Search Results (2,727)

Background/Objectives: Discharging patients after hospitalization for an acute exacerbation of chronic obstructive pulmonary disease (COPD) is a critical transition in care associated with a high risk of early readmission. This survey aimed to describe physician-reported discharge practices following COPD exacerbations, identify perceived gaps and organizational barriers, explore attitudes toward structured COPD discharge summaries, and use a SWOT analysis as an interpretative framework. Methods: In this cross-sectional observational survey, 100 physicians involved in COPD care were recruited from the official mailing list of the Respiratory Society of Serbia, which represents approximately 71% of the Society’s members. The survey assessed discharge procedures, multidisciplinary practices, patient education, comorbidity management, perceived causes of readmission, and barriers to structured discharge summaries. Data were analyzed descriptively and complemented with a structured SWOT (Strengths, Weaknesses, Opportunities, Threats) analysis. Results: Most respondents worked in tertiary care settings and were involved in managing patients hospitalized for COPD exacerbations. Although 24% of physicians routinely used structured discharge summaries, 45% reported never using them. The most frequently perceived contributors to 30-day readmissions were active smoking (90%), poor treatment adherence (81%), comorbidities (77%), and incorrect inhaler technique (72%). Major barriers to implementing structured discharge summaries included the lack of standardized templates, time constraints, poor coordination across healthcare levels, and technical limitations. Willingness to implement structured discharge tools was high (mean score 8.86/10). SWOT analysis identified strong professional support for discharge standardization alongside organizational and system-level barriers to implementation. Conclusions: This exploratory survey identified important gaps between recommended and routine COPD discharge practices and highlighted organizational barriers to implementation. The findings may inform future evaluation and development of structured discharge tools in this healthcare setting. Full article

Background: Sarcopenia and frailty are highly prevalent extrapulmonary manifestations of chronic obstructive pulmonary disease (COPD) and are strongly associated with reduced exercise tolerance, exacerbation risk, hospitalizations, and mortality. Beyond inflammation, oxidative stress, and physical inactivity, emerging evidence highlights nutrition as a major modifiable driver of muscle deterioration in COPD. Nutritional deficits impair anabolic signaling, exacerbate proteolysis, worsen mitochondrial dysfunction, and contribute to frailty progression. Methods: This narrative review synthesizes evidence from PubMed, Embase, Scopus, and Web of Science up to 2025, integrating mechanistic, metabolic, nutritional, and biomarker-related pathways underlying muscle dysfunction in COPD. Studies examining inflammation, hypoxemia, oxidative stress, hormonal imbalance, nutrition, and emerging biomarkers were included. Results: COPD-related sarcopenia results from converging inflammatory (TNF-α, IL-6), catabolic (FOXO, UPS), metabolic, and vascular mechanisms, compounded by energy deficiency, protein insufficiency, and micronutrient deficits. Inadequate intake of protein, vitamin D, antioxidants, and omega-3 fatty acids increase anabolic resistance, enhance muscle catabolism, and worsen frailty. Nutritional interventions, particularly high-protein supplementation, leucine-enriched formulas, vitamin D repletion, omega-3 fatty acids, and multimodal nutrition–exercise programs, demonstrate benefits in muscle mass, strength, and physical performance. Biomarkers such as GDF-15, CAF22, and specific microRNAs reflect nutritional status and correlate with muscle health in COPD. Conclusions: Sarcopenia and frailty in COPD arise from a complex interplay of inflammatory, metabolic, nutritional, and lifestyle-related factors. Integrating nutritional assessment and targeted dietary interventions with exercise and pulmonary rehabilitation is essential to counteract anabolic resistance and improve functional outcomes. Advances in biomarker research may support earlier diagnosis and personalized nutrition-based therapeutic strategies. Full article

Background: Patient activation is associated with both health outcomes and the utilization of healthcare resources. Since various factors influence activation levels among older ill adults, further exploration of this topic is needed. Specifically, we aim to examine the extent to which changes over time in self-rated symptoms of depression are associated with changes in patient activation and to what extent self-rated health status and satisfaction of basic psychological needs (autonomy, relatedness, and competence) have a mediation effect. Methods: A longitudinal and correlational design was employed in which two hundred and seven participants with heart failure or chronic obstructive pulmonary disease were recruited from two hospitals in the middle of Sweden. The sample used in this study is the same as that used in a randomized controlled trial. A questionnaire was administered at baseline, and at 30-, 90-, and 180 days post-discharge, involving ratings of depression, patient activation, self-rated health, and satisfaction of basic psychological needs (autonomy, relatedness, and competence). As the results from the original study showed no difference between the two randomized groups in patient activation, the analysis in this study was conducted using a combined sample in which the intervention and control groups were merged. For estimation of the direct effects and the components of indirect effects, we employed multilevel modeling using a linear mixed model, and to test mediation, the stand-alone program RMediation was used. Results: Over time, increases in depressive symptoms were associated with reduced patient activation, with this relationship mediated by declines in relatedness and competence. No evidence was found showing that autonomy or self-rated health had a mediation effect. Conclusions: The results indicate that older chronically ill individuals may benefit from interventions targeting psychological mediators to improve and sustain activation. Full article

Background/Objectives: Given rising lung cancer incidence and limited data on pulmonologist-performed ultrasound-guided transthoracic core biopsy (US-TTCB), in this study, we evaluated diagnostic yield and safety for pleural or pulmonary lung masses, using Clavien–Dindo classification to standardize complication reporting. Methods: We retrospectively reviewed single-center pulmonologist-performed US-TTCB using a MEDONE biopsy gun with a 16 G/18 G Tru-Cut needle between January 2019 and December 2025. The primary endpoints were diagnostic yield, defined as specific malignant or benign histology, and complication rate. Non-diagnostic results were assessed using available clinical/imaging follow-up. Univariate analyses screened candidate correlates, and a prespecified computer tomography (CT)-completed subanalysis (n = 67) used multivariable logistic regression and receiver operating characteristic (ROC) analysis to assess CT lesion size discrimination. Results: Diagnostic yield was 84.2% (202/240); complications occurred in 12.1% (29/240), including one Clavien–Dindo Grade III event (0.4%). In the CT-completed subset (n = 67), diagnostic yield was independently associated with CT lesion size (aOR 1.03/mm, 95% CI 1.00–1.05; p = 0.022) and Chronic Obstructive Pulmonary Disease (COPD) (aOR 2.30, 95% CI 1.06–4.96; p = 0.034); CT lesion size showed an area under the curve (AUC) of 0.717 for predicting yield. Diagnostic yield remained stable over time (84.2% in first vs. second half; p = 1.00), with no association between case order and yield (OR 0.999; p = 0.64). Conclusions: US-TTCB of pleural/pulmonary masses achieved a high diagnostic yield with minimal major complications. Large CT dimension and COPD were associated with higher diagnostic success, and CT size provided fair discrimination for predicting yield; findings should be interpreted in the context of the retrospective single-center design and the restricted CT-completed subset. Full article

Cigarette smoke is a major inducer of oxidative stress, promoting reactive oxygen species (ROS) accumulation and contributing to the pathogenesis of chronic obstructive pulmonary disease (COPD) and lung cancer. Heated tobacco products (HTP) and e-cigarettes are promoted as reduced-risk alternatives; however, their impact on cellular redox regulation remains unclear. Here, we investigated the effects of conventional cigarette smoke extract (CSE), HTP, and e-cigarette extracts on hydrogen peroxide (H₂O₂) permeability mediated by aquaporins (peroxiporins) and on the activity of key antioxidant enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in ATII-like cells. Eight aquaporins were detected at the mRNA level, and seven were confirmed at the protein level. CSE markedly inhibited H₂O₂ permeability across plasma, mitochondrial, and nuclear membranes. HTP extract impaired H₂O₂ transport across the plasma membrane and nuclear envelope, while mitochondrial permeability was preserved. Both CSE and HTP extract reduced superoxide dismutase and glutathione peroxidase activities. In contrast, e-cigarette extract exerted minimal effects on membrane H₂O₂ permeability and selectively decreased superoxide dismutase activity. Overall, our findings identify a graded pattern of oxidative toxicity (CSE > HTP > e-cigarette) and highlight peroxiporins as critical regulators of intracellular redox homeostasis. Although less harmful than cigarettes, alternative nicotine delivery systems are not biologically inert. Full article

Background: Respiratory diseases (RDs), including asthma, COVID-19, chronic obstructive pulmonary disease (COPD), and pneumonia, remain a major global health challenge, contributing substantially to global morbidity and mortality. Conventional diagnosis relies heavily on clinicians’ expertise to interpret respiratory sounds and radiographic images, a process that can be subjective, time-consuming, and prone to inter-observer variability. Recent advances in artificial intelligence (AI) and machine learning (ML) have enabled automated diagnostic approaches that can improve the efficiency, consistency, and scalability of respiratory disease detection. However, existing research remains fragmented across different data modalities. Methods: This review systematically analyzes recent studies on AI-based respiratory disease detection using both visual modalities (e.g., chest X-rays, computed tomography (CT) scans, and ultrasound) and audio modalities (e.g., cough and breath sounds). To provide a comprehensive perspective, the reviewed literature is organized using a unified taxonomy that categorizes existing approaches into three main groups: audio-based, visual-based, and audio–visual-based methods. In addition, two conceptual frameworks are proposed to illustrate representative pipelines for audio-based and visual-based respiratory disease classification. Results: The analysis reveals that most existing studies focus on single-modality approaches, while multimodal integration remains relatively underexplored. Only a limited number of studies combine audio and visual data within unified frameworks, primarily due to the scarcity of synchronized multimodal datasets collected from the same patients. The proposed taxonomy and conceptual frameworks provide a structured basis for comparing existing methods, identifying methodological trends, and highlighting key research gaps in multimodal respiratory disease detection. Conclusions: Future research should prioritize the development of multimodal datasets, robust evaluation protocols, and interpretable and lightweight AI models suitable for real-world clinical deployment. Advancing multimodal integration has the potential to significantly enhance the accuracy, reliability, and clinical applicability of AI-driven respiratory disease diagnosis systems. Full article

Background: Penetrating keratoplasty (PK) is a technically demanding corneal transplant procedure frequently performed in elderly patients with substantial systemic comorbidities. In this population, an anesthetic strategy that ensures hemodynamic stability, cooperative sedation, adequate analgesia, and preserved spontaneous ventilation is highly desirable. Dexmedetomidine, a highly selective alpha2-adrenergic agonist, provides “cooperative” sedation with minimal risk of respiratory depression and additional sympatholytic benefits. Methods: This single-center retrospective observational case series included 50 consecutive patients (American Society of Anesthesiologists [ASA] II–III, age 50–90 years) undergoing PK under sub-Tenon block combined with continuous dexmedetomidine infusion. Dexmedetomidine was administered without a loading bolus at 0.7 mcg/kg/h for 10–15 min, then reduced to 0.5 mcg/kg/h, targeting a Ramsay Sedation Scale (RSS) score of 2–3. The sub-Tenon block was performed using a mixture of levobupivacaine 0.5% and lidocaine 2% (3–5 mL). Heart rate (HR), mean arterial pressure (MAP), oxygen saturation (SpO₂) and RSS were recorded in nine predefined perioperative phases. Data were analyzed descriptively. Results: The mean age was 72 ± 9 years; 52% of patients were ASA III. Hypertension was present in all patients; 30% had cardiovascular disease, 28% diabetes mellitus type II, and 30% chronic obstructive pulmonary disease. Progressive, controlled bradycardia was observed (mean HR decreased from 76 to 57 beats/min during graft transplantation), while MAP gradually decreased from hypertensive baseline values (150–160 mmHg) to an optimal intraoperative range of 115–130 mmHg, without episodes of clinically significant hypotension. SpO₂ remained stable at 98–99% throughout all phases, with no episodes of desaturation or need for airway intervention or supplemental oxygen. Target sedation (RSS 2–3) was achieved in all patients (median RSS 3), with preserved spontaneous breathing and cooperation. Sub-Tenon block-related bulging occurred in 6% of cases. No episodes of clinically significant bradycardia, malignant arrhythmia, respiratory compromise, or need to discontinue dexmedetomidine were recorded. No opioids or non-steroidal analgesics were required intraoperatively or in the early postoperative period. Conclusions: The combination of sub-Tenon block and continuous dexmedetomidine sedation without a loading bolus represents a hemodynamically stable and respiratory-safe anesthetic strategy for PK in elderly, high-risk patients. These preliminary, hypothesis-generating findings suggest that the protocol provides stable surgical conditions and a favorable safety profile, justifying future prospective randomized controlled trials to establish its comparative efficacy against general anesthesia or standard sedative regimens. Full article

Background/Objective: To identify respiratory pathology, automated cough counting is frequently proposed. A trial validating an early warning system for exacerbations in chronic obstructive pulmonary disease (COPD) patients was recently concluded successfully. This paper aims to review the critical design choices for converting a cough counter into a patient-friendly continual cough monitor. Furthermore, it provides a basis for a practical reliability metric for continual cough monitoring. Methods: Design choices made in the development of a cough-based alert mechanism called XACT are discussed. A practical approach for reliability assessment is outlined based on cough counts, day-to-day variation and specificity data. Results: In post hoc analysis, it is shown that the described approach enables differentiation between high-quality cough estimates and less reliable data. The approach is used to underpin an earlier cohort subdivision into patients with and without increased cough during exacerbation. Conclusions: The validated alert mechanism has various patient-oriented design choices (unobtrusiveness, privacy-preserving). The examples illustrate how to screen for potential issues in automated cough count data without resorting to laborious annotation. It creates a practical basis for confidence metrics of medical inferences made from cough data, e.g., exacerbation forecasts. The proposed concepts need further validation. Full article

Background: Chronic Obstructive Pulmonary Disease (COPD) is a progressive, incurable condition marked by irreversible airflow limitation and systemic inflammation. Cardiovascular comorbidities, particularly pulmonary hypertension (PH), exacerbate disease severity. While cigarette smoke is a well-known trigger, non-smoking-related inflammatory pathways remain underexplored. This study investigates vascular remodeling in a murine model of inflammation induced by chronic exposure to house dust mite Farinae (HDM). Methods: Female C57BL/6 mice were sensitized with HDM in Freund’s Complete Adjuvant and challenged intranasally with HDM for six weeks. Lung inflammation, mucus hypersecretion, and vascular remodeling were evaluated via BAL, histology, immunofluorescence, echocardiography, gene expression, proteomics, and FlexiVent pulmonary function tests (FlexiVent system). Results: HDM exposure induced a mixed inflammatory response, with elevated neutrophils, monocytes, and lymphocytes in BALF. Mucus hyperproduction (increase in MUC5AC/MUC5B) and impaired lung function (reduced FEV0.1/FVC) were observed. Vascular remodeling was evidenced by increased wall thickness, α-SMA expression, and collagen deposition. Proteomic analysis revealed dysregulation of endothelial markers and protease/antiprotease imbalance. HIF1-α was significantly upregulated in lung tissue and correlated with vascular and epithelial remodeling. Conclusions: Chronic HDM exposure in mice recapitulates key features observed in subsets of COPD and PH, including inflammation-driven airway and vascular remodeling. HIF1-α emerges as a central regulator, linking hypoxia to structural changes. This model offers insights into the effect of non-smoking-related inflammatory pathways on bronchial and vascular remodeling that are potentially relevant for subgroups of COPD patients and highlights HIF1-α as a potential therapeutic target. Full article

LY104 (previously designated as B7) is a selective phosphodiesterase 4 inhibitor with promising activity against chronic obstructive pulmonary disease. We previously reported its single-dose pharmacokinetics and tissue distribution in rats. In the present study, a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed and validated for the simultaneous quantification of LY104 and its major metabolite M1 in rat plasma following ICH M10 guidelines. The method showed excellent linearity over 20–1200 ng/mL for both analytes, with retention times of 2.85 min (LY104) and 3.22 min (M1). Using this method, we extended our previous work in several directions. Re-analysis of previously published single-dose pharmacokinetic and tissue distribution data revealed no significant sex differences for LY104. Newly generated multiple-dose studies (1 mg/kg daily for 7 days) demonstrated no accumulation of LY104 or M1. The pharmacokinetic profile of M1 was quantified for the first time. Comprehensive in vitro investigations included plasma and liver microsomal stability, plasma protein binding, and excretion studies. This systematic preclinical pharmacokinetic characterization of LY104 and M1, incorporating re-analysis of existing data with sex stratification, newly generated multiple-dose and metabolite data, excretion studies, and comprehensive in vitro investigations, provides useful information to support further drug development and clinical trial design. Full article

Background: Near-infrared spectroscopy (NIRS)-based wearable devices offer non-invasive, continuous monitoring of muscle oxygenation, providing direct microvascular and metabolic information that complements indirect indices of intensity such as heart rate and accelerometry. Their clinical applicability in chronic non-communicable diseases (NCDs) remains under active development. Methods: A structured narrative review was conducted in PubMed, Scopus, Web of Science, and IEEE Xplore (January 2010–January 2026) using pre-specified search strings combining NIRS, muscle oxygenation, SmO₂, StO₂, wearable, exercise intensity, ventilatory/lactate threshold, and individual chronic disease terms. Eligible studies addressed technical validation of wearable NIRS, NIRS-derived exercise intensity estimation, clinical applications in NCDs, or rehabilitation implementation. Evidence was synthesized thematically; quality of validation studies was appraised against AMSTAR-2-informed, COSMIN-informed, or Cochrane RoB-2 criteria. Results: Wearable continuous-wave NIRS shows acceptable concurrent validity with frequency-domain laboratory systems (r = 0.79; range 0.69–0.88; ±8% SmO₂ agreement in 95% of measurements) and good test–retest reliability for moderate-to-severe domains (ICC 0.72–0.91). NIRS-derived breakpoints align more reliably with the second ventilatory/lactate threshold (ICC = 0.80) than with the first (ICC = 0.53), constraining its use for prescribing lower-intensity domains. In chronic obstructive pulmonary disease, peripheral arterial disease, chronic respiratory failure and selected cardiovascular conditions, wearable NIRS detects disease-specific patterns of muscle deoxygenation and post-exercise reoxygenation that track responses to rehabilitation. Conclusions: Current evidence supports wearable NIRS as a complementary, intensity-aware monitoring tool—particularly for delineating the heavy/severe-intensity boundary and detecting peripheral metabolic limitations—rather than as a stand-alone replacement for ventilatory or lactate thresholds. Because much of the evidence derives from small, single-sex or athlete-only cohorts, these findings should be regarded as a promising basis requiring further validation in broader NCD populations. Implementation in NCDs requires standardized placement and calibration protocols, sex- and body composition-stratified reference values, motion-artifact mitigation, and adequately powered longitudinal trials in clinical populations. Full article

Chronic obstructive pulmonary disease (COPD) extends beyond the respiratory system and is closely linked to an increased risk of cardiovascular complications. Exacerbations represent critical periods of cardiovascular vulnerability, with a marked rise in major adverse cardiovascular events observed in the early post-exacerbation phase. This narrative review synthesizes current evidence on the epidemiology, pathophysiological mechanisms, and therapeutic implications of cardiovascular risk following COPD exacerbations. A structured literature search was conducted to identify relevant studies in this setting. Cardiovascular risk is elevated following exacerbations, particularly within the first weeks, and remains increased for months thereafter. Multiple pathophysiological mechanisms contribute to this vulnerable window. Systemic inflammation, marked by elevated cytokines such as IL-6, IL-8, and CRP, promotes endothelial dysfunction, vascular oxidative stress, and impaired nitric oxide bioavailability. Despite the well-established link, cardiovascular disease remains overlooked and undertreated in patients with COPD, and the use of guideline-directed cardiovascular therapies is suboptimal. A more systematic, integrated approach to cardiovascular assessment and management in patients with COPD is warranted to improve outcomes. Full article

Background and objective: Hypoxemia and respiratory failure (RF) in chronic obstructive pulmonary disease (COPD) are associated with exacerbations, comorbidities and increased mortality. However, the prevalence of hypoxemia and RF in stable COPD is unknown. We aimed at investigating the prevalence and determining predictive factors for chronic gas exchange abnormalities in COPD patients. Methods: A retrospective cohort study that enrolled clinically stable COPD patients referring to a pulmonary outpatient clinic. Anthropometrics, clinical characteristics, blood gas analysis and lung function were analyzed. Patients were grouped according to hypoxemia (PaO₂ <80 and ≥60 mmHg), type 1 (PaO₂ < 60 mmHg) or type II (PaO₂ < 60 and PaCO₂ > 45 mmHg) RF. A sensitivity analysis adopting an age-adjusted definition of hypoxemia was performed. Predictive factors for hypoxemia or RF were assessed with multifactorial analysis. Results: We analyzed data from 515 patients. Fixed-ratio hypoxemia, RF type 1 and type 2 were observed in 352 (68.3%), 27 (5.2%) and 43 (8.3%) patients, respectively. Risk of hypoxemia was associated with preserved alveolar volume, residual volume/total lung capacity, and lung diffusion capacity. Heart failure, ischemic heart disease, atrial fibrillation, and metabolic syndrome were predictive factors for RF. Patients with age-adjusted hypoxemia (n = 321 patients, 62.3%) showed no difference in terms of anthropometrics, lung function, and clinical characteristics as compared with fixed-threshold hypoxemia. Conclusions: Hypoxemia is frequent in stable COPD. Lung function parameters and comorbidities can support the identification of patients at risk of RF. Blood gas analysis should be always performed in patients with COPD to allow for personalized therapy and management. Full article

Assessing autophagy may offer insights into the pathogenesis of chronic obstructive pulmonary disease (COPD). However, measuring the dynamic aspect of autophagy is challenging, and sample manipulation can cause signal fluctuations that deviate from physiological conditions. We applied an organotypic method to quantify autophagy in COPD, where it frequently demonstrates disease-related dysregulation. Blood from control and COPD participants was treated with or without chloroquine. Microtubule-associated protein 1 light chain 3B II (LC3B-II) abundance was quantified in peripheral blood mononuclear cells (PBMCs), and findings were validated by transmission electron microscopy. Our observations show that while basal LC3B-II abundance was similar between groups (p = 0.60), autophagic flux was significantly lower in the COPD cohort, suggesting disruption in the regulatory factors that direct autophagosome clearance (p = 0.004). This was supported by less frequent observations of autophagy-related vacuoles in the cytosol of COPD-derived PBMCs. Our findings indicate that the suppression of autophagy can be detected in the blood of individuals with COPD, which warrants further investigation into its contribution to extrapulmonary disease processes. Full article

Background/Objectives: Daytime sleepiness in obstructive sleep apnea (OSA) shows substantial variability and is not fully explained by disease severity. This study aimed to evaluate whether a history of cancer is associated with subjective daytime sleepiness independently of respiratory burden. Methods: In this observational cohort study, 402 untreated patients with OSA were included. Cancer history was defined as a documented diagnosis of malignancy prior to baseline polygraphy. Daytime sleepiness was assessed using the Epworth Sleepiness Scale (ESS). Multivariable linear and logistic regression models were used to evaluate the association between cancer history and ESS (continuous and dichotomized as >10), adjusting for age, sex, body mass index, smoking status, chronic obstructive pulmonary disease, and apnea–hypopnea index (AHI). Sensitivity analyses additionally adjusted for heart disease and nocturnal hypoxic burden. Results: Sixty-two patients (15%) had a history of cancer. OSA severity and hypoxemia indices were comparable between groups. In multivariable analysis, cancer history was independently associated with modestly lower ESS scores (B = −1.66, 95% confidence interval [CI] −2.96 to −0.37; p = 0.012) and a reduced likelihood of excessive daytime sleepiness (ESS > 10) (odds ratio [OR] = 0.25, 95% CI 0.07 to 0.85; p = 0.027). Conclusions: In this real-world cohort of untreated patients with OSA, cancer history is associated with modestly lower subjective daytime sleepiness despite comparable disease severity, supporting a potential dissociation between physiological burden and symptom perception. These findings indicate that reliance on subjective sleepiness alone may contribute to under-recognition of clinically relevant OSA in patients with a cancer history. Full article