Journal of cellular biochemistry最新文献

{"title":"RETRACTION: Silencing of HAS2-AS1 Mediates PI3K/AKT Signaling Pathway to Inhibit Cell Proliferation, Migration, and Invasion in Glioma","authors":"","doi":"10.1002/jcb.30650","DOIUrl":"10.1002/jcb.30650","url":null,"abstract":"<p><b>RETRACTION:</b> Z. Zhao, T. Liang, and S. Feng,<b> </b>“Silencing of HAS2-AS1 Mediates PI3K/AKT Signaling Pathway to Inhibit Cell Proliferation, Migration, and Invasion in Glioma,” <i>Journal of Cellular Biochemistry</i> 120, no. 7 (2019): 11510-11516, https://doi.org/10.1002/jcb.28430.</p><p>The above article, published online on 20 February 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, image elements in Figure 4 were found to have been previously published in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid. The authors have been informed of the decision of retraction but unavailable for a final confirmation.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 11","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30650","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EXPRESSION OF CONCERN: Ap1 Mediates uPA/uPAR Induced FUT4 Expression and Trophoblast Invasion","authors":"","doi":"10.1002/jcb.30657","DOIUrl":"10.1002/jcb.30657","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: Q. Zheng, Y. Yang, X. Cui, D. Zhang, S. Liu, and Q. Yan, “AP1 Mediates uPA/uPAR Induced FUT4 Expression and Trophoblast Invasion,” <i>Journal of Cellular Biochemistry</i> 119, no. 8 (2018): 6442-6451, https://doi.org/10.1002/jcb.26648.</p><p>This Expression of Concern is for the above article, published online on 26 December 2017 in Wiley Online Library (wileyonlinelibrary.com), has been issued by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals, LLC.</p><p>The Expression of Concern has been agreed due to concerns raised by third parties regarding the data presented in the article. Specifically, overlaps have been detected in the invasion assay images between the “uPAR+c-Fos siRNA” and “uPAR+TIIA” groups in Figure 5C. Further investigation by the publisher revealed additional overlaps in the migration assay images between the “uPAR+SP600125” and “uPAR+TIIA” groups in the same figure. The authors explained that these overlaps occurred due to errors during the figure assembly and provided revised images to correct the mistakes. However, the replacement images provided by the authors failed to reproduce the results of the originally published images. Consequently, the journal has decided to issue this Expression of Concern to inform and alert readers.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 11","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30657","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Assay Reveals the Early Setting-Up of Membrane Repair Machinery in Human Skeletal Muscle Cells","authors":"Léna d'Agata,&nbsp;Phoebe Rassinoux,&nbsp;Céline Gounou,&nbsp;Flora Bouvet,&nbsp;Dounia Bouragba,&nbsp;Kamel Mamchaoui,&nbsp;Anthony Bouter","doi":"10.1002/jcb.30662","DOIUrl":"10.1002/jcb.30662","url":null,"abstract":"<p>Defect in membrane repair contributes to the development of muscular dystrophies such as limb girdle muscular dystrophy (LGMD) type R2 or R12. Nevertheless, many other muscular dystrophies may also result from a defect in this process. Identifying these pathologies requires the development of specific methods to inflict sarcolemma damage on a large number of cells and rapidly analyze their response. We adapted a protocol hitherto used to study the behavior of cancer cells to mechanical constraint. This method is based on forcing the passage of cells through a thin needle, which induces shear stress. Due to size considerations, this method requires working with mononuclear muscle cells instead of myotubes or muscle fibers. Although functional sarcolemma repair was thought to be restricted to myotubes and muscle fibers, we show here that 24h-differentiated myoblasts express a complete machinery capable of addressing membrane damage. At this stage, muscle cells do not yet form myotubes, revealing that the membrane repair machinery is set up early throughout the differentiation process. When submitted to the shear-stress assay, these cells were observed to repair membrane damage in a Ca²⁺-dependent manner, as previously reported. We show that this technique is able to identify the absence of membrane resealing in muscle cells from patient suffering from LGMDR2. The proposed technique provides therefore a suitable method for identifying cellular dysregulations in membrane repair of dystrophic human muscle cells.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the Inhibitory Potential of Pregnenolone Sulfate on Pentraxin 3 in Diabetic Kidney Disease: A Molecular Docking and Simulation Study","authors":"Soumik Das,&nbsp;Gnanasambandan Ramanathan","doi":"10.1002/jcb.30661","DOIUrl":"10.1002/jcb.30661","url":null,"abstract":"<div>\u0000 \u0000 <p>Diabetic Kidney Disease (DKD), a frequent consequence of diabetes, has substantial implications for both morbidity and mortality rates, prompting the exploration of new metabolic biomarkers due to limitations in current methods like creatinine and albumin measurements. Pentraxin 3 (PTX3) shows promise for assessing renal inflammation in DKD. This study investigates how DKD metabolites could influence PTX3 expression through molecular docking, ADMET profiling, and dynamic simulation. Network and pathway analyses were conducted to explore metabolite interactions with DKD genes and their contributions to DKD pathogenesis. Thirty-three DKD-associated metabolites were screened, using pentoxifylline (PEN) as a reference. The pharmacokinetic properties of these compounds were evaluated through molecular docking and ADMET profiling. Molecular dynamics simulations over 200 ns assessed the stability of PTX3 (apo), the PRE-PTX3 complex, and PEN-PTX3 across multiple parameters. Cytoscape identified 1082 nodes and 1381 edges linking metabolites with DKD genes. KEGG pathway analysis underscored PTX3's role in inflammation. Molecular docking revealed pregnenolone sulfate (PRE) with the highest binding affinity (−6.25 kcal/mol), followed by hydrocortisone (−6.03 kcal/mol) and 2-arachidonoylglycerol (−5.92 kcal/mol), compared to PEN (−5.35 kcal/mol). ADMET profiling selected PRE for dynamic simulation alongside PEN. Analysis of RMSD, RMSF, RG, SASA, H-bond, PCA, FEL, and MM-PBSA indicated stable complex behavior over time. Our findings suggest that increasing PRE levels could be beneficial in managing DKD, potentially through isolating PRE from fungal sources, synthesizing it as dietary supplements, or enhancing endogenous PRE synthesis within the body.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: MiR-125a Suppresses Malignancy of Multiple Myeloma by Reducing the Deubiquitinase USP5","authors":"","doi":"10.1002/jcb.30628","DOIUrl":"10.1002/jcb.30628","url":null,"abstract":"<p><b>RETRACTION:</b> L. Wu, C. Zhang, M. Chu, Y. Fan, L. Wei, Z. Li, Y. Yao, and W. Zhuang, “MiR-125a Suppresses Malignancy of Multiple Myeloma by Reducing the Deubiquitinase USP5,” <i>Journal of Cellular Biochemistry</i> 121, no. 1 (2020): 642-650, https://doi.org/10.1002/jcb.29309.</p><p>The above article, published online on 26 August 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC.</p><p>The retraction has been agreed upon the authors' request. In the following investigation performed by the journal, several inconsistencies between results presented and experimental methods described were found. Specifically, the experimental methods were found to lack or have unavailable supporting data, making the experiments not comprehensible nor reproducible to readers. Additionally, evidence of editing was found in the Western Blot images presented in the article. The authors were unable to provide comprehensive raw data upon request. Accordingly, the conclusions of this article are considered invalid by the editors.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30628","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Septins: Structural Insights, Functional Dynamics, and Implications in Health and Disease","authors":"Aurosikha Das,&nbsp;Ambarish Kunwar","doi":"10.1002/jcb.30660","DOIUrl":"10.1002/jcb.30660","url":null,"abstract":"<div>\u0000 \u0000 <p>Septins are a class of proteins with diverse and vital roles in cell biology. Structurally, they form hetero-oligomeric complexes and assemble into filaments, contributing to the organization of cells. These filaments act as scaffolds, aiding in processes like membrane remodeling, cytokinesis, and cell motility. Functionally, septins are essential to cell division, playing essential roles in cytokinetic furrow formation and maintaining the structural integrity of the contractile ring. They also regulate membrane trafficking and help organize intracellular organelles. In terms of physiology, septins facilitate cell migration, phagocytosis, and immune responses by maintaining membrane integrity and influencing cytoskeletal dynamics. Septin dysfunction is associated with pathophysiological conditions. Mutations in septin genes have been linked to neurodegenerative diseases, such as hereditary spastic paraplegias, underscoring their significance in neuronal function. Septins also play a role in cancer and infectious diseases, making them potential targets for therapeutic interventions. Septins serve as pivotal components of intracellular signaling networks, engaging with diverse proteins like kinases and phosphatases. By modulating the activity of these molecules, septins regulate vital cellular pathways. This integral role in signaling makes septins central to orchestrating cellular responses to environmental stimuli. This review mainly focuses on the human septins, their structural composition, regulatory functions, and implication in pathophysiological conditions underscores their importance in fundamental cellular biology. Moreover, their potential as therapeutic targets across various diseases further emphasizes their significance.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revisiting Luteolin Against the Mediators of Human Metastatic Colorectal Carcinoma: A Biomolecular Approach","authors":"Ankita Chakraborty,&nbsp;Advaitha Midde,&nbsp;Pritha Chakraborty,&nbsp;Sourin Adhikary,&nbsp;Simran Kumar,&nbsp;Navpreet Arri,&nbsp;Nabarun Chandra Das,&nbsp;Parth Sarthi Sen Gupta,&nbsp;Aditi Banerjee,&nbsp;Suprabhat Mukherjee","doi":"10.1002/jcb.30654","DOIUrl":"10.1002/jcb.30654","url":null,"abstract":"<div>\u0000 \u0000 <p>Metastatic colorectal carcinoma (mCRC) is one of the prevalent subtypes of human cancers and is caused by the alterations of various lifestyle and diet-associated factors. β-catenin, GSK-3β, PI3K-α, AKT1, and NF-κB p50 are known to be the critical regulators of tumorigenesis and immunopathogenesis of mCRC. Unfortunately, current drugs have limited efficacy, side effects and can lead to chemoresistance. Therefore, searching for a nontoxic, efficacious anti-mCRC agent is crucial and of utmost interest. The present study demonstrates the identification of a productive and nontoxic anti-mCRC agent through a five-targets (β-catenin, GSK-3β, PI3K-α, AKT1, and p50)-based and three-tier (binding affinity, pharmacokinetics, and pharmacophore) screening strategy involving a series of 30 phytocompounds having a background of anti-inflammatory/anti-mCRC efficacy alongside 5-fluorouracil (FU), a reference drug. Luteolin (a phyto-flavonoid) was eventually rendered as the most potent and safe phytocompound. This inference was verified through three rounds of validation. Firstly, luteolin was found to be effective against the different mCRC cell lines (HCT-15, HCT-116, DLD-1, and HT-29) without hampering the viability of non-tumorigenic ones (RWPE-1). Secondly, luteolin was found to curtail the clonogenicity of CRC cells, and finally, it also disrupted the formation of colospheroids, a characteristic of metastasis. While studying the mechanistic insights, luteolin was found to inhibit β-catenin activity (a key regulator of mCRC) through direct physical interactions, promoting its degradation by activating GSK3-β and ceasing its activation by inactivating AKT1 and PI3K-α. Luteolin also inhibited p50 activity, which could be useful in mitigating mCRC-associated proinflammatory milieu. In conclusion, our study provides evidence on the efficacy of luteolin against the critical key regulators of immunopathogenesis of mCRC and recommends further studies in animal models to determine the effectiveness efficacy of this natural compound for treating mCRC in the future.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network Pharmacology, Molecular Docking, and Molecular Dynamics Study to Explore the Effect of Resveratrol on Type 2 Diabetes","authors":"Fernando Martínez-Esquivias,&nbsp;Juan Manuel Guzmán-Flores,&nbsp;Andrés Reyes-Chaparro,&nbsp;Sergio Sánchez-Enríquez,&nbsp;Luis Miguel Anaya-Esparza","doi":"10.1002/jcb.30655","DOIUrl":"10.1002/jcb.30655","url":null,"abstract":"<div>\u0000 \u0000 <p>This network pharmacology study represents a significant step in understanding the potential of Resveratrol as an antidiabetic agent and its molecular targets. Targets for Type 2 diabetes were obtained from the MalaCards and DisGeNET databases, while targets for Resveratrol were sourced from the STP and CTD databases. Subsequently, we performed matching to identify common disease-compound targets. The identified genes were analyzed using the ShinGO-0.76.3 database for functional enrichment analysis and KEGG pathway mapping. A protein−protein interaction network was then constructed using Cytoscape software, and hub genes were identified. These hub genes were subjected to molecular docking and dynamic simulations using AutoDock Vina and Gromacs software. According to functional enrichment and KEGG pathway analysis, Resveratrol influences insulin receptors, endoplasmic reticulum functions, and oxidoreductase activity and is involved in the estrogen and HIF-1 pathways. Ten hub genes were identified, including <i>ESR1</i>, <i>PTGS2</i>, <i>SRC</i>, <i>NOS3</i>, <i>MMP9</i>, <i>IGF1R</i>, <i>CYP19A1</i>, <i>MTOR</i>, <i>MMP2,</i> and <i>PIK3CA</i>. The proteins associated with these genes exhibited high interaction with Resveratrol in the molecular docking analysis, and molecular dynamics showed a stable interaction of Resveratrol with ESR1, MMP9, PIK3CA, and PTGS2. In conclusion, our work enhances the understanding of the antidiabetic activity of Resveratrol, which future studies should experimentally corroborate.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of Sigma-2/TMEM97 Involvement in Cholesterol Metabolism","authors":"Martina Parente,&nbsp;Claudia Tonini,&nbsp;Sara Caputo,&nbsp;Marco Fiocchetti,&nbsp;Valentina Pallottini","doi":"10.1002/jcb.30645","DOIUrl":"10.1002/jcb.30645","url":null,"abstract":"<div>\u0000 \u0000 <p>Extensive research has focused on cellular cholesterol and its regulation, primarily due to its crucial physiological roles and its association with numerous diseases resulting from dysregulated homeostasis. Consequently, investigating cholesterol metabolism and the network of regulating proteins remains an ongoing challenge for biomedical research seeking new molecular targets to manage aberrant cholesterol levels in pathologic conditions. There is evidence that Sigma-2/TMEM97 receptor regulates cholesterol metabolism. However, the mechanisms remain incompletely understood to date. Therefore, this study aimed to employ a pharmacological approach based on selective Sigma-2/TMEM97 agonists, rimcazole and siramesine, to uncover the contribution of this receptor to cholesterol homeostasis. Our results indicate that Sigma-2/TMEM97 activation modulates cholesterol uptake by altering key proteins involved in, leading to free cholesterol and neutral lipids accumulation. This sheds light on potential mechanisms implied, contributing a new piece to the intricate puzzle of cholesterol metabolism homeostasis.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repurposing Non-Nucleosidic Reverse Transcriptase Inhibitors (NNRTIs) to Overcome EGFR T790M-Mediated Acquired Resistance in Non-Small Cell Lung Cancer","authors":"Iqrar Ahmad,&nbsp;Harun M. Patel","doi":"10.1002/jcb.30653","DOIUrl":"10.1002/jcb.30653","url":null,"abstract":"<div>\u0000 \u0000 <p>This study investigates the repurposing potential of non-nucleosidic reverse transcriptase inhibitors (NNRTIs), specifically Rilpivirine and Etravirine, as L858R/T790M tyrosine kinase inhibitors for addressing acquired resistance in non-small cell lung cancer (NSCLC). Using in silico molecular docking, Rilpivirine demonstrated a docking score of −7.534 kcal/mol, comparable to established epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) like Osimertinib and WZ4002. Molecular dynamics (MD) simulations over 200 ns revealed the stability of the Rilpivirine–EGFR complex, with RMSD values ranging from 2.5 to 3.5 Å. The in vitro antiproliferative assays showed that Rilpivirine had an IC₅₀ value of 2.3 µM against H1975 cells, while WZ4002 had an IC₅₀ of 0.291 µM, indicating moderate efficacy. Enzymatic assays revealed that Rilpivirine inhibited the double mutant epidermal growth factor receptor tyrosine kinase (EGFR TK) with an IC₅₀ value of 54.22 nM and spared the wild-type EGFR TK with an IC₅₀ of 22.52 nM. These findings suggest Rilpivirine's potential as a therapeutic agent for NSCLC with EGFR L858R/T790M mutations</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}