Pub Date : 2025-12-11DOI: 10.1183/13993003.02091-2025
Vickram Tejwani,Arunangshu Sarkar,Claire J Guo,Satria Sajuthi,Peter Castaldi,Laura E Crotty Alexander,Igor Z Barjaktarevic,Alejandro P Comellas,Jennifer Dawson,Dawn L DeMeo,Craig P Hersh,Lisa Ruvuna,Sunita Sharma,Edwin K Silverman,Katherine A Pratte,Max Seibold,Katerina Kechris,Russell P Bowler
{"title":"Nasal epithelium and blood transcriptomic signatures associations with smoking and exacerbations.","authors":"Vickram Tejwani,Arunangshu Sarkar,Claire J Guo,Satria Sajuthi,Peter Castaldi,Laura E Crotty Alexander,Igor Z Barjaktarevic,Alejandro P Comellas,Jennifer Dawson,Dawn L DeMeo,Craig P Hersh,Lisa Ruvuna,Sunita Sharma,Edwin K Silverman,Katherine A Pratte,Max Seibold,Katerina Kechris,Russell P Bowler","doi":"10.1183/13993003.02091-2025","DOIUrl":"https://doi.org/10.1183/13993003.02091-2025","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"2 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145728575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-05DOI: 10.1183/13993003.02083-2025
Hans-Willem Snoeck
Idiopathic pulmonary fibrosis (IPF) is a progressive, fibrotic lung disease for which the only definitive treatment is lung transplantation. Currently available pharmacological treatments target the most obvious component of the disease, the accumulating mesenchymal tissue, and delay but do not prevent its relentlessly progressive course. It is now understood, however, that IPF is a consequence of aberrant, fibrotic repair in response to epithelial injury or to increased epithelial susceptibility to injury. The diversity of genetic and environmental risk factors underlying IPF raises the question whether mechanisms of epithelial dysfunction shared across all etiologies for IPF exist. Deeper understanding of such mechanisms could lead to causative, disease-modifying treatments, but first requires insight into the identity of the epithelial drivers of IPF. Two schools of thought exist that are not mutually exclusive. One focuses on type 2 alveolar epithelial (AT2) cells, the surfactant-producing cells in the alveoli that can also function as alveolar stem cells. The second school of thought sees a contribution of the distal airways to IPF pathogenesis. Here, I summarize the arguments in favor of each proposition, discuss the limitations of mouse models, which have supported a role for AT2 cells, and argue based on studies in human lungs and organoid models that the epithelium of the most distal airway branches, which are absent in rodents, may play a major role in IPF pathogenesis.
{"title":"Advances in our understanding of distal progenitors in idiopathic pulmonary fibrosis: implications for novel therapeutics.","authors":"Hans-Willem Snoeck","doi":"10.1183/13993003.02083-2025","DOIUrl":"https://doi.org/10.1183/13993003.02083-2025","url":null,"abstract":"Idiopathic pulmonary fibrosis (IPF) is a progressive, fibrotic lung disease for which the only definitive treatment is lung transplantation. Currently available pharmacological treatments target the most obvious component of the disease, the accumulating mesenchymal tissue, and delay but do not prevent its relentlessly progressive course. It is now understood, however, that IPF is a consequence of aberrant, fibrotic repair in response to epithelial injury or to increased epithelial susceptibility to injury. The diversity of genetic and environmental risk factors underlying IPF raises the question whether mechanisms of epithelial dysfunction shared across all etiologies for IPF exist. Deeper understanding of such mechanisms could lead to causative, disease-modifying treatments, but first requires insight into the identity of the epithelial drivers of IPF. Two schools of thought exist that are not mutually exclusive. One focuses on type 2 alveolar epithelial (AT2) cells, the surfactant-producing cells in the alveoli that can also function as alveolar stem cells. The second school of thought sees a contribution of the distal airways to IPF pathogenesis. Here, I summarize the arguments in favor of each proposition, discuss the limitations of mouse models, which have supported a role for AT2 cells, and argue based on studies in human lungs and organoid models that the epithelium of the most distal airway branches, which are absent in rodents, may play a major role in IPF pathogenesis.","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"29 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145704418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-05DOI: 10.1183/13993003.00729-2025
Diane M Gray,Anhar Ullah,Shaakira Chaya,Carvern Jacobs,Maresa Botha,Zoltán Hantos,Nicola Marozva,Dan J Stein,Mark P Nicol,Adnan Custovic,Heather J Zar
BACKGROUNDImpaired lung function trajectories from childhood are associated with lifelong health risk. However, data are lacking on trajectories in infancy and preschool years, a time of critical lung growth with potential for interventions. We investigated lung function trajectories from birth through 6-years, and their determinants, in the Drakenstein Child Health study, an African birth cohort.METHODSChildren were followed from birth, with lung function (intra-breath oscillometry) measured at six timepoints (six-weeks to six-years). Comprehensive exposure information was longitudinally collected from the antenatal period through childhood. Longitudinal data on resistance (Ree) and reactance at end expiration (Xee) were jointly modelled using Group-based multi-trajectory modelling to derive trajectories of respiratory system impedance.FINDINGS830 children with ≥two lung function measures were included. A model comprising 5-trajectories was the optimal solution: Normal (70.2%); Persistent low (2.4%); Early normal-declines (8.4%); Early low-catch up (5.8%); Decline and recovery (13.1%). Ninety (11%) children had low trajectories (Persistent low or Early normal-decline); risk factors were Respiratory syncytial virus-lower respiratory tract infection, preterm birth and postnatal maternal psychological distress. One hundred and fifty seven children (19%) showed catch-up to normal lung function (Early low-catch-up or Decline and recovery) through six years. Spirometry at 6-years differed by trajectory: children in the Normal trajectory had the highest FEV1 and FVC, and those in the Persistent low, the lowest.INTERPRETATIONSpecific early life lung function trajectories show potential for healthy lung development and recovery in early childhood. Modifiable factors including prematurity, RSV-LRTI and maternal psychological distress negatively impact on lung trajectories.
{"title":"Lung function trajectories and determinants from birth to 6-years in an African birth cohort: extending trajectories through infancy using oscillometry.","authors":"Diane M Gray,Anhar Ullah,Shaakira Chaya,Carvern Jacobs,Maresa Botha,Zoltán Hantos,Nicola Marozva,Dan J Stein,Mark P Nicol,Adnan Custovic,Heather J Zar","doi":"10.1183/13993003.00729-2025","DOIUrl":"https://doi.org/10.1183/13993003.00729-2025","url":null,"abstract":"BACKGROUNDImpaired lung function trajectories from childhood are associated with lifelong health risk. However, data are lacking on trajectories in infancy and preschool years, a time of critical lung growth with potential for interventions. We investigated lung function trajectories from birth through 6-years, and their determinants, in the Drakenstein Child Health study, an African birth cohort.METHODSChildren were followed from birth, with lung function (intra-breath oscillometry) measured at six timepoints (six-weeks to six-years). Comprehensive exposure information was longitudinally collected from the antenatal period through childhood. Longitudinal data on resistance (Ree) and reactance at end expiration (Xee) were jointly modelled using Group-based multi-trajectory modelling to derive trajectories of respiratory system impedance.FINDINGS830 children with ≥two lung function measures were included. A model comprising 5-trajectories was the optimal solution: Normal (70.2%); Persistent low (2.4%); Early normal-declines (8.4%); Early low-catch up (5.8%); Decline and recovery (13.1%). Ninety (11%) children had low trajectories (Persistent low or Early normal-decline); risk factors were Respiratory syncytial virus-lower respiratory tract infection, preterm birth and postnatal maternal psychological distress. One hundred and fifty seven children (19%) showed catch-up to normal lung function (Early low-catch-up or Decline and recovery) through six years. Spirometry at 6-years differed by trajectory: children in the Normal trajectory had the highest FEV1 and FVC, and those in the Persistent low, the lowest.INTERPRETATIONSpecific early life lung function trajectories show potential for healthy lung development and recovery in early childhood. Modifiable factors including prematurity, RSV-LRTI and maternal psychological distress negatively impact on lung trajectories.","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"30 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145704421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-05DOI: 10.1183/13993003.00560-2025
Gaurav Veer Singh,Huma Asghar,Sophie É Collins,Daniel Genkin,James C Hogg,Jean Bourbeau,Wan C Tan,Michael K Stickland,Miranda Kirby
INTRODUCTIONExisting computed tomography (CT) vascular pruning measures rely on volumes, such as the proportion of blood volume in vessels with cross-sectional area (CSA)<5 mm2 or <10 mm2/total blood volume (BV5/TBV, BV10/TBV, respectively), but may underestimate vascular pruning due to blood redistribution to larger vessels in individuals with milder chronic obstructive pulmonary disease (COPD). We aim to develop a novel CT vessel measure, the total vessel count (TVC), quantify small and combined small/intermediate vessel count percentages, and compare these measures with BV5/TBV and BV10/TBV in terms of associations with lung function and its decline. As a secondary aim, associations with exercise capacity and COPD symptoms will be investigated.METHODSCanCOLD participants underwent CT imaging. BV5/TBV and BV10/TBV were generated using vessel segmentation. TVC, and small (CSA<5 mm2, VC≤5/TVC) and combined small/intermediate (CSA<10 mm2, VC≤10/TVC) vessel count percentages were calculated. Fully adjusted regression models assessed associations with forced expiratory volume in 1 s (FEV1), FEV1/forced vital capacity (FEV1/FVC), carbon monoxide diffusing capacity (DLCO), accelerated FEV1 decline over 3-years, maximal oxygen consumption (VO2peak), 6-minute walk distance (6MWD) and Medical Research Council (MRC).RESULTS1254 CanCOLD participants were investigated. TVC, VC≤5/TVC and VC≤10/TVC were associated with FEV1/FVC (p<0.05), DLCO (p<0.05) and FEV1 decline (p<0.05); VC≤10/TVC was associated with VO2peak (p<0.05) and both VC≤5/TVC and VC≤10/TVC were associated with MRC (p<0.05). BV5/TBV and BV10/TBV were only associated with 6MWD (p<0.05) and MRC (p<0.05).CONCLUSIONPulmonary vessel count percent, a measure of vasculature narrowing/loss, is associated with lung function and its decline, reduced exercise capacity and increased symptoms in COPD.
{"title":"CT Total vessel count and vessel count percentages: associations with exercise capacity, symptoms, and rapid FEV1 decline in COPD.","authors":"Gaurav Veer Singh,Huma Asghar,Sophie É Collins,Daniel Genkin,James C Hogg,Jean Bourbeau,Wan C Tan,Michael K Stickland,Miranda Kirby","doi":"10.1183/13993003.00560-2025","DOIUrl":"https://doi.org/10.1183/13993003.00560-2025","url":null,"abstract":"INTRODUCTIONExisting computed tomography (CT) vascular pruning measures rely on volumes, such as the proportion of blood volume in vessels with cross-sectional area (CSA)<5 mm2 or <10 mm2/total blood volume (BV5/TBV, BV10/TBV, respectively), but may underestimate vascular pruning due to blood redistribution to larger vessels in individuals with milder chronic obstructive pulmonary disease (COPD). We aim to develop a novel CT vessel measure, the total vessel count (TVC), quantify small and combined small/intermediate vessel count percentages, and compare these measures with BV5/TBV and BV10/TBV in terms of associations with lung function and its decline. As a secondary aim, associations with exercise capacity and COPD symptoms will be investigated.METHODSCanCOLD participants underwent CT imaging. BV5/TBV and BV10/TBV were generated using vessel segmentation. TVC, and small (CSA<5 mm2, VC≤5/TVC) and combined small/intermediate (CSA<10 mm2, VC≤10/TVC) vessel count percentages were calculated. Fully adjusted regression models assessed associations with forced expiratory volume in 1 s (FEV1), FEV1/forced vital capacity (FEV1/FVC), carbon monoxide diffusing capacity (DLCO), accelerated FEV1 decline over 3-years, maximal oxygen consumption (VO2peak), 6-minute walk distance (6MWD) and Medical Research Council (MRC).RESULTS1254 CanCOLD participants were investigated. TVC, VC≤5/TVC and VC≤10/TVC were associated with FEV1/FVC (p<0.05), DLCO (p<0.05) and FEV1 decline (p<0.05); VC≤10/TVC was associated with VO2peak (p<0.05) and both VC≤5/TVC and VC≤10/TVC were associated with MRC (p<0.05). BV5/TBV and BV10/TBV were only associated with 6MWD (p<0.05) and MRC (p<0.05).CONCLUSIONPulmonary vessel count percent, a measure of vasculature narrowing/loss, is associated with lung function and its decline, reduced exercise capacity and increased symptoms in COPD.","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"3 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145704416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUNDChildhood interstitial lung diseases (chILD) encompass a diverse group of rare, chronic respiratory disorders. While treatment options are limited, evaluating health related quality of life (HrQoL) has become a vital approach for clinical monitoring. This study aims to enhance our understanding of the medical and socio-demographic factors influencing HrQoL in chILD.METHODSThis study used prospectively obtained data from the chILD EU Register. Caregivers were handed validated, age-specific HrQoL questionnaires (the chILD specific and generic PedsQL™ 4.0 questionnaire) and the scores calculated. We used exploratory univariate analyses and multivariable ordinary least squares (OLS) regression models on cross-sectional data to investigate the associations between subjectś clinical features and HrQoL scores.RESULTS424 patients from 10 European countries and 48 study sites were included in the final analysis. The most relevant factors associated with lower HrQoL scores for the chILD specific questionnaire and the Total Score, as identified in the univariate analysis and confirmed in the multivariable OLS regression model, were "inpatient medical care in the last 3 months" (-13.6; p<0.0001 and -11.4; p<0.0001) and "failure to thrive" (-9.1; p=0.0014 and -12.1; p<0.0001). Among subjects old enough for pulmonary function testing (PFT) (n=162), we observed only a weak correlation between PFT results and different HrQoL scores.CONCLUSIONSMain factors linked to reduced HrQoL scores were prior inpatient treatment and failure to thrive. Further interventional studies should determine whether addressing these factors can enhance HrQoL scores and potentially improve quality of life in chILD.
{"title":"Health-Related Quality of Life in Childhood Interstitial Lung Disease.","authors":"Matthias Griese,Mandy Niemitz,Katrin Erlewein,Srdjan Micic,Julia Rodler,Julia Carlens,Honorata Marczak,Joanna Lange,Katarzyna Krenke,Nagehan Emiralioğlu,Miriam Rassenhofer,Jörg Fegert,Steve Cunningham,Susanne Hämmerling,Florian Stehling,Anna Zschocke,Alexander Möller,Nicolaus Schwerk,Elias Seidl, ","doi":"10.1183/13993003.01777-2025","DOIUrl":"https://doi.org/10.1183/13993003.01777-2025","url":null,"abstract":"BACKGROUNDChildhood interstitial lung diseases (chILD) encompass a diverse group of rare, chronic respiratory disorders. While treatment options are limited, evaluating health related quality of life (HrQoL) has become a vital approach for clinical monitoring. This study aims to enhance our understanding of the medical and socio-demographic factors influencing HrQoL in chILD.METHODSThis study used prospectively obtained data from the chILD EU Register. Caregivers were handed validated, age-specific HrQoL questionnaires (the chILD specific and generic PedsQL™ 4.0 questionnaire) and the scores calculated. We used exploratory univariate analyses and multivariable ordinary least squares (OLS) regression models on cross-sectional data to investigate the associations between subjectś clinical features and HrQoL scores.RESULTS424 patients from 10 European countries and 48 study sites were included in the final analysis. The most relevant factors associated with lower HrQoL scores for the chILD specific questionnaire and the Total Score, as identified in the univariate analysis and confirmed in the multivariable OLS regression model, were \"inpatient medical care in the last 3 months\" (-13.6; p<0.0001 and -11.4; p<0.0001) and \"failure to thrive\" (-9.1; p=0.0014 and -12.1; p<0.0001). Among subjects old enough for pulmonary function testing (PFT) (n=162), we observed only a weak correlation between PFT results and different HrQoL scores.CONCLUSIONSMain factors linked to reduced HrQoL scores were prior inpatient treatment and failure to thrive. Further interventional studies should determine whether addressing these factors can enhance HrQoL scores and potentially improve quality of life in chILD.","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"29 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145704417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-05DOI: 10.1183/13993003.01638-2025
Ryosuke Imai,Rene S Bermea,Sophia H Zhao,Anjali Singh,Andrew J Synn,Bess M Flashner,Julia K Munchel,Mary B Rice,Barry S Shea,Robert W Hallowell
{"title":"Low forced vital capacity is associated with poor prognosis in physiologically stable non-IPF interstitial lung disease.","authors":"Ryosuke Imai,Rene S Bermea,Sophia H Zhao,Anjali Singh,Andrew J Synn,Bess M Flashner,Julia K Munchel,Mary B Rice,Barry S Shea,Robert W Hallowell","doi":"10.1183/13993003.01638-2025","DOIUrl":"https://doi.org/10.1183/13993003.01638-2025","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"3 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145704420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-04Print Date: 2025-12-01DOI: 10.1183/13993003.01880-2025
Yogesh N V Reddy, Robert P Frantz, Alexander C Egbe, William R Miranda, Tomonari Harada, Tatsuro Ibe, Hilary M Dubrock, Hector Cajigas, Barry A Borlaug
{"title":"Inhaled treprostinil improves cardiac output during exertion in interstitial lung disease.","authors":"Yogesh N V Reddy, Robert P Frantz, Alexander C Egbe, William R Miranda, Tomonari Harada, Tatsuro Ibe, Hilary M Dubrock, Hector Cajigas, Barry A Borlaug","doi":"10.1183/13993003.01880-2025","DOIUrl":"10.1183/13993003.01880-2025","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-04DOI: 10.1183/13993003.01687-2025
Miguel Angel Martinez-Garcia,Joan B Soriano
{"title":"The expanding and accelerating universe of bronchiectasis.","authors":"Miguel Angel Martinez-Garcia,Joan B Soriano","doi":"10.1183/13993003.01687-2025","DOIUrl":"https://doi.org/10.1183/13993003.01687-2025","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"29 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145673683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-04Print Date: 2025-12-01DOI: 10.1183/13993003.00130-2025
Jeisson Osorio, Olga Tura-Ceide, Javier Pavía, Ivan Vollmer, Isabel Blanco, Aida Niñerola-Baizán, Pilar Paredes, Francisco Lomeña, Jesús Ruiz-Cabello, Manel Castellà, Victor Ivo Peinado, Joan Albert Barberà
{"title":"Increased lung [<sup>18</sup>F]-FDG uptake in chronic thromboembolic pulmonary hypertension with distal involvement.","authors":"Jeisson Osorio, Olga Tura-Ceide, Javier Pavía, Ivan Vollmer, Isabel Blanco, Aida Niñerola-Baizán, Pilar Paredes, Francisco Lomeña, Jesús Ruiz-Cabello, Manel Castellà, Victor Ivo Peinado, Joan Albert Barberà","doi":"10.1183/13993003.00130-2025","DOIUrl":"10.1183/13993003.00130-2025","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12675955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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