Pub Date : 2026-02-01DOI: 10.1016/j.opresp.2026.100559
Sara Pischedda , Alberto Gomez-Carballa , Jacobo Pardo-Seco , Sandra Viz-Lasheras , Alba Camino-Mera , Xabier Bello , María José Curras-Tuala , Irene Rivero-Calle , Ana I. Dacosta-Urbieta , Federico Martinon-Torres , Antonio Salas , GENDRES Consortium
Background
Respiratory syncytial virus (RSV) poses significant morbidity and mortality risks in childhood, particularly among previously healthy infants hospitalized without predisposing risk factors for severe disease. This study aimed to investigate the role of the host epigenome in RSV infection severity using non-invasive buccal swabs from sixteen hospitalized infants.
Methods
Eight patients exhibited severe symptoms, while eight had mild to moderate symptoms. DNA methylation analysis was performed using the Illumina EPIC BeadChip on DNA isolated from saliva samples. A cohort of healthy children served as controls to assess baseline DNA methylation levels of identified biomarkers. Candidate gene methylation levels were further validated by pyrosequencing in both the discovery and validation cohorts.
Results
A panel of differentially methylated positions (DMPs) distinguishing severe from mild to moderate RSV symptoms in infants was identified. DMPs were determined using a threshold of adjusted P-value (false discovery rate, FDR) < 0.01 and an absolute DNA methylation difference (delta beta) > 0.10. Differentially methylated regions (DMRs) were identified in genes implicated in asthma, pulmonary disease, and viral infections. The differential DNA methylation of these genes was validated in an independent replication cohort. A weighted correlation network analysis highlighted the pivotal role of a module with a hub gene crucial in regulating viral infections.
Conclusions
Oral mucosa methylation may contribute to RSV disease severity in infants.
{"title":"EPIGENETIC SIGNATURES OF SEVERE RSV INFECTION IN INFANTS: EVIDENCE FROM NON-INVASIVE SALIVA SAMPLES","authors":"Sara Pischedda , Alberto Gomez-Carballa , Jacobo Pardo-Seco , Sandra Viz-Lasheras , Alba Camino-Mera , Xabier Bello , María José Curras-Tuala , Irene Rivero-Calle , Ana I. Dacosta-Urbieta , Federico Martinon-Torres , Antonio Salas , GENDRES Consortium","doi":"10.1016/j.opresp.2026.100559","DOIUrl":"10.1016/j.opresp.2026.100559","url":null,"abstract":"<div><h3>Background</h3><div>Respiratory syncytial virus (RSV) poses significant morbidity and mortality risks in childhood, particularly among previously healthy infants hospitalized without predisposing risk factors for severe disease. This study aimed to investigate the role of the host epigenome in RSV infection severity using non-invasive buccal swabs from sixteen hospitalized infants.</div></div><div><h3>Methods</h3><div>Eight patients exhibited severe symptoms, while eight had mild to moderate symptoms. DNA methylation analysis was performed using the Illumina EPIC BeadChip on DNA isolated from saliva samples. A cohort of healthy children served as controls to assess baseline DNA methylation levels of identified biomarkers. Candidate gene methylation levels were further validated by pyrosequencing in both the discovery and validation cohorts.</div></div><div><h3>Results</h3><div>A panel of differentially methylated positions (DMPs) distinguishing severe from mild to moderate RSV symptoms in infants was identified. DMPs were determined using a threshold of adjusted P-value (false discovery rate, FDR) < 0.01 and an absolute DNA methylation difference (delta beta) > 0.10. Differentially methylated regions (DMRs) were identified in genes implicated in asthma, pulmonary disease, and viral infections. The differential DNA methylation of these genes was validated in an independent replication cohort. A weighted correlation network analysis highlighted the pivotal role of a module with a hub gene crucial in regulating viral infections.</div></div><div><h3>Conclusions</h3><div>Oral mucosa methylation may contribute to RSV disease severity in infants.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100559"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01DOI: 10.1016/j.opresp.2026.100562
Adrián Gómez-Del Rosario , Carolina Cubillos-Zapata , Aitana Alonso González , José Miguel Lorenzo-Salazar , Almudena Corrales , Beatriz Guillen-Guio , María Molina-Molina , Laura Ciuffreda , Francisco García Río , Carlos Flores
Introduction
Critical care patients who survive to severe COVID-19 are at higher risk of developing interstitial lung disease (ILD). Identifying protein biomarkers of lung sequelae may help to clarify the underlying pathophysiology and contribute to the development of precision medicine strategies.
Objectives
Here, we aimed to identify a set of proteins that could be used as biomarkers of ILD in post-COVID patients.
Methods
Protein levels from plasma samples collected at 6 months post-ICU discharge of 40 post-COVID patients that survived severe ARDS was obtained via the Olink® Explore assay (3,072 proteins). ILD was assessed by CT scans, quantitative analysis of lung attenuation and of different pulmonary function parameters with a follow-up at 6 months after ICU discharge. Protein prioritization was based on Student's t-test and principal component analysis to identify those contributing more to the differentiation of patients evidencing ILD. Spearman correlation analysis was used to reduce protein information redundancy. Functional enrichment analysis was performed using EnrichR.
Results
A total of 203 proteins showed nominally significant differences between ILD and non-ILD patients at six months. Further analyses prioritized 10 non-redundant proteins of this set. These proteins are involved in key mechanisms of immune regulation, inflammatory signalling, and tissue remodelling.
Conclusions
We identified a set of proteins that may serve as biomarkers for post-COVID ILD. Validation in independent patients is needed.
{"title":"INTERSTITIAL LUNG DISEASE PROTEIN BIOMARKERS IN POST-COVID PATIENTS","authors":"Adrián Gómez-Del Rosario , Carolina Cubillos-Zapata , Aitana Alonso González , José Miguel Lorenzo-Salazar , Almudena Corrales , Beatriz Guillen-Guio , María Molina-Molina , Laura Ciuffreda , Francisco García Río , Carlos Flores","doi":"10.1016/j.opresp.2026.100562","DOIUrl":"10.1016/j.opresp.2026.100562","url":null,"abstract":"<div><h3>Introduction</h3><div>Critical care patients who survive to severe COVID-19 are at higher risk of developing interstitial lung disease (ILD). Identifying protein biomarkers of lung sequelae may help to clarify the underlying pathophysiology and contribute to the development of precision medicine strategies.</div></div><div><h3>Objectives</h3><div>Here, we aimed to identify a set of proteins that could be used as biomarkers of ILD in post-COVID patients.</div></div><div><h3>Methods</h3><div>Protein levels from plasma samples collected at 6 months post-ICU discharge of 40 post-COVID patients that survived severe ARDS was obtained via the Olink® Explore assay (3,072 proteins). ILD was assessed by CT scans, quantitative analysis of lung attenuation and of different pulmonary function parameters with a follow-up at 6 months after ICU discharge. Protein prioritization was based on Student's t-test and principal component analysis to identify those contributing more to the differentiation of patients evidencing ILD. Spearman correlation analysis was used to reduce protein information redundancy. Functional enrichment analysis was performed using EnrichR.</div></div><div><h3>Results</h3><div>A total of 203 proteins showed nominally significant differences between ILD and non-ILD patients at six months. Further analyses prioritized 10 non-redundant proteins of this set. These proteins are involved in key mechanisms of immune regulation, inflammatory signalling, and tissue remodelling.</div></div><div><h3>Conclusions</h3><div>We identified a set of proteins that may serve as biomarkers for post-COVID ILD. Validation in independent patients is needed.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100562"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01DOI: 10.1016/j.opresp.2026.100564
Sara M. Exojo-Ramírez , Israel David Duarte-Herrera , Paula Martín-Vicente , Cecilia López-Martínez , Karla Miravete-Lagunes , Irene Ordoñez , Diego Parra , Juan Gómez , Natalia Campo Ortiz de Zárate , Manuel Chacón , Guillermo M. Albaiceta , Laura Amado-Rodríguez
Introduction
Mechanical ventilation triggers a complex molecular response that may lead to ineffective lung repair and fibrosis. Our objective is to study the impact of ex-vivo mechanical stretch on repair processes involving epithelial and mesenchymal cells.
Methods
Bronchoalveolar lavage fluid (BALF) was collected from patients under protective mechanical ventilation (MV, 6-8 ml/kg, PEEP 5 cmH2O) or continuous positive airway pressure (CPAP) of 5 cmH2O, during scheduled cardiac surgery. Wound healing assays were performed on epithelial (BEAS-2B) and fibroblast (MRC5) cells supplemented with these samples. RNA was extracted and sequenced, to identify differences in gene expression, molecular pathways and interactions, related to mechanical stretch. Targeted drug modulation experiments were performed to evaluate the identified molecular mechanisms. An interaction analysis of genes allowed us to exclude pharmacological treatment in MV condition.
Results
Cyclic stretch condition resulted in a slower wound closure rate in epithelial cells, compared to the static condition. Fibroblasts exhibited the opposite behavior. Differential expression analysis identified dysregulation in the IL6 and EGFR gene pathways in BEAS-2B, as well as in LIF, IL6, and TGFβ1 in MRC5. The use of tocilizumab reverses the wound closure rates in both cell lines. Interaction RNA analysis highlighted upregulation of PPIA in epithelial cells under cyclic conditions and cellular stretching. Cyclosporine treatment reduced PPIA and IL6 expression.
Conclusions
Tidal ventilation promotes a delay in epithelial repair and fibroproliferative response, mediated by IL-6 pathway activation and enhanced TGFβ1 expression. Upstream modulation of stretch-induced expression of PPIA could promote effective tissue regeneration during mechanical ventilation.
{"title":"THE ROLE OF PPIA GENE IN LUNG REPAIR DURING MECHANICAL VENTILATION","authors":"Sara M. Exojo-Ramírez , Israel David Duarte-Herrera , Paula Martín-Vicente , Cecilia López-Martínez , Karla Miravete-Lagunes , Irene Ordoñez , Diego Parra , Juan Gómez , Natalia Campo Ortiz de Zárate , Manuel Chacón , Guillermo M. Albaiceta , Laura Amado-Rodríguez","doi":"10.1016/j.opresp.2026.100564","DOIUrl":"10.1016/j.opresp.2026.100564","url":null,"abstract":"<div><h3>Introduction</h3><div>Mechanical ventilation triggers a complex molecular response that may lead to ineffective lung repair and fibrosis. Our objective is to study the impact of ex-vivo mechanical stretch on repair processes involving epithelial and mesenchymal cells.</div></div><div><h3>Methods</h3><div>Bronchoalveolar lavage fluid (BALF) was collected from patients under protective mechanical ventilation (MV, 6-8 ml/kg, PEEP 5 cmH2O) or continuous positive airway pressure (CPAP) of 5 cmH2O, during scheduled cardiac surgery. Wound healing assays were performed on epithelial (BEAS-2B) and fibroblast (MRC5) cells supplemented with these samples. RNA was extracted and sequenced, to identify differences in gene expression, molecular pathways and interactions, related to mechanical stretch. Targeted drug modulation experiments were performed to evaluate the identified molecular mechanisms. An interaction analysis of genes allowed us to exclude pharmacological treatment in MV condition.</div></div><div><h3>Results</h3><div>Cyclic stretch condition resulted in a slower wound closure rate in epithelial cells, compared to the static condition. Fibroblasts exhibited the opposite behavior. Differential expression analysis identified dysregulation in the <em>IL6</em> and <em>EGFR</em> gene pathways in BEAS-2B, as well as in <em>LIF, IL6,</em> and <em>TGFβ1</em> in MRC5. The use of tocilizumab reverses the wound closure rates in both cell lines. Interaction RNA analysis highlighted upregulation of <em>PPIA</em> in epithelial cells under cyclic conditions and cellular stretching. Cyclosporine treatment reduced <em>PPIA</em> and <em>IL6</em> expression.</div></div><div><h3>Conclusions</h3><div>Tidal ventilation promotes a delay in epithelial repair and fibroproliferative response, mediated by IL-6 pathway activation and enhanced TGFβ1 expression. Upstream modulation of stretch-induced expression of <em>PPIA</em> could promote effective tissue regeneration during mechanical ventilation.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100564"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01DOI: 10.1016/j.opresp.2026.100572
Viviane de Cássia Oliveira , Amanda Carolina Souza Delfino da Rocha , Alba Soler-Comas , Guillen Macip , Miguel Ferrer , Antoni Torres , Laia Fernandez-Barat
Introduction
Phage-antibiotic synergy (PAS) results in bacterial killing beyond the efficacy of either agent alone. Although the main candidates for therapeutic PAS are lytic phages, temperate phages have been re-evaluated in light of PAS. This study explored the potential use of combined temperate phage and ceftolozane/tazobactam (CT) against a carbapenem-resistant Pseudomonas aeruginosa (CRPA).
Methods
Lytic and temperate phages were isolated and characterized in terms of host range, functional genomics and morphology. Afterwards, 48h biofilms were grown on endotracheal tubes using a CRPA. Biofilms were treated with 2 different phage cocktails (108PFU/mL of four phages), either alone or combined with 5 µg/mL of CT. One cocktail (CK6) consisted exclusively of temperate phages, whereas the other (CK8) included a lytic phage in addition to temperate ones. Repeated treatment doses were administered every 12h. Bacterial counts (log10CFU/mL) were assessed every 24h up to 192h. In parallel, the minimal inhibitory concentration of CT was evaluated throughout different treatment groups and timepoints.
Results
Phage cocktails and CT alone had only a slight effect on biofilm viability over the treatment period. The combined treatment using both cocktails reduced biofilm viability by 3 logs up to 120h. Emergence of resistance to CT was delayed from 96h with CT alone to 120h with the combined treatment with the CK8. CK6 had no impact on the emergence of resistance to CT.
Conclusions
The combination of temperate and lytic phages and CT showed synergistic effects reducing CRPA-biofilm; however, the presence of a lytic phage delayed the emergence of resistance to CT compared to the cocktail that combined only temperate phages.
Genomic map overview of a temperate and lytic phage used in the study. (C-D) Biofilm viability (CFU/mL) according to the different groups and timepoints. (E-F) Minimal inhibitory concentrations of CT assessed throughout different treatment groups and timepoints.
{"title":"FORMULATING PHAGE COCKTAILS AS ADJUVANT THERAPY IN CARBAPENEM-RESISTANT PSEUDOMONAS AERUGINOSA","authors":"Viviane de Cássia Oliveira , Amanda Carolina Souza Delfino da Rocha , Alba Soler-Comas , Guillen Macip , Miguel Ferrer , Antoni Torres , Laia Fernandez-Barat","doi":"10.1016/j.opresp.2026.100572","DOIUrl":"10.1016/j.opresp.2026.100572","url":null,"abstract":"<div><h3>Introduction</h3><div>Phage-antibiotic synergy (PAS) results in bacterial killing beyond the efficacy of either agent alone. Although the main candidates for therapeutic PAS are lytic phages, temperate phages have been re-evaluated in light of PAS. This study explored the potential use of combined temperate phage and ceftolozane/tazobactam (CT) against a carbapenem-resistant <em>Pseudomonas aeruginosa</em> (CRPA).</div></div><div><h3>Methods</h3><div>Lytic and temperate phages were isolated and characterized in terms of host range, functional genomics and morphology. Afterwards, 48h biofilms were grown on endotracheal tubes using a CRPA. Biofilms were treated with 2 different phage cocktails (10<sup>8</sup>PFU/mL of four phages), either alone or combined with 5 µg/mL of CT. One cocktail (CK6) consisted exclusively of temperate phages, whereas the other (CK8) included a lytic phage in addition to temperate ones. Repeated treatment doses were administered every 12h. Bacterial counts (log<sub>10</sub>CFU/mL) were assessed every 24h up to 192h. In parallel, the minimal inhibitory concentration of CT was evaluated throughout different treatment groups and timepoints.</div></div><div><h3>Results</h3><div>Phage cocktails and CT alone had only a slight effect on biofilm viability over the treatment period. The combined treatment using both cocktails reduced biofilm viability by 3 logs up to 120h. Emergence of resistance to CT was delayed from 96h with CT alone to 120h with the combined treatment with the CK8. CK6 had no impact on the emergence of resistance to CT.</div></div><div><h3>Conclusions</h3><div>The combination of temperate and lytic phages and CT showed synergistic effects reducing CRPA-biofilm; however, the presence of a lytic phage delayed the emergence of resistance to CT compared to the cocktail that combined only temperate phages.</div><div>Genomic map overview of a temperate and lytic phage used in the study. (C-D) Biofilm viability (CFU/mL) according to the different groups and timepoints. (E-F) Minimal inhibitory concentrations of CT assessed throughout different treatment groups and timepoints.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100572"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146162085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sarcopenia is common in chronic respiratory diseases. Several biological processes are involved in its onset. In the muscles of patients with non-cystic fibrosis bronchiectasis, the underlying mechanisms have not yet been described. We hypothesized that markers of inflammation and oxidative stress are elevated in this patients.
Objectives
To assess nutritional status, pulmonary and muscle function, markers of inflammation and oxidative stress, and correlations between biological and clinical variables.
Methods
In blood samples from 20 stable patients with bronchiectasis and functionally confirmed sarcopenia and 10 healthy subjects, the following biomarkers were quantified:
1. Oxidants and antioxidants: 3-nitrotyrosine, protein carbonylation, malondialdehyde protein adducts, Trolox equivalent antioxidant capacity (TEAC), reduced glutathione (GSH), superoxide dismutase (SOD) activity, and catalase activity.
2. Systemic inflammation: myeloperoxidase, cyclooxygenase-2 (COX-2), transforming growth factor beta 1 (TGF-β1), vascular endothelial growth factor A (VEGF-A), and interleukin-6 (IL-6), using ELISA.
Results
Compared to controls, patients with bronchiectasis showed significantly reduced body composition, lung function, and muscle function (sarcopenia). Systemic levels of inflammation biomarkers, oxidants, and antioxidants were significantly increased in patients.
In these patients, quadriceps strength and handgrip strength were negatively correlated with systemic levels of 3-nitrotyrosine (r = -0.558, p = 0.013), SOD (r = -0.454, p = 0.044), and IL-6 (r = -0.520, p = 0.022), respectively.
Conclusions
This study demonstrates that in bronchiectasis, sarcopenia affects both upper and lower limb muscles. The increased systemic levels of oxidative stress and inflammation, along with their correlations with muscle strength, suggest these factors are likely involved in the pathophysiology. These findings could be important for designing therapeutic strategies in pulmonary rehabilitation.
肌少症是慢性呼吸系统疾病的常见病。它的发生涉及几个生物过程。在非囊性纤维化支气管扩张患者的肌肉中，其潜在机制尚未被描述。我们假设这些患者的炎症和氧化应激标志物升高。目的评估营养状况、肺和肌肉功能、炎症和氧化应激标志物以及生物学和临床变量之间的相关性。方法对20例稳定的支气管扩张合并功能性肌少症患者和10例健康受试者的血液样本进行以下生物标志物的定量分析：氧化剂和抗氧化剂：3-硝基酪氨酸、蛋白质羰基化、丙二醛蛋白质加合物、Trolox等效抗氧化能力（TEAC）、还原型谷胱甘肽（GSH）、超氧化物歧化酶（SOD）活性和过氧化氢酶活性。全体性炎症：髓过氧化物酶、环氧化酶-2 （COX-2）、转化生长因子- 1 （TGF-β1）、血管内皮生长因子A （VEGF-A）、白细胞介素-6 (IL-6)， ELISA检测。结果与对照组相比，支气管扩张患者的身体组成、肺功能和肌肉功能显著降低（肌肉减少症）。患者全身炎症生物标志物、氧化剂和抗氧化剂水平显著升高。在这些患者中，股四头肌力量和握力分别与全身3-硝基酪氨酸（r = -0.558, p = 0.013）、SOD （r = -0.454, p = 0.044）和IL-6 （r = -0.520, p = 0.022）水平呈负相关。结论支气管扩张时，肌肉减少会同时影响上肢和下肢肌肉。全身氧化应激和炎症水平的增加，以及它们与肌肉力量的相关性，表明这些因素可能与病理生理学有关。这些发现可能对设计肺部康复治疗策略具有重要意义。
{"title":"SYSTEMIC INFLAMMATION AND OXIDATIVE STRESS IN BRONCHIECTASIS PATIENTS WITH SARCOPENIA: IMPLICATIONS FOR MUSCLE FUNCTION AND PULMONARY REHABILITATION STRATEGIES","authors":"Cinta Cumplí Gargallo , Adriana Núñez-Robainas , Mariela Alvarado-Miranda , Marina Sáinz , Esther Barreiro","doi":"10.1016/j.opresp.2026.100545","DOIUrl":"10.1016/j.opresp.2026.100545","url":null,"abstract":"<div><h3>Introduction</h3><div>Sarcopenia is common in chronic respiratory diseases. Several biological processes are involved in its onset. In the muscles of patients with non-cystic fibrosis bronchiectasis, the underlying mechanisms have not yet been described. We hypothesized that markers of inflammation and oxidative stress are elevated in this patients.</div></div><div><h3>Objectives</h3><div>To assess nutritional status, pulmonary and muscle function, markers of inflammation and oxidative stress, and correlations between biological and clinical variables.</div></div><div><h3>Methods</h3><div>In blood samples from 20 stable patients with bronchiectasis and functionally confirmed sarcopenia and 10 healthy subjects, the following biomarkers were quantified:</div><div>1. Oxidants and antioxidants: 3-nitrotyrosine, protein carbonylation, malondialdehyde protein adducts, Trolox equivalent antioxidant capacity (TEAC), reduced glutathione (GSH), superoxide dismutase (SOD) activity, and catalase activity.</div><div>2. Systemic inflammation: myeloperoxidase, cyclooxygenase-2 (COX-2), transforming growth factor beta 1 (TGF-β1), vascular endothelial growth factor A (VEGF-A), and interleukin-6 (IL-6), using ELISA.</div></div><div><h3>Results</h3><div>Compared to controls, patients with bronchiectasis showed significantly reduced body composition, lung function, and muscle function (sarcopenia). Systemic levels of inflammation biomarkers, oxidants, and antioxidants were significantly increased in patients.</div><div>In these patients, quadriceps strength and handgrip strength were negatively correlated with systemic levels of 3-nitrotyrosine (r = -0.558, p = 0.013), SOD (r = -0.454, p = 0.044), and IL-6 (r = -0.520, p = 0.022), respectively.</div></div><div><h3>Conclusions</h3><div>This study demonstrates that in bronchiectasis, sarcopenia affects both upper and lower limb muscles. The increased systemic levels of oxidative stress and inflammation, along with their correlations with muscle strength, suggest these factors are likely involved in the pathophysiology. These findings could be important for designing therapeutic strategies in pulmonary rehabilitation.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100545"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01DOI: 10.1016/j.opresp.2026.100575
Victor Guerra-Ruiz , M.F. Pilia , D. Soler-Segovia , D. Espejo Castellanos , C.E. Romero Mesones , A. Goitisolo Oyon , I. Ojanguren Arranz , X. Muñoz Gall , M.J. Cruz
Introduction
Soybean hull (SH), was identified as the cause of the asthma epidemics reported in Barcelona in the 1980s and 90s. During soybean unloading in ports, SH-rich dust is released to the air, potentially causing asthma exacerbations. This study aims to establish a method for the detection of SH specific IgE in patients with asthma and to identify the current sensitisation to this aeroallergen in Barcelona.
Methods
A dissociation-enhanced lanthanide fluorescence immunoassay (DELFIA) was standardised on plates coated with SH extract. The results were reported as fluorescence counts (FC). A ROC curve was generated comparing the results from healthy control patients (HCP) and sensitised asthmatic patients (SAP) to set the limit value for positivity of the method. Then, we analysed sera samples from asthmatic patients recruited in our centre to assess the current degree of sensitisation to SH.
Results
A value of 3256 CF showed sensitivity 78.3% and specificity 93% to discriminate between SAP and HCP. To determine the current degree of sensitisation, the study population consisted of 104 patients with asthma (74 women, mean age 51 years) and 31 healthy individuals as control group (15 women, mean age 35 years). In four patients (3.9%) values >3256 CF were obtained, median (range), 1282.9 (0-3709.3). In the control group five individuals (16%) had values >3256 CF, median (range) 1531.6 (0-3618.3).
Conclusions
The standardised method has enough sensitivity and specificity to discriminate between SH-sensitised and non-sensitised patients. Current sensitisation to SH in asthmatic population of Barcelona is low.
{"title":"STANDARDISATION OF A METHOD FOR THE DETERMINATION OF SPECIFIC IGE TO SOYBEAN HULL AEROALLERGEN","authors":"Victor Guerra-Ruiz , M.F. Pilia , D. Soler-Segovia , D. Espejo Castellanos , C.E. Romero Mesones , A. Goitisolo Oyon , I. Ojanguren Arranz , X. Muñoz Gall , M.J. Cruz","doi":"10.1016/j.opresp.2026.100575","DOIUrl":"10.1016/j.opresp.2026.100575","url":null,"abstract":"<div><h3>Introduction</h3><div>Soybean hull (SH), was identified as the cause of the asthma epidemics reported in Barcelona in the 1980s and 90s. During soybean unloading in ports, SH-rich dust is released to the air, potentially causing asthma exacerbations. This study aims to establish a method for the detection of SH specific IgE in patients with asthma and to identify the current sensitisation to this aeroallergen in Barcelona.</div></div><div><h3>Methods</h3><div>A dissociation-enhanced lanthanide fluorescence immunoassay (DELFIA) was standardised on plates coated with SH extract. The results were reported as fluorescence counts (FC). A ROC curve was generated comparing the results from healthy control patients (HCP) and sensitised asthmatic patients (SAP) to set the limit value for positivity of the method. Then, we analysed sera samples from asthmatic patients recruited in our centre to assess the current degree of sensitisation to SH.</div></div><div><h3>Results</h3><div>A value of 3256 CF showed sensitivity 78.3% and specificity 93% to discriminate between SAP and HCP. To determine the current degree of sensitisation, the study population consisted of 104 patients with asthma (74 women, mean age 51 years) and 31 healthy individuals as control group (15 women, mean age 35 years). In four patients (3.9%) values >3256 CF were obtained, median (range), 1282.9 (0-3709.3). In the control group five individuals (16%) had values >3256 CF, median (range) 1531.6 (0-3618.3).</div></div><div><h3>Conclusions</h3><div>The standardised method has enough sensitivity and specificity to discriminate between SH-sensitised and non-sensitised patients. Current sensitisation to SH in asthmatic population of Barcelona is low.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100575"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01DOI: 10.1016/j.opresp.2026.100542
Júlia Plá-Salom , José Luis Gómez Ribelles , Manuel Mata Roig
Introduction
The interaction of tumour cells with the tumour microenvironment (TME) is key for survival, proliferation, migration and drug resistance. In vitro 2D models fail to reproduce TME complexity, highlighting the need for 3D biomimetic models. This work aims to develop an adaptive biomimetic culture platform for lung cancer.
Methods
Alginate microspheres produced by emulsion were surface functionalized with relevant biomolecules of lung cancer stroma (collagen I, fibronectin, laminin, heparan sulphate, hyaluronic acid). A mixture of coated microspheres, called a microgel, was then used to culture H460 cancer cells for up to 7 days. Live/Dead and DNA quantification assays were performed.
Results
Within the microgel, H460 cells formed aggregates1 (Fig. 1a). DNA quantification assays showed sustained cell growth in the microgel (Fig. 1b), while Live/Dead assay confirmed that cell viability was significantly higher in the collagen or the matrix protein mix microgel than in the control group (Fig. 1c).
Conclusions
In summary, the 3D model provides a supportive, biomimetic environment for lung cancer culture. Future work will incorporate additional tumour niche components and evaluate response to drugs commonly used in the treatment of lung cancer, such as docetaxel or doxorubicin.
{"title":"IN VITRO BIOMIMETIC MICROGEL MODEL FOR LUNG CANCER","authors":"Júlia Plá-Salom , José Luis Gómez Ribelles , Manuel Mata Roig","doi":"10.1016/j.opresp.2026.100542","DOIUrl":"10.1016/j.opresp.2026.100542","url":null,"abstract":"<div><h3>Introduction</h3><div>The interaction of tumour cells with the tumour microenvironment (TME) is key for survival, proliferation, migration and drug resistance. <em>In vitro</em> 2D models fail to reproduce TME complexity, highlighting the need for 3D biomimetic models. This work aims to develop an adaptive biomimetic culture platform for lung cancer.</div></div><div><h3>Methods</h3><div>Alginate microspheres produced by emulsion were surface functionalized with relevant biomolecules of lung cancer stroma (collagen I, fibronectin, laminin, heparan sulphate, hyaluronic acid). A mixture of coated microspheres, called a microgel, was then used to culture H460 cancer cells for up to 7 days. Live/Dead and DNA quantification assays were performed.</div></div><div><h3>Results</h3><div>Within the microgel, H460 cells formed aggregates<span><span><sup>1</sup></span></span> (Fig. 1a). DNA quantification assays showed sustained cell growth in the microgel (Fig. 1b), while Live/Dead assay confirmed that cell viability was significantly higher in the collagen or the matrix protein mix microgel than in the control group (Fig. 1c).</div></div><div><h3>Conclusions</h3><div>In summary, the 3D model provides a supportive, biomimetic environment for lung cancer culture. Future work will incorporate additional tumour niche components and evaluate response to drugs commonly used in the treatment of lung cancer, such as docetaxel or doxorubicin.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100542"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Muscle dysfunction or sarcopenia is a systemic manifestation of chronic respiratory diseases such as COPD and non-cystic fibrosis (non-CF) bronchiectasis. Alterations in the endoplasmic reticulum (ER) as a signaling mechanism, as well as markers of proteolysis and autophagy, are increased in the vastus lateralis (VL) of COPD patients. Until now, it has not been demonstrated that these events occur in patients with bronchiectasis. The hypothesis is that expression of ER stress, proteolysis, and autophagy markers may be increased in the VL of patients with non-CF bronchiectasis-associated sarcopenia.
Objectives
To evaluate biomarkers of ER stress, proteolysis, and autophagy and explore correlations between biological findings and clinical muscle assessment parameters.
Methods
In 20 stable patients with non-CF bronchiectasis and functionally confirmed sarcopenia, and 10 healthy subjects, levels of ER stress biomarkers (chaperone molecules and the IRE1, PERK, and ATF6 pathways), proteolysis markers (ubiquitin-proteasome system), and autophagy markers were quantified. Associations between clinical and biological variables were also assessed (Pearson correlation coefficient).
Results
Compared to controls, the VL of patients showed higher expression of ER stress markers (XBP1, ATF4), proteolysis markers (MURF1 and 20S proteasome), and autophagy marker (p62). In patients, BiP and calreticulin levels correlated negatively with fat-free mass index (FFMI) (r = -0.449, p = 0.047) and quadriceps strength (r = -0.443, p = 0.045), respectively.
Conclusions
Protein degradation pathways, autophagy, and ER-mediated signalling are relevant in the pathophysiology of sarcopenia in patients with stable bronchiectasis. These findings may help explain the reduced response to exercise training in chronic respiratory patients.
肌肉功能障碍或肌肉减少症是慢性呼吸系统疾病如COPD和非囊性纤维化（非cf）支气管扩张的全身性表现。内质网（ER）作为信号机制的改变，以及蛋白水解和自噬的标志物，在COPD患者的股外侧肌（VL）中增加。到目前为止，还没有证明这些事件发生在支气管扩张患者身上。假设内质网应激、蛋白水解和自噬标志物的表达可能在非cf支气管扩张相关肌少症患者的VL中增加。目的评价内质网应激、蛋白水解和自噬的生物标志物，探讨生物学结果与临床肌肉评估参数之间的相关性。方法对20例稳定的非cf支气管扩张合并功能性肌少症患者和10例健康受试者进行内质网应激生物标志物（伴侣分子和IRE1、PERK和ATF6通路）、蛋白水解标志物（泛素-蛋白酶体系统）和自噬标志物水平的定量分析。临床变量和生物学变量之间的关联也被评估（Pearson相关系数）。结果与对照组相比，VL患者内质网应激标志物（XBP1、ATF4）、蛋白水解标志物（MURF1、20S蛋白酶体）和自噬标志物（p62）表达较高。在患者中，BiP和钙网蛋白水平分别与无脂质量指数（FFMI） （r = -0.449, p = 0.047）和股四头肌力量（r = -0.443, p = 0.045）呈负相关。结论蛋白质降解途径、自噬和er介导的信号通路与稳定型支气管扩张患者肌少症的病理生理有关。这些发现可能有助于解释慢性呼吸系统患者对运动训练的反应降低。
{"title":"PROTEOLYSIS AND AUTOPHAGY IN THE VASTUS LATERALIS OF PATIENTS WITH BRONCHIECTASIS-ASSOCIATED SARCOPENIA: ROLE IN TRAINING PROGRAMS","authors":"Cinta Cumplí Gargallo , Adriana Núñez-Robainas , Mariela Alvarado-Miranda , Marina Sáinz , Esther Barreiro","doi":"10.1016/j.opresp.2026.100546","DOIUrl":"10.1016/j.opresp.2026.100546","url":null,"abstract":"<div><h3>Introduction</h3><div>Muscle dysfunction or sarcopenia is a systemic manifestation of chronic respiratory diseases such as COPD and non-cystic fibrosis (non-CF) bronchiectasis. Alterations in the endoplasmic reticulum (ER) as a signaling mechanism, as well as markers of proteolysis and autophagy, are increased in the vastus lateralis (VL) of COPD patients. Until now, it has not been demonstrated that these events occur in patients with bronchiectasis. The hypothesis is that expression of ER stress, proteolysis, and autophagy markers may be increased in the VL of patients with non-CF bronchiectasis-associated sarcopenia.</div></div><div><h3>Objectives</h3><div>To evaluate biomarkers of ER stress, proteolysis, and autophagy and explore correlations between biological findings and clinical muscle assessment parameters.</div></div><div><h3>Methods</h3><div>In 20 stable patients with non-CF bronchiectasis and functionally confirmed sarcopenia, and 10 healthy subjects, levels of ER stress biomarkers (chaperone molecules and the IRE1, PERK, and ATF6 pathways), proteolysis markers (ubiquitin-proteasome system), and autophagy markers were quantified. Associations between clinical and biological variables were also assessed (Pearson correlation coefficient).</div></div><div><h3>Results</h3><div>Compared to controls, the VL of patients showed higher expression of ER stress markers (XBP1, ATF4), proteolysis markers (MURF1 and 20S proteasome), and autophagy marker (p62). In patients, BiP and calreticulin levels correlated negatively with fat-free mass index (FFMI) (r = -0.449, p = 0.047) and quadriceps strength (r = -0.443, p = 0.045), respectively.</div></div><div><h3>Conclusions</h3><div>Protein degradation pathways, autophagy, and ER-mediated signalling are relevant in the pathophysiology of sarcopenia in patients with stable bronchiectasis. These findings may help explain the reduced response to exercise training in chronic respiratory patients.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100546"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01DOI: 10.1016/j.opresp.2026.100554
Pilar Alonso-Moreno , Antonio Ferruelo , Carolina Gotera Rivera , Raquel Murillo , Luis A. de Benito-Rodríguez , María de los Ángeles Zambrano Chacón , Raquel Herrero , Germán Peces-Barba Romero , José A. Lorente , Jose L. Izquierdo-Garcia
Introduction
COVID-19 pandemic highlighted the need for diagnostics and track respiratory diseases, especially in Intensive Care Units (ICUs). Nuclear Magnetic Resonance (NMR)-based metabolomics offers unique metabolic fingerprinting for respiratory disease detection and characterization, but conventional NMR systems are limited by size and cost. Benchtop NMR (b-NMR) spectrometers have emerged as promising alternatives for clinical applications.
Objectives
The aim of this study is to assess the potential of b-NMR techniques as a valuable tool for clinical implementation, focusing on ICU applications.
Methods
In this project, serum samples from Madrid hospitals during early COVID-19 pandemic were analyzed. Metabolomics analysis was conducted in 128 cases (83 mild, 15 moderate, 6 severe and 24 very severe) using both conventional (500 MHz Bruker AVIII) and benchtop (80 MHz Magritek Spinsolve Ultra) NMR spectrometers. NMR spectra were processed for multivariate statistical analyses.
Results
Our results demonstrated the ability to stratify patients by disease severity using both equipment, with an excellent group separation in Principal Component Analysis (PCA). Partial Least Squares Discriminant Analysis (PLS-DA) achieved perfect classification performance with near perfect accuracy (99.23% for the conventional and 85.93% for b-NMR) and robust cross-validation metrics. A stratification model accurately distinguished mild cases from hospitalized patients (moderate, severe and very severe cases), achieving an AUC-ROC value of 0.999 (CI95%: 0.994-1) with 100% sensitivity and 97.59% specificity using conventional instrument, and an AUC-ROC of 0.996 (CI95%: 0.984-1), 95.56% sensitivity and 96% specificity using b-NMR. Moreover, we identified 21 biomarkers associated with respiratory failure, revealing significant alterations in metabolic pathways.
Conclusions
These studies demonstrate that b-NMR is a reliable and cost-effective tool for clinical metabolomics, especially for COVID-19 respiratory infection in hospital settings.
{"title":"METABOLIC FINGERPRINTING OF COVID-19: BENCHTOP NMR SPECTROSCOPY FOR PRECISION DIAGNOSTICS IN HOSPITALS","authors":"Pilar Alonso-Moreno , Antonio Ferruelo , Carolina Gotera Rivera , Raquel Murillo , Luis A. de Benito-Rodríguez , María de los Ángeles Zambrano Chacón , Raquel Herrero , Germán Peces-Barba Romero , José A. Lorente , Jose L. Izquierdo-Garcia","doi":"10.1016/j.opresp.2026.100554","DOIUrl":"10.1016/j.opresp.2026.100554","url":null,"abstract":"<div><h3>Introduction</h3><div>COVID-19 pandemic highlighted the need for diagnostics and track respiratory diseases, especially in Intensive Care Units (ICUs). Nuclear Magnetic Resonance (NMR)-based metabolomics offers unique metabolic fingerprinting for respiratory disease detection and characterization, but conventional NMR systems are limited by size and cost. Benchtop NMR (b-NMR) spectrometers have emerged as promising alternatives for clinical applications.</div></div><div><h3>Objectives</h3><div>The aim of this study is to assess the potential of b-NMR techniques as a valuable tool for clinical implementation, focusing on ICU applications.</div></div><div><h3>Methods</h3><div>In this project, serum samples from Madrid hospitals during early COVID-19 pandemic were analyzed. Metabolomics analysis was conducted in 128 cases (83 mild, 15 moderate, 6 severe and 24 very severe) using both conventional (500 MHz Bruker AVIII) and benchtop (80 MHz Magritek Spinsolve Ultra) NMR spectrometers. NMR spectra were processed for multivariate statistical analyses.</div></div><div><h3>Results</h3><div>Our results demonstrated the ability to stratify patients by disease severity using both equipment, with an excellent group separation in Principal Component Analysis (PCA). Partial Least Squares Discriminant Analysis (PLS-DA) achieved perfect classification performance with near perfect accuracy (99.23% for the conventional and 85.93% for b-NMR) and robust cross-validation metrics. A stratification model accurately distinguished mild cases from hospitalized patients (moderate, severe and very severe cases), achieving an AUC-ROC value of 0.999 (CI95%: 0.994-1) with 100% sensitivity and 97.59% specificity using conventional instrument, and an AUC-ROC of 0.996 (CI95%: 0.984-1), 95.56% sensitivity and 96% specificity using b-NMR. Moreover, we identified 21 biomarkers associated with respiratory failure, revealing significant alterations in metabolic pathways.</div></div><div><h3>Conclusions</h3><div>These studies demonstrate that b-NMR is a reliable and cost-effective tool for clinical metabolomics, especially for COVID-19 respiratory infection in hospital settings.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100554"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-01DOI: 10.1016/j.opresp.2026.100538
Verónica Barroso-García , Fernando Vaquerizo-Villar , Gonzalo C. Gutiérrez-Tobal , Ehab Dayyat , David Gozal , Timo Leppänen , Roberto Hornero
Introduction
Approaches based on single-channel airflow show great potential for simplifying pediatric obstructive sleep apnea (OSA) diagnosis, but most analyses have relied on feature-engineering, limiting recognition of complex respiratory patterns and lowering performance in automated models. We propose deep learning and explainable artificial intelligence to estimate pediatric OSA severity from airflow while ensuring transparent predictions.
Methods
We used 3,672 recordings from four datasets. A convolutional neural network (CNN)-based regression model was trained to estimate the apnea-hypopnea index (AHI) and predict severity. We evaluated Gradient-Weighted Class Activation Mapping (Grad-CAM) and SHapley Additive exPlanations (SHAP) to identify airflow regions guiding CNN predictions.
Results
The model showed strong concordance between actual and estimated AHI (intraclass correlation coefficient 0.69–0.87 in the test group) and high diagnostic performance: four-class Cohen's kappa 0.37–0.43 and accuracies of 82.03%, 97.09%, and 99.03% for 1, 5, and 10 events/h in the test group. Interpretability analysis revealed that the CNN accurately identified apneic events by focusing on their onset and offset. While Grad-CAM highlighted abrupt signal changes, SHAP captured subtler, noisier patterns.
Conclusions
Accordingly, our model enables automatic pediatric OSA detection and provides clinicians with explainable outputs that enhance credibility and usability, paving the way for clinical translation in early diagnosis.
{"title":"AN EXPLAINABLE DEEP-LEARNING APPROACH TO DETECT PEDIATRIC SLEEP APNEA FROM SINGLE-CHANNEL AIRFLOW","authors":"Verónica Barroso-García , Fernando Vaquerizo-Villar , Gonzalo C. Gutiérrez-Tobal , Ehab Dayyat , David Gozal , Timo Leppänen , Roberto Hornero","doi":"10.1016/j.opresp.2026.100538","DOIUrl":"10.1016/j.opresp.2026.100538","url":null,"abstract":"<div><h3>Introduction</h3><div>Approaches based on single-channel airflow show great potential for simplifying pediatric obstructive sleep apnea (OSA) diagnosis, but most analyses have relied on feature-engineering, limiting recognition of complex respiratory patterns and lowering performance in automated models. We propose deep learning and explainable artificial intelligence to estimate pediatric OSA severity from airflow while ensuring transparent predictions.</div></div><div><h3>Methods</h3><div>We used 3,672 recordings from four datasets. A convolutional neural network (CNN)-based regression model was trained to estimate the apnea-hypopnea index (AHI) and predict severity. We evaluated Gradient-Weighted Class Activation Mapping (Grad-CAM) and SHapley Additive exPlanations (SHAP) to identify airflow regions guiding CNN predictions.</div></div><div><h3>Results</h3><div>The model showed strong concordance between actual and estimated AHI (intraclass correlation coefficient 0.69–0.87 in the test group) and high diagnostic performance: four-class Cohen's <em>kappa</em> 0.37–0.43 and accuracies of 82.03%, 97.09%, and 99.03% for 1, 5, and 10 events/h in the test group. Interpretability analysis revealed that the CNN accurately identified apneic events by focusing on their onset and offset. While Grad-CAM highlighted abrupt signal changes, SHAP captured subtler, noisier patterns.</div></div><div><h3>Conclusions</h3><div>Accordingly, our model enables automatic pediatric OSA detection and provides clinicians with explainable outputs that enhance credibility and usability, paving the way for clinical translation in early diagnosis.</div></div>","PeriodicalId":34317,"journal":{"name":"Open Respiratory Archives","volume":"8 ","pages":"Article 100538"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146161794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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