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Journal articleAsamoah K, Yang F, Adcock IM, et al., 2026,
Trajectory-based clustering to identify asthma subgroups responsive to the selective CXCR2 antagonist, AZD5069
, Allergy, Vol: 81, Pages: 297-299, ISSN: 0105-4538 -
Journal articleFeleszko W, Caminati M, Gern JE, et al., 2026,
Effect of tezepelumab on asthma exacerbations co-occurring with infection-attributed acute respiratory illnesses.
, Ann Allergy Asthma Immunol, Vol: 136, Pages: 61-65.e1BACKGROUND: Tezepelumab, a human monoclonal antibody, blocks the activity of thymic stromal lymphopoietin. In the phase 2b PATHWAY (NCT02054130) and phase 3 NAVIGATOR (NCT03347279) studies, tezepelumab reduced exacerbations and improved lung function, asthma control, and health-related quality of life vs placebo in patients with severe, uncontrolled asthma. OBJECTIVE: To evaluate the incidence of asthma exacerbations co-occurring with documented acute respiratory illnesses attributed to infections. METHODS: Patients were randomized 1:1 to receive tezepelumab 210 mg subcutaneously or placebo every 4 weeks for 52 weeks. The incidence of asthma exacerbations co-occurring with respiratory illness-related adverse events (AEs) was assessed. Co-occurrence was defined as at least 1 day of overlap between a respiratory illness-related AE and the asthma exacerbation period beginning 7 days before the start of the exacerbation until the end of the asthma exacerbation. RESULTS: Of the 1334 patients (tezepelumab, n = 665; placebo, n = 669) included, 312 experienced at least 1 asthma exacerbation co-occurring with a respiratory illness-related AE attributed to an infection. The incidence of asthma exacerbation co-occurring with a respiratory illness-related AE was lower in the tezepelumab group than in the placebo group overall (18.2% vs 28.6%; exposure-adjusted incidence difference [EAID], -11.1 [95% CI: -15.75, -6.41]) and among patients with perennial allergy (EAID, -11.6 [95% CI: -17.44, -5.69]) and without perennial allergy (EAID, -10.2 [95% CI: -18.16, -2.10]). CONCLUSION: Tezepelumab reduced asthma exacerbations attributed to respiratory infections in patients with severe, uncontrolled asthma compared with placebo, irrespective of perennial allergy status. TRIAL REGISTRATION: This is a pooled analysis of 2 studies registered at Clinicaltrials.gov: PATHWAY (NCT02054130) and NAVIGATOR (NCT03347279).
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Journal articleChung KF, Mazzone SB, 2026,
Chronic Cough Hypersensitivity as a Neuropathic Disorder: Implications for Management and New Treatments.
, Annu Rev Med, Vol: 77, Pages: 449-462Chronic cough can coexist with or without pulmonary and extrapulmonary conditions and can be refractory to therapies that improve these associated conditions. It is underlined by cough hypersensitivity, which is characterized by increased cough responses to stimuli that affect the airways and vagally innervated tissues as well as by excessive cough responses to innocuous stimuli, and it is caused by neuroinflammatory and neuropathic mechanisms at both peripheral and central levels. The management of chronic cough starts with exclusion of associated conditions, followed by use of neuromodulators and speech and language therapy. This is progressing toward personalized management, with new approaches to endotype to treat these patients with the introduction of novel antitussive therapies.
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Journal articleCucco A, Pearce N, Simpson A, et al., 2026,
Exploring geographic differences in IgE response through network and manifold analyses.
, J Allergy Clin Immunol, Vol: 157, Pages: 262-272BACKGROUND: Component-resolved diagnostics allow detailed assessment of IgE sensitization to multiple allergenic molecules (component-specific IgEs, or c-sIgEs) and may be useful for asthma diagnosis. However, to effectively use component-resolved diagnostics across diverse settings, it is crucial to account for geographic differences. OBJECTIVE: We investigated spatial determinants of c-sIgE networks to facilitate development of diagnostic algorithms applicable globally. METHODS: We used multiplex component-resolved diagnostics array to measure c-sIgE to 112 proteins in an international collaboration of several studies: WASP (World Asthma Phenotypes; United Kingdom, New Zealand, Brazil, Ecuador, and Uganda), U-BIOPRED (Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes; 7 European countries), and MAAS (Manchester Asthma and Allergy Study, a UK population-based birth cohort). Hierarchical clustering on low-dimensional representation of co-occurrence networks ascertained sensitization and c-sigE clusters across populations. Cross-country comparisons focused on a common subset of 18 c-sIgEs. We investigated sensitization networks across regions in relation to asthma severity. RESULTS: Sensitization profiles shared similarities across regions. For 18 c-sIgEs shared across study populations, the response structure enabled differentiation between different geographic areas and study designs, revealing 3 clusters: (1) Uganda, Ecuador, and Brazil, (2) U-BIOPRED children and adults, and (3) New Zealand, United Kingdom, and MAAS. Spectral clustering identified differences between clusters. We observed constant, almost parallel shifts between severe and nonsevere asthma in each country. CONCLUSIONS: Patterns of c-sIgE response reflect geographic location and study design. However, despite geographic differences in c-sIgE networks, there is a remarkably consistent shift between networks of subjects with nonsevere and severe asthma.
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Journal articleSiddiqui S, Di Paola AS, Brown T, et al., 2026,
Lessons learned from a UK platform trial during the COVID-19 pandemic and beyond: The BEAT-Severe Asthma Trial
, Efficacy and Mechanism Evaluation, Pages: 1-21<jats:sec id="abs1-1"> <jats:title>Background</jats:title> <jats:p>It is estimated that around 5% of people with asthma have severe asthma. Severe asthma typically presents with poor symptom control, impaired lung function and asthma exacerbations, despite regular inhaled steroids and additional controller medications. In the BEyond Allergic Th2-Severe Asthma clinical trials programme, we worked with severe asthma specialist centres in the United Kingdom to identify patients who experienced frequent asthma attacks (two or more per year), who were potentially eligible for stratified asthma treatments.</jats:p> </jats:sec> <jats:sec id="abs1-2"> <jats:title>Objectives</jats:title> <jats:p>There are currently two recognised subtypes of severe asthma which can be characterised by their level of eosinophils (a type of white blood cells). In the BEyond Allergic Th2-Severe Asthma clinical trial programme, we aimed to test whether a simple, once-daily oral antibiotic (doxycycline) can reduce asthma attacks in individuals with lower levels of eosinophils in peripheral blood (T2-Low arm: < 300 cells/µl). We also aimed to test whether a simple twice-daily oral drug (dexpramipexole) can reduce asthma attacks in individuals with high levels of eosinophils in peripheral blood (T2-High arm : ≥ 300 cells/µl). The trial was established using a master protocol and platform trial design with study protocols for the T2-High and T2-Low cohorts.</jats:p> </jats:sec> <jats:sec id="abs1-3"> <jats:title>Study outcomes</jats:title> <jats:p>The trial platform was successfully set up during the COVID-19 pandemic and opened across 13 sites in the United Kingdom
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Journal articleSadatsafavi M, Miravitlles M, Quint JK, et al., 2025,
Development and validation of PRECISE-X model: predicting first severe exacerbation in COPD.
, ThoraxOBJECTIVES: In patients with chronic obstructive pulmonary disease (COPD), severe exacerbations (ECOPDs) impose significant morbidity and mortality. Current guidelines emphasise using ECOPD history to inform preventive treatments but offer limited guidance for risk stratification for the first severe ECOPD. METHODS: We developed and validated PRECISE-X using a cohort of newly diagnosed COPD patients from the UK's Clinical Practice Research Datalink (2004-2022), to predict first severe ECOPD over 5 years (primary outcome) and 12 months (secondary outcome). Predictors were selected via clinical expertise and data-driven methods. Internal-external cross-validation was performed across practice regions to evaluate the model's out-of-sample performance in terms of discrimination (c-statistic), calibration and net benefit. RESULTS: The study included 2 19 015 patients (mean age 66.0; 42.4% female). Observed risk of first severe ECOPD was 29.5% at 5 years (4.2% at 1 year). The final model included four mandatory predictors (sex, age, Medical Research Council dyspnoea score and forced expiratory volume in 1 second) and 28 optional predictors. In internal-external cross-validation, the average out-of-sample c-statistic was 0.836 (95% CI 0.827 to 0.846) for 5-year prediction and 0.756 (95% CI 0.746 to 0.766) for 1-year prediction. Calibration across regions was robust, and the model showed positive NB across a wide range of risk thresholds. In a secondary validation assessment among those with available spirometry data with confirmed airflow obstruction, the model was well calibrated and had only a modest decline in discriminatory performance. CONCLUSIONS: PRECISE-X accurately predicts the first severe COPD exacerbation using routine clinical data, supporting earlier risk stratification and proactive disease management.
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Journal articleSousa-Pinto B, Louis R, Anto JM, et al., 2025,
Adherence to inhaled corticosteroids and long-acting β2-agonists in asthma: A MASK-air study
, PULMONOLOGY, Vol: 31, ISSN: 2531-0437- Cite
- Citations: 11
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Journal articleNamporn T, Manopwisedjaroen S, Ngodngamthaweesuk M, et al., 2025,
Evidence of Mpox clade IIb infection in primary human alveolar epithelium
, EMERGING MICROBES & INFECTIONS, Vol: 14 -
Journal articleTran XN, Bai K-J, Suk C-W, et al., 2025,
Interaction effects of environmental factors with white blood cell profiles on mycobacterial pulmonary diseases: a case-control study.
, BMC Infect Dis, Vol: 26BACKGROUND: Mycobacterial pulmonary diseases remain a significant global health concern. This study investigates the interaction effects of relative humidity (RH), temperature, and fine particular matter (PM2.5) with immune profiles, reflected by white blood cell (WBC) counts, on pulmonary drug-susceptible tuberculosis (DS-TB), multidrug-resistant TB (MDR-TB), and non-tuberculous mycobacteria (NTM) disease. METHODS: This case-control study of 1,398 participants, including 409 cases (203 DS-TB, 151 MDR-TB, and 55 NTM) and 989 controls, assessed individual exposure to RH, temperature, and PM2.5, in mean and difference over 1-month interval, using radial basis function interpolation. Logistic regression models evaluated the associations between environmental exposures and these mycobacterial diseases while also analyzing their interaction effects with WBCs. Generalized additive models with penalized splines were used to explore potential non-linear associations. RESULTS: Higher mean RH was associated with a 0.92-fold decreased OR for DS-TB (95% CI: 0.88, 0.96), while higher temperature daily difference and PM2.5 were associated with higher ORs across all mycobacterial disease groups. Non-linear models illustrated U-shape associations for those environmental factors. Additionally, elevated neutrophil levels attenuated the impact of temperature daily difference on NTM disease, while higher lymphocyte levels amplified temperature daily difference-related effects for DS-TB and MDR-TB. CONCLUSION: This study highlights the role of WBC profiles in modifying the relationship between short-term temperature exposure and mycobacterial pulmonary disease, underscoring the interplay between environmental triggers and immune profiles in disease pathogenesis. Understanding these associations may enhance strategies for TB prevention and early detection. CLINICAL TRIAL NUMBER: Not applicable.
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Journal articlePham DD, Kwon H-S, Song W-J, et al., 2025,
Type 2 Biomarkers as Mediators of Clinical Remission With Biologics in Severe Asthma
, ALLERGY, ISSN: 0105-4538 -
Journal articleWilliams P, Buttery S, Perkins A, et al., 2025,
Exploring the predictors and barriers to accepting smoking cessation support within a targeted lung health check setting
, BMJ Open Respiratory Research, ISSN: 2052-4439Background: The Quit Smoking Lung Health Intervention Trials (QuLIT-1 and -2) and other studies show that providing immediate smoking cessation within lung cancer screening services substantially improves quit rates. However, in the QuLIT2 trial only around half of those offered smoking cessation support actually accepted it. Understanding what underpins this and how to facilitate higher smoking cessation rates would enhance the health impact of the Targeted Lung Health Check programme.Method: We compared characteristics of participants in the intervention arm of the QuLIT-2 study who accepted or declined the offer of smoking cessation support and conducted thematic analysis of interviews with 15 smokers who had declined it. Results: Of 152 randomised to smoking cessation support (61.3±4.8 years, 42% female), 80 declined the offer and 15 dropped out after the initial session leaving 57 “accepters”. Accepters were more likely to be female [53% vs 40% AOR: 3.30, 95%CI 1.47-7.48], younger [AOR: 0.90(0.80-0.98)] and were more likely to live in areas of medium or low deprivation, [AOR: 5.30(1.86-22.85)]. Thematic analysis of the interviews revealed four main barriers to acceptance: concerns about mental health, beliefs about quitting smoking and about the effectiveness of interventions, and negative past experiences of smoking cessation support.Discussion: Cessation services embedded in lung screening clinics need to anticipate barriers such as mental health concerns, past experiences and personal beliefs. Efforts should be made to design and offer equitable services that meet the needs of this population. Trial registration: This study is registered online: ISRCTN12455871.What is already known on this topic- Intensive smoking cessation support embedded within lung cancer screening services significantly increases 3 and 12 month quit rates among this high-risk population. What this study adds- Despite the success of cessation embedded into screening, a
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Journal articleNigro M, Behring GE, Aliverti A, et al., 2025,
Accuracy, comprehensiveness and understandability of AI-generated answers to questions from people with COPD: the AIR-COPD Study.
, Respir Res, Vol: 27BACKGROUND: Chronic obstructive pulmonary disease (COPD) remains an underestimated and underdiagnosed condition due to low disease awareness. Generative Artificial Intelligence (AI) chatbots are convenient and accessible sources of medical information, but evaluation of the quality of answers provided by patient-generated questions about COPD has not been performed to date. OBJECTIVE: To assess and compare accuracy, comprehensiveness, understandability and reliability of different AI chatbots in response to patient-generated questions on the clinical management of COPD. METHODS: A cross-sectional study was conducted in collaboration with the European Respiratory Society (ERS), the European Lung Foundation (ELF), and the ERS CONNECT Clinical Research Collaboration (CRC). Fifteen real questions formulated by ELF COPD patient representatives were divided into three difficulty tiers (easy, medium, difficult) and submitted to ChatGPT (version 3.5), Bard, and Copilot. Experts assessed accuracy and comprehensiveness on a 0–10 scale; patients assessed understandability using the same scale. Reliability was assessed by two investigators. Reviewers were blinded to which AI system generated the answers, and only those who completed all evaluations were included in the analysis. RESULTS: ChatGPT responses were the most reliable (14/15), followed by Copilot (12/15) and Bard (11/15). ChatGPT scored higher for accuracy (8.0 [7.0 – 9.0]) and comprehensiveness (8.0 [6.8 – 9.0]) than Bard (6.0 [5.0 – 8.0] and 6.0 [5.0 – 7.0]) and Copilot (6.0 [5.0 – 7.3] and 6.0 [5.0 – 8.0]) (both P < 0.001). Understandability was similar across all software (ChatGPT: 8.0 [8.0–10.0]; Bard: 9.0 [8.0–10.0]; Copilot: 9.0 [8.0–10.0]) (P = 0.53). No significant effect was detected according to the difficulty of the question. CONCLUSION: Our findings suggest that AI chatbots, particularly ChatGPT, can provide accurat
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Journal articleBloom C, Yang F, Mcclean M, et al., 2025,
Global prevalence of eligibility for biologic therapy in ATS/ERS-defined severe asthma: A Systematic Review
, World Allergy Organization Journal, ISSN: 1939-4551 -
Journal articleAntao J, Rodrigues G, Zounemat-Kermani N, et al., 2025,
Proteomic and Transcriptomic Signatures of Poor Asthma Symptom Control in the U-BIOPRED Cohort
, ALLERGY, ISSN: 0105-4538 -
Journal articleTahmasebi S, Amani D, Adcock IM, et al., 2025,
Harnessing miR-145 in NSCLC: mechanistic roles, diagnostic-prognostic utility, and therapeutic potential
, Cancer Cell International, Vol: 26, ISSN: 1475-2867Non-small cell lung cancer (NSCLC) is responsible for most lung cancer diagnoses and causes elevated worldwide mortality rates, mostly due to late detection and the development of resistance against medicines. This review summarizes evidence regarding miR-145, a downregulated NSCLC microRNA, and emphasizes the multifaceted tumor-suppressor activity of miR-145 involving the repression of oncogenes such as c-Myc, epidermal growth factor receptor (EGFR), and octamer-binding transcription factor 4 (OCT4) to restrict cell growth, stemness, epithelial-to-mesenchymal-transition (EMT), metastasis via Phosphoinositide 3-kinases (PI3Ks)/ activation of protein kinase B (AKT, Mitogen‑activated protein kinase (MAPK), and transforming growth factor beta (TGF-β)/Smad signaling. miR-145 also exhibits potential diagnostic specificity in distinguishing NSCLC cases from controls through serum/plasma testing, with greater sensitivity/specificity in multi-miRNA sets, and prognostic value predicting resistance, survival, and disease advancement. Therapeutically, miR-145 enhances responses to chemotherapies, targeted therapies, radiotherapy, and immunotherapies by counteracting resistance networks. Utilizing novel delivery platforms, such as nanoparticles, exosomes, and chemical modifications, may overcome stability and targeting issues that exist with miRNA therapies. Through the integration of preclinical and clinical information, this review helps identify crucial research gaps, such as incompletely defined regulatory networks and the need for large-scale studies, and calls for the application of advanced techniques to expedite the integration of miR-145-based treatments with personalized NSCLC therapy for improved outcomes.
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Journal articleFeng Y, Weng J, Li C, et al., 2025,
FUNDC1 promoted ferroptosis via JNK pathway in cigarette smoking-induced chronic obstructive pulmonary disease
, Lung, Vol: 203, ISSN: 0341-2040BackgroundCigarette smoking (CS), the major risk factor for chronic obstructive pulmonary disease (COPD), induces oxidative stress, mitophagy, and ferroptosis. Because FUN14 domain-containing protein 1 (FUNDC1), a mitophagy receptor, may drive the onset and progression of COPD, we investigated its role in CS-induced ferroptosis in COPD and to explore the underlying cellular signaling mechanisms.MethodsWild-type (C57BL/6J background) and FUNDC1-knockdown (KD) mice were exposed to CS for 12 weeks. FUNDC1-KD and FUNDC1-overexpressing (OE) alveolar epithelial A549 cells were exposed to CS extracts (CSE) in the presence and absence of the JNK inhibitor, SP6001 (10 mM). Oxidative stress, inflammation, mitochondrial function, and ferroptosis were measured.ResultsFUNDC1 expression was increased in lung tissues from COPD patients and CS-exposed mice. CS exposure induced airway inflammation, reduced lung function, and enhanced ferroptosis in mice. FUNDC1-KD prevented CS-induced lung injury in mice. Similarly, CSE exposure up-regulated FUNDC1 expression, promoted ferroptosis, inflammation, oxidative stress, lipid peroxidation, and mitochondrial damage in A549 cells. FUNDC1-KD prevented CSE-induced cellular damage. Transcriptomic data indicated that FUNDC1 mediated ferroptosis through the JNK pathway. These in vitro results were further confirmed by pretreatment with the JNK inhibitor SP6001.ConclusionFUNDC1 plays an important role in CS-exposed alveolar epithelial cells and in a mouse model of COPD through the JNK-ferroptosis pathway.
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Journal articleAlimohammadi M, Amani D, Adcock IM, et al., 2025,
Dual role of mir-146a in non-small cell lung cancer progression: molecular mechanisms and clinical potential
, Cellular Signalling, Vol: 136, ISSN: 0898-6568Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality. 2.48 million new cases were reported globally in 2022, driven by rising adenocarcinoma rates linked to environmental factors such as air pollution. MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression by targeting messenger RNA for degradation or translational repression. Emerging studies highlight miR-146a as a molecular pivot with dual functionality that acts as a tumor suppressor by inhibiting NF-κB signaling to reduce inflammation and chemoresistance while paradoxically exhibiting oncogenic potential through immune modulation in specific microenvironments. The expression of miR-146a has been associated with numerous pathological and physiological alterations in cancer cells, including the modulation of various signaling pathways such as TNF-α, NF-κB, MEK-1/2, and JNK-1/2. miR-146a can act exogenously through extracellular vesicles and thereby reprogram tumor-associated macrophages to either promote or inhibit metastasis depending on cellular context. The diagnostic potential of miR-146a is underscored by expression patterns correlating with disease progression and treatment response in NSCLC, whilst preclinical studies suggest therapeutic promise when combined with checkpoint inhibitors. In this review, we first discuss the biogenesis and function of miR-146a in NSCLC development, with emphasis on recent findings that underscore the dual role of miR-146a in the regulation of cell proliferation, invasion, inflammation, immune responses, and chemoresistance in NSCLC. We also describe the possible function of miR-146a as a biomarker for cancer diagnosis, prognosis, and therapeutic target.
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Journal articleSousa-Pinto B, Schleich F, Louis G, et al., 2025,
Daily digital biomarkers in the follow-up and clustering of patients with asthma
, Pulmonology, Vol: 31, ISSN: 2531-0429Background and Research questionWe aimed to assess whether levels of digital biomarkers can reflect monthly patterns of asthma controlStudy design and methodsWe performed a longitudinal study on patients with asthma and comorbid rhinitis who filled ≥26 days of data in a month in the MASK-air® app and who reported at least 1 day of treatment with an inhaled corticosteroid with or without a long-acting β2-agonist (ICS ± LABA). We applied k-means cluster analysis to define clusters of months according to daily asthma control and medication use. Clusters were compared using digital biomarkers (visual analogue scale [VAS] on asthma symptoms and electronic daily asthma control score [e-DASTHMA]). We compared patients who did not switch with patients who switched their ICS ± LABA.ResultsWe assessed 243 patients and 1358 months. We identified three clusters of poor asthma control despite high ICS ± LABA adherence, one cluster of poor asthma control and poor ICS ± LABA adherence, one cluster of good asthma control and high ICS ± LABA adherence and one cluster of good asthma control despite poor ICS ± LABA adherence. These clusters displayed relevant differences in VAS asthma and e-DASTHMA levels. Similar clusters were found in ‘non-switchers’ versus ‘switchers’.ConclusionLevels of digital biomarkers reflect asthma control patterns and might be used to monitor patients with asthma.
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Journal articleLee YJ, Birring SS, Chung KF, et al., 2025,
Chronic cough: nomenclature and classification
, Ers Monograph, Vol: 2025-December, Pages: 1-10, ISSN: 2312-508XCC imposes a significant burden on patients and remains a frequent challenge in routine practice. Current evidence indicates that CC is not merely a symptom, but represents a distinct disease entity characterised by dysregulation of the cough reflex. Nevertheless, current classification remains restricted to symptom duration (e.g. >8 weeks), lacking terminology that reflects underlying mechanisms or informs clinical decision-making. Accurate disease naming and classification are essential for effective communication between clinicians and patients, appropriate diagnostic coding and reimbursement, policy development and epidemiological tracking. In ICD-10, cough is listed solely as a symptom code. The advent of ICD-11 enables a more accurate and mechanism-based representation of diseases, as seen in the reclassification of chronic pain and allergic conditions. Many patients with CC demonstrate intrinsic pathophysiological features such as cough reflex hypersensitivity, which are not adequately captured by existing terms such as RCC or UCC. These labels may also carry unintended connotations of therapeutic failure or diagnostic ambiguity. This chapter outlines a rationale for redefining CC as a disease entity, grounded in recent advances in pathophysiology and clinical phenotyping. It proposes updated diagnostic terminology and a roadmap for future integration into classification systems such as ICD-11, aiming to improve patient care, resource allocation and research frameworks.
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Journal articleMazzone SB, Chung KF, Cho PSP, et al., 2025,
Future directions for clinical and research development in chronic cough
, Ers Monograph, Vol: 2025-December, Pages: 317-325, ISSN: 2312-508XThis Monograph provides a comprehensive review of CC, highlighting significant progress in the field over recent years. The contributing chapters also demonstrate key future directions that warrant attention. This includes reclassifying cough, for example into chronic primary cough and chronic secondary cough, to reflect that it can be both a disease and a symptom; developing new diagnostic tools and biomarkers to identify specific CC endotypes based on different underlying mechanisms; creating targeted therapies for these endotypes; improving clinical trial design with better endpoints and digital monitoring tools; and expanding our understanding of the full patient burden. Effective progression of these future priority areas will benefit from greater efforts to incorporate patient perspectives. There is also an additional and distinct need for research investigating CC in children, as much of our current understanding comes from studies in adults. Addressing these future directions will progress the field further towards effective management strategies for patients impacted by CC.
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