Translational Research最新文献

{"title":"Targeting RIG-I alleviates renal tubular epithelial cells PANoptosis during post-traumatic rhabdomyolysis","authors":"Ning Li ,&nbsp;Yuru Wang ,&nbsp;Ou Qiao ,&nbsp;Herui Hao ,&nbsp;Xinyue Wang ,&nbsp;Zeyu Jiang ,&nbsp;Jiale Chen ,&nbsp;Lu Han ,&nbsp;Zizheng Li ,&nbsp;Zichuan Liu ,&nbsp;Yanhua Gong","doi":"10.1016/j.trsl.2026.02.002","DOIUrl":"10.1016/j.trsl.2026.02.002","url":null,"abstract":"<div><div>Post-traumatic rhabdomyolysis poses a significant threat to human life and health, primarily due to crush syndrome-associated acute kidney injury (CS-AKI). A critical factor contributing to this condition is the destruction of the tubular epithelial barrier, which results from the death of tubular epithelial cells (TECs) caused by myoglobin (Mb) accumulation. In this study, we identified a novel programmed cell death (PCD), termed PANoptosis, occurring in TECs in both <em>in vivo</em> and <em>in vitro</em> CS-AKI models. This process is induced by Mb, with RIG-I serving as the apical sensor molecule for damage-associated molecular patterns (DAMPs). RIG-I transfers Mb insult signals into the cell, where it aggregates with ASC, caspase-1, caspase-8, FADD, RIPK1, and RIPK3 forming the RIG-I PANoptosome. Attenuating RIG-I expression not only disrupts PANoptosome assembly and inhibits PANoptosis but also mitigates TECs damage. Consequently, targeting RIG-I activity may offer a promising avenue for developing novel therapies for post-traumatic rhabdomyolysis and other Mb-associated diseases that trigger cell death and pathology.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"288 ","pages":"Pages 49-63"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146128042","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":"Ligand–receptor hotspots in dendritic–T cell niches expose targets in autoimmunity","authors":"Caio Santos Bonilha","doi":"10.1016/j.trsl.2026.01.006","DOIUrl":"10.1016/j.trsl.2026.01.006","url":null,"abstract":"<div><h3>Background</h3><div>Dendritic cell–T cell (DC–T) co-signalling pathways are central switches directing immunity, tolerance, or evasion. Despite characterisation of known pathways, additional mediators that may contribute uniquely to regulating T-cell responses remain to be defined.</div></div><div><h3>Objective</h3><div>To identify emerging mediators of DC–T communication associated with autoimmune skin inflammation.</div></div><div><h3>Methods</h3><div>Spatial transcriptomic data from atopic dermatitis (AD) and psoriasis (PsO) skin were integrated with single-cell RNA sequencing to resolve ligand–receptor (LR) networks operating at DC–T interaction sites, including regions of DC–T co-occupation, defined as spots simultaneously enriched for DC and T-cell transcriptional signatures. LR-based ranking was used to prioritise canonical and emerging co-signalling mediators linked to autoimmune inflammation, which were subsequently validated in independent spatial and CITE-seq datasets.</div></div><div><h3>Results</h3><div>Top-ranked genes F11R and CDH3 localised to the epidermis, an area enriched in highly interactive DC–T regions, and correlated with PsO severity, establishing a link between spatial communication strength and clinical outcome. Among these, F11R also associated with cytokine signalling in severe PsO, linking its spatial enrichment to enhanced inflammatory states within interaction-rich niches. CITE-seq analysis showed that F11R RNA and protein expression correlate in PsO patients, with no upregulation observed in circulating DCs or T cells. In contrast, both F11R and co-signalling molecules were elevated in the arthritic form of the disease, characterised by systemic immune activation.</div></div><div><h3>Conclusion</h3><div>This study establishes a spatial framework for identifying immune communication mediators and highlight F11R as a potential target linked to autoimmune skin inflammation severity.</div></div><div><h3>Capsule summary</h3><div>Mapping dendritic–T cell communication in psoriasis identifies F11R as a spatially enriched signature associated with disease severity, offering insight into local immune amplification and highlighting potential targets for precision modulation of autoimmune inflammation.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"288 ","pages":"Pages 21-32"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146081012","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":"Targeting lipid metabolism in CAFs: A therapeutic opportunity in solid tumors","authors":"Qi Ai ,&nbsp;Bin Wang ,&nbsp;Wei Zhang ,&nbsp;Xin-Yun Xu","doi":"10.1016/j.trsl.2026.02.003","DOIUrl":"10.1016/j.trsl.2026.02.003","url":null,"abstract":"<div><div>Cancer-associated fibroblasts (CAFs), representing the predominant stromal cell population within the solid tumor microenvironment (TME), are thought to play a significant role in facilitating tumorigenesis and progression. Nonetheless, recent experimental efforts to eradicate CAFs in solid tumors have inadvertently resulted in tumor progression, potentially due to the tumor-suppressive effects exhibited by specific CAF subtypes. Therefore, strategies that selectively target pro-tumorigenic CAFs may yield more favorable outcomes. Emerging evidence indicates that CAFs are instrumental in reprogramming lipid metabolism within TME, fostering a high-fat, immunosuppressive environment. To adapt to the hypoxic and nutrient-limited conditions of TME, cancer cells alter their metabolic processes, which subsequently influences the behavior of CAFs. The variability among CAF populations affects the metabolic pathways of cancer cells and neighboring immune cells. Despite the importance of these interactions, the discussion regarding lipid metabolism crosstalk between CAFs and the TME remains insufficiently explored in the literature. As a result, this study systematically reviews the various origins and heterogeneity of CAFs and closely investigates their roles in lipid metabolism reprogramming within the TME. Additionally, we analyze the metabolic interactions between CAFs and different components of the TME in solid tumors. Ultimately, we discuss potential therapeutic strategies and the challenges of targeting CAF lipid metabolism.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"288 ","pages":"Pages 33-48"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146127707","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":"Author Guidelines","authors":"","doi":"10.1016/S1931-5244(26)00039-3","DOIUrl":"10.1016/S1931-5244(26)00039-3","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"288 ","pages":"Pages iii-iv"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147399639","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":"Information for Readers","authors":"","doi":"10.1016/S1931-5244(26)00040-X","DOIUrl":"10.1016/S1931-5244(26)00040-X","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"288 ","pages":"Page IBC"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147399641","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":"Integrating plasma proteomics and cytokine profiles identifies immunopathogenic biomarkers for early acute-stage ANE in children","authors":"Chaonan Fan ,&nbsp;Zhihong Song ,&nbsp;Kechun Li ,&nbsp;Fei Li ,&nbsp;Guangyuan Zhao ,&nbsp;Feng Huo ,&nbsp;Jing He ,&nbsp;Danqun Jin ,&nbsp;Yufeng Huo ,&nbsp;Huaili Wang ,&nbsp;Zheng Li ,&nbsp;Quan Wang ,&nbsp;Suyun Qian","doi":"10.1016/j.trsl.2026.02.001","DOIUrl":"10.1016/j.trsl.2026.02.001","url":null,"abstract":"<div><div>Acute necrotizing encephalopathy (ANE) in children is a critical condition characterized by rapid progression, high mortality rates and potentially cytokine storm imvolvement. Early-stage ANE lacks distinctive clinical features, and its initial symptoms resemble those of febrile seizures (FS) despite differing outcomes. In this study, we utilized FS as a control to identify plasma biomarkers associated with the cytokine storm in ANE through plasma proteomic analysis. We identified 398 differentially expressed proteins in ANE patients, including 345 upregulated and 53 downregulated proteins, which were enriched in biological pathways such as antigen processing and presentation, cell chemotaxis, immune responses, metabolism, and cell matrix adhesion. Using weighted gene co-expression network analysis (WGCNA), we further identified protein modules and hub proteins related to the cytokine storm and ultimately selected eight key proteins (APOE, GAPDH, TPI1, SPP1, ENO1, COL1A1, LUM, and A2M) as immunopathogenic biomarkers. These findings were validated in an independent cohort using targeted quantitative proteomics, with ROC analysis demonstrating their diagnostic potential. This study provides a foundation for early ANE diagnosis and highlights promising targets for therapeutic intervention.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"288 ","pages":"Pages 64-74"},"PeriodicalIF":5.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146145122","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":"Predicting exercise pulmonary hypertension: the right-net machine learning model a pilot study","authors":"Francesco Ferrara ,&nbsp;Rossana Castaldo ,&nbsp;Luna Gargani ,&nbsp;Nicola Benjamin ,&nbsp;Andreina Carbone ,&nbsp;Erberto Carluccio ,&nbsp;Antonio Cittadini ,&nbsp;Veronica Codullo ,&nbsp;Anna D’Agostino ,&nbsp;Michele D’Alto ,&nbsp;Ekkehard Grünig ,&nbsp;Alessandra Maria Esposito ,&nbsp;Giovanni Esposito ,&nbsp;Stefano Ghio ,&nbsp;Jaroslaw D. Kasprzak ,&nbsp;Graziella Lacava ,&nbsp;Alberto Maria Marra ,&nbsp;Marco Matucci-Cerinic ,&nbsp;Antonella Moreo ,&nbsp;Eugenio Picano ,&nbsp;Monica Franzese","doi":"10.1016/j.trsl.2025.12.007","DOIUrl":"10.1016/j.trsl.2025.12.007","url":null,"abstract":"<div><h3>Background</h3><div>Exercise-transthoracic Doppler echocardiography (Ex-TTE) determination of mean pulmonary arterial pressure (mPAP)/cardiac output (CO) slope may offer key diagnostic and prognostic information in cardiorespiratory diseases. However, its applicability and reliability in routine clinical practice remain to be established. Herein, the aim of the present study was to apply a machine learning (ML) model to predict abnormal exercise TTE-derived mPAP/CO slope (&gt;3 mmHg/L·min) in individuals at risk of pulmonary hypertension (PH), based only on clinical and resting TTE parameters.</div></div><div><h3>Methods</h3><div>The study population (221 healthy adults and 196 patients with connective tissue disease) was grouped according to mPAP/CO slope ≤3 vs. &gt;3 mmHg/L·min (<em>n</em> = 222 and <em>n</em> = 195, respectively). Three different ML models (Elastic Net-Regularized Generalized Linear Model, Classification and Regression Tree, LogitBoost) were trained on resting clinical and TTE parameters to predict mPAP/CO slope &gt;3 mmHg/L·min. Data were split into training/test sets to evaluate performance. The model with the highest area under the curve (AUC) on the test set was selected.</div></div><div><h3>Results</h3><div>The Elastic Net model achieved the best performance (AUC=0.92). Lower tricuspid annular plane systolic excursion/systolic PAP ratio, female sex, and smaller left ventricular outflow tract diameter were the key features predicting TTE-derived mPAP/CO slope &gt;3 mmHg/L·min.</div></div><div><h3>Conclusions</h3><div>An ML algorithm using resting clinical and TTE parameters can effectively predict exercise TTE-derived mPAP/CO slope &gt;3 mmHg/L·min, supporting its use as a noninvasive tool to identify individuals at risk of exercise PH.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"287 ","pages":"Pages 12-21"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890849","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":"B-cell activation underpins Rituximab response in focal segmental glomerulosclerosis","authors":"Liangjian Lu ,&nbsp;Chang Yien Chan ,&nbsp;Mya Than ,&nbsp;Sharon Teo ,&nbsp;Perry YW Lau ,&nbsp;Kong-Peng Lam ,&nbsp;Kar Hui Ng ,&nbsp;Hui Kim Yap","doi":"10.1016/j.trsl.2026.01.002","DOIUrl":"10.1016/j.trsl.2026.01.002","url":null,"abstract":"<div><div>The pathogenesis of primary focal segmental glomerulosclerosis (FSGS) is incompletely understood, and outcomes remain poor. Some patients respond to Rituximab, especially patients who have hyporesponsive T-cells, but the underlying mechanism is unknown. This study aimed to investigate the association between B-cell activation and T-cell hypo-responsiveness as well as Rituximab response. A cohort of 33 patients with childhood-onset FSGS receiving Rituximab were recruited. T-cell hypo-responsiveness was defined as stimulated T-cell IFNγ &lt;2.5%, and B-cell activation was characterized by CD80 expression and cytokine production. T-cell hypo-responsiveness was associated with Rituximab response (OR: 5.4 (95% CI: 1.2-25), <em>p</em> = 0.028). Compared to T-cell normo-responsive patients, T-cell hypo-responsive patients had elevated activated CD19+CD80+ <em>B</em>-cells (16% (IQR 6-25) vs 5% (IQR: 1-9), <em>p</em> = 0.009), and upregulation in resting B-cell cytokine production (15/27 cytokines, <em>p</em> &lt; 0.05). Rituximab selectively restored T-cell responsiveness and abolished elevated B-cell CD80 expression and resting cytokine production in these patients, although nascent B-cell activation could still be detected on <em>in vitro</em> stimulation (6/27 cytokines, <em>p</em> &lt; 0.05). Resting B-cell culture supernatants from patients with hypo-responsive T-cells (<em>p</em> = 0.02) but not normo-responsive T-cells were able to induce cytoskeletal rearrangements in cultured podocytes. Together with T-cell responsiveness, resting B-cell cytokine production was able to strongly predict Rituximab response (AUC 0.922±0.077, <em>p</em> = 0.002), and also the duration of Rituximab response (AUC 0.958±0.062, <em>p</em> = 0.019). Rituximab response in childhood-onset FSGS occurs in a subgroup of patients with B-cell mediated disease characterized by B-cell activation and the production of podocyte damaging factors. Resting B-cell cytokine production can predict Rituximab response, and if it will be long-lasting.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"287 ","pages":"Pages 1-11"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145936872","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":"Inhibiting CCR3 expands cancer stem cells via c-Myc–NTSR1 axis and associates with tumor innervation features","authors":"Ta-Jung Peng ,&nbsp;Wei-Lun Hwang ,&nbsp;Wan-Hsuan Sun ,&nbsp;Shye-Jye Tang ,&nbsp;Kuang-Hui Sun","doi":"10.1016/j.trsl.2025.12.005","DOIUrl":"10.1016/j.trsl.2025.12.005","url":null,"abstract":"<div><div>Cancer stem cells (CSCs) drive intra-tumor heterogeneity, therapy resistance, and relapse. Chemokines regulate cancer stemness via intercellular signaling within the tumor microenvironment. However, the role and clinical relevance of CCR3 in tumor subpopulations remain unexplored. In this study, we enriched CSCs by serum-free spheroid culture as spheroid-derived CSCs (SDCSCs). Cell proliferation, clonogenicity, migration/invasion, tumorsphere formation, chemo-drug resistance, in vivo tumorigenicity, signaling activity, and transcriptomic landscape were characterized. TCGA databases were analyzed for clinical relevance. We found that CCR3 silencing increased self-renewal capability, stemness markers expression, chemoresistance, and <em>in vivo</em> tumorigenicity in SDCSCs; however, it inhibited proliferation, colony formation, and invasion in parental cancer cells. Transcriptomic analysis revealed that CCR3 silencing induced pro-tumoral features in SDCSCs, while it resulted in anti-proliferative and anti-invasive profiles in parental cancer cells by oppositely regulating oncogenic signaling, including c-Myc, KRAS, mTORC, and HIF pathways. In SDCSCs, CCR3 silencing induced c-Myc nuclear expression and transcriptional activation, leading to NTSR1 upregulation and enhanced cancer stemness, which was hindered by a c-Myc inhibitor (10058-F4). Clinically, tumors with low CCR3 expression exhibited a transcriptomic landscape with enhanced cell growth and suppressed immune surveillance, accompanied by activated stemness-related signalings and tumor innervation signatures. High NTSR1 expression further exacerbated the poorer survival in patients with low CCR3 expression. In summary, CCR3 inhibition elicits divergent functional and transcriptomic responses in tumor subpopulations and is associated with stemness- and innervation-related signatures that predict poor prognosis. Combined targeting of CCR3 and the c-Myc–NTSR1 axis may eliminate CSCs.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"287 ","pages":"Pages 55-68"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145835806","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":"Neutrophil extracellular traps exacerbate endothelial tight junction dysfunction via the Wnt7a/β-catenin/HDAC5 pathway in sepsis-associated lung injury","authors":"Qianya Hong ,&nbsp;Shuainan Zhu ,&nbsp;Chenning Li ,&nbsp;Heyang Sun ,&nbsp;Zhenzhen Zhan ,&nbsp;Hao Zhang ,&nbsp;Kefang Guo","doi":"10.1016/j.trsl.2026.01.001","DOIUrl":"10.1016/j.trsl.2026.01.001","url":null,"abstract":"<div><div>Sepsis is a complicated clinical disease caused by an infection-related host response, which results in acute organ dysfunction and a high mortality risk. Among the affected organs, the lungs are particularly susceptible to sepsis. Sepsis-induced acute lung injury (SI-ALI) is a common and severe complication observed among septic patients. Neutrophil extracellular traps (NETs) serve a significant role in immune and inflammatory regulation. Our previous studies have shown a close association between NETs and SI-ALI. However, the mechanism by which NETs mediate the interaction between endothelial cell (EC) barrier integrity and inflammatory responses remains incompletely understood. By reanalyzing our RNA-seq data, we discovered that NET-stimulated HUVECs had an increased cell adhesion molecules pathway, and the differentially expressed genes Wnt7a, HDAC5, and Claudin-5 were screened out. The relationships between differentially expressed genes were further established by STRING analysis. The expression levels of Claudin-5 and Wnt7a/β-catenin/HDAC5 signaling pathway proteins were evaluated by quantitative PCR (qPCR), western blotting, and immunofluorescence staining. At the same time, a cecal ligation and puncture (CLP) model was used to induce sepsis in mice to investigate the function of NETs in vivo. In our research, we demonstrated that NETs activate HDAC5 gene expression through the Wnt7a/β-catenin signaling activation, which subsequently downregulated the expression of tight junction (TJ) proteins, including Claudin-5, ZO-1, and Occludin. This led to impaired barrier function in lung microvascular endothelial cells and worsened the prognosis in a murine model of SI-ALI. Moreover, the NETs disruption and Wnt7a or HDAC5 inhibition mitigated the degradation of tight junction proteins in endothelial cells and improved outcomes in septic mice. In conclusion, our findings indicate that NETs contribute to lung endothelial barrier dysfunction via the Wnt7a/β-catenin/HDAC5 axis during the progression of SI-ALI.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"287 ","pages":"Pages 22-37"},"PeriodicalIF":5.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145936953","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}