American Journal of Respiratory Cell and Molecular Biology最新文献

{"title":"Clinical Translation of Inhaled Vitamin A in Preterm Infants: Considering Extrapulmonary Safety.","authors":"Nezihe Köker Özer, Ercan Yılmaz, Erdem Topal","doi":"10.1093/ajrcmb/aanag200","DOIUrl":"https://doi.org/10.1093/ajrcmb/aanag200","url":null,"abstract":"","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102983","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":"A Novel Precision-cut lung slice stretch model using removable inflation materials.","authors":"Cassidy J Potter, Jeannie Haak, David Dean, Andrew M Dylag, Jared A Mereness","doi":"10.1093/ajrcmb/aanag196","DOIUrl":"10.1093/ajrcmb/aanag196","url":null,"abstract":"<p><p>Mechanical stretch is an important biomechanical stimulus that facilitates tissue development in the respiratory system by programming the epithelium, endothelium, mesenchyme, and immune cells. Lung tissue undergoes stretch-induced lung differentiation under normal prenatal and postnatal development. Furthermore, supraphysiological and aberrant stretch responses are known mechanisms of acute lung injury and ECM disruption. Current in vitro and ex vivo human tissue cyclic mechanical stretch (CMS) models suffer from significant, well-recognized disadvantages and are poorly validated in vivo for longer-term study. Ex vivo precision-cut lung slice (PCLS) models maintain lung tissue architecture and the variety of cell types present in the lung, allowing for a more realistic imitation of the lung microenvironment and the study of cell-cell interactions while under stretch that are not possible in single-cell-type stretch models. 3 Existing agarose-inflated PCLS models are hindered by retention of agarose media in the tissue, which affects material properties and complicates stretch studies, and damaging methods of anchoring the PCLS for stretch. Herein, we present a novel and innovative PCLS system that includes a removable agarose-inflation media and supportive poly(ethylene glycol) (PEG) hydrogel for embedding that can be used to apply CMS to PCLS. We will demonstrate and validate, for the first time, that PCLS can undergo CMS for 24 hours, remain viable, and demonstrate activation of CMS pathways through transcriptomics.</p>","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102980","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":"Myeloid TLR2 signaling amplifies immunopathology in influenza-infected murine neonates.","authors":"Abhishek S Rao, Abigail P Onufer, Ogan Kumova, Linda T N Roberts, Roschanak Mossabeb, Judy Pascasio, Alison J Carey","doi":"10.1093/ajrcmb/aanag050","DOIUrl":"10.1093/ajrcmb/aanag050","url":null,"abstract":"<p><p>We previously demonstrated that pretreatment with intranasal Lactobacillus rhammosus GG (LGG) prior to influenza viral (IAV) infection protected murine neonates through toll-like receptor (TLR) priming. Based on these results, we hypothesized that neonates had impaired TLR activation in response to IAV. However, translational studies with human neonatal monocytes stimulated with IAV exhibited comparable IL-6 production and sustained TLR2 expression compared to adults. Next, to further investigate the role of TLR2, transgenic mice lacking the TLR2 gene (TLR2-/-) were intranasally infected with IAV. TLR2-/- neonates displayed improved survival over C57BL/6 neonates after IAV infection, with reduced neutrophil recruitment at 6-days post-infection. To test the role of neutrophils in increasing mortality, neutrophil depletion was performed in C57BL/6 neonates; survival was improved. Additionally, treatment with an anti-TLR2 blocking antibody improved survival in the C57BL/6 neonates. Similarly, myeloid-specific TLR2-deficient mice demonstrated enhanced survival with improved histopathology and decreased neutrophil-associated pro-inflammatory cytokines and chemokines (IL-6, TNF-α, MCP-1, CXCL1), despite no changes in immune cell recruitment. Moreover, conditional knockout neonates did not amplify production of pro-inflammatory cytokines and chemokines from 3 days post-infection to 6-days post-infection, compared to the age-matched neonatal control group. These findings suggest that myeloid TLR2 signaling exacerbates neonatal susceptibility to respiratory viral infections by driving increased pulmonary inflammation over the first week of infection.</p>","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":"1440-1450"},"PeriodicalIF":5.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13261744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832477","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":"E protein-driven iNKT subset modulation shapes early immune responses during influenza A virus infection.","authors":"Justyna A Luczak, Oliwia Milek, Hannah Carter, Christopher M Schafer, Erola Ainsua-Enrich, Courtney T Griffin, Matthew S Walters, Susan Kovats, José Alberola-Ila","doi":"10.1093/ajrcmb/aanag054","DOIUrl":"10.1093/ajrcmb/aanag054","url":null,"abstract":"<p><p>Invariant natural killer T (iNKT) cells play a critical role in the early phases of the response to influenza A virus (IAV) infection by influencing inflammation and immune regulation, but the impact of the different iNKT functional subsets (iNKT1, iNKT2, and iNKT17) in these responses is unclear. We used genetically altered mouse strains with normal numbers of iNKT cells but different iNKT subset representation (NKTWT and NKTET2) to analyze the impact of different iNKT functional subsets on IAV infection outcomes. We show that IAV-infected NKTET2 mice have reduced weight loss, diminished myeloid recruitment and activation, and a 40% reduction in lung-infected areas compared with controls. This was accompanied by lower expression of inflammatory mediators (Ifna, Isg15, Ifit1) and chemoattractants Ccl2 and Cxcl2, along with elevated levels of type III interferon (Ifnl3). Single-cell RNA sequencing analysis of iNKTs suggests that these changes are driven by quantitative differences in iNKT responses, which are predominantly type I in NKTWT mice but type 17 in NKTET2 mice. These differences correlate with higher levels of Il22b and Il1b in NKTET2 mice lungs. Altogether, our results indicate that changes in iNKT subset representation impact the outcome of IAV infections by changing the character of the early immune response, and suggests that selective activation of iNKT subsets could be used to improve vaccination strategies in the future.</p>","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":"1418-1430"},"PeriodicalIF":5.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13151994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832368","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":"Temporal type I IFN signaling orchestrates protective and pathogenic inflammation post-influenza.","authors":"Md Bashir Uddin, Michael McKelvey, Sunil Palani, Shengjun Shao, Yuejin Liang, Keer Sun","doi":"10.1093/ajrcmb/aanag057","DOIUrl":"10.1093/ajrcmb/aanag057","url":null,"abstract":"<p><p>Secondary bacterial pneumonia following influenza A virus (IAV) infection markedly exacerbates lung inflammation and contributes to acute respiratory distress syndrome (ARDS); however, the immunologic pathways that drive lung injury and determine protective versus pathogenic inflammation remain incompletely defined. Using a clinically relevant murine model of sublethal IAV infection followed by methicillin-resistant Staphylococcus aureus challenge under antibiotic therapy, this study investigated the dynamic role of type I interferon (IFN-I) signaling in disease progression. The findings demonstrate that IFN-I exerts dual and contrasting effects on the host inflammatory response: it enhances myeloid-derived TNF-α while indirectly suppressing T cell-derived IFN-γ. Reporter mouse models identified recruited monocytes and dendritic cells (DCs) as the primary IFN-I-targeted populations, whereas neutrophils, T cells, and alveolar macrophages exhibited limited direct responsiveness. Myeloid-specific deletion of IFNAR1 reduced TNF-α production, restrained inflammatory monocyte differentiation, and improved survival without disrupting IFN-γ and IL-10 balance. Temporal IFNAR1 blockade further revealed that early IFN-I signaling supports alveolar macrophage maintenance and primes monocytes/DCs for immune activation, whereas sustained signaling during bacterial superinfection drives persistent monocyte chemoattractant production, excessive monocyte activation, and delayed resolution of inflammation. Collectively, these findings position IFN-I as a temporal immune rheostat-protective during acute viral infection but pathogenic when prolonged-and define a therapeutic window in which selective IFNAR inhibition enhances host antibacterial defense, either alone or in combination with antibiotic therapy. These insights highlight a promising immunomodulatory strategy to improve outcomes in severe viral-bacterial pneumonia and ARDS.</p>","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":"1451-1462"},"PeriodicalIF":5.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832600","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":"Current insight into the molecular mechanisms of lymphangioleiomyomatosis.","authors":"Amina Jouida, Michael P Keane, Cormac McCarthy","doi":"10.1093/ajrcmb/aanag042","DOIUrl":"10.1093/ajrcmb/aanag042","url":null,"abstract":"<p><p>Lymphangioleiomyomatosis (LAM) is a rare, progressive lung disease that predominantly affects women, particularly during their reproductive years. It is characterized by the proliferation of abnormal smooth muscle-like cells that infiltrate the lungs, leading to cystic destruction of lung tissue and a decline in respiratory function. The pathogenic defect in LAM occurs due to mutations in the tuberous sclerosis complex genes, resulting in failure to suppress the mTOR pathway activation, which drives abnormal cell proliferation and lymphangiogenesis. Although mTOR inhibitors, such as sirolimus, have improved clinical management by slowing disease progression, they are not curative and do not reverse existing lung damage. Recent research has expanded our understanding of LAM pathogenesis by revealing substantial genetic and cellular heterogeneity within LAM lesions. Beyond mTOR dysregulation, pathways involving estrogen signaling, metabolic adaptation, and immune evasion contribute to disease development. These insights open new avenues for treatment. A better understanding of these pathways will pave the way for more durable and individualized treatments for LAM.</p>","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":"1352-1363"},"PeriodicalIF":5.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832436","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":"Metabolic alterations in cystic fibrosis lymphocyte memory accompany restoration of CFTR function.","authors":"Milene T Saavedra, Noel M Rysavy, Katie R Poch, Silvia M Caceres, Sonia M Leach, Curtis Laborda, Fatjon Leti, Kendra N Walton, Thomas Danhorn, Julie A Reisz, Angelo D'Alessandro, Jennifer L Taylor-Cousar, Jerry A Nick, R Lee Reinhardt, Preston E Bratcher, Brian E Vestal","doi":"10.1093/ajrcmb/aanag081","DOIUrl":"10.1093/ajrcmb/aanag081","url":null,"abstract":"<p><strong>Rationale: </strong>Elexacaftor/tezacaftor/ivacaftor (ETI) broadly improves outcomes in cystic fibrosis (CF). Cystic fibrosis transmembrane conductance regulator (CFTR) correction by ETI is incomplete, and patients with established disease continue to experience infection. We hypothesized that CFTR restoration by ETI would modify T-cell memory, providing a basis for improved infectious outcomes after treatment.</p><p><strong>Objectives: </strong>To evaluate ETI modification of lymphocyte signatures using transcriptomics and metabolomics in blood samples taken from adults with CF (awCF).</p><p><strong>Methods and main results: </strong>Circulating CD3+ T cells from awCF (n = 18) before and after ETI initiation were evaluated by cellular indexing of transcriptomes and epitopes by sequencing. Single-cell data profiled multiple T-cell populations, including naive, memory, and effector states, with the most extensive changes occurring in CD4+ T-cell populations. Simultaneous plasma metabolomic measurements were analyzed in association with CD4+ T-cell metabolic gene signatures. The relationships between clinical outcomes, cell-specific gene expression, and metabolomics were evaluated using generalized linear mixed models. The effect of reduced CFTR in lymphocytes was evaluated in vitro using CRISPR/Cas9-mediated CFTR knockdown in primary human lymphocyte cultures, as well as in splenocytes harvested from CFTR knockout mice.</p><p><strong>Conclusions: </strong>We reveal that altered metabolism occurs within the CD4+ T memory compartment following CFTR modulation, identifying multiple previously unrecognized changes in memory functions. Memory T-cell metabolic switches are highly related to a reduction in hospitalizations after treatment. Adaptive immune memory in awCF after modulator therapy is highly associated with improved outcomes from CF pulmonary infections, with variation seen in individuals experiencing lesser benefit after modulators.</p>","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":"1389-1406"},"PeriodicalIF":5.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147925511","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":"Immune regulation by CD55 in chronic beryllium disease.","authors":"Li Li, Sucai Liu, Zhe Lei, Joshua Macaluso, Shujin Guo, Kristyn MacPhail, Margaret M Mroz, Clara I Restrepo, Ivana Y Yang, Lisa A Maier","doi":"10.1093/ajrcmb/aanag063","DOIUrl":"10.1093/ajrcmb/aanag063","url":null,"abstract":"<p><p>CD55 is an immune regulator that inhibits T-cell activation and also binds to CD97, a molecule involved in immune cell migration and signaling. While CD55 expression is reduced in chronic beryllium disease (CBD), its functional role in disease pathogenesis remains unclear. We hypothesized that CD55 downregulation in peripheral blood mononuclear cells (PBMCs) contributes to heightened beryllium (Be)-specific immune responses in CBD. To test this, we characterized CD55 expression and function in PBMCs from patients with CBD and individuals with beryllium sensitization (BeS), as well as in a human Be-specific T-cell model. CD55, soluble CD55 (sCD55), and CD97 mRNA expression was quantified by qRT-PCR in PBMCs from CBD (n = 25), BeS (n = 36), and control (n = 7) participants. BeSO4 (beryllium sulfate) stimulation was used to assess CD55, STAT1, JAK2, and TNF-α expression over time in CBD PBMCs (n = 8). Serum sCD55 was measured by ELISA in an independent cohort. Functional studies using anti-CD55 neutralizing antibodies and the JAK2 inhibitor TG101348 evaluated effects on TNF-α production and lymphocyte proliferation (beryllium lymphocyte proliferation test [BeLPT]) in PBMCs, and IL-2 production in a Jurkat-Be cell model. CD55, sCD55, and CD97 were significantly downregulated in CBD PBMCs compared to BeS (P < .001). Serum sCD55 was also reduced in CBD (P < .05). BeSO4 stimulation further downregulated CD55 and upregulated STAT1. CD55 blockade increased TNF-α production and BeLPT responses in CBD (P < .001) and BeS (P < .05); these effects were reversed by JAK2 inhibition. In the Be-cell model, CD55 inhibition enhanced IL-2 production (P < .01), attenuated by JAK2 blockade. These findings suggest that CD55 downregulation amplifies Be-induced immune responses in CBD via JAK2/STAT1 signaling.</p>","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":"1431-1439"},"PeriodicalIF":5.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13479807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832370","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":"Regional micro-computed tomography analysis enables longitudinal detection of compensatory ventilation effects in a mouse model of pulmonary fibrosis.","authors":"Martina Buccardi, Francesca Pennati, Erica Ferrini, Davide Buseghin, Eugenia Polverini, Nicola Sverzellati, Andrea Aliverti, Franco Fabio Stellari","doi":"10.1093/ajrcmb/aanag036","DOIUrl":"10.1093/ajrcmb/aanag036","url":null,"abstract":"<p><p>Accurate lung function assessment is essential in preclinical idiopathic pulmonary fibrosis (IPF) research, yet conventional whole-lung endpoints overlook spatial heterogeneity and compensatory mechanisms. We present a micro-computed tomography (µCT)-based pipeline for longitudinal, regional quantification of structural and functional changes in a murine bleomycin (BLM)-induced fibrosis model to improve evaluation of disease progression and therapeutic effects. C57BL/6 mice received triple oropharyngeal administrations of saline or BLM. Respiratory-gated µCT scans were acquired in free-breathing at baseline and days 7, 14, and 21. A deep-learning algorithm segmented the lungs into left and right lobes, further subdivided into apical and caudal regions using airway landmarks. Regional volumes, aeration compartments, and ventilation maps were extracted to assess structural and functional alterations. Saline-treated mice showed stable metrics over time, with minimal interanimal variability, demonstrating the robustness and physiological consistency of our segmentation procedure. BLM-treated animals exhibited early and heterogeneous fibrotic changes, with the apical regions appearing as most affected. The caudal-right region displayed a compensatory functional increase of respiratory parameters derived from multivolume µCT. µCT-based regional analysis can detect localized dysfunction and compensatory effects not captured by whole-lung measurements. This strategy is applicable to different models of heterogeneous lung disease and may contribute to reduce the translational gap in IPF research.</p>","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":"1342-1351"},"PeriodicalIF":5.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832570","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":"MLKL regulates intracellular trafficking of neutrophil elastase to promote lung epithelial cell senescence.","authors":"Rong Liu, Aifang Zhang, Steven D Shapiro, Dongshi Chen","doi":"10.1093/ajrcmb/aanag072","DOIUrl":"10.1093/ajrcmb/aanag072","url":null,"abstract":"<p><p>Neutrophil elastase (NE) is a key contributor to the pathogenesis of chronic obstructive pulmonary disease (COPD), driving airway inflammation and tissue destruction. While the receptor-interacting protein kinase 3 (RIPK3)/mixed lineage kinase domain-like protein (MLKL)-mediated necroptosis has been implicated in cigarette smoke-induced COPD, its role in NE-mediated lung injury remains undefined. In this study, we demonstrate that NE does not induce necroptosis in lung epithelial cells in vitro. Although genetic deletion of RIPK3 or MLKL did not prevent NE-induced apoptosis, the absence of MLKL significantly reduced NE-induced cellular senescence. Mechanistically, we found that after NE is internalized into endosomes, MLKL facilitates its escape into the cytoplasm and subsequent translocation to the nucleus, where it induces DNA damage and senescence. In contrast, MLKL deficiency retains NE within endosomes, promoting its degradation via lysosomal trafficking. Furthermore, Mlkl knockout mice were protected from porcine pancreatic elastase-induced emphysema, highlighting the pathological relevance of this mechanism. Collectively, our findings reveal a novel, necroptosis-independent function of MLKL in regulating intracellular NE trafficking, suggesting a new therapeutic target for protease-driven lung injury in COPD.</p>","PeriodicalId":7655,"journal":{"name":"American Journal of Respiratory Cell and Molecular Biology","volume":" ","pages":"1407-1417"},"PeriodicalIF":5.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832484","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}