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Journal articleChung KF, Song WJ, 2025,
Use of digital monitoring technologies to measure chronic cough: “cough-omics”
, Ers Monograph, Vol: 2025-December, Pages: 296-305, ISSN: 2312-508XObjective measurement of cough frequency has been developed over the past 25 years. Current cough monitors are semi-automatic, limited to 24 h recordings using microphone detection and portable sound recorders, and have provided valuable information on cough frequency in patients with CC, which is modestly correlated with patient-reported outcomes. Their main use at the current time is in clinical trials for assessment of novel antitussives. Automatic analysis of cough events using machine learning has allowed for the use of digital tools and devices that in turn has led to the continuous unobtrusive recordings over long periods of time. The process of “cough-omics”, which is the analysis of large amount of data thus derived, has shown wide variability of daily cough counts in CC at an individual level and the lack of predictability of the cough counts in some for monitoring the effects of antitussives. There will be a greater understanding of the pathophysiology of cough with the analysis of cough-omics on how to use these new monitors efficiently both for clinical trials and in the clinic.
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Journal articleSong WJ, Chung KF, 2025,
Recent developments in the antitussive area
, Ers Monograph, Vol: 2025-December, Pages: 306-316, ISSN: 2312-508XRecent advances in CC research have led to a shift in perspective, with RCC and UCC recognised as forms of CHS. This condition is characterised by maladaptive sensitisation in both peripheral and central neural pathways. Key peripheral targets include transient receptor potential (TRP) channels, voltage-gated sodium channels, and purinergic (P2X3) receptors. Central mechanisms have been revealed through neuroimaging studies and clinical responses to neuromodulators, such as gabapentin and low-dose opioids. The clinical development of gefapixant, a P2X3 antagonist, validated the P2X3-ATP pathway as a therapeutic target, although limitations (e.g. taste disturbances and modest efficacy) led to the exploration of more selective agents. Emerging therapies include more selective P2X3 antagonists, TRPM8 agonists, neurokinin-1 receptor antagonists, N-methyl-D-aspartate receptor blockers, and novel opioid receptor modulators like nalbuphine. However, several challenges remain, including the lack of validated in vitro and in vivo experimental models, and limited access to nerve tissues. The heterogeneity of underlying mechanisms also complicates trial outcome and supports the need for better patient stratification. Furthermore, large placebo effects and the limitations of current efficacy end-points, such as 24-h cough frequency, hinder the detection of meaningful treatment effects. Future research must focus on identifying reliable biomarkers, refining trial methodologies and tailoring therapies to specific patient subgroups to improve CC treatment outcome.
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Journal articleButton B, Chung KF, Edwards DA, 2025,
Airway mucosal mediation of chronic cough and cough hypersensitivity
, Ers Monograph, Vol: 2025-December, Pages: 83-93, ISSN: 2312-508XCough plays a critical role in the clearance of mucus in respiratory disease. Recent findings suggest that mucus may also play a key role in the origins of cough itself. Recent in vitro and in vivo studies indicate that protracted mucosal collapse or intermittent collapse over long periods of tidal breathing can initiate an inflammatory cascade that triggers cough by multiple pathways, upregulating the expression of genes associated with cough hypersensitivity. Recent clinical data in RCC patients, and experimental data collected in airway lining interface cultures of human bronchial epithelial cells, indicate that reversing mucosal collapse with salt ions and buffers endogenous to the airways, while mimicking airway surface liquid pH fluctuations that occur in healthy human airways, diminishes airway epithelial cell compression, reduces cough frequency in RCC, and potentially lessens cough hypersensitivity.
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Journal articleAli N, Katsouli J, Auyang E, et al., 2025,
Microplastic and nanoplastic pollution and associated potential disease risks
, The Lancet Planetary Health, Vol: 9, ISSN: 2542-5196Microplastics and nanoplastics (MNPs) are emerging pollutants widely dispersed in the environment, with humans primarily exposed through ingestion and inhalation. Although their biological effects are being increasingly studied, their potential effect on human health and disease risk remains uncertain. This Review summarises evidence on potential disease risks of human exposure to MNPs, while highlighting key limitations and research gaps. Evidence suggests that MNP exposure might elevate the risk of various diseases, including metabolic, respiratory, cardiovascular, neuroendocrine, hepatic, renal, and skin disorders, as well as infectious diseases, cancer, and ageing-related disorders. Despite extensive evidence of adverse effects in animal models and cell cultures, direct evidence linking MNP exposure to human disease risk remains scarce. A key challenge on research of MNPs lies in the scarcity of robust human exposure data and the narrow scope of existing studies on specific types of MNPs, leaving several environmentally prevalent plastic particles understudied. Addressing these gaps will require investigating the mechanisms of toxicity, relevant biomarkers, and disease pathways associated with MNP exposure. Such efforts will be essential to clarify human health risks and inform future regulatory and mitigation strategies.
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Journal articleSong WJ, McGarvey L, Cho PSP, et al., 2025,
Introduction
, Ers Monograph, Vol: 2025-December, Pages: x-xiii, ISSN: 2312-508X -
Journal articleRoofchayee ND, Heshmatnia J, Jamatti H, et al., 2025,
Transcription Factor and Cytokine Profiles in Peripheral Blood T Helper Cells in Patients with Idiopathic Pulmonary Fibrosis
, IRANIAN JOURNAL OF ALLERGY ASTHMA AND IMMUNOLOGY, Vol: 24, Pages: 786-798, ISSN: 1735-1502 -
Journal articleHopkinson NS, 2025,
A lesson from Nye Bevan on the roots of fascism
, The BMJ, Vol: 391, ISSN: 0959-8146 -
Journal articleUsmani OS, Toumpanakis D, Meah S, et al., 2025,
Whole lung directed anti-muscarinic therapy improves small airway dysfunction in COPD patients
, European Respiratory Journal, ISSN: 0903-1936 -
Journal articleManeechotesuwan K, Kanokkantapong C, Boonpromkul C, et al., 2025,
The association of defective pleural sRAGE production with the recurrence of malignant pleural effusion after Talc pleurodesis
, Scientific Reports, Vol: 15, ISSN: 2045-2322Symptomatic malignant pleural effusions (MPE) are treated with chemical pleurodesis to prevent recurrence. The serum soluble receptor for advanced glycation end products (sRAGE) has been linked to lung cancer progression but its role in predicting talc pleurodesis failure is unclear. A prospective cohort study was conducted from November 2023 to December 2024, encompassing subjects with confirmed MPE. Pleural fluid samples were collected prior to intercostal drainage (ICD) insertion for the measurement of sRAGE, ADAM10, MMP9, and HMGB1 levels. Participants were monitored for 90-day post-pleurodesis failure, pleural interventions, and survival. Among seventy-three adults (median age 66 [IQR 53–74 years]) with MPE who received pleurodesis, lung adenocarcinoma was the most common. Talc pleurodesis failure (24.7%) was associated with greater pleural fluid output, multiple pleurodesis attempts, longer ICD retention, and lower pH and lymphocyte fraction. Pleural sRAGE and MMP9 levels were significantly diminished (p = 0.0033 and p = 0.029, respectively), whereas HMGB1 levels were substantially elevated (p = 0.019) in the failure cases. Among biomarkers, pleural sRAGE had the most predictive value for talc pleurodesis failure, followed by HMGB1 and MMP9. However, pleural sRAGE and MMP-9 lacked prognostic significance for 90-day mortality. The present study demonstrated that lower pleural sRAGE is a potential predictive biomarker for talc pleurodesis failure despite inferiority to pleural acidity. Imbalance between sRAGE and HMGB1 in MPE may be associated with the underlying mechanism for talc pleurodesis failure.
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Journal articleLaverty A, Parnham J, Filippos T F, et al., 2025,
Social media use and child cigarette smoking and e-cigarette use: a cohort study 2015-2023
, Tobacco Induced Diseases, ISSN: 1617-9625IntroductionThere are growing concerns that advertising and promotion on social media are driving youth use of tobacco and e-cigarettes. The UK provides an instructive example as it has high levels of e-cigarette use, high levels of social media use and a restrictive tobacco control environment. Existing evidence in the UK however, has not focused on children, has not been updated to reflect changes in patterns of social media use and in the use of these products. The aim of this study is to assess the associations of social media use with smoking and vaping.MethodsUsing data from the United Kingdom Household Longitudinal Study on 10–17-year-olds between 2015-2023, Generalised Estimating Equation (GEE) models estimated relationships between time spent on social media and likelihood of smoking tobacco and using e-cigarettes. Models were controlled for possible confounders including socio-demographics and whether children lived in a home with e-cigarette use or tobacco smoking. ResultsWe included data from 9,359 participants with 25,704 observations. Current cigarette smoking was reported by 4.9% of the sample and current e-cigarette use by 3.1% of the sample. Our adjusted models found strong relationships between time spent on social media and both smoking and vaping (p value for trend <0.001). For example, use of social media for ≥7 hours/day was linked to greater odds of tobacco (Adjusted Odds Ratio (AOR) 5.13, 95% Confidence Interval (CI) 3.32-7.95) and e-cigarette use (AOR 4.26, CI 2.25-8.08). ConclusionsThis study finds associations between time spent on social media and both smoking and vaping among children. Enforcing regulations on content and restricting the duration of social media use may be warranted to protect children’s health.
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Journal articleSanchez-Burgos I, Tejedor AR, Collepardo-Guevara R, et al., 2025,
Molecular insights on the mechanism of α1-antitrypsin condensate formation and maturation
, PLoS Computational Biology, Vol: 21, ISSN: 1553-734XThe deficiency of -antitrypsin protein is a genetic disorder characterized by the accumulation of misfolded protein aggregates within hepatocytes, leading to liver dysfunction. In the lung, it is found in macrophages, bronchial and epithelial alveolar cells type 2, leading to pulmonary emphysema. Despite extensive research, the precise mechanism underlying the formation of -antitrypsin inclusion bodies remain elusive. In this study, we combine equilibrium and non-equilibrium molecular dynamics simulations to elucidate the intricate process of -antitrypsin condensate formation and maturation. Our mechanistic model explains cluster accumulation—specifically the onset of this pathogenesis—through the emergence of phase-separated liquid-like protein droplets, which subsequently undergo inter-protein β-sheet transitions between misfolded variants, resulting in solid-like clusters. We find that this mechanism only applies to the misfolded variant, Z--antitrypsin, which phase-separates driven by its disordered C-terminus. In contrast, the native protein, M--antitrypsin, shows much lower propensity to phase-separate and later form kinetically trapped aggregates. Furthermore, we explore how Z--antitrypsin exhibits an increased capacity to form condensates near external walls with different types of interactions. Such conditions can be similar to those found within the endoplasmic reticulum membrane, where phase separation and hardening take place. Overall, our results shed light on the molecular basis of -antitrypsin-related disorders and provide valuable microscopic insights for the development of therapeutic strategies targeting protein misfolding and aggregation-related disorders.
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Journal articleAdesibikan A, Williams P, Cumella A, et al., 2025,
The relationship of material deprivation with emergency or unplanned healthcare utilisation in adults with Chronic Obstructive Pulmonary Disease: analysis from an Asthma + Lung UK survey
, BMJ Open Respiratory Research, ISSN: 2052-4439Background Various forms of deprivation have been linked to poor health. Emergency and unplanned healthcare utilisation (EUHU) is inefficient and represents suboptimal chronic disease management. Understanding the relationship between material deprivation – the inability to afford certain basic items of living – and EUHU in COPD may identify intervention targets. However, research is limited. This study investigates the relationship between material deprivation and the frequency of EUHU.MethodsData were analysed from 3472 individuals with COPD who completed an online Asthma + Lung UK survey (January-March2024). The relationship was assessed between material deprivation (nine-item European Union Statistics on Income and Living Conditions survey) and self-reported frequency of EUHU in the preceding year in 5 categories. ResultsPeople experiencing material deprivation had higher odds of reporting a higher frequency of emergency and unplanned healthcare utilisation compared to those who were not (OR:1.27, 95%CI:1.08-1.49, p=0.005), independent of identified confounders. Associations were also seen with six of the nine individual items including not being able to afford mortgage/rent/utility bills, cars, unexpected expenses, heating, decent meal, or a holiday. Living in cold/or damp housing was associated with increased emergency and unplanned healthcare utilisation.Discussion and ConclusionMaterial deprivation is associated with more frequent emergency and unplanned healthcare utilisation in COPD. Interventions targeting material deprivation may improve health outcomes and reduce emergency and unplanned healthcare utilisation.
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Journal articleDeng Z, Xia T, Lu C, et al., 2025,
Quantitative Computed Tomographic Clusters in C-BIOPRED Asthma Cohort: Association with Sputum Proteomics
, MEDCOMM, Vol: 6 -
Journal articleGreen CG, Bempong J, Ong MLY, et al., 2025,
Evaluating short-chain fatty acids in breath condensate as surrogate measurements for systemic levels and investigation into alternative respiratory sample matrices
, Clinical Science, Vol: 139, Pages: 1287-1300, ISSN: 0143-5221Short-chain fatty acids (SCFAs) are metabolic by-products from microbial fermentation of complex carbohydrates and protein. They have gained clinical interest for their protective effects, including within the lung microenvironment. SCFAs are detectable in circulation and exhaled breath condensate (EBC), posing questions as to whether exhaled SCFAs originate from the gut and/or lung microbiota. Mapping SCFAs from the lung could improve our understanding of microbial activity in respiratory conditions. SCFA measurements in EBC were evaluated using a validated gas chromatography-mass spectrometry assay. Six healthy participants ingested sodium acetate, calcium propionate and sodium butyrate to acutely increase circulating SCFAs. EBC samples were collected alongside venous draws, with circulating and exhaled levels compared. A series of additional respiratory sample matrices from patient samples was investigated to gain novel insights into SCFAs within different respiratory biofluids. Serum SCFAs were increased in line with known responses. However, these increases were not observed in EBC, indicating a lack of correlation between circulating and exhaled SCFAs. SCFAs were detected in all additional respiratory biosamples, with EBC and sputum reporting the highest concentrations. Interestingly, branched-chain moieties were notably abundant in sputum, indicating the potential for their local production by bacterial fermentation of lung mucus proteins. SCFAs in EBC do not reflect circulatory levels and, therefore, are not a suitable surrogate measurement to inform on systemic load. These data suggest that exhaled SCFAs are potentially derived from lung microbial metabolism, supporting the need for further investigation into SCFA production, function and diagnostic utility in respiratory health.
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Journal articleWelham B, Bennett M, Ostridge K, et al., 2025,
A novel SPECT-CT imaging platform for quantifying in vivo lung cytokine signals in COPD
, ERJ OPEN RESEARCH, Vol: 11 -
Journal articleMarei I, Vinokurova M, Qiucheng L, et al., 2025,
Impact of type 1 diabetes on endothelial cells derived from living donors
, FASEB BioAdvances, Vol: 7, ISSN: 2573-9832Endothelial colony forming cells (ECFCs) derived from peripheral blood have been shown to retain disease phenotype in several conditions thus possessing great translational potential for regenerative medicine. Hyperglycaemia may alter the phenotype of ECFCs yet the characteristics of ECFCs isolated from people with type 1 diabetes (T1D) have not been described. Here, we establish whether ECFCs can be successfully isolated from donors with T1D and we characterize their functional properties. Human ECFCs were isolated from peripheral blood of up to 9 control and T1D donors. Expression of cell markers and cytokines was analyzed using immunocytochemistry, RT-PCR and ELISA. Ca2+ signaling and contraction were studied using Fluo-4-AM in cells treated with serial concentrations of histamine (1 × 10−7-1 × 10−4M). T1D ECFCs showed robust endothelial marker expression and displayed normal morphology but had a reduced size compared to those from control donors. In response to inflammatory stimuli, T1D ECFCs exhibited exaggerated pro-atherogenic/pro-inflammatory cytokine (IL-6 and MCP-1) and adhesion molecule gene induction (VCAM-1 and ICAM-1) but suppressed induction of interferon signaling markers (IP-10). Histamine stimulated a concentration-dependent increase in Ca2+ influx in ECFCs which was significantly reduced in ECFCs from T1D donors, independent of differences in H1 receptor expression levels. Histamine-induced contraction was significantly enhanced in T1D ECFCs. ECFCs from control and T1D donors exhibit distinct phenotypic differences redolent of the vascular pathologies associated with T1D. This establishes the utility of T1D ECFCs for modeling vascular complications but also highlights the need to understand the potential limitations of autologous ECFCs to treat diabetic complications.
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Journal articleTahmasebi S, Amani D, Salimi B, et al., 2025,
LncRNA-mediated miR-145 sponging drives FN1 and CCND1 expression: prognostic and therapeutic targets in NSCLC
, Biomolecules, Vol: 15, ISSN: 2218-273XBackground: Non-small cell lung cancer (NSCLC) progression is driven by dysregulated competing endogenous RNA (ceRNA) networks, where non-coding RNAs sequester miR-NAs to modulate oncogene expression. The tumor-suppressor miR-145 is frequently downregulated in NSCLC, but its lncRNA-mediated regulation remains incompletely characterized. Methods: Integrated transcriptomic analysis of NSCLC datasets (GSE135304: blood RNA from 712 patients; GSE203510: plasma miRNAs) was used to identify dysregulated genes (|log2FC| > 0.1, p < 0.05) and miRNAs (|log2FC| > 1, p < 0.05). Experimentally validated targets from miRTarBase/TarBase were intersected with dysreg-ulated genes, followed by WikiPathways/GO enrichment. ceRNA networks were con-structed via co-expression analysis. RT-qPCR validated miR-145-3p expression in A549/MRC-5 cells and NSCLC tissues. GEPIA assessed FN1/CCND1 clinical relevance. Results: We identified 8271 dysregulated genes and 52 miRNAs. miR-145-3p, critical in immune regulation, was significantly downregulated (log2FC = −1.24, p = 0.036). Intersec-tion analysis revealed 27 miR-145-3p targets (e.g., FN1, CCND1, SMAD3) enriched in im-mune pathways (FDR < 0.05) and TGF-β-mediated EMT within the dysregulated geneset. Six immune-linked hub genes emerged. LncRNAs LOC729919 and LOC100134412 showed strong co-expression with hub genes and competitively bind miR-145-3p, dere-pressing the expression of the metastasis drivers FN1 (ECM regulator) and CCND1 (cell cycle controller). This ceRNA axis operates within a broader dysregulation of ATM-de-pendent DNA damage, Hippo signaling, and cell cycle pathways. RT-qPCR confirmed significant miR-145-3p suppression in NSCLC models (p < 0.05). GEPIA revealed a signif-icant FN1-CCND1 co-expression (p = 0.0017). Conclusion: We characterize a novel LOC729919/LOC100134412–miR-145–FN1/CCND1 ceRNA axis in NSCLC pathogenesis. FN1’s prognostic value and functional linkage to CCND1 underscor
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Journal articlePham DD, Lee J-H, Kwon H-S, et al., 2025,
Reply to “Optimizing FeNO and blood eosinophil stratification in eosinophilic asthma study: Adjusting for smoking history and blood sampling time”
, Journal of Allergy and Clinical Immunology: In Practice, Vol: 13, Pages: 3161-3163, ISSN: 2213-2198 -
Journal articleZimmer AJ, Das R, Lopez PE, et al., 2025,
Objective cough counting in clinical practice and public health: a scoping review.
, Lancet Digit Health, Vol: 7Quantifying cough can offer value for respiratory disease assessment and monitoring. Traditionally, patient-reported outcomes have provided subjective insights into symptoms. Novel digital cough counting tools now enable objective assessments; however, their integration into clinical practice is limited. The aim of this scoping review was to address this gap in the literature by examining the use of automated and semiautomated cough counting tools in patient care and public health. A systematic search of six databases and preprint servers identified studies published up to Feb 12, 2025. From 6968 records found, 618 full-text articles were assessed for eligibility, and 77 were included. Five clinical use cases were identified-disease diagnosis, severity assessment, treatment monitoring, health outcome prediction, and syndromic surveillance-with scarce available evidence supporting each use case. Moderate correlations were found between objective cough frequency and patient-reported cough severity (median correlation coefficient of 0.42, IQR 0·38 to 0·59) and quality of life (median correlation coefficient of -0·49, -0·63 to -0·44), indicating a complex relationship between quantifiable measures and perceived symptoms. Feasibility challenges include device obtrusiveness, monitoring adherence, and addressing patient privacy concerns. Comprehensive studies are needed to validate these technologies in real-world settings and show their clinical value. Early feasibility and acceptability assessments are essential for successful integration.
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Journal articlePramanik SK, Sreedharan S, Kandoth N, et al., 2025,
Transition metal complexes as optical probes for super-resolution microscopy
, NATURE REVIEWS CHEMISTRY, Vol: 9, Pages: 733-748
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