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Journal articleFreeman A, Rink S, Bansal AT, et al., 2026,
Multimorbidity phenotypes and associated characteristics in severe asthma: an observational study of European severe asthma registries.
, Lancet Reg Health Eur, Vol: 63BACKGROUND: The phenotypic nature of multimorbidity in severe asthma is poorly understood. Our aims in this study were to define multimorbidity phenotypes and their characteristics in severe asthma across Europe by identifying and characterising co-aggregation of comorbidities. METHODS: Cross-sectional patient data were analysed from the pan-European Severe Heterogenous Asthma Research Collaboration: Patient Centred (SHARP) Central database of national severe asthma registries. Patients were grouped by four European regions (North, South, East, and West). Hierarchical clustering of comorbidities was applied to characterise the correlation structure of the ten commonest comorbidities within these geographical regions. Subsequent multimorbidity phenotypes (MMP) and their clinical features were then defined. FINDINGS: Data were available for 2690 severe asthma patients and 23 comorbidities from 11 countries. Three comorbidity clusters were consistently seen across the four European regions: 1) osteoporosis plus steroid-induced weight gain, 2) eczema plus rhinitis, and 3) chronic sinusitis plus nasal polyps. Four further comorbidities (obesity, bronchiectasis, gastro-oesophageal reflux disease, psychological factors) showed variable clustering. Multimorbidity was ubiquitous. Patients were assigned multimorbidity phenotypes (MMP) according to comorbidity cluster alignment. MMP sn (sinonasal-associated) and MMP u (no specific cluster alignment) were commonest. MMP ster (steroid-associated multimorbidity) had highest maintenance oral steroid (m-OCS) use, and Body Mass Index, plus worst lung function, asthma control, and asthma exacerbation frequency. MMP max (maximal multimorbidity) showed high prevalence of variably assigned comorbidities, higher m-OCS and biologic treatment needs. INTERPRETATION: Multimorbidity is common in severe asthma and can be classified into replicable novel phenotypes with characteristic clinical traits and outcomes. Recognising these phenotypes c
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Journal articleWen H, Kole T, Carpaij OA, et al., 2026,
Nasal Airway Transcriptome Reflects Selected Asthma-Associated Gene Signatures in the Lower Airways.
, AllergyBACKGROUND: Transcriptomic analysis of bronchial brushes reveals asthma-associated gene signatures but is limited by the invasiveness of bronchoscopy. Based on the "united airways" hypothesis, we evaluated whether and to what extent nasal brushes reflect asthma-associated transcriptomic changes in the lower airways. METHODS: In the ARMS study, we included 26 asthma patients and 28 healthy controls, all fully clinically characterized. Nasal and bronchial brushes were collected for RNA sequencing. We used edgeR and WGCNA to identify asthma-associated genes and modules in bronchial brushes. We assessed their expression patterns in ARMS nasal brushes and validated the findings in the independent ATLANTIS study (n = 427). RESULTS: We identified 51 asthma-associated genes in the lower airways, of which 40 were up-regulated and 11 were down-regulated in asthma compared to healthy controls. Seven of the 40 up-regulated genes were also up-regulated in ARMS nasal brushes and validated in ATLANTIS: CLCA1, FETUB, CST1, NTRK2, CDH26, TPSAB1, and DHX35. WGCNA revealed two modules that were consistently elevated in asthma across bronchial and nasal brushes in ARMS and confirmed in ATLANTIS. One module represents IL-13 related inflammation, whereas the other represents mast cell activity. CONCLUSION: The asthma-associated gene signatures of the lower and upper airways show a limited but biologically coherent overlap, with seven genes and two gene modules consistently elevated in asthma. The shared gene signatures reflect two separate components of type 2 inflammation: IL-13 related inflammation and mast cell activity. Selected nasal gene signatures offer a non-invasive tool to identify asthma endotypes with distinct molecular mechanisms driving underlying disease biology.
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Journal articlePuttur F, Lloyd CM, 2026,
Sex Differences in Lung Immunity.
, Immunol Rev, Vol: 338Biological sex has a significant impact on how the immune system develops and responds to foreign and self-antigens. Sex differences exist in innate and adaptive immune cells, both at homeostasis and in the context of infection and inflammatory diseases such as asthma, cancer, and autoimmune disorders. Women generate stronger immune responses and are more susceptible to developing autoimmune conditions, while males are more prone to acute viral infections and developing certain cancers. Some immunological differences persist throughout life, while others emerge only after puberty and before reproductive senescence. Additionally, environmental exposures can affect the influence of biological sex in regulating immune function. This is particularly pertinent at mucosal surfaces such as the lungs, where lung immune defenses are constantly exposed to foreign material during respiration. Consequently, environmental factors together with genetics, age and sex hormones play a vital role in governing lung tissue immune responses between the sexes. In this context, we highlight studies that support the need for considering sex as an important biological variable in lung immunological research. This knowledge will provide a benchmark for understanding sex-driven immunological mechanisms that underpin disease development and may inform new avenues targeted for generating sex-specific therapies in lung disease.
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Journal articleSiddiqui SH, Wilson-Morkeh H, Monti S, et al., 2026,
Early Diagnosis and Treatment in Patients With Eosinophilic Granulomatosis With Polyangiitis.
, J Allergy Clin Immunol Pract, Vol: 14, Pages: 599-610Eosinophilic granulomatosis with polyangiitis (EGPA), originally termed Churg-Strauss syndrome, represents the rarest form of antineutrophil cytoplasmic antibody-associated vasculitis. It is characterized by the presence of asthma, rhinosinusitis with or without nasal polyps, eosinophilic inflammation of the blood, and tissues and necrotizing vasculitis of small to medium-sized blood vessels. Owing to its rare, multisystemic nature with diverse symptom presentation, diagnosis is complex, requiring a multidisciplinary approach and a careful array of diagnostic and clinical assessments. Conventional therapy is composed of the use of oral glucocorticoids, which are associated with long-term adverse effects, and other immunomodulatory drugs. However, earlier diagnosis and prompt tailored treatment can improve clinical outcomes and reduce drug-related toxicity. The initiation of biologic therapies, such as those blocking IL-5 or its receptor, which have recently been approved for the treatment of non-severe relapsing EGPA, has emerged as a paradigm shift in management. An illustrative case is used to present a comprehensive representation of the diagnosis, pathophysiology, and management of EGPA.
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Journal articleKahai R, Castelli G, Danzo F, et al., 2026,
Specialist Dietary Intervention in Patients With Fibrotic Interstitial Lung Disease Experiencing Unintentional Weight Loss: A Pilot Randomized Controlled Trial.
, Chest, Vol: 169, Pages: 687-697BACKGROUND: Weight loss in patients with fibrotic interstitial lung disease (F-ILD) is associated with poor prognosis, yet the impact of dietary input is unknown. RESEARCH QUESTION: What is the feasibility of a randomized controlled trial of specialist dietary intervention in F-ILD? STUDY DESIGN AND METHODS: Patients with F-ILD experiencing low weight or weight loss were randomized 1:1 to either a 12-week specialist dietary intervention or a dietary information sheet by computer-generated sequence using random block design with stratification by antifibrotic drugs. The primary outcome was feasibility of recruitment, randomization, and retention. A key predefined exploratory outcome was weight change from baseline. RESULTS: Of 128 screened patients, 40 patients (31%) were randomized, 19 to diet and 21 to control arm. The target number of patients was reached within 7 months, suggesting feasibility of a larger trial. All randomized patients completed the study. In the diet arm, 8 of 19 (42%) vs 1 of 21 (4.8%) participants in the control arm gained ≥ 1 kg at 12 weeks (OR, 14.2; 95% CI, 1.4-141.8; P = .02). Analysis of the exploratory outcome of weight change revealed that after a 4-week lag, the estimated rate of weight change between 4 and 12 weeks was -0.25 kg/month (95% CI, -0.61 to 0.12) in the control and +0.40 kg/month (95% CI, 0.02 to 0.78) in the diet group, with a difference of +0.65 kg/month (95% CI, 0.15 to 1.14) in favor of the diet group (P = .01). INTERPRETATION: Based on the encouraging results of this pilot trial of dietary intervention in F-ILD, a definitive multicenter randomized controlled trial is warranted. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov; No.: NCT06016959; URL: www. CLINICALTRIALS: gov).
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Journal articleTian K, Labeur-Iurman L, Walker SA, et al., 2026,
Inhaled Acinetobacter lwoffii exposure promotes lung PD-L1+ neutrophils and dampens viral-induced type 2 immunity
, Mucosal Immunology, ISSN: 1933-0219 -
Journal articleKumar A, Chan R, Zounemat-Kermani N, et al., 2026,
Small Airways Dysfunction and Remission in Adults With Asthma: A Longitudinal Exploratory Analysis of the AssessmenT of smalL Airways involvemeNT In aSthma (ATLANTIS) Study.
, AllergyBACKGROUND: Asthma remission is a feasible treatment goal. However, remission definitions vary, and predictive biomarkers remain underexplored. METHODS: We conducted a post hoc analysis of ATLANTIS (NCT02123667), a multinational prospective study including 684 adult asthmatics. Remission was defined by 3-component (3C) and 4-component (4C) criteria. 3C remission included: (1) ACQ-6 < 1.5, (2) no maintenance oral corticosteroids, (3) no exacerbations. An absolute decline < 10% in pre-bronchodilator FEV1% predicted, was added for the 4C definition. Multivariate logistic regression identified remission predictors. A novel Low Disease Activity (LDA) score was developed using factor analysis of five clinical variables (ACQ-6, FeNO, BEC, and FEV1) including an innovative small airways dysfunction questionnaire tool (SADT). Nasal transcriptomics were analysed for differential gene expression and pathway enrichment and were replicated in U-BIOPRED (NCT01976767) using sputum transcriptomics. U-BIOPRED was included only to study omics replication of remission pathways identified in ATLANTIS. FINDINGS: Remission occurred in 48% (3C) and 45% (4C) of patients. Predictors included male sex, better lung function, fewer previous exacerbations, and higher SADT (fewer small airways symptoms). LDA identified milder disease and was associated with remission [OR 3C 4.43 (2.80, 7.10) and 4C 3.46 (2.23, 5.43)], improved QoL [OR 2.07 (1.65, 2.60)], and fewer future exacerbations [OR 0.43 (0.22, 0.85)]. Transcriptomic analyses revealed remission-associated upregulation of interleukin 4/13 signalling and downregulation of coagulation pathways, in both ATLANTIS and U-BIOPRED. INTERPRETATION: SAD was associated with reduced asthma remission. A novel LDA tool demonstrated clinical utility in stratifying prospective asthma risk. Key immunologic and haemostatic pathways may underpin remission, offering potential targets for future intervention.
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Journal articleChen W, Shao Y, Durham SR, et al., 2026,
Comparative Efficacy of Biologicals for Chronic Rhinosinusitis With Nasal Polyps: A Systematic Review and Bayesian Network Meta-Analysis.
, Clin Exp Allergy -
Journal articleArasi S, Bärhold F, Alvaro-Lozano M, et al., 2026,
Correspondence: First Peanut (Arachis hypogaea) Allergen Oral Immunotherapy Product Out of Sale-A Major Drawback for Food Allergy Immunotherapy?
, Allergy -
Journal articleWang D, Hadad N, Moss S, et al., 2026,
Assessment of mosaic loss of chromosome Y in pulmonary fibrosis reveals limited association with susceptibility or disease severity.
, BMJ Open Respir Res, Vol: 13BACKGROUND: Pulmonary fibrosis (PF) is a rare lung disease with diverse pathogenesis and biological mechanisms. Mosaic loss of chromosome Y (mLOY) has been reported to be associated with increased risk of fibrotic diseases. However, the exact role of mLOY in the development of PF remains to be elucidated. METHODS: Copy number on chromosome Y was used to estimate mLOY comparing patients in PROFILE and gnomAD cohorts and between cases and control patients from the GE100KGP cohort. Correlation of mLOY with demographic and clinical variables was tested using patients from the PROFILE cohort. Lung single-cell transcriptomic data were analysed to assess the cell types implicated in mLOY. Mendelian randomisation was performed to examine the causal relationship between mLOY, idiopathic pulmonary fibrosis (IPF) and telomere length. RESULTS: The genetic analysis suggests that mLOY is found in PF from both case cohorts but when compared with an age matched population the effect is minimal (p=0.00316, median: 0.288 vs 0.291). mLOY is related to age (p=0.000214) and shorter telomere length (p=0.00815) rather than PF severity or progression. Single-cell analysis indicates that mLOY appears to be found primarily in immune cells. Mendelian randomisation demonstrates that mLOY is not on the causal pathway for IPF, but partial evidence supports that telomere shortening is on the causal pathway for mLOY. CONCLUSIONS: Our study confirms the existence of mLOY in PF patients, suggests that mLOY is not a major driver of IPF, and might support a triangulation model where telomere shortening leads to both IPF and mLOY.
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Journal articleMay J, Jenkins G, 2026,
Idiopathic Pulmonary Fibrosis: An Overview.
, Br J Hosp Med (Lond), Vol: 87Idiopathic pulmonary fibrosis (IPF) is the prototypical fibrosing interstitial lung disease, characterised by its unrelenting progressive course and poor prognosis. The incidence of IPF is rising and is becoming a major public health concern. Debilitating dyspnoea and respiratory failure results. Death occurs on average 3-5 years from the time of diagnosis. Clearer understanding of the pathobiology of the condition continues to advance and although we may now better understand disease mechanisms, our therapeutic approach remains limited. In the UK, only two treatments are licensed for IPF, and both can only slow the process down. An ideal silver bullet would halt and ideally reverse established fibrosis. New therapies are showing promise; however, lung transplant remains the only treatment that can substantially increase both duration and quality of life. Here we will provide a comprehensive overview of IPF to summarise definitions, epidemiology, mechanisms, diagnostics, and management.
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Journal articleOldham J, Molyneaux P, Maddali M, et al., 2026,
Prioritizing Therapeutic Targets for Interstitial Lung Disease: A Causal Mediation Analysis.
, Res SqProgressive interstitial lung disease (ILD) leads to declining lung function and death. New therapies to treat ILD are urgently needed. Here we performed a secondary analysis of proteomic data from ten ILD cohorts across the United States, Canada, and United Kingdom. Causal mediation analysis was used to estimate the effect of plasma proteins previously linked to organ fibrosis in mechanistic studies (exposure) on survival (outcome) through lung function decline (mediator). Of 102 proteins tested in a discovery cohort (n = 1963), 47 were mediated by declining lung function. Of these 47 proteins, 7 showed sustained mediation in an independent validation cohort (n = 1172). Proteins with the strongest mediated effect were amphiregulin and integrin beta six. Sensitivity analysis showed that results were robust to unmeasured confounding. Here we provide epidemiological evidence implicating seven proteins as potentially causal of progressive ILD. These findings build upon mechanistic studies showing a causal link between these proteins and organ fibrosis, supporting their prioritization for therapeutic consideration.
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Journal articleMorelli T, Purcell M, Panaguiton J, et al., 2026,
Understanding risk of poor outcomes in adults hospitalised with respiratory syncytial virus infection: evidence from a multicentre UK cohort.
, ThoraxBACKGROUND: Respiratory syncytial virus (RSV) causes substantial winter pressure on adult services. In the UK, RSV vaccination currently targets adults aged ≥75 years and care home residents; it remains uncertain whether this age criterion alone meaningfully discriminates risk of poor outcome among adults hospitalised with RSV. METHODS: We pooled three UK hospital cohorts (one prospective, two retrospective) of adults admitted with acute respiratory infection (ARI) and PCR-confirmed RSV. The primary outcome was intensive care unit/high dependency unit (ICU/HDU) admission or all-cause mortality within 60 days. Prespecified predictors (age, sex and comorbidities) entered a least absolute shrinkage and selection operator (LASSO) penalised logistic regression; selected variables were refitted using standard logistic regression. Discrimination, calibration and decision-analytic performance were assessed using 1000-bootstrap internal validation and decision-curve analysis. RESULTS: Among 334 adults, 37 (11.1%) experienced the primary outcome. An age-only rule mirroring current UK vaccine age-eligibility (≥75 years) demonstrated only modest discrimination (optimism-adjusted area under the receiver operating characteristic curve (AUC) 0.58, 95% CI 0.48 to 0.65) and a compressed distribution of predicted risks. A four-predictor model-including age, COPD, active/previous cancer and dementia-achieved higher discrimination AUC (0.77 (0.69 to 0.85)), a wider spread of predicted risks and the greatest net benefit across clinically plausible escalation thresholds (5-20%). CONCLUSIONS: In adults hospitalised with RSV-associated ARI, simple age-based heuristics-including the UK ≥75-year threshold-showed only modest ability to discriminate risk of ICU/HDU admission/60-day mortality once hospitalised. Comorbidity-inclusive approaches may provide more informative hospital-level risk stratification and warrant evaluation in future RSV vaccine-effectiveness and outcome st
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Journal articleSory DR, Heyraud ACM, Jones JR, et al., 2026,
SiO2-CaOCME/Poly(Tetrahydrofuran)/Poly(Caprolactone) 3D-Printed Scaffolds Drive Human-Bone Marrow Stromal Cell Osteogenic Differentiation.
, Adv Healthc MaterThis article addresses the unmet clinical need of scaffolds for bone regeneration that can combine osteogenic properties, such as the promotion of bone marrow stem cell differentiation into osteoblasts, with the ability to withstand cyclic loading. In our previous study, we demonstrated that discs of SiO2-CaOCME/poly(tetrahydrofuran)/poly(caprolactone) hybrids or their dissolution products can drive terminal osteogenic differentiation of human bone marrow stromal cells (h-BMSCs) in vitro. The current study shows that the 3D-printed hybrid scaffolds with physiologically relevant 3D architecture further promote h-BMSC osteogenesis. The 3D-printed scaffolds support spatially organized cell behavior in an environment mirroring conditions relevant to off-the-shelf implant applications. Primary cellular functions, including viability, adhesion, and proliferation, were maintained across 3D scaffold surfaces and within inter-strut regions. osteogenic commitment was evidenced by the upregulation of lineage-specific transcripts, hydroxyapatite deposition, and the organized assembly of extracellular matrix (ECM) proteins. Our results demonstrate that 3D-printed scaffolds drive osteogenesis by modulating cell metabolism, inducing osteogenic morphological transitions, and promoting the expression of osteocalcin and collagen type I alpha 1 chain, alongside hydroxyapatite matrix mineralization. Collectively, our findings highlight the SiO2-CaOCME/poly(tetrahydrofuran)/poly(caprolactone) scaffold's strong osteogenic properties-driven by composition, surface architecture, and ion release - and its promise for clinical bone regeneration.
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Journal articleKlimek L, Mullol J, Hummel T, et al., 2026,
The Unmet Need of Olfactory Testing in Inflammatory Disorders of the Upper Airways-An EAACI Position Paper.
, AllergyThe sense of smell, with its extensive evolutionary history, is highly prone to disorders that can have a profound impact on daily life. Anosmia affects approximately 5% of the population, with an additional 15% exhibiting reduced olfactory function. The prevalence of olfactory dysfunction (OD) varies by population and age group, and standardized testing reveals a broad range of impacts. OD includes various causes, most commonly aging, inflammation of the olfactory epithelium, upper respiratory tract infections (URTI), traumatic brain injury, and neurological conditions. The recent COVID-19 pandemic has highlighted the association between viral infections and olfactory dysfunction, with severe hyposmia/anosmia being an early marker of infection. Despite its importance, the assessment of olfactory function remains inconsistent across clinical practices. Psychophysical smell tests, while vital for diagnosis and patient management, are underutilized, especially outside of specialized centers. Standardized testing methods are crucial for objective diagnosis, but significant challenges, including test variability, lack of comparability, and healthcare reimbursement issues, persist. The European Academy of Allergy and Immunology (EAACI) advocates for improvements in the quality and standardization of chemosensory assessments. Future efforts must prioritize education, incentives for better testing, and the integration of digital tools to expand access to olfactory testing and diagnosis in remote or quarantine situations. However, office-based testing remains irreplaceable, even with advancements in telemedicine.
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Journal articleStewart I, John A, Bin L, et al., 2026,
Residual lung abnormality following COVID-19 hospitalisation is characterised by biomarkers of epithelial injury
, EBioMedicine, Vol: 124, ISSN: 2352-3964Some survivors of acute COVID-19 infection have long-term symptoms that could suggest ongoing lung impairment. Searches performed in MEDLINE and Embase for SARS-COV-2 studies with radiological lung follow-up estimated that 50% of participants had inflammatory patterns and 29% had fibrotic patterns at a median of 3 months post infection. Analysis of the UK nationwide Post-hospitalisation COVID-19 Study at 5-months follow-up suggested that up to 11% of people discharged from hospital following COVID-19 infection were at-risk of radiological residual lung abnormalities, such as ground glass opacity and reticulation. In people with pulmonary fibrosis, these radiological patterns are often consistent with persistent epithelial lung injury. Biomarker studies have identified associations with COVID-19 severity, however there are few studies that explore the relationship between biomarkers of epithelial injury and parenchymal lung abnormalities post-hospitalisation.
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Journal articleShamji MH, Boyle RJ, 2026,
Advancing Allergy Research Through Innovative Methodologies and Epithelial Immunology.
, Clin Exp Allergy, Vol: 56, Pages: 121-123 -
Journal articleO'Brien H, O'Callaghan M, Comerford L, et al., 2026,
Assessment of mTOR pathways in diffuse idiopathic neuroendocrine cell hyperplasia.
, Eur Respir J, Vol: 67 -
Journal articleBousquet J, Sousa-Pinto B, Vieira RJ, et al., 2026,
Methodology for the Development of the Allergic Rhinitis and Its Impact on Asthma (ARIA)-EAACI 2024-2025 Guidelines: From Evidence-to-Decision Frameworks to Digitalised Shared Decision-Making Algorithms.
, Allergy, Vol: 81, Pages: 427-453The Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines produced their first edition in 1999, with subsequent revisions in 2008, 2010, 2016 and 2019. A new iteration of ARIA-ARIA 2024-2025-in collaboration with EAACI is currently being developed, focusing on the management of allergic rhinitis. ARIA 2024-2025 follows the GRADE framework and is endorsed by the European Academy of Allergy and Clinical Immunology (EAACI). A set of approaches has been used to develop guideline questions, including surveying key opinion leaders and using artificial intelligence (AI)-based tools to analyse web searches on allergic rhinitis and to generate questions. Each prioritised guideline question is assessed through an Evidence-to-Decision (EtD) framework. EtDs support the systematic and transparent formulation of recommendations, comprising 12 criteria for which the best available evidence should be sought. In the context of ARIA-EAACI 2024-2025, such evidence is derived not only from randomised controlled trials but also-among others-from patient-generated data sources that better reflect the affected individuals' perspectives. Moreover, ARIA-EAACI 2024-2025 incorporates evidence on planetary health. Developed guideline recommendations will support the creation of digitalised decision algorithms and care pathways. This paper describes the methodology used to develop the person-centred, digitally enabled and AI-assisted ARIA-EAACI 2024-2025. Among others, it describes (i) the development and prioritisation of guideline questions, (ii) sources of evidence for EtDs and (iii) the development of digitalised decision algorithms and care pathways.
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Journal articleKong E, Cucco A, Custovic A, et al., 2026,
Machine learning in allergy research: A bibliometric review
, IMMUNOLOGY LETTERS, Vol: 277, ISSN: 0165-2478
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