Results
- Showing results for:
- Reset all filters
Search results
-
Journal articleDiaz-Nicieza C, Sahyoun L, Michalaki C, et al., 2026,
Correction: Ageing results in an exacerbated inflammatory response to LPS by resident lung cells.
, Immun Ageing, Vol: 23, ISSN: 1742-4933 -
Journal articleCawthorne W, Zhang Y, Val N, et al., 2026,
Unmasking programmed cell death in rhinovirus-driven asthma pathology
, Biochemical Society Transactions, Vol: 54, Pages: 1359-1373, ISSN: 0300-5127Rhinovirus (RV) infection is responsible for the majority of cases of viral exacerbations of asthma. Understanding the cellular and molecular mechanisms that cause asthma exacerbations is an absolute requirement for the development of effective treatments. Emerging literature suggests that cell death may have an important role in RV-induced exacerbations. Several types of programmed cell death (PCD) have been implicated in asthma, including apoptosis, necroptosis, pyroptosis, and ferroptosis. Increased presence of apoptotic airway epithelial cells in the sputum of adult and paediatric asthma patients is suggestive of defects in apoptosis. Elevated levels of phosphorylated mixed lineage kinase domain-like protein and receptor-interacting serine/threonine-protein kinase 3, markers of active necroptosis, have been found in the serum of asthmatic patients. Gasdermin B, a member of the gasdermin family of pyroptosis executioner proteins, has a strong genetic linkage to severe asthma. Expression level of GSDMB correlated with asthma exacerbations and antiviral pathways. Lipid peroxidation and increased airway iron levels, both suggestive of ferroptosis, have been observed in asthma patients. RV infection of epithelial cells triggers an inflammatory response, which can provide the necessary pro-inflammatory chemokines and cytokines to initiate PCD, such as tumour necrosis factor-α. RV exploits PCD such as apoptosis, necroptosis, pyroptosis, and ferroptosis to aid its replication and release, while modulating them probably to limit immune response. In the present review, we investigate the concept that pro-inflammatory PCD pathways modulated by RV infection in the context of asthma lead to prolonged inflammatory and immune responses that are key to asthma exacerbations.
-
Journal articleFore F, Bagley DC, Martinez-Nunez RT, et al., 2026,
Airway epithelia clear rhinovirus infection via two waves of cell extrusion.
, Sci Adv, Vol: 12Epithelial barriers represent the first line of defense against pathogens, yet their role in innate immunity is typically relegated to pathogen detection and immune cell recruitment. This perspective ignores a fundamental biological principle: Epithelia defended against pathogens long before complex immune systems evolved. Here, we demonstrate that human bronchial epithelium retains this ancestral capacity, autonomously clearing rhinovirus (RV) within 24 hours by selectively extruding infected cells, a process that we term virus-induced cell extrusion (VICE). VICE occurs in two waves: a rapid response occurring independently of complete virus entry, followed by a replication-dependent wave. Barrier-defective epithelia that cannot extrude do not eliminate RV. While VICE maintains barrier integrity and reduces local infection, it also expels virus-laden cells, which can infect fresh epithelia. Thus, VICE enables leukocyte-independent epithelial defense while inadvertently promoting viral spread, redefining epithelia as central to viral pathogenesis and host protection.
-
Journal articleMa J, Burney P, Mannino D, et al., 2026,
Generational changes in lung function in adults from several world regions: results from the burden of Obstructive Lung Disease study
, Thorax, ISSN: 0040-6376This study estimated birth cohort effects on lung function using BOLD data from 28,569 adults born between 1902 and 1976 across 41 sites in 34 countries. Forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and the FEV1/FVC increased across successive birth cohorts in both high-income countries (HICs) and low- and middle-income countries (LMICs), with mean values rising steadily with later birth year. In fully adjusted models, FVC increased by 21.4 mL, FEV1 by 24.6 mL, and FEV1/FVC by 0.25% per birth year. These positive associations were consistent across sex, smoking status, and country-income subgroups (HICs and LMICs).
-
Journal articleConway F, Finney L, 2026,
Knowing when to stop: the challenge of macrolide discontinuation in chronic airways disease.
, Thorax -
Journal articleGuo H, Li J, Lei M, et al., 2026,
The circadian rhythm gene BHLHE40 regulates inflammation in asthma patients and promotes ferroptosis through PTGS2 and SERPINB2 in lung fibroblast cells
, BMC Pulmonary Medicine, ISSN: 1471-2466BackgroundCircadian rhythm transcription factor basic helix-loop-helix family member e40 (BHLHE40) is a core regulator in the transcriptional response in immunoglobulin class switching to IgE. We describe here the results of our systematic investigations of BHLHE40 in inflammatory responses in lung epithelial cells and fibroblast cells, and particularly for its role in ferroptosis.MethodsBHLHE40 levels in serum and transcript levels in human peripheral blood mononuclear cells (PBMC) from asthma patients and healthy controls were quantified. BHLHE40 was silenced by siRNAs in human airway epithelial A549 cells and human lung fibroblast MRC5 cells. RNA sequencing was performed with BHLHE40-silenced MRC5 cells. Gene silencing or overexpression models for BHLHE40, PTGS2 and SERPINB2 were established with MRC5 cells. MRC5 cells were co-stimulated by lipopolysaccharide (LPS) and IL-13. Apoptosis, reactive oxygen species (ROS), Fe2+, lipid peroxide (LPO), malondialdehyde (MDA) and glutathione (GSH) levels were quantified. Levels of HMGB-1, IL-4, IL-6 and TNF-α in supernatants were measured by ELISAs. Expression levels of BHLHE40, GPX4, SLC7A11, PTGS2, and SERPINB2 were determined by qPCRs and Western blotting. RNA immunoprecipitation and dual-luciferase reporter assays were applied to detect gene interactions.ResultsBHLHE40 protein levels in serum and BHLHE40 transcript levels in PBMC were higher in asthma patients compared to the control group (P<0.001 and P<0.0001, respectively). BHLHE40 transcript levels were correlated with neutrophil counts in blood, FEV1%pred, PEF and FeNO levels in asthma patients. Silencing BHLHE40 in A549 and MRC5 cells resulted in a decrease of IL-6 and IL-8 levels after stimulation of IL-1β. Transcriptomic analysis for BHLHE40-silenced MRC5 cells showed 506 up-regulating genes and 512 down-regulated genes, which contained PTGS2 and SERPINB2. PTGS2 and SERPINB2 were highly expressed in asthma samples and positively correlated
-
Journal articleOzoh O, Owusu SK, Nantanda R, et al., 2026,
Prevalence of asthma among African children and adolescents: findings from the chronic respiratory disease observatory for Africa (CHEST-Africa)
, Thorax, ISSN: 0040-6376 -
Journal articleMa J, Quintero Santofimio V, Potts J, et al., 2026,
Alcohol consumption and small airways obstruction
, Chest, Vol: 170, Pages: 752-754, ISSN: 0012-3692 -
Journal articleMoffatt MF, Nishimura T, Cox MJ, et al., 2026,
Airway microbiome diversity, intra-mucosal bacteria, and spatial immunity in asthmatics and controls
, American Journal of Respiratory and Critical Care Medicine, Vol: 212, Pages: 1962-1974, ISSN: 1073-449XRationaleAsthma is characterized by disruption of the thoracic airway mucosae and loss of microbial diversity. Spatial profiling of the mucosal transcriptome may systematically discover mechanisms for microbial influences on immunity.ObjectivesWe investigated relationships between clinical measures, microbial communities, and the host mucosal transcriptome within different strata of bronchial biopsies in subjects with and without asthma.MethodsWe bronchoscoped 65 adult asthmatics and 44 healthy controls, quantifying bacterial operational taxonomic units (OTUs) in bronchial brushings by 16S rRNA gene amplicon sequences. Biopsy histologic features were scored blind to diagnosis. Following 16S rRNA in situ hybridization of 44 biopsies, bacterial foci were scored in epithelium, basement membrane and stroma. Global human gene expression was quantified in epithelial and stromal compartments using Digital Spatial Profiling.Measurements and main resultsClinical asthma was independently predicted by basement membrane abnormalities (BaseMA), endobronchial bacterial diversity and circulating eosinophil counts, but not by specific OTU abundances. 16S rRNA staining revealed bacteria within epithelium and mucosa of all biopsies. Intra-mucosal bacteria (IMCBs) counts correlated negatively with spatially organized co-expression networks encoding antigen-specific immunity, neutrophil functions, and matrix activation, whereas BaseMA correlated positively with the adaptive immunity module. Eosinophil counts correlated with epithelial bacterial counts and senescence pathways. Clinical asthma was accompanied by upregulation of a Treg cell network.ConclusionsAsthma and its related phenotypes are accompanied by complex mucosal events that extend beyond eosinophilic pathways. Components of diverse airway microbiota may modify immunity by beneficial interactions within the mucosa.
-
Journal articleBaraldi F, Mah JSY, Almuhanna A, et al., 2026,
Mucus plug formation is associated with eosinophilic activation in chronic obstructive pulmonary disease.
, Am J Respir Crit Care Med, Vol: 212, Pages: 2071-2074 -
Journal articleThorarinsdottir E, Benediktsdóttir B, Aspelund T, et al., 2026,
Screening for obstructive sleep apnoea in the general population in Iceland and uptake of positive airway pressure treatment: a prospective cohort study
, BMJ Open, Vol: 16, ISSN: 2044-6055Objectives To estimate uptake of obstructive sleep apnoea (OSA) screening and initiation and long-term use of positive airway pressure (PAP) treatment in a middle-aged and older general population cohort.Design Prospective population-based cohort study.Setting Icelandic arm of the multinational Burden of Obstructive Lung Disease follow-up study II (2019–2021)Participants 378 non-institutionalised adults aged 54–91 years were invited from a general population cohort. 26 with prior OSA diagnosis were excluded. Of the remaining participants, 334 (88.4%) completed a technically adequate home sleep apnoea test.Interventions Those with an apnoea–hypopnoea index (AHI)≥15 events/hour were invited for clinical evaluation and when appropriate, referred for PAP treatment. Adherence was assessed 2 years after PAP initiation.Main outcome measures Primary outcomes were screening uptake and PAP initiation. Secondary outcomes included long-term PAP use and objective adherence 2 years after referral.Results AHI≥15 was identified in 132/334 participants (39.5%). Of these, 123 (93.2%) attended clinical evaluation and 99 (75.0%) were referred for PAP treatment. Of those not referred, six declined PAP and the remainder were advised alternative management or reassessment. At 2-year follow-up, 53/99 (53.5%) were long-term PAP users, 43/99 (43.4%) had discontinued and 3/99 (3.0%) never initiated PAP. Objective adherence data were available for 47/53 long-term users; 21/47 (44.7%) met adherence criteria (≥4 hours/night on ≥70% of nights in the preceding 30 days).Conclusions Most adults accepted OSA screening when offered. Among those with moderate-to-severe OSA identified through population screening, most accepted evaluation and PAP treatment, with approximately half becoming long-term users. These findings suggest that population-based detection of OSA followed by routine clinical management is feasible. Future studies should identify subgroups most li
-
Journal articleJackson R, Bentley S, Davies JC, et al., 2026,
Keeping up with CFTR modulator eligibility.
, Paediatr Respir Rev, Vol: 59, Pages: 12-19The availability of highly effective cystic fibrosis transmembrane conductance regulator (CFTR) modulators has transformed outcomes for people with cystic fibrosis (pwCF). Eligibility, conferred initially by clinical trial data, has evolved through advances in in vitro 'theratyping' and use of real‑world evidence. Since ivacaftor's approval for a single gating variant in 2012, eligibility has broadened to over 180 variants with the highly effective therapies elexacaftor/tezacaftor/ivacaftor and recently launched vanzacaftor/tezacaftor/deutivacaftor. Regulatory authorities have increasingly accepted non‑traditional evidence, notably the FDA's 2017 ivacaftor extension based on cell‑based assays and, in 2025, the EMA's decision to extend elexacaftor/tezacaftor/ivacaftor to people ≥2 years with at least one non class I variant. However, clinical response remains variable, influenced in part by baseline characteristics, pharmacokinetics, pharmacogenetics, and environmental exposures. We outline evolving approaches to determining eligibility and strategies to improve methods to predict, verify, and monitor clinical response in an era of personalised medicine.
-
Journal articleBell RV, Faulkner NB, Sinadinos A, et al., 2026,
Assessment of F/HN-pseudotyped lentiviral vector following intravenous delivery to mice.
, Gene Ther, Vol: 33, Pages: 586-595In pursuit of a gene transfer agent with efficient pulmonary transduction, the UK Respiratory Gene Therapy Consortium has developed a lentiviral vector pseudotyped with the envelope proteins, F and HN from Sendai virus (rSIV.F/HN). In contrast to other viral vectors, pulmonary rSIV.F/HN delivery achieves sustained gene expression ( ~ 2 years in mice) in the lungs and systemic circulation following a single dose. Here, we investigate the application of the rSIV.F/HN vector-platform for wider indications, including systemic disorders that require serum expression of therapeutic proteins. To assess the potential for rSIV.F/HN to produce systemic proteins, intravenous vector delivery was characterised and compared against intrapulmonary administration, achieved via 'nasal sniffing'. Both delivery routes achieved sustained (at least 1 year) systemic expression of the secreted reporter protein Gaussia luciferase. Systemic rSIV.F/HN delivery resulted in widespread protein expression across multiple organs, accompanied by the generation of significant anti-vector neutralising antibodies limiting vector readministration. Conversely, localised airway transduction was observed following pulmonary administration, which we have previously shown is not an impediment to efficient vector readministration. These data support intrapulmonary rSIV.F/HN delivery for systemic protein production, with sustained high-level transgene expression and feasible readministration.
-
Journal articleJohannson KA, Barnes H, Peters CE, et al., 2026,
An Evidence-Based Exposure Questionnaire for Interstitial Lung Disease: EXPO-ILD.
, CHEST Pulm, Vol: 4BACKGROUND: Many interstitial lung diseases (ILDs) are associated directly or indirectly with inhaled environmental and/or occupational exposures; exposure identification is critical for diagnosis and clinical management. However, there are currently few evidence-informed exposure questionnaires for ILD, and none are in widespread systematic use. This study sought to develop an evidence-informed ILD exposure questionnaire, leveraging international expert-based consensus on exposures that present relevant risk for ILD development. RESEARCH QUESTION: What environmental and occupational exposures are risk factors for the development of ILD and should be included on ILD-specific exposure questionnaires? STUDY DESIGN AND METHODS: Participants with expertise in ILD, occupational respiratory medicine, or exposure assessment were invited to complete 2 rounds of a modified Delphi survey to identify relevant exposures associated with the risk of developing ILD. Items in the first Delphi round were informed by prior data, including a systematic review/meta-analysis and scoping review of questionnaires. Items not meeting consensus in the first round were carried over to the second round, with additional items added or modified as suggested by participants. Well-established causal exposures were not included. A priori definitions of consensus were applied, indicating response distribution. RESULTS: A total of 38 of 43 experts (88%) participated in the Delphi survey, with 37 of 38 (97%) completing both rounds. A total of 11 exposures met consensus for agreement as relevant risk factors for ILD, whereas 9 met consensus for disagreement as being irrelevant to ILD risk. Six exposures did not achieve consensus. Incorporating these findings with prior evidence syntheses, we developed 2 exposure questionnaires (EXPO-ILD-Short and EXPO-ILD-Long) for ILD for application in both clinical and research settings. INTERPRETATION: This international modified Delphi identified clinically releva
-
Journal articleFinney LJ, Conway FM, Sethi DK, 2026,
COPD Biologics: Right Patient, Right Pathway, Right Time.
, Pulm Ther, Vol: 12, Pages: 763-783Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease that is entering a new era in precision medicine. Advances in disease endotyping have challenged the traditional view of COPD as a uniformly neutrophilic disorder and revealed biologically distinct subgroups in whom targeted immunomodulation may be effective. Reproducible signatures of type 2 (T2) inflammation and epithelial-derived alarmin activation have emerged as actionable pathways, reshaping therapeutic development in COPD. This narrative review synthesises mechanistic insights and clinical trial evidence for biologic therapies targeting key T2 cytokines such as interleukin-5 (IL-5) IL-4/IL-13 and upstream epithelial alarmins, including interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP). We examine why earlier approaches targeting neutrophilic inflammation failed, and how biomarker-driven trial design has enabled success in selected populations. Across these programmes, therapeutic efficacy has depended not only on the pathway targeted but also on patient selection, disease stage and timing of intervention. We propose that the future of biologics in COPD lies in integrating biomarkers, treatable traits and longitudinal phenotyping to align the right patient with the right pathway at the right time, closing persistent treatment gaps in this common, overlooked and burdensome disease.
-
Journal articleAndersson LI, Kupczyk M, Dahlén B, et al., 2026,
Adipokines in Obese Asthma: A Complex Relationship Influenced More by Sex, Weight, and Oral Steroid Treatment Than Disease Severity.
, Allergy, Vol: 81, Pages: 3206-3220BACKGROUND: Obesity-related asthma (OBA) is a distinct asthma phenotype, with increased severity. Adipokine release from excessive adipose tissue is suggested to be a key feature of OBA pathophysiology. However, it is unclear how the clinical characteristics of severe asthma associate with adipokine mediators. We examined systemic adipokine levels and evaluated relationships with disease severity, weight, sex, and steroid treatment in asthma. METHODS: A multiplex immunoassay for nine adipokines with proposed involvement in obesity-related inflammation (adiponectin, adipsin, BAFF, chemerin, FGF-21, leptin, lipocalin-2/NGAL, osteonectin and resistin) was designed. Plasma adipokines were measured in 127 patients with mild-to-moderate asthma (MMA) or severe asthma (SA) from the European BIOAIR cohort at baseline and after a controlled 2-week oral corticosteroid (OCS) intervention. RESULTS: Leptin and chemerin were significantly increased in patients with SA vs. MMA. Leptin, adiponectin, adipsin, and NGAL were affected by sex, whereas leptin and adipsin were strongly affected by weight. OCS increased leptin and adiponectin, decreased adipsin and BAFF, and did not affect osteonectin, resistin, or chemerin. No adipokines showed positive associations with exhaled NO, blood or sputum eosinophils, although certain correlations with serum CRP, blood, and sputum neutrophils were observed. CONCLUSIONS: Overall, we observe variable relationships between the nine adipokines, obesity and asthma severity. There were no relationships between adipokine levels and type-2 airway inflammation, yet associations with systemic neutrophilic inflammation were seen. Although one adipokine, chemerin, was independently associated with asthma severity, deciphering the role of adipokines in OBA is complex due to the influence of sex, BMI, and OCS.
-
Journal articleLawton A, Hughes D, 2026,
Artificial intelligence in paediatric respiratory medicine.
, Paediatr Respir Rev, Vol: 59, Pages: 44-49Proponents of artificial intelligence (AI) believe that it will revolutionise the modern world, affecting how healthcare is delivered and improve both the clinical care we provide and the ease with which we perform our work. In this paper we explain what is meant by 'artificial intelligence' and explore how this technology has been implemented, or might be implemented, with respect to paediatric respiratory medicine. We review the current literature on how AI has been used to improve diagnostics - including examples in radiology, primary ciliary dyskinesia (PCD) diagnostics, sleep medicine, and pulmonary function tests. We also review how AI has been applied to therapeutics and drug discovery, how it will impact evidence-based medicine and literature review, and how clinician support tools will assist us in our work.
-
Journal articleHowlett P, Durairaj A, Gan J, et al., 2026,
Adjusting for the diagnostic accuracy of CXR in the dose-response relationship between cumulative silica exposure and silicosis in miners.
, Occup Environ Med, Vol: 83, Pages: 287-290INTRODUCTION: A recent meta-analysis confirmed that chest X-ray (CXR) has low sensitivity for diagnosing silicosis. We re-estimated previously published dose-response relationships between cumulative respirable crystalline silica (RCS) exposure and silicosis risk, under the assumptions that sensitivity was either fixed or relative to the population proportion of severe silicosis. METHODS: We combined unpublished logistic regression models from Scottish coal miners with meta-analysis results to model how CXR sensitivity changed according to cumulative RCS exposure. We assumed specificity was 0.95. Among mining cohorts, we calculated the difference in the cumulative risk of silicosis between the unadjusted and fixed and relative scenarios. Finally, we re-estimated a published dose-response meta-analysis and associated absolute risk reductions (ARR). RESULTS: The cumulative risk of silicosis was substantially higher in both the fixed and relative sensitivity scenarios compared with the unadjusted estimate in all mining cohorts. This was most pronounced in the relative scenario and when cumulative RCS exposures were below approximately 6 mg/m³-years. A reduction in cumulative RCS exposure from 4 to 2mg/m³-years corresponded to larger ARRs in the fixed and relative scenarios than the unadjusted scenario; 382 (95% CI 361 to 399) and 529 (95% CI 353 to 592) cases per 1000 miners compared with 313 (95% CI 288 to 333) cases per 1000 miners, respectively. DISCUSSION: We relied on a single estimate of the proportion of severe disease to link sensitivity and cumulative RCS exposure. Nevertheless, adjusting for the reduced diagnostic accuracy of CXR for silicosis suggests the burden of silicosis is underestimated in published mining cohorts.
-
Journal articleCarter EC, Hill H, Solórzano C, et al., 2026,
High respiratory syncytial virus burden in children under 3 years of age across all care levels in England.
, BMJ Open Respir Res, Vol: 13OBJECTIVES: This prospective surveillance study aimed to estimate the burden of laboratory-confirmed respiratory syncytial virus (RSV) in under 3-year-olds in the United Kingdom. SETTING: The study was implemented in Merseyside and Bristol, encompassing 11 primary care sites, 5 walk-in centres, 2 secondary care hospitals and 2 tertiary care hospitals. PARTICIPANTS: Children aged under 3 years presenting with lower respiratory tract infection (LRTI) symptoms were included, with a substudy in primary care recruiting children with upper respiratory tract infection (URTI). PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome of the study was the prevalence of RSV infection in primary, secondary and tertiary healthcare settings. Secondary outcomes included severity outcomes (rates of hospitalisation and high dependency care admissions), risk factors for severe disease, economic burden of disease and coinfection prevalence. RESULTS: 2000 children were included in the analysis (410 primary care and 1590 secondary/tertiary care). 318 were included in the URTI substudy. RSV prevalence was 50.0% (95% CI 46.7% to 53.3%) in children admitted to hospital via emergency departments (ED), 36.3% (95% CI 31.7% to 41.0%) in ED discharges, 36.5% (95% CI 24.7% to 49.6%) in primary care (LRTI) and 12.7% (95% CI 8.6% to 17.9%) in primary care URTI. Healthy term-born children accounted for 70.1% of RSV hospitalisations. Risk factors for severe disease included any level of prematurity, age <3 months and congenital cardiac disease. RSV-positive cases incurred a higher mean cost per participant (£1811, 95% CI £1720 to £1903) than RSV-negative cases (£1295, 95% CI £1220 to £1370). CONCLUSIONS: The findings revealed a substantial burden associated with RSV. Even moderate prematurity was a risk factor for severe disease, and these children may not benefit from maternal RSV vaccination due to missed late gestation antibody transfer. Fur
-
Journal articleRosenheim J, Bender B, Gilmour J, et al., 2026,
Conference report: airway mucosal sampling and immune analysis.
, Vaccine, Vol: 88Respiratory pathogens cause substantial global morbidity, mortality, and pandemic risk. While parenteral vaccines can effectively reduce severe disease for some respiratory infections, they are often less effective at preventing infection and onward transmission. Vaccines delivered directly to the airways have the potential to induce protective mucosal immunity at the site of pathogen entry. However, progress in mucosal vaccine development has been constrained by limited understanding of airway immune mechanisms, the technical challenges of sampling respiratory tissues, and the lack of standardised, validated immunological assays capable of defining mucosal correlates of protection. To address these challenges, the Novo Nordisk Foundation and Wellcome Trust convened a workshop on airway mucosal sampling and immunological assays, bringing together researchers, clinicians, funders, and representatives from major research consortia. Participants reviewed approaches to sampling the upper and lower respiratory tract, assay technologies, and regulatory considerations for integrating mucosal endpoints into vaccine development. Discussions highlighted major barriers including variability in sampling techniques, low and inconsistent cell yields, limited assay standardisation, and insufficient cross-study comparability. The workshop produced a set of recommendations in four priority areas (i.e., Collaboration, Communication, Consistency and Conduct of research) to share knowledge, accelerate standardisation and validation, and generate evidence supporting mucosal vaccine development. Together, these advances will help strengthen the scientific and regulatory foundations needed to realize the full potential of airway-delivered vaccines for the prevention of respiratory diseases.
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.