Cell Regeneration最新文献

{"title":"Advances in the application of human amniotic membrane for tissue repair.","authors":"Jiatong Han, Xinyue Yang, Arooj Khabbir, Chun Hu, Yidan Gao, Xinran Liu, Renping Liu, Yuyang Zhang, Yang Lei","doi":"10.1186/s13619-026-00290-0","DOIUrl":"https://doi.org/10.1186/s13619-026-00290-0","url":null,"abstract":"<p><p>Human amniotic membrane (hAM) is a widely used biomaterial with longstanding utility in ophthalmology and emerging therapeutic promise across orthopaedics, obstetrics and gynaecology, and dermatology. Clinically available biological tissue repair materials primarily encompass autologous, allogeneic, and xenogeneic tissues. However, autologous materials are limited by availability, while allogeneic and xenogeneic tissues often present challenges related to immunocompatibility. As a commonly used allogeneic biomaterial, the hAM is regarded as a highly promising tissue repair material owing to its favourable immunological profile and exceptional tissue-regenerative properties. HAM is the innermost natural barrier of the placenta and possesses unique structural and biological characteristics that facilitate tissue repair and regeneration. This review summarizes recent advances and clinical applications of hAM in orthopaedics, obstetrics and gynaecology, and dermatology, specifically focusing on its roles in promoting tendon repair, alleviating osteoarthritis, repairing endometrial injury, treating diabetic foot ulcer, and enhancing burn wound healing. With the continued development of regenerative medicine, hAM is expected to play an increasingly important role in diverse tissue repair and regenerative medicine applications.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular senescence in skeletal muscle regeneration.","authors":"Xingyuan Liu, Huating Wang","doi":"10.1186/s13619-026-00287-9","DOIUrl":"10.1186/s13619-026-00287-9","url":null,"abstract":"<p><p>Skeletal muscle possesses a remarkable capacity for regeneration, driven by the activation and proliferation of Pax7-positive muscle stem cells within a dynamic niche that includes immune cells, fibro-adipogenic progenitors, endothelial cells, pericytes, and neural elements. Cellular senescence, a stress-induced program featuring stable cell-cycle arrest and the senescence-associated secretory phenotype (SASP), has emerged as a critical yet paradoxical regulator of this process. Accumulating evidence indicates that transient senescence, particularly in FAPs, macrophages, and other niche cells during acute muscle injury, plays a beneficial role in supporting muscle regeneration. These senescent cells promote cellular plasticity, enhance myoblast differentiation, facilitate phagocytic clearance of debris, and modulate inflammation and repair via timely SASP factor secretion. However, conflicting findings suggest that senescent cells exert detrimental effects, impairing regeneration by establishing a sustained pro-inflammatory and pro-fibrotic niche, especially when senescence persists in aged or dystrophic muscle. This review synthesizes the complex and contradictory roles of cellular senescence in skeletal muscle regeneration, underscores the distinction between transient pro-regenerative and persistent deleterious senescence, highlights the importance of cell-type-specific contributions, and emphasizes the need for precise characterization of senescent cell dynamics and fate. Resolving these discrepancies will be critical for developing targeted senotherapeutic strategies to enhance muscle regeneration in aging and degenerative diseases.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MSI1-FTHL17C-iron circuit couples metabolic and epigenetic control of pluripotency in mouse embryonic stem cells.","authors":"Qianyan Li, Yi Li, Jiazhen Han, Liming Cheng, Gufa Lin, Youwei Chen","doi":"10.1186/s13619-026-00288-8","DOIUrl":"10.1186/s13619-026-00288-8","url":null,"abstract":"<p><p>Maintenance of pluripotency in embryonic stem cells (ESCs) requires coordinated integration of transcriptional, metabolic, and epigenetic programs. Here, we identify a post-transcriptional regulatory axis linking the RNA-binding protein Musashi-1 (MSI1) to iron dependent DNA demethylation via the ferritin like gene Fthl17c. Genetic ablation of MSI1 and its short isoform MSI1-C in mESCs induced spontaneous differentiation and was accompanied by downregulation of Fthl17 family genes. Among these, Fthl17c was directly bound and stabilized by MSI1, and its depletion reduced intracellular ferrous iron (Fe²⁺), impaired ten eleven translocation (TET) enzyme activity, and increased global 5-methylcytosine (5mC) levels. Restoration of Fthl17c expression rescued TET activity, reduced DNA methylation, and reinstated pluripotency associated gene expression, whereas extracellular Fe²⁺ supplementation alone was insufficient. In contrast, vitamin C, which preserves redox active Fe²⁺, effectively restored DNA demethylation, highlighting the requirement for bioavailable iron in TET mediated epigenetic regulation. Biochemical and imaging analyses further revealed that FTHL17C interacts with TET1 in the nucleus, supporting a role in facilitating iron dependent catalysis. Together, these findings define an MSI1-FTHL17C-Fe²⁺-TET axis that integrates post transcriptional control of iron homeostasis with epigenetic remodeling to preserve the pluripotent and plastic state of embryonic stem cells.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances in TGF-β signaling: insights into regulation, pathophysiological function, and clinical translation.","authors":"Xiaohua Yan, Junyu Zhang, Carl-Henrik Heldin, Xin-Hua Feng, Ye-Guang Chen","doi":"10.1186/s13619-026-00286-w","DOIUrl":"https://doi.org/10.1186/s13619-026-00286-w","url":null,"abstract":"<p><p>Cytokines from the transforming growth factor-β (TGF-β) superfamily are essential regulators of cell growth, survival, and differentiation, playing a pivotal role in mammalian embryonic development, adult tissue homeostasis, and progression of human diseases. Recently, an international symposium on TGF-β Signaling in Development and Diseases was held in Nanchang, China, from October 21 to 23, 2025. This event showcased the latest advances in TGF-β signaling and its pathophysiological functions. Over ten presentations at the symposium offered new insights on Smad-dependent and non-Smad TGF-β signaling, its spatiotemporal regulation, and multifaceted roles of TGF-β family cytokines in various pathophysiological contexts. The symposium also addressed potential strategies and opportunities for targeting the TGF-β pathway in the treatment of human diseases.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13121644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HUMSCs repair CCl₄-induced chronic liver injury in rats via metabolic regulation.","authors":"Changpeng Xie, Yiming Dong, Xinxin Yin, Jin Zeng, Zhanhai Su, Haiyan Wang, Jing Zhao, Qiong Wu, Panjian Wei, Ziyu Wang, Meng Gu, Xudong Zhang, Xianzong Ma, Yong Deng, Yuanming Pan, Juan An","doi":"10.1186/s13619-026-00282-0","DOIUrl":"10.1186/s13619-026-00282-0","url":null,"abstract":"<p><strong>Background and aims: </strong>To explore the therapeutic effects of human umbilical cord mesenchymal stem cells (HUMSCs) on repairing CCl₄-induced chronic liver injury in rats via intravenous injection and to identify the associated key metabolites.</p><p><strong>Methods: </strong>Cell experiments: THLE-2 cells were divided into blank control, CCl₄-treated, and CCl₄ + Exos groups. Cell viability was assessed using the CCK-8 assay, while levels of AST, ALT, and MDA were determined using commercial kits. Targeted metabolomics analysis was employed to identify differentially expressed metabolites. Transmission electron microscopy (TEM) was used to evaluate mitochondrial morphology, and immunofluorescence staining was performed to examine the colocalization of Exos with mitochondria. Animal experiments: 24 healthy SPF SD rats were randomly divided into healthy, CCl₄, and CCl₄ + HUMSCs groups (n = 8 per group). Serum samples were collected for biochemical detection and targeted metabolomics analyses, while liver tissues underwent histopathological examination. Immunofluorescence staining was employed to monitor HUMSCs enrichment.</p><p><strong>Results: </strong>In the CCl₄ + Exos group, cell viability was significantly restored, and the elevated levels of AST, ALT, and MDA were reversed, while mitochondrial ultrastructure was ameliorated with successful Exos-mitochondria colocalization. Targeted metabolomics confirmed the presence of differentially expressed metabolites exhibiting consistent trends in both cellular and animal models. In the animal study, the CCl₄ group showed significant liver dysfunction and hepatic pathology characterized by hepatocyte steatosis and fibrous tissue hyperplasia. In contrast, the CCl₄ + HUMSCs group demonstrated markedly improved liver function and reduced pathological changes. Biochemical analysis revealed significant differences in ALT, AST, ALB, TBIL, TP, UREA, CR, and UA levels between the CCl₄ + HUMSCs and CCl₄ groups. Serum metabolomics analysis showed that compared with the CCl₄ group, 1,7-Dimethylxanthine and Xanthosine were significantly upregulated, while Succinic Acid, (S)-2-Hydroxybutanoic Acid, oxidized glutathione, and 3'-Sialyllactose were significantly downregulated in the CCl₄ + HUMSCs group.</p><p><strong>Conclusion: </strong>HUMSCs treatment significantly reduced hepatic steatosis and fibrosis compared with the CCl₄ group alone. Metabolomic analysis suggests that the underlying mechanisms may involve upregulation of propanoate metabolism and increased taurochenodeoxycholic acid levels, which warrant further investigation.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12996463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ACSS2-mediated lysine crotonylation attenuates senescence and enhances the therapeutic efficacy of adipose-derived stem cells in inflammatory bowel disease.","authors":"Ming Yuan, Senmao Li, Shaopeng Chen, Minghui Zhu, Runfeng Yu, Junfeng Huang, Guanzhan Liang, Chi Zhang, Xiaowen He, Ping Lan, Xianrui Wu","doi":"10.1186/s13619-026-00285-x","DOIUrl":"10.1186/s13619-026-00285-x","url":null,"abstract":"<p><strong>Background: </strong>Inflammatory bowel disease (IBD) remains a significant clinical challenge with limited curative options. Adipose-derived mesenchymal stem cells (ADSCs) hold therapeutic promise, but their anti-inflammatory efficacy is often compromised by cellular senescence. This study investigates the role of lysine crotonylation (Kcr) in ADSCs senescence and explores its therapeutic potential.</p><p><strong>Methods: </strong>We analyzed Pan-Kcr levels in senescent ADSCs and evaluated the effects of sodium crotonate (NaCr), a crotonyl-CoA precursor, on senescence, proliferation, and anti-inflammatory function. A murine colitis model was used to assess therapeutic efficacy. Molecular mechanisms focusing on ACSS2-mediated Kcr regulation and H3K9 crotonylation (H3K9cr) at the ACSS2 promoter.</p><p><strong>Results: </strong>Senescent ADSCs exhibited a marked decline in Pan-Kcr levels. NaCr treatment ameliorated senescence, enhanced proliferation, and improved anti-inflammatory capacity. ACSS2, a key regulator of Kcr, was downregulated in senescent ADSCs. Moreover, the anti-senescence effect of NaCr depended on ACSS2-mediated crotonylation. NaCr promoted H3K9cr modification at the ACSS2 promoter, forming a positive feedback loop that elevated Kcr levels. Mechanistically, ACSS2-mediated Kcr suppressed the NF-κB pathway to delay ADSCs senescence.</p><p><strong>Conclusion: </strong>Our findings reveal an epigenetic pathway (ACSS2-Kcr-H3K9cr) regulating ADSCs senescence and propose Kcr modulation as a novel strategy to enhance ADSC-based therapy for IBD.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12950121/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lgr5⁺ cells regulate small intestinal morphogenesis before villification.","authors":"Lianzheng Zhao, Yuchen Xie, Wanlu Song, Yonghui Shen, Huidong Liu, Shiwen Luo, Ye-Guang Chen","doi":"10.1186/s13619-026-00284-y","DOIUrl":"10.1186/s13619-026-00284-y","url":null,"abstract":"<p><p>Lgr5 marks both adult intestinal stem cells and embryonic intestinal stem/progenitor cells. However, the stemness properties and physiological roles of embryonic intestinal Lgr5⁺ cells prior to villification (PVLCs) remain largely unknown. In this study, we show that PVLCs in the embryonic small intestine exhibit region-specific stemness, with progressively enhanced stemness potential from the proximal to distal region. Through inducible cell ablation and gene knockout experiments, we demonstrate that PVLCs regulate small intestinal morphogenesis via Hedgehog signaling in a region-dependent manner, with distal morphogenesis being more dependent on this mechanism. This study reveals the stemness and functional roles of PVLCs in the embryonic small intestine prior to villification, highlighting regionalized cellular heterogeneity as a critical determinant of intestinal morphogenesis.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12946557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147289376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FRZB regulates the osteogenic differentiation of periodontal ligament stem cells in an inflammatory microenvironment through Wnt5a-mitochondrial axis.","authors":"Yuanmeng Su, Houpeng Wang, Tao Luo, Junyao Liu, Xiaoping Hu","doi":"10.1186/s13619-026-00283-z","DOIUrl":"10.1186/s13619-026-00283-z","url":null,"abstract":"<p><p>The Wnt signaling pathway critically regulates the osteogenic differentiation in periodontal ligament stem cells (PDLSCs). However, the functional contributions of this pathway under inflammatory conditions remain unclear. This study investigated the effect and underlying mechanisms of the FRZB-Wnt5a-mitochondrial axis on the osteogenic differentiation capacity of PDLSCs under inflammatory conditions. PDLSCs were isolated from healthy teeth and exposed to lipopolysaccharide (LPS) to mimic an inflammatory microenvironment. The Wnt pathway-related molecules were assessed, and the osteogenic differentiation capacity and mitochondrial function of PDLSCs were evaluated. To elucidate its regulatory role, we employed gene transfection to establish an FRZB (Frizzled-Related Protein) overexpression model. Results showed that inflammation significantly impaired osteogenic differentiation and activated Wnt/β-catenin signaling. Mitochondrial dysfunction was also observed, including reduced membrane potential, increased calcium and reactive oxygen species (ROS) levels, suppressed autophagic flux, and altered mitochondrial morphology. Notably, FRZB overexpression partially restored mitochondrial function and the osteogenic differentiation capacity of PDLSCs. These results demonstrated that FRZB serves as a pivotal regulator of osteogenic differentiation in PDLSCs. We found that inflammation downregulates FRZB expression, thereby activating Wnt/β-catenin signaling, which leads to mitochondrial dysfunction and ultimately impairs osteogenesis. These findings reveal a mechanism by which inflammation suppresses osteogenesis in PDLSCs and highlight FRZB as a promising therapeutic target for periodontitis.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":"9"},"PeriodicalIF":4.7,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12881248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MRG15 decline in aged/injured MuSCs hinders regeneration via differentiation defects.","authors":"Zhuoyang Li, Mei Ma, Siyi Shen, Ruisen Ma, Wenqing Kong, Yuting Wu, Qiurong Ding, Hao Ying, Yuying Li","doi":"10.1186/s13619-026-00279-9","DOIUrl":"10.1186/s13619-026-00279-9","url":null,"abstract":"<p><p>Skeletal muscle aging is characterized by a functional decline in muscle stem cells (MuSCs), yet the key regulatory mechanisms driving this deterioration remain poorly understood. By integrating transcriptomic profiles from aged MuSCs with data from C2C12 cells exposed to spaceflight conditions (which mimic an aging-like phenotype), we identified MORF4-related gene on chromosome 15 (MRG15) as a putative epigenetic regulator involved in age-related myogenic decline. Using a MuSC-specific inducible knockout (iKO) mouse model, we found that loss of MRG15 severely compromises myogenic differentiation and muscle regeneration. Subsequent RNA sequencing of iKO MuSCs, combined with ChIP-seq analysis of histone modifications, revealed that MRG15 modulates the chromatin landscape of myogenic genes through interaction with MyoD, thereby facilitating transcriptional activation and differentiation. Our findings establish MRG15 as a critical epigenetic regulator that cooperates with MyoD to orchestrate chromatin remodeling, thereby promoting transcriptional activation of the myogenic program. Dysregulation of MRG15 may underlie impaired muscle regeneration during aging.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":"8"},"PeriodicalIF":4.7,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12831727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146043769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dual recombinase-mediated endothelial cell-specific lineage tracing and ablation.","authors":"Jie Li, Mingjun Zhang, Xiuxiu Liu, Zhenqian Zhang, Mengyang Shi, Wenjuan Pu, Bin Zhou","doi":"10.1186/s13619-026-00280-2","DOIUrl":"10.1186/s13619-026-00280-2","url":null,"abstract":"<p><p>The precise ablation of specific cell lineages is crucial for functional studies in vivo. Conventional methods, like the Cre-dependent iDTR system, are constrained by the off-target effects and variable efficiency of single-recombinase approaches. Here, we present a novel Cdh5-RL-DTRGFP mouse model that requires both Dre and Cre recombinases to activate diphtheria toxin receptor (DTR) and GFP expression specifically in endothelial cells. This dual-recombinase logic ensures tight control over transgene expression. We demonstrate that diphtheria toxin administration in recombined mice leads to efficient endothelial cell ablation, resulting in severe vascular leakage, rapid organ failure, and mortality. The Cdh5-RL-DTRGFP line thus provides a robust and precise platform for the genetic dissection of endothelial cell function in physiological and pathological contexts.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":"7"},"PeriodicalIF":4.7,"publicationDate":"2026-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12830524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146040611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}