Respiratory Research最新文献

{"title":"ECG-based identification of COPD patients at risk for atrial fibrillation and its impact on adverse clinical outcomes-a subgroup analysis of the prospective multicenter COSYCONET cohort.","authors":"Martin Eichenlaub, Björn Christian Frye, Heiko Lehrmann, Frank Biertz, Amir Sherwan Jadidi, Klaus Kaier, Thomas Melzer, Peter Alter, Henrik Watz, Benjamin Waschki, Barbara Christine Weckler, Franziska Christina Trudzinski, Julia Dorothea Michels-Zetsche, Frederik Trinkmann, Felix Josef-Friedrich Herth, Hans-Ulrich Kauczor, Kathrin Kahnert, Rudolf Jörres, Robert Bals, Dirk Westermann, Thomas Arentz, Claus Franz Vogelmeier, Daiana Stolz, Sebastian Fähndrich","doi":"10.1186/s12931-025-03342-2","DOIUrl":"10.1186/s12931-025-03342-2","url":null,"abstract":"<p><strong>Background: </strong>Atrial fibrillation (AF) frequently occurs in patients with chronic obstructive pulmonary disease (COPD) and is associated with adverse clinical outcomes. We aimed to identify patients at risk for AF using amplified p-wave duration (APWD) analysis on electrocardiogram (ECG) as non-invasive tool to diagnose an atrial cardiomyopathy (AtCM) which is an established risk factor for AF.</p><p><strong>Methods: </strong>This subgroup analysis of the prospective COSYCONET cohort included 2,385 COPD patients from 31 study centers with baseline sinus rhythm ECG and at least one follow-up examination. Of these, 73 patients showed AF during follow-up and were propensity-score matched to controls. APWD was measured at baseline and future major adverse cardiac and cerebrovascular events (MACCE) and health related outcome were assessed.</p><p><strong>Results: </strong>219 COPD patients (70 [64-74] years, 79.5% male) were analyzed during a follow-up of 586 (210-1137) days. APWD was significantly longer in patients with AF occurrence compared to controls (132 [125-141] ms vs. 124 [117-133] ms, p < 0.001) and remained significant in multivariate regression analysis (OR: 1.05 [1.01-1.09], p = 0.03). An APWD ≥ 131 ms was identified as best cut-off for AF prediction (62% sensitivity, 70% specificity, OR: 3.91 [2.58 to 5.95], p < 0.001). Patients with AF had a significantly higher MACCE rate (24.7% versus 8.2%, p = 0.001) and a significantly lower physical activity score (1,074 [264-4,776] vs. 2,706 [975-7,339], p = 0.008).</p><p><strong>Conclusions: </strong>This study demonstrates that ECG-based AtCM diagnosis identifies COPD patients at risk for AF, which was associated with a substantially elevated MACCE rate and a significantly reduced physical activity. This easy, cost-effective and widely available digital biomarker might enable early therapy initiation and prevention of adverse clinical outcomes.</p><p><strong>Trial registration: </strong>NCT01245933 on Clinical-Trials.gov (Registration date: 22.11.2010).</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"272"},"PeriodicalIF":5.8,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12442265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145082209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Computed tomography morphological assessments of central airways in interstitial lung abnormalities and idiopathic pulmonary fibrosis.","authors":"Tomoki Maetani, Naoya Tanabe, Kiminobu Tanizawa, Ryo Sakamoto, Yusuke Shiraishi, Yusuke Hayashi, Michihiro Uyama, Atsushi Matsunashi, Susumu Sato, Katsuhiro Suzuki, Izuru Masuda, Motonari Fukui, Shizuo Kaji, Tomohiro Handa, Toyohiro Hirai","doi":"10.1186/s12931-025-03346-y","DOIUrl":"10.1186/s12931-025-03346-y","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"271"},"PeriodicalIF":5.8,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12434911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145070905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Amitriptyline inhibits bronchoconstriction and directly promotes dilatation of the airways.","authors":"Paulina Hempel, Virag Klein, Anna Michely, Svenja Böll, Annette D Rieg, Jan Spillner, Till Braunschweig, Saskia von Stillfried, Norbert Wagner, Christian Martin, Klaus Tenbrock, Eva Verjans","doi":"10.1186/s12931-025-03353-z","DOIUrl":"10.1186/s12931-025-03353-z","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"270"},"PeriodicalIF":5.8,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12427097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145055545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Altered immune surveillance of B and T cells in patients with persistent residual lung abnormalities 12 months after severe COVID-19.","authors":"Julio Flores-Gonzalez, Ivette Buendia-Roldan, Fernanda Téllez-Quijada, Carlos Peña-Bates, Lucero A Ramón-Luing, Armando Castorena-Maldonado, Ramcés Falfán-Valencia, Gloria Pérez-Rubio, Moisés Selman, Leslie Chavez-Galan","doi":"10.1186/s12931-025-03351-1","DOIUrl":"10.1186/s12931-025-03351-1","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"269"},"PeriodicalIF":5.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12421738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145031098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of the COVID-19 pandemic on the research productivity of K-awardees.","authors":"Nupur Gupta, Shikha Gupta, Alison Morris, Divay Chandra","doi":"10.1186/s12931-025-03301-x","DOIUrl":"10.1186/s12931-025-03301-x","url":null,"abstract":"<p><p>The COVID-19 pandemic disrupted many aspects of academic research, particularly for early career investigators striving for independence. This study examines geographic heterogeneity in the pandemic's impact on the publication productivity of recipients of National Heart, Lung, and Blood Institute K01, K08, and K23 awards within Departments of Medicine across different states in the US using data from the National Institutes of Health RePORTER and the Centers for Disease Control and Prevention COVID data tracker from 2015 to 2022. Findings indicate that while publication productivity increased steadily until 2020, it plateaued soon after. K-awardees in states with an early peak in COVID-19-related deaths maintained relatively stable productivity levels post-2020, whereas those in states with a late peak experienced a decline. The observed geographic differences may stem from variations in pandemic response measures, resource availability, and institutional support. These findings highlight the need for careful consideration of geographic heterogeneity when designing targeted interventions, such as funding support and tenure extensions, to mitigate the pandemic's impact on early career investigators. Addressing additional factors, including career stage, personal responsibilities, and institutional environments, is essential for a comprehensive understanding of disparities in publication productivity.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"268"},"PeriodicalIF":5.8,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12406337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144976024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trends in influenza- and pneumonia-related mortality in lung cancer patients from 1999 to 2022: a retrospective CDC WONDER analysis.","authors":"Kate Woods, Mustafa Beidas, Vikram Murugan, Taylor Billion, Abubakar Tauseef, Mohsin Mirza","doi":"10.1186/s12931-025-03336-0","DOIUrl":"10.1186/s12931-025-03336-0","url":null,"abstract":"","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"267"},"PeriodicalIF":5.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12403505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144976019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The LPAR1 antagonist, PIPE-791 produces antifibrotic effects in models of lung fibrosis.","authors":"Michael Poon, Kym Lorrain, Alexander Broadhead, Karin Stebbins, Didier Bagnol, Geraldine Edu, Gregory Joseph, Christopher Baccei, Jeffrey Roppe, Thomas Schrader, Lino Valdez, Yifeng Xiong, Austin Chen, Daniel Lorrain","doi":"10.1186/s12931-025-03340-4","DOIUrl":"https://doi.org/10.1186/s12931-025-03340-4","url":null,"abstract":"<p><strong>Background: </strong>Idiopathic pulmonary fibrosis (IPF) is a chronic progressive form of interstitial lung disease (ILD) characterized by significant extracellular matrix deposition, alveolar damage, and tissue remodeling. Antagonists against the G-protein coupled receptor, lysophosphatidic acid receptor 1 (LPAR1) have shown efficacy in lung fibrosis preclinically and clinically. Here, we profile PIPE-791, a small molecule, orally bioavailable LPAR1 receptor antagonist, and show its effectiveness in several lung fibrosis-related contexts.</p><p><strong>Methods: </strong>In vitro, we used human lung fibroblasts and precision cut lung slices (PCLS) derived from donors with pulmonary fibrosis to test PIPE-791 efficacy in reducing markers of fibrosis. In vivo, we used bleomycin-induced lung fibrosis models to demonstrate PIPE-791 efficacy.</p><p><strong>Results: </strong>In vitro PIPE-791 reduced LPA-induced collagen expression (IC₅₀ 1.1 nM) in human lung fibroblasts. We also show that LPAR1 is elevated in IPF lung tissue and that PIPE-791 significantly reduced several markers of lung fibrosis in PCLS as measured by gene expression and secreted biomarkers. Using in vivo receptor occupancy, we found that PIPE-791 has long association kinetics resulting in a 20-fold increase in potency when dosed 3 versus 24 h prior to radioligand administration. At 3 mg/kg, PIPE-791 was effective in significantly reducing markers of fibrosis and collagen expression in mouse bleomycin models.</p><p><strong>Conclusions: </strong>We show that PIPE-791 effectively reduces fibrosis and fibrotic markers in vitro and in vivo and that it has slow association and dissociation kinetics. Taken together, our data support clinical testing of PIPE-791 in the context of fibrotic conditions such as IPF.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"265"},"PeriodicalIF":5.8,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144976045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A mouse model of E-cigarette or vaping product use-associated lung injury (EVALI) induced by nose-only exposure to aerosolized vitamin E acetate and associated macrophage dysfunction.","authors":"Xuanrong Bao, Hanbing Hu, Yu Dun, Yuedong Tang, Fuli Liu, Jian Zhou, Weichun Mo, Jie Shen","doi":"10.1186/s12931-025-03343-1","DOIUrl":"10.1186/s12931-025-03343-1","url":null,"abstract":"<p><strong>Background: </strong>E-cigarette or vaping product use-associated Lung Injury (EVALI) has become a public health concern since 2019, with vitamin E acetate (VEA) identified as a potential causative agent. While previous studies have used whole-body VEA aerosol exposure or intratracheal instillation models, these approaches may introduce confounding exposure routes or do not fully reflect real-world vaping conditions. To better understand VEA-induced EVALI, there remains a need for an animal model that isolates airway exposure and closely mimics human vaping behaviour.</p><p><strong>Methods: </strong>We utilized a nose-only exposure system to develop a mouse model of EVALI, with VEA aerosol generated by a commercially available vaping device. Puffs were generated at a volume of 55 mL over 3 s, delivered every 30 s for 1 h per day, up to 6 consecutive days. Lung injury was assessed through histopathological analysis, and airway function was measured via invasive airway function test. Ultrastructural changes in mouse alveoli were analyzed with transmission electron microscopy. Alveolar macrophages were assessed for pro-inflammatory polarization and functional impairment. Potential pathogenic mechanisms were explored with RNA-seq analysis.</p><p><strong>Results: </strong>Our findings revealed acute lung injuries, characterized by pulmonary edema and typical histopathological findings. Additionally, we observed changes in airway functions with altered respiratory patterns and decreased lung dynamic compliance. Transmission electron microscopy further revealed type II pneumocyte hypertrophy, type I pneumocyte swelling, and prolonged activation of alveolar macrophages with electron-dense phagocytic contents. We also demonstrated macrophage dysfunction with sustained pro-inflammatory polarization and impaired efferocytosis function. The persistent inflammation of the lung was also characterized by the increased level of pro-inflammatory cytokines in the bronchoalveolar lavage fluid, especially IL-6. RNA-seq analysis highlighted pathways related to T cell activation, cytokine signaling, and leukocyte migration.</p><p><strong>Conclusion: </strong>This study established a mouse model using a nose-only VEA aerosol exposure system to examine the respiratory effects of VEA in EVALI. Our results revealed that VEA inhalation triggered acute lung injury, accompanied by early signs of airway dysfunction. The findings support the hypothesis that VEA drives EVALI pathogenesis through both direct cytotoxic effects and macrophage-mediated inflammation. Our findings offer new insights into the mechanisms of EVALI and present a valuable model for future research.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"263"},"PeriodicalIF":5.8,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144975942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Divergent biological pathways distinguish community-acquired pneumonia from COVID-19 despite similar plasma cytokine profiles.","authors":"Douglas D Fraser, Logan R Van Nynatten, David Tweddell, Mark Daley, James A Russell","doi":"10.1186/s12931-025-03331-5","DOIUrl":"https://doi.org/10.1186/s12931-025-03331-5","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary infections, ranging from mild respiratory issues to severe multiorgan failure, pose a major global health threat. The immune response in community-acquired pneumonia (CAP) and COVID-19 influences disease severity and outcomes, but molecular pathogenesis differs across pathogens. Comparisons of plasma cytokine profiles between CAP and COVID-19 are limited. Analyzing these profiles with machine learning and bioinformatics could reveal subtle patterns and improve our understanding of immune responses in both conditions.</p><p><strong>Methods: </strong>We conducted a novel case-control study to profile cytokine levels in patients with CAP and COVID-19. Age- and sex-matched cohorts included 39 patients with CAP, 39 with COVID-19, and 20 healthy controls. We measured 384 plasma cytokine levels using proximity extension assays and analyzed differences between cohorts with conventional statistical methods, bioinformatics and machine learning.</p><p><strong>Results: </strong>Median ages of the cohorts were comparable (P = 0.797). COVID-19 patients exhibited a higher prevalence of hematologic disease (P = 0.047), increased corticosteroid use (P = 0.040), and reduced antibiotic use (P = 0.012). Clinical outcomes, including mortality, ICU admission, invasive mechanical ventilation, renal replacement therapy, acute respiratory distress syndrome, and acute kidney injury, were similar between groups. Both cohorts showed comparable absolute circulating cytokine profiles but distinct profiles relative to healthy controls. Machine learning identified a model of twelve cytokines that distinguished CAP from COVID-19 with a classification accuracy of 0.71 (SD 0.20). Gene ontology and enrichment analysis revealed differences in cytosolic and nuclear functions, intracellular signaling, stress responses, and cell cycle processes between patient cohorts and healthy controls. Enriched GO pathways showed that CAP pathways were positively associated with leukocyte counts and ARDS development, while COVID-19 pathways were negatively associated with ARDS and positively with platelet counts.</p><p><strong>Conclusions: </strong>This case-control study provides insights into cytokine profiles related to CAP and COVID-19 pathogenesis. Although absolute circulating cytokine levels showed no significant differences between the groups, machine learning identified a model of twelve proteins that effectively distinguished the cohorts. Gene ontology and enrichment analyses also revealed distinct dysregulated pathways with differing associations with clinical variables in each cohort. These findings underscore the complexity and variability of cytokine responses in pulmonary infections.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"264"},"PeriodicalIF":5.8,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144975988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Yanghe Pingchuan granules inhibit cellular senescence in airway smooth muscle cells to improve bronchial asthma via modulating Nrf2 acetylation.","authors":"Dezhi Yuan, Xing Yang, Bangfu He, Yanquan Han, Yongzhong Wang, Deling Wu, Lingyu Pan","doi":"10.1186/s12931-025-03345-z","DOIUrl":"https://doi.org/10.1186/s12931-025-03345-z","url":null,"abstract":"<p><strong>Background: </strong>Bronchial asthma (BA) is regarded as one of the most prevalent chronic respiratory diseases worldwide. Yanghe Pingchuan Granules (YPG), a traditional Chinese medicine (TCM) compound, has been employed extensively in treating BA. However, the precise mechanism by which it exerts its therapeutic effects remains to be fully elucidated. This study aimed to investigate the therapeutic mechanisms of YPG in BA model rats, focusing on the interventional effects on cellular senescence of airway smooth muscle cells (ASMCs) in vivo and in vitro.</p><p><strong>Methods: </strong>In this study, OVA was utilized to induce the replication of an asthmatic rat model, α-smooth muscle actin (α-SMA) was employed to identify ASMCs, and a series of in vitro experiments were conducted. These experiments included β-galactosidase (β-gal), Enzyme-linked immunosorbent assay (ELISA), biochemical assay, western blotting, Co-Immunoprecipitation (CO-IP), overexpression/silencing of Sirtuin 1 (SIRT1) and Nuclear factor E2-related factor 2 (Nrf2) was studied in ASMCs. Subsequently, Hematoxylin and Eosin (H&E), Masson, Alcian Blue-Periodic Acid Schiff (AB-PAS), ELISA, biochemical assay, western blotting, Co-Immunofluorescence (CO-IF), and CO-IP were employed to examine the histopathological damage, acetylation, oxidative stress, senescence-related protein expression, and senescence-associated secretion phenotype (SASP) secretion of bronchial tubes in asthmatic rats. This comprehensive approach was undertaken to elucidate the mechanism by which YPG inhibits the senescence of ASMCs.</p><p><strong>Results: </strong>The results of in vivo and in vitro experiments demonstrated that SIRT1 overexpression and YPG inhibited the senescence of ASMCs and significantly reduced P16 and P21 proteins, as well as cellular SASP (Interleukin-1β (IL-1β), Interleukin-4 (IL-4), and Interleukin-17 (IL-17)). Moreover, YPG demonstrated a substantial reduction in histopathological alterations in BA rats. Furthermore, the study observed a decline in Malondialdehyde (MDA) expression, concomitant with an augmentation in the expression levels of SIRT1, Nrf2, oxygenase-1 (HO-1), Superoxide dismutase (SOD), and Catalase (CAT). It substantiated the interaction of SIRT1 with Nrf2 and the decrease in the expression level of Nrf2 acetylation.</p><p><strong>Conclusions: </strong>These results suggest that YPG can activate the SIRT1/Nrf2/HO-1 signaling pathway by regulating the expression level of SIRT1 to regulating the acetylated expression level of Nrf2, to inhibit the senescence of ASMCs, leading to the treatment of asthma.</p>","PeriodicalId":49131,"journal":{"name":"Respiratory Research","volume":"26 1","pages":"266"},"PeriodicalIF":5.8,"publicationDate":"2025-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144975994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}