COPD-OSA overlap syndrome (OVS) is defined by the coexistence of chronic obstructive pulmonary disease and obstructive sleep apnea syndrome in the same patient; it affects 28.3% of patients evaluated for either condition and is associated with significantly higher mortality compared to either pathology in isolation. Current therapeutic approaches, involving PAP therapy and bronchodilation, treat this syndrome as a homogeneous entity and ignore the biological heterogeneity of this patient population.

This review proposes a systematic framework for the endotypic classification of biological interactions between COPD and OSA, integrating current literature on the pathophysiological mechanisms underlying the OVS, clinically accessible biomarkers, and emerging therapies.

A narrative review based on available literature, focusing on studies published between 2010 and 2026 identified via searches in PubMed, PMC, and Dove Medical Press using the terms: COPD-OSA overlap syndrome, endotype, precision medicine, phenotype, biomarker, dupilumab, and incretin-based therapies.

Four clinical phenotypes (obese-metabolic, emphysematous, bronchitic-hypoxemic, and hypercapnic) and three molecular endotypes (Th2/eosinophilic, neutrophilic/oxidative, and metabolic-adipokine) are proposed, each with distinct pathophysiological mechanisms and specific therapeutic implications. The interaction between the two conditions generates a unique, pronounced hypoxemic profile. We propose the "double-hit hypoxemia" model as a conceptual framework characterized by amplified systemic inflammation and increased cardiovascular risk compared to either pathology in isolation. This proposed model has not yet been prospectively validated. Dupilumab (approved for an inflammatory phenotype in COPD patients characterized by eosinophil counts ≥ 300 cells/μL) represents a promising option, though currently unsupported in the OVS population, that could nonetheless be relevant to the Th2/eosinophilic endotype of this syndrome and tirzepatide (which reduced the AHI by up to 23.8 events/hour versus placebo in the SURMOUNT-OSA trial, conducted in patients with obesity and moderate-to-severe OSA, rather than in patients with confirmed OVS) could represent a promising therapy for the metabolic-adipokine endotype of obese patients with OVS. A minimal biomarker panel, comprising blood eosinophils, FeNO, daytime PaCO₂, BMI, and T90, allows for a practical approach to identifying the dominant endotype.

Endotyping of OVS may provide a framework for moving beyond a uniform therapeutic approach toward more individualized management based on the dominant underlying biological mechanism. Randomized clinical trials focusing on endotypic stratification and OVS cohorts remain research priorities.

Background/Objective: The morphology of the flow-volume curve has emerged as a potential source of additional functional information by enabling the analysis of concavity, slope-based metrics, area-derived measures, and mathematical models extracted from the expiratory tracing. Therefore, the aim of this study was to map and describe the available evidence on morphological analysis methods of the expiratory flow-volume curve for the identification and characterization of fixed airflow obstruction. Methods: A scoping review was conducted following the methodological frameworks proposed by Arksey and O'Malley, Levac et al., the Joanna Briggs Institute, and the PRISMA Extension for Scoping Reviews (PRISMA-ScR). Studies published between 1 January 1990, and 31 December 2025, that evaluated morphological flow-volume curve metrics for the diagnosis or characterization of Chronic Obstructive Pulmonary Disease (COPD) were included, without language restrictions. Searches were performed in PubMed/MEDLINE, Embase, Scopus, Web of Science, IEEE Xplore, OpenGrey, and Google Scholar. Study selection was conducted by independent reviewers, with disagreements resolved by consensus, and data extraction was performed using a standardized form. Results were synthesized narratively and organized according to metric families. Results: The search identified 13,577 records; after duplicate removal and screening, 24 studies met the inclusion criteria. The evidence included observational studies, diagnostic validation studies, longitudinal cohorts, and methodological modeling studies. Identified metrics were grouped into four main categories: concavity and geometric indices of the flow-volume curve, expiratory slope and flow-decay metrics, area-based or volumetric-derived measures, and mathematical or computational models applied to the tracing. Concavity indices, the β-angle, slope-ratio, Peak Index, and the D parameter showed consistent associations with airflow obstruction, emphysema, small airway disease, or functional impairment. Expiratory slope metrics and Flow Decay demonstrated high diagnostic performance in several studies, whereas area-based measures such as AEX, AEX-FV, AreaFE%, and AUC3/AT3 integrated the overall loss of expiratory flow during forced expiration. Mathematical and computational models suggested that the complete shape of the curve contains additional diagnostic and prognostic information, although methodological variability and the need for external validation remain important limitations. Conclusions: Morphological analysis of the flow-volume curve represents a promising approach to complement conventional spirometry in the identification and characterization of fixed airflow obstruction. These metrics may provide additional information regarding airflow limitation, non-uniform lung emptying, emphysema, small airway disease, hyperinflation, and clinically relevant outcomes.

Chronic obstructive pulmonary disease (COPD) is a heterogeneous respiratory disorder driven by neutrophilic and eosinophilic inflammation, structural changes, and airflow limitation. Shared pathophysiology makes cardiovascular disease a prevalent COPD comorbidity, necessitating an integrated cardiopulmonary assessment. Screening questionnaires may aid early COPD detection. CT imaging can supplement spirometry to characterise structural changes. Recent advances have shifted COPD management toward phenotype-directed approaches that incorporate novel biomarkers and emerging targeted therapies.

This narrative review summarises recent advances in COPD management. Relevant literature was identified through database searches focusing on COPD guidelines, randomised controlled trials, systematic reviews, and emerging therapies.

Current management emphasises smoking and e-cigarette cessation, vaccination against respiratory pathogens, and early recognition of disease phenotypes. Blood eosinophils and other biomarkers correlate with corticosteroid responsiveness. Dual long-acting bronchodilator therapy (LABA/LAMA) remains foundational for maintenance treatment, while triple therapy (ICS/LABA/LAMA) reduces exacerbations in patients with recurrent exacerbations and eosinophilic inflammation. Advances in targeted therapies include biologics such as dupilumab and mepolizumab that improve outcomes in patients with eosinophilic COPD. Phosphodiesterase inhibitors provide additional therapeutic options including ensifentrine, which combines bronchodilator and anti-inflammatory effects, and roflumilast, which reduces frequent exacerbations and chronic bronchitis. Emerging therapies that target inflammatory pathways including tezepelumab, and IL-33 inhibitors such as astegolimab, itepekimab, and tozorakimab, are under investigation.

COPD management is evolving toward precision medicine, guided by inflammatory phenotypes, biomarkers, and individualised risk profiles. Continued investigation into targeted biologics, anti-inflammatory agents, and incorporating biomarkers into clinical practice may improve outcomes and reduce disease burden.

Pneumocystis jirovecii pneumonia (PJP) is an increasingly recognised opportunistic infection among non-HIV immunocompromised patients receiving prolonged corticosteroid and immunosuppressive therapy who may present with progressive dyspnoea and fever and are initially treated for community-acquired pneumonia. Rapid clinical deterioration led to respiratory failure requiring invasive mechanical ventilation. Imaging revealed diffuse ground-glass opacities with bilateral pneumothoraces. Microbiological testing of sputum confirmed PJP. Despite targeted antimicrobial therapy and pleural drainage, the clinical course was complicated by persistent air leak, ventilator-associated pneumonia and refractory hypoxaemia, resulting in death. This case highlights the importance of early suspicion for PJP in non-HIV immunosuppressed patients and underscores bilateral pneumothorax as a rare but life-threatening complication. Consideration of prophylaxis and prompt evaluation for structural complications are essential to improve outcomes in high-risk populations.

The schematic workflow illustrates next-generation sequencing of lung-derived mesenchymal stromal cells (MSCs) from IPF patients and controls. Rather than broad epigenetic reprogramming, IPF-MSCs exhibit a remarkably restricted down-regulation of only three critical microRNAs: hsa-miR-373-3p, hsa-miR-486-5p, and hsa-miR-449a. This selective dysregulation leads to the targeted upregulation of key profibrotic genes (SMAD4, BCL2, TGF-β, CXCL12, VEGF), driving TGF-β cascade activation, altered autophagy, and profibrotic and proangiogenic signaling.

Swine are a crucial species in influenza A virus (IAV) ecology, capable of supporting replication and consequently evolution of human, avian, and swine strains. They are also the source of the 2009 pandemic H1N1 virus (H1N1pdm09). Understanding how swine IAV breach the species barrier is essential for detection of potentially pandemic viruses, but is often overlooked compared to avian IAV. We hypothesize that the HA-NA balance of (pre)pandemic swine viruses is a key feature that needs adjustment as swine and humans differ in their sialoglycome. We focused on a set of (pre)pandemic swine viruses collected in Mexico following the H1N1pdm09 emergence. Phylogenetic analysis showed that the emergence was preceded by substitutions in HA and NA predicted to affect their function. Thus, HA acquired substitution A227E, previously shown to reduce receptor binding in H1N1pdm09, while NA obtained substitution S369N in the 2nd sialic acid binding site (2SBS) predicted to reduce NA cleavage. The substitutions' effect on the HA-NA balance, was confirmed with biolayer interferometry using recombinant proteins attached to nanoparticles. Engineering recombinant attenuated influenza viruses with swine HA and NA with/without the mentioned substitutions, showed that the 2SBS substitution negatively affected replication in primary human and swine cultures. Interestingly, replication was restored by the HA substitution. Overall, we show that the emergence of H1N1pdm09 in humans was preceded by substitutions in HA and NA that were acquired in swine and adjusted the HA-NA balance. We hypothesize that adjustment of the HA-NA balance was a critical step for crossing the host-species barrier.

SARS-CoV-2 infection during pregnancy has been associated with higher rates of preeclampsia (PE). While placental abnormalities resembling PE have been reported in COVID-19 pregnancies, the molecular mechanisms underlying the association remain unclear.

We conducted bulk RNA sequencing on placental tissues from four pregnancy groups: uneventful prepandemic (preCOVID-19), prepandemic PE (preCOVID-19 PE), COVID-19 without PE (COVID no PE), and COVID-19 complicated by PE or other hypertensive disorders (COVID PE). Differential expression was analyzed using Deseq2 likelihood ratio test (LRT), and gene set enrichment analysis identified dysregulated pathways.

Clustering of LRT-significant differentially expressed genes (DEGs) identified a set of 16 genes (defined by the false discovery rate adjusted p-value < 0.05) across the four pregnancy groups, showing stepwise expression changes-lowest in preCOVID-19 uneventful, followed by those in COVID-19 without PE, then preCOVID-19 PE, and highest in COVID PE. This cluster included genes associated with placental dysfunction, such as LAMA5 and BTNL9. While morphogenesis-related pathways were enriched across all pathological groups, immune activation pathways were predominantly enriched in COVID PE, moderately in preCOVID-19 PE, and absent in COVID no PE.

Our findings identify a COVID-19-associated placental signature that mirrors PE features and shows a progressive expression pattern defining a continuum of placental stress, with maternal SARS-CoV-2 infection potentially exacerbating underlying dysfunction.

Intracranial aneurysms are dilatations of cerebral arteries that may rupture, leading to subarachnoid hemorrhage and high mortality. Endovascular coiling is widely used to prevent rupture; however, many treated aneurysms experience recanalization, which often necessitates follow-up interventions or surgical clipping. Despite its clinical importance, the segmentation and morphological characterization of recanalized coiled aneurysms remain largely unexplored. In this study, we introduce an automated framework for the segmentation of recanalized coiled aneurysms from three-dimensional rotational angiography (3D-RA) images and the extraction of morphological descriptors relevant to surgical planning. The method is based on the nnU-Net architecture, trained to segment the vascular tree, coil mass, and recanalized lumen. Quantitative postprocessing enables the computation of clinically relevant parameters, including coil-neck distance, recanalization volume, and maximum neck diameter, which contribute to the assessment of clipping feasibility. Preliminary results show encouraging segmentation performance and consistent estimation of morphological parameters across the evaluated cases, supporting the potential of the proposed framework for preoperative assessment of recanalized coiled aneurysms.

Heart failure is a chronic, progressive condition with a high symptom burden and a high mortality rate.

To explore the experiences of heart failure nurses in delivering palliative care to patients with heart failure.

A qualitative study using semi-structured interviews.

Three main themes emerged: the heart failure nurse's role in advance care planning; challenges and barriers to the provision of palliative care; and the positive impact of education and collaboration. Participants reflected on the shift in mindset with palliative care originally seen as outside their scope of practice to a care pathway and now being integral to their role. This was underpinned by the provision of specific training, sharing of practice and growing exposure to clinical practice across settings which facilitated this process.

Heart failure nurses are in a unique position to provide palliative care for their patients, but they highlight that current palliative care provision fails to meet the specific needs of patients with heart failure at a systems level. Palliative care services are inconsistent across and within systems and professions which is attributed to both a lack of resources and a lack of understanding. A collaborative model which integrates palliative care, cardiology and primary care teams is required to lead to more holistic patient care. Further research is needed to ascertain the most effective models to integrate palliative care into the management of people with heart failure and assess patient and caregiver perspectives.

Palliative care should be integrated into routine heart failure management through clear referral pathways and multidisciplinary collaboration. Targeted education and training can support heart failure nurses in advance care planning, symptom management and end-of-life care, enabling earlier and more person-centred support for patients and caregivers.

Health care crises may be associated with changes in in-hospital cardiac arrest (IHCA) care and resuscitation practices. Whether prolonged health care workforce shortage is associated with termination of resuscitation (TOR) practices remains unclear.

To determine whether a nationwide resident resignation in South Korea was associated with differences in IHCA characteristics, resuscitation trajectories, and TOR practices.

A retrospective cohort study conducted at a single tertiary teaching hospital in South Korea of adults aged 18 years or older who underwent cardiopulmonary resuscitation (CPR) for IHCA between March 1, 2023, and February 28, 2025.

IHCA occurring before vs during a workforce crisis precipitated by mass resident physician resignations.

Primary outcomes were return of spontaneous circulation (ROSC) and TOR without ROSC, analyzed as competing events over CPR duration. Secondary outcomes included CPR duration, 24-hour survival, 30-day survival, favorable neurological status, and survival to discharge.

A total of 383 patients with 469 IHCA events were included (median [IQR] age, 69 [61-79] years; 238 [62.1%] male). Overall IHCA incidence did not differ between periods (2.30 vs 2.50 incidents per 1000 admissions; P = .36). The median CPR duration was 8 minutes in both periods. CPR exceeding 35 minutes was less frequent during vs before the crisis (12 of 180 events [6.7%] vs 38 of 289 events [13.1%]; P = .03). ROSC, neurological outcomes, and survival outcomes did not differ statistically. In adjusted competing-risk analyses, the crisis period was not associated with ROSC (adjusted hazard ratio [aHR], 0.93; 95% CI, 0.72-1.19) but was associated with higher hazard of TOR without ROSC (aHR, 1.66; 95% CI, 1.14-2.42). Standardized cumulative incidence analyses showed a higher cumulative incidence of TOR without ROSC, with an absolute risk difference of 4.9 percentage points at 35 minutes.

In this retrospective cohort study, the crisis period was associated with fewer prolonged CPR attempts, with no significant differences in ROSC or survival outcomes. These findings suggest that prolonged health care workforce shortage and associated resuscitation-system adaptations may have influenced TOR practices, underscoring the need for standardized TOR decision-making.