus data as contributing factors for the final model. Six machine learning and logistic regression tools were used to evaluate the performance of the model. A light gradient boosted machine (LGBM) afforded the best predictive power with an area under the curve (AUC) of 0.935 and an F1 score of 0.653. Similar favorable predictive performance was observed for the 2151 individuals in the external validation dataset. Daily prediction of the COPD exacerbation risk may help patients to rapidly assess their risk of exacerbation and will guide them to take appropriate intervention in advance. This might lead to reduction of the personal and socioeconomic burdens associated with exacerbation.
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http://dx.doi.org/10.1038/s41598-023-45835-4 | DOI Listing |
Am J Respir Crit Care Med
September 2025
Temple University Hospital, Pulm & Crit Care Medicine, Philadelphia, Pennsylvania, United States.
Rationale: AIRFLOW-3 was a 1:1 randomized, double blind, sham controlled trial of the d'Nerva Targeted Lung Denervation (TLD) System in patients with COPD.
Objective: Evaluate the impact of TLD on COPD exacerbations compared to optimal medical treatment.
Methods: AIRFLOW-3 patients were symptomatic (CAT ≥10) with moderate to very severe airflow obstruction (25% ≤ FEV ≤ 80% predicted) and GOLD E status (≥2 moderate or ≥1 severe exacerbation over prior 12 months).
Ann Am Thorac Soc
September 2025
University of California Los Angeles David Geffen School of Medicine, Medicine, Los Angeles, California, United States.
Rationale: Inflammation is central to chronic obstructive pulmonary disease (COPD) pathogenesis but incompletely represented in COPD prognostic models. Neutrophil to lymphocyte ratio (NLR) is a readily available inflammatory biomarker.
Objectives: To explore the associations of NLR with smoking status, clinical features of COPD, and future adverse outcomes.
PLoS Negl Trop Dis
September 2025
Unit of Clinical and Molecular Medicine, ICMR-Vector Control Research Centre (VCRC), Indira Nagar, Puducherry, India.
Background: Filarial lymphedema, caused by lymphatic filariasis, is characterized by chronic swelling and recurrent skin infections. Acute adenolymphangitis (ADL) episodes significantly exacerbate morbidity. Diabetes mellitus (DM) increases susceptibility to infections; however, the relationship between diabetes and ADL frequency and severity in filarial lymphedema patients remains unclear.
View Article and Find Full Text PDFAdv Sci (Weinh)
September 2025
Postgraduate training base Alliance of Wenzhou Medical University (Zhejiang Cancer Hospital), Hangzhou, 310022, China.
Asthma is a chronic inflammatory respiratory disease influenced by genetic and environmental factors. Emerging evidence suggests that microplastics and nanoplastics (NPs) pose significant health risks. When inhaled, these tiny particles can accumulate in the lungs, triggering inflammation, oxidative stress, and other disruptions in pulmonary function.
View Article and Find Full Text PDFFerroptosis, an iron-dependent cell death pathway driven by lipid peroxidation, has emerged as a critical pathophysiological mechanism linking cancer and inflammatory diseases. The seemingly distinct pathologies exhibit shared microenvironmental hallmarks-oxidative stress, immune dysregulation, and metabolic reprogramming-that converge on ferroptosis regulation. This review synthesizes how ferroptosis operates at the intersection of these diseases, acting as both a tumor-suppressive mechanism and a driver of inflammatory tissue damage.
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