American journal of physiology. Lung cellular and molecular physiology最新文献

{"title":"Mechanisms of lung crosstalk with end organs: scientific session V-ReSPIRE 2025.","authors":"Navneet Singh, Ceren Koçana, Eric P Schmidt, Mark L Hepokoski, Michael A Matthay, Troy Stevens","doi":"10.1152/ajplung.00175.2025","DOIUrl":"10.1152/ajplung.00175.2025","url":null,"abstract":"<p><p>Session V of the inaugural biennial Research Symposium on Pulmonary Injury and Repair of the Endothelium showcased cutting-edge research on pulmonary endothelial crosstalk with end organs and its role in vascular disease. Growing evidence suggests that communication between injured organs and distal vascular beds plays a critical role in the pathogenesis of complex conditions such as sepsis, acute respiratory distress syndrome, pulmonary arterial hypertension, and heart failure with preserved ejection fraction. Circulating mediators-including heparan sulfate fragments, proinflammatory cytokines, mitochondrial damage-associated molecular patterns, bone morphogenetic protein 9, bile acids, and nitric oxide-have emerged as key factors linking pulmonary endothelial dysfunction to neural impairment, acute kidney injury, subclinical liver injury, and left-sided heart disease. This review highlights recent advances in the field, identifies critical knowledge gaps, and outlines future research directions aimed at elucidating mechanisms of multiorgan dysfunction and identifying novel therapeutic targets.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L419-L427"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computer model-based injury prediction and evaluation of lung function in mice with acute and ventilator-induced lung injuries.","authors":"Elizabeth Kaye, Alexander Sosa, Katharine Drayton Warner, David J Albers, Peter D Sottile, Bradford J Smith","doi":"10.1152/ajplung.00248.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00248.2025","url":null,"abstract":"<p><p>Invasive mechanical ventilation is a lifesaving intervention for acute respiratory distress syndrome (ARDS) patients but also causes ventilator-induced lung injury (VILI) that can be challenging to avoid due to inter-patient and temporal heterogeneity. Thus, the aim of this study was to characterize and predict experimental VILI using readily available measures of lung function. Initially healthy (CTL) and hydrochloric acid (HCL) lung-injured mice were ventilated for four hours at PEEP = 1, 3, or 8 cmH₂O to produce graded VILI severity as measured in lung function, alveolocapillary leak, and inflammation. Optimally protective PEEP was found to be 8 and 3 cmH₂O in the HCL and CTL groups, respectively. A novel computational model was fit to the data to investigate elastance dynamics described by the \"compliance factor\" (C_F) which was also used to predict VILI over four subsequent hours of ventilation. The model C_F is a sensitive measure of injury-induced alterations in the pressure- and pressure-history dependence of lung elastance that are known to correlate with recruitment and derecruitment dynamics. The C_F was then combined with PEEP and plateau pressures calculated from 10 minutes at the start of prolonged ventilation and used to accurately predict VILI outcomes measured four hours later. This model outperformed other commonly utilized measures of injury such as driving pressure and mechanical power. The computer model provides a new tool for understanding lung dynamics and for predicting VILI. In future work, this approach could be used to guide identification of lung protective ventilation settings.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scar Wars: The Viral Menace.","authors":"Sara Kass-Gergi, Nicolas P Holcomb, Michael M Maiden, Laurence C Eisenlohr, Andrew E Vaughan","doi":"10.1152/ajplung.00189.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00189.2025","url":null,"abstract":"<p><p>Pulmonary fibrosis (PF) is a severe consequence of respiratory infections, characterized by excessive extracellular matrix deposition and irreversible lung architectural damage. Once considered a rare condition, PF is now increasingly recognized in the wake of viral infections, particularly among survivors of viral-induced acute respiratory distress syndrome (ARDS). The COVID-19 pandemic has highlighted in bold relief the observation that many survivors of severe viral pneumonia do not recover fully but develop chronic fibrotic changes that impair lung function. This review examines the clinical evidence and underlying mechanisms linking viral infections-COVID-19, influenza, and other respiratory viruses-to the onset of pulmonary fibrosis. By probing the mechanisms of cellular injury, immune dysregulation, and aberrant repair mechanisms, we aim to illuminate the pathways that transform an acute viral insult into a chronic, fibrotic disease.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145123879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sorted-Cell Proteomics Reveals an AT1-Associated Epithelial Cornification Phenotype and Suggests Endothelial Redox Imbalance in Human Bronchopulmonary Dysplasia.","authors":"Mereena George Ushakumary, William B Chrisler, Gautam Bandyopadhyay, Heidie L Huyck, Brittney L Gorman, Naina Almazbekovna Beishembieva, Ariana Pitonzo, Zhenli J Lai, Thomas L Fillmore, Isaac Kwame Attah, Gail Deutsch, Jeffrey M Purkerson, Andrew M Dylag, Ravi S Misra, James P Carson, Joshua N Adkins, Gloria Pryhuber, Geremy C Clair","doi":"10.1152/ajplung.00098.2025","DOIUrl":"10.1152/ajplung.00098.2025","url":null,"abstract":"<p><p>Bronchopulmonary dysplasia (BPD) is a neonatal lung disease characterized by inflammation and scarring leading to long-term tissue damage. Previous whole tissue proteomics identified BPD-specific proteome changes and cell type shifts. Little is known about the proteome-level changes within specific cell populations in disease. Here, we sorted epithelial (EPI) and endothelial (ENDO) cell populations based on their differential surface markers from normal and BPD human lungs. Using a low-input compatible sample preparation method (MicroPOT), proteins were extracted and digested into peptides and subjected to Liquid Chromatography-tandem Mass Spectrometry (LC-MS/MS) proteome analysis. Of the 4,970 proteins detected, 293 were modulated in abundance or detection in the EPI population and 422 were modulated in ENDO cells. Modulation of proteins associated with actin-cytoskeletal function such as SCEL, LMO7, and TBA1B were observed in the BPD EPIs. Using confocal imaging and analysis, we validated the presence of aberrant multilayer-like structures comprising SCEL and LMO7, known to be associated with epidermal cornification, in the human BPD lung. This is the first report of accumulation of cornification-associated proteins in BPD. Their localization in the alveolar parenchyma, primarily associated with alveolar type 1 (AT1) cells, suggests a role in the BPD post-injury response. In the ENDOs, redox balance and mitochondrial function pathways were modulated. Alternative mRNA splicing and cell proliferative functions were elevated in both populations suggesting potential dysregulation of cell progenitor fate. This study characterized the proteome of epithelial and endothelial cells from the BPD lung for the first time, identifying population-specific changes in BPD pathogenesis.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aerosolized Vitamin D Attenuates Ozone-Induced Inflammation and Transcriptional Responses Via Membrane Antioxidant Effects in Human Bronchial Epithelial Cells.","authors":"Kevin D Schichlein, Syed Masood, Hye-Young H Kim, Benjamin Hawley, Arunava Ghosh, James M Samet, Ned A Porter, Gregory J Smith, Ilona Jaspers","doi":"10.1152/ajplung.00233.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00233.2025","url":null,"abstract":"<p><p>Ozone exposure increases the risk of infection, worsens lung diseases, and causes systemic health issues. As ambient ozone levels continue to rise globally, effective interventions are needed to reduce these harmful effects. Vitamin D, known for its anti-inflammatory properties, has been inversely linked to various lung conditions, including ozone-induced airway inflammation and reduced lung function. However, oral vitamin D supplementation has shown inconsistent results, possibly due to poor delivery to lung tissues. This study explores a novel approach using vitamin D aerosols to counter ozone-induced damage in primary human bronchial epithelial cells. Cells were pre-treated with vitamin D aerosols apically or as bulk addition basolaterally before ozone exposure at the air-liquid interface. Both treatment routes significantly reduced the ozone-induced secretion of the inflammatory cytokine IL-8. Furthermore, vitamin D suppressed the ozone-induced expression of inflammation- and oxidative stress-related genes, including IL-8, FFAR2, COX-2, and NFKB2. Gene set enrichment analysis (GSEA) indicated that vitamin D reversed ozone-driven pathways related to inflammation, oxidative stress, and immune dysfunction. Additionally, vitamin D pre-treatment reduced lipid peroxidation, glutathione oxidation, and formation of ozone-derived oxysterols, suggesting a membrane antioxidant effect. These findings support vitamin D's potential as a protective agent against inhaled oxidants and highlight inhaled delivery as a promising therapeutic strategy for treating lung diseases.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Airway sympathectomy attenuates inflammation, transcriptional ratios of Muc5ac and Muc5b, and airway mechanic deficits in mice delivered intranasal IL-13.","authors":"Pedro Trevizan-Baú, Amy L Fagan, Shanil P Amin, Leah R Reznikov","doi":"10.1152/ajplung.00139.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00139.2025","url":null,"abstract":"<p><p>Excessive mucus in the airways is an underlying pathological feature of many airway diseases, including asthma. Therapeutic options to reduce mucus production in the airways remain limited. One possible therapeutic target is the airway sympathetic nerves. Although lung sympathetic innervation has been considered sparse, sympathetic nerves secrete neurotransmitters that act on adrenergic receptors, including β₂-adrenergic receptor (β₂AR). Interestingly, in experimental models, chronic use β₂AR agonists can augment mucus secretion. Thus, in the present study, we tested the hypothesis that airway sympathetic nerves regulate mucus production in the airway in response to the type 2 cytokine interleukin 13 (IL-13). We performed airway sympathectomy using intranasal instillation of the synthetic neurotoxin 6-hydroxydopamine (6-OHDA). Airway sympathectomy attenuated multiple IL-13-mediated airway deficits, including density of goblet cells containing neutral mucins, transcriptional ratio of mucin 5ac (Muc5ac) to mucin 5b (Muc5b) and airway elastance and tissue damping. Although total <i>Muc5ac</i> and <i>Muc5b</i> transcript levels and Muc5ac and Muc5b protein levels in bronchoalveolar lavage were not significantly altered, these changes suggest that airway sympathectomy modifies goblet cell phenotype and mucin composition. Airway sympathectomy also dampened IL-13 mediated increases in total lung transcripts important for regulating allergic responses, including interleukin 6, complement component 3, and colony stimulating factor. This study reveals that airway sympathetic nerves regulate physiologic, molecular, and inflammatory responses to type 2 (IL-13-mediated) airway inflammation and raises the possibility that they may serve as potential targets for therapeutic intervention.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145051570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Untangling the nets - a roadmap to standardized sampling and analysis of exhaled volatile organic compounds powered by <i>in silico</i> medicine.","authors":"Robin Curnow, Carl A Whitfield, Waqar Ahmed, Ran Wang, Stephen J Fowler","doi":"10.1152/ajplung.00056.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00056.2025","url":null,"abstract":"<p><p>Biomarkers based on volatile organic compounds (VOCs) measured in human breath have been investigated in a wide range of diseases. However, the excitement surrounding such biomarkers has not yet translated to the discovery of any that are ready for clinical implementation. A lack of standardisation in sampling and analysis has been identified as a key obstacle to the validation of potential biomarkers in in multi-centre studies. Some progress towards standardisation has been made, but further progress is required to optimise sampling protocols and account for the confounding factors identified. This review highlights the important role that <i>in silico</i> (<i>i.e.</i> computational modelling) methods can play in addressing these gaps. Moreover, we discuss their potential for targeting and validating disease biomarkers by mechanistically linking them to the underlying metabolomic processes. We explore pertinent examples of mathematical, computational and machine learning models, that have proven useful in similar contexts, such as the development of fractional exhaled nitric oxide sampling standards. We then propose a roadmap outlining how existing and new modelling approaches can be applied to the problem of standardisation in breathomics research.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145028716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal Stromal Cell Extracellular Vesicles Reduce <i>Pseudomonas</i> Biofilm Formation, and let-7b-5p Loading Confers Additional Anti-Inflammatory Effects.","authors":"Sharanya Sarkar, Roxanna Barnaby, Amanda B Nymon, Lily A Charpentier, Lily Taub, Matthew J Wargo, Daniel J Weiss, Tracey L Bonfield, Bruce A Stanton","doi":"10.1152/ajplung.00187.2025","DOIUrl":"10.1152/ajplung.00187.2025","url":null,"abstract":"<p><p>Cystic Fibrosis (CF) is a multiorgan disease caused by mutations in the <i>CFTR</i> gene, leading to chronic pulmonary infections and hyperinflammation. Among pathogens colonizing the CF lung, <i>Pseudomonas aeruginosa</i> is predominant, infecting over 50% of adults with CF, and becoming antibiotic-resistant over time. Current therapies for CF, while providing tremendous benefits, fail to eliminate persistent bacterial infections, chronic inflammation, and irreversible lung damage, necessitating novel therapeutic strategies. Our group engineered mesenchymal stromal cell derived extracellular vesicles (MSC EVs) to carry the microRNA let-7b-5p as a dual anti-infective and anti-inflammatory treatment. MSC EVs are low-immunogenicity platforms with innate antimicrobial and immunomodulatory properties, while let-7b-5p reduces inflammation. This study demonstrates that MSC EVs effectively blocked the formation of antibiotic-resistant <i>P</i>. <i>aeruginosa</i> biofilms on primary Human Bronchial Epithelial Cells (pHBECs), and let-7b-5p loading into MSC EVs conferred additional anti-inflammatory effects by reducing <i>P</i>. <i>aeruginosa</i>-induced IL-8 secretion by pHBECs. This approach holds promise for improving outcomes for people with CF, and future work will focus on optimizing delivery strategies and expanding the clinical applicability of MSC EVs to target other CF-associated pathogens.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGFβ induces excessive pulmonary IL-6 secretion in cystic fibrosis via PI3K.","authors":"Grace Scharf, Cynthia R Davidson, Vladimir Ustiyan, Lauren G Falkenberg, Amulya Adavalli, Jessica Meeker, Hunter Morgan, Alicia J Ostmann, Kristin M Hudock, John J Brewington, John P Clancy, Elizabeth L Kramer","doi":"10.1152/ajplung.00183.2025","DOIUrl":"10.1152/ajplung.00183.2025","url":null,"abstract":"<p><p>Cystic Fibrosis (CF) is characterized by impaired mucociliary clearance and pulmonary infections. Accumulating evidence suggests that fundamentally abnormal inflammatory responses also contribute to CF pathology. TGFβ, a pleiotropic cytokine, is a modifier of CF lung disease; its mechanism of action in CF is unclear. Previous studies have shown that TGFβ induces IL-6 secretion from lung epithelium, which may drive worse pulmonary outcomes in CF and other lung diseases. However, the nature of the TGFβ/IL-6 relationship in CF is not fully understood. In this study, we demonstrated that TGFβ and IL-6 concentration were positively associated in bronchoalveolar lavage fluid from children with CF. Furthermore, pulmonary TGFβ exposure in a CF mouse model induced heightened IL-6 secretion when compared with non-CF mice. CF airway epithelial cells had increased IL-6 secretion and PI3K signaling after TGFβ exposure. In wild type airway epithelium, TGFβ exposure and CFTR inhibition synergistically provoked IL-6 secretion. Restoration of CFTR function by a CFTR modulator and inhibition of PI3K signaling both normalized IL-6 secretion from CF airway epithelial cells. These data indicate that TGFβ drives abnormal IL-6 secretion via the PI3K pathway in the CF airway, demonstrating an inherent inflammatory abnormality in CF and suggesting potential therapeutic targets.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022675","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":"Regulation of Inflammatory Lung Injury by Transforming Growth Factors.","authors":"Mrinmay Chakrabarti, Mollie Phillips, Rana Dhar, Ansley Herron, Jason L Kubinak, Kiesha Wilson, E Angela Murphy, Mohamad Azhar, Colin Evans","doi":"10.1152/ajplung.00154.2025","DOIUrl":"10.1152/ajplung.00154.2025","url":null,"abstract":"<p><p>Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) are inflammatory conditions with substantial rates of morbidity and mortality, but no effective treatments. The lack of effective treatments and unacceptably high mortality rates for ARDS are partly due to an incomplete understanding of the mechanisms that control ALI/ARDS and subsequent vascular repair. Transforming growth factors (TGFs) are a class of growth factors that regulate the vascular response to inflammation, including migration, proliferation, and differentiation of cells comprising the lung vasculature. Here we review studies that describe the impact of the TGF family on inflammatory lung injury and subsequent vascular repair and fibrosis. We highlight gaps in understanding TGF isoform-specific roles in ALI/ARDS and outline directions for future research in the field of TGF-dependent regulation of inflammatory lung injury and vascular repair. Functional roles of the TGFs have been investigated in ALI/ARDS pathogenesis and pulmonary fibrosis, with a predominance for studies showing a pro-injurious and pro-fibrotic impact of TGF-β1. Studies have also shown that TGF-α is positively associated with inflammatory lung injury and fibrosis. However, the contributions of TGF-β2 and TGF-β3 to ALI/ARDS are unclear, and the contributions of all the TGF isoforms to vascular repair after ALI/ARDS are unknown. Improved understanding of the regulation of inflammatory lung injury and repair by the TGFs could lead to the development of a safe and effective treatment strategy for patients with ALI/ARDS.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}