生物学最新文献

{"title":"Non-parametric differential methylation analysis characterizes histotype-specific promoter regions in epithelial ovarian cancer.","authors":"Hugo Swenson, Ella Ittner, Lucas Werner, Elisabeth Werner Rönnerman, Szilárd Nemes, Toshima Z Parris, Khalil Helou","doi":"10.1080/15592294.2026.2720990","DOIUrl":"10.1080/15592294.2026.2720990","url":null,"abstract":"<p><p>Epithelial ovarian cancer (EOC) is a heterogenous disease with frequent late-stage diagnosis and high mortality rates, for which no reliable screening tests exist. In recent years, epigenetic biomarkers in the form of DNA methylation in CpG-rich regions have gained increased attention in the scientific community due to their robust nature and accessibility, allowing for diagnosis without the need for invasive surgery. In this study, we investigated the aberrant methylation of promoter regions in early stage EOC through non-parametric methods, with the purpose of characterizing candidate epigenetic biomarkers. The approach was used on a cohort of early stage EOC samples, and results were compared to existing programs for differential methylation. Significant regions were then used to construct a CpG panel for stratifying EOC histotypes through predictive classification in external data. Identified promoter regions were highly reproducible across cohorts, and the constructed CpG model stratified histotypes in external cohorts through predictive classification. Comparisons against other DMP and DMR callers showed a degree of homogeneity between results but also revealed promoter regions that were overlooked despite clear signs of aberrant methylation. Finally, EOC histotypes were found to differ in their methylation distribution types, and results indicate that methods sensitive to non-normally distributed data may be poorly suited to compare groups with different distribution types. The non-parametric approach identified aberrantly methylated promoter regions that were highly reproducible across cohorts. Results from predictive classification indicate that these regions may be useful for the purpose of EOC histotype stratification.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2720990"},"PeriodicalIF":3.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148873483","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":"pgRNA-m⁶A levels associate with HBV replication and liver function.","authors":"Chaoqi Yang, Shanshan Qin, Rui-Huan Gao, Anling Li, Shihui Song, Yidan Zhou, Song-Mei Liu","doi":"10.1080/15592294.2026.2726628","DOIUrl":"10.1080/15592294.2026.2726628","url":null,"abstract":"<p><p>m⁶A modification has been shown to play a role in regulating HBV RNA expression. However, it remains unclear whether the m⁶A levels of HBV pregenomic RNA (pgRNA) are related to HBV replication and liver function. Serum HBV pgRNA-m⁶A levels were determined by T3 DNA ligase assay. HBV DNA copy numbers and gene expression were detected by TaqMan assay and RT-qPCR, respectively. Liver function was evaluated using clinical laboratory indicators. The TET-off stable HBV-producing cell line HepAD38 and targeted pgRNA demethylation by SunTag system (TRADES) were used for the site-specific m⁶A editing. Flow cytometry was used to measure the cytokine levels in the supernatant of cell culture. Serum HBV pgRNA-m⁶A levels were positively correlated with HBV DNA copy number, pgRNA expression and liver function indicators (all <i>p</i> < 0.05). Both pgRNA-m⁶A levels and pgRNA expression were significantly increased in patients with high virus load (HBV DNA > 1.0 × 10⁷ IU/mL). Site-specific demethylation of pgRNA1907-m⁶A significantly reduced HBV DNA, hepatitis B e antigen (HBeAg) and HBV pgRNA, while induced levels of interferon alfa 2 (IFN-α2) and apolipoprotein B mRNA editing enzyme catalytic subunit 3A (APOBEC3A). pgRNA-m⁶A modification of HBV associates with viral replication and liver function indicators. Site-specific m⁶A demethylation of pgRNA provides novel insight into anti-HBV treatment.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2726628"},"PeriodicalIF":3.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13556976/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900392","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":"Bistable wave speed of a diffusive three-species Lotka-Volterra competition model.","authors":"Jia Guo, Binxiang Dai","doi":"10.1080/17513758.2026.2672784","DOIUrl":"10.1080/17513758.2026.2672784","url":null,"abstract":"<p><p>In this paper, we investigate the propagation speed of bistable traveling waves in a diffusive three-species Lotka-Volterra competition model. By constructing a novel pair of upper and lower solutions, we derive sufficient conditions that determine whether the bistable wave speed is positive or negative. These criteria offer a theoretical foundation for predicting the direction of wave propagation in such systems. The validity and applicability of our theoretical results are further confirmed through several numerical examples.</p>","PeriodicalId":48809,"journal":{"name":"Journal of Biological Dynamics","volume":"20 1","pages":"2672784"},"PeriodicalIF":2.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147934614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The behavioural spillover effect: modelling behavioural interdependencies in multi-pathogen dynamics.","authors":"Leah LeJeune, Omar Saucedo, Lauren M Childs, Navid Ghaffarzadegan","doi":"10.1080/17513758.2026.2676366","DOIUrl":"10.1080/17513758.2026.2676366","url":null,"abstract":"<p><p>During the recent pandemic, a rise in COVID-19 cases was followed by a decline in influenza. In the absence of cross-immunity, a potential explanation for the observed pattern is behavioural: non-pharmaceutical interventions (NPIs) designed and promoted for one disease also reduce the spread of others. We study short-term and long-term dynamics of two pathogens where NPIs targeting one pathogen indirectly influence the spread of another - a phenomenon we term <i>behavioural spillover</i>. We examine how perceived risk of and response to one disease substantially alter the spread of other pathogens, revealing how waves of different pathogens emerge over time as a result of behavioural interdependencies and human response. Our analysis identifies the parameter space where two diseases simultaneously co-exist, and where shifts in prevalence occur. Our findings are consistent with observations from the COVID-19 pandemic, where NPIs contributed to significant declines in infections such as influenza, pneumonia, and Lyme disease.</p>","PeriodicalId":48809,"journal":{"name":"Journal of Biological Dynamics","volume":"20 1","pages":"2676366"},"PeriodicalIF":2.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148036638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Linking oxidative stress defense to biofilm architecture: Ohr mediates strain-dependent persistence in <i>Acinetobacter baumannii</i>.","authors":"Rong Yu, Mona Mohamed Al-Shamiri, Sirui Zhang, Pu Li, Cheng Lei, Haiping Liu, Lirui Xue, Kai Luo, Bei Han, Meng Xun, E Yang, Lei Han","doi":"10.1080/21505594.2026.2664989","DOIUrl":"10.1080/21505594.2026.2664989","url":null,"abstract":"<p><p>Biofilm formation is critical for the persistence of <i>Acinetobacter baumannii</i>, yet its directional correlation with antimicrobial resistance remains paradoxical. Here, we confirmed our prior finding that drug-sensitive and multidrug-resistant (MDR) strains employ distinct, temporally regulated biofilm developmental programs: susceptible strains excel at rapid biomass accumulation but undergo early collapse, while MDR strains delay biofilm initiation and optimize for the maintenance and reinforcement of mature biofilms. Transcriptomic profiling identified the organic hydroperoxide resistance protein (Ohr) as a crucial contributor mediating this strain-specific biofilm divergence, with its deletion resulting in severe biofilm defects. Metabolomics analyses further revealed that Ohr maintains biofilm integrity through dual mechanisms: by modulating redox homeostasis and regulating extracellular polymeric substance (EPS) production through control of AdeAB and AdeFG efflux pumps. Moreover, we identified indole-3-lactic acid as a potent biofilm inhibitor. Our findings suggest Ohr as a linchpin in <i>A. baumannii</i> biofilm development, elucidate the basis of temporal phenotypic divergence, and unveil promising therapeutic targets against biofilm-associated infections.</p>","PeriodicalId":23747,"journal":{"name":"Virulence","volume":"17 1","pages":"2664989"},"PeriodicalIF":6.8,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13114124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147782765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein disulphide isomerase protects against ALS/FTD phenotypes associated with cyclin F in zebrafish and cellular models.","authors":"Sina Shadfar, Sonam Parakh, Emma Perri, Cyril Jones Jagaraj, Sara Assar Kashani, Keelin Beyers, Audrey M G Ragagnin, Angela S Laird, Julie D Atkin","doi":"10.1080/13510002.2026.2732775","DOIUrl":"https://doi.org/10.1080/13510002.2026.2732775","url":null,"abstract":"<p><strong>Background: </strong>Mutations in <i>CCNF</i>, encoding cyclin F, cause a small proportion of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) cases. Mutant cyclin F mislocalises from the nucleus to the cytoplasm, impairs the ubiquitin proteasome system, disrupts endoplasmic reticulum (ER) to Golgi transport, and triggers ER stress and apoptosis. Protein disulphide isomerase (PDI), a redox-active ER chaperone of the thioredoxin superfamily, protects against ALS phenotypes induced by mutant SOD1, TDP-43, and FUS, but its activity against mutant cyclin F has not been examined.</p><p><strong>Objectives: </strong>To test whether PDI overexpression prevents the cellular and behavioural phenotypes induced by the ALS/FTD-associated cyclin F^S621G mutation.</p><p><strong>Methods: </strong>Neuro-2a cells were co-transfected with mCherry-tagged wild-type or mutant cyclin F^S621G and V5-tagged PDI or empty vector. Subcellular localisation, XBP-1 and CHOP activation, proteasome reporter (GFPu) accumulation, nuclear morphology, and cleaved caspase-3 immunoreactivity were assessed by confocal microscopy. Transient transgenic zebrafish larvae generated by mRNA co-injection of cyclin F and PDI were assessed by photomotor response at 48 h post-fertilisation.</p><p><strong>Results: </strong>Mutant cyclin F^S621G induced cytoplasmic mislocalisation, ER stress (assessed by XBP-1 and CHOP activation), proteasome dysfunction (indicated by GFPu accumulation), and apoptosis (assessed by nuclear condensation and caspase-3 activation), all of which were significantly attenuated by PDI co-expression. Zebrafish larvae expressing cyclin F^S621G swam significantly shorter distances than uninjected or wildtype controls, and co-expression of PDI restored motor function to near-wildtype levels.</p><p><strong>Conclusion: </strong>PDI protects against ALS/FTD-associated mutant cyclin F in both cellular and <i>in vivo</i> zebrafish models, identifying PDI as a redox-based therapeutic target for <i>CCNF</i>-linked ALS/FTD.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2732775"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modelling and analyzing the transmission dynamics of HIV/AIDS epidemic in China.","authors":"Lili Su, Weide Li, Yumei Ma","doi":"10.1080/17513758.2026.2622439","DOIUrl":"10.1080/17513758.2026.2622439","url":null,"abstract":"<p><p>Based on the considerations of round-trip in the treatment process, this paper presents a mathematical model aimed at studying the dynamic behaviour and epidemiological trends of HIV/AIDS. We first calculate the basic reproduction number <math><msub><mover><mi>R</mi><mo>̅</mo></mover><mn>0</mn></msub></math> and discuss the stability of equilibrium points and the existence of forward bifurcations, validating the theoretical results through numerical simulations. Subsequently, using cumulative HIV/AIDS case data reported in China, we estimate model parameters using the least squares method, achieving a good fit. Furthermore, sensitivity analyses were performed on the model parameters to explain the dependence of the parameters on the infection variables. Finally, the model is applied to evaluate the control effects of treatment coverage at different stages of infection. The results suggest that reducing HIV/AIDS exposure, improving HIV/AIDS screening, promoting infectious disease treatment and increasing disease prevention awareness are the most effective measures to prevent HIV/AIDS infection.</p>","PeriodicalId":48809,"journal":{"name":"Journal of Biological Dynamics","volume":"20 1","pages":"2622439"},"PeriodicalIF":2.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146114724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma proteomics implicates NOX-driven redox imbalance in degenerative cervical myelopathy: findings from the Australian MYelopathy Natural History Registry [AO Spine RECODE-DCM research priority number 5].","authors":"Nashwa Najib, Valerie C Wasinger, Ryan O'Hare Doig, Muhammad Alsherbiny, Stone Sima, Ashish D Diwan","doi":"10.1080/13510002.2026.2649669","DOIUrl":"10.1080/13510002.2026.2649669","url":null,"abstract":"<p><strong>Objectives: </strong>To identify disease-relevant pathways and biomarkers in degenerative cervical myelopathy (DCM) patients from the MYelopathy Natural History Registry.</p><p><strong>Methods: </strong>Shotgun bottom-up proteomics (DCM <i>n</i> = 20; controls <i>n</i> = 20) was performed using LC-MS/MS in DDA mode. Peptides were eluted over 90 min on an in-house manufactured C18 column. Differential proteins were validated using parallel reaction monitoring (PRM) on the same instrument over a 60-min gradient. Bioinformatics was conducted in Skyline and ELISA using Ella™.</p><p><strong>Results: </strong>Discovery proteomics highlighted acute phase and cytokine signalling with STAT1/STAT3 involvement. Targeted assays showed higher IL-6 and IFN-γ in DCM, consistent with a pro-inflammatory state. PRM indicated upregulation of NADPH oxidase complex cytochrome b-245 α-chain (p22 phox or CYBA) and glutathione reductase, alongside downregulation of extracellular glutathione peroxidase, a pattern consistent with NOX-driven reactive oxygen species generation and impaired glutathione redox homeostasis. Together, this provides human plasma evidence of systemic redox imbalance in DCM and nominate a mechanistic framework linking cytokine signalling to oxidative stress via NOX activation and disrupted glutathione cycling.</p><p><strong>Conclusion: </strong>Findings support the feasibility of a plasma 'liquid biopsy' to augment diagnosis and monitoring. The modest cohort size and potential confounding by age and adiposity, absolute quantification, multivariate adjustment, and external validation are warranted to establish specificity and clinical utility.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"31 1","pages":"2649669"},"PeriodicalIF":6.9,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13034710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147575182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dnmt1 associated <i>Gja1</i> promoter methylation changes are implicated in Cx43 remodeling during acute myocardial ischemia/reperfusion injury.","authors":"Yang Liu, Zijun Wang, Youxiao Zhao, Yanyan Ma, Jing Yi, Yingnan Song, Yanqiu Liu, Li An, Zhijun Pan, Hong Gao, Ying Cao","doi":"10.1080/15592294.2026.2694817","DOIUrl":"10.1080/15592294.2026.2694817","url":null,"abstract":"<p><p>DNA methylation has traditionally been regarded as a stable epigenetic modification. However, emerging evidence indicates that oxidative and genotoxic stress can induce locus-specific methylation changes that modulate transcriptional responses. The contribution of such dynamic regulation to cardiac gene expression during myocardial ischemia/reperfusion injury (MIRI) remains incompletely understood. This study investigated whether altered methylation changes within the <i>Gja1</i> promoter region are associated with connexin43 (Cx43) remodeling during MIRI. Male C57BL/6 mice were underwent global hypothermic I/R using a Langendorff-perfused heart model, with or without pretreatment using the DNA methyltransferase inhibitor 5-azacytidine (5-Aza, 3 μg/g body weight, i.p.). <i>Gja1</i> promoter methylation was analyzed by BSP and MSP, while Dnmt1 enrichment was assessed by chromatin immunoprecipitation. Cx43 expression and localization were examined by qRT-PCR, Western blotting, and immunofluorescence, together with electrophysiological and histological analyses. MIRI was associated with Dnmt1 upregulation and nuclear enrichment, accompanied by altered methylation signals at selected CpG sites within the examined <i>Gja1</i> promoter region and transcriptional repression. These changes coincided with reduced Cx43 expression, altered subcellular localization, impaired electrical conduction and increased arrhythmia susceptibility. Pretreatment with 5-Aza partially attenuated <i>Gja1</i> promoter methylation signals and preserved Cx43 expression and localization during subsequent MIRI. These findings support an association between Dnmt1 enrichment, altered<i>Gja1</i>promoter CpG methylation, and Cx43 remodeling under reperfusion stress, suggesting that methylation-related epigenetic regulation may participate in Gja1 transcriptional responses during MIRI. Further temporal and gene-specific validation will be required to establish the kinetics and causal specificity of this pathway.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"21 1","pages":"2694817"},"PeriodicalIF":3.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13336278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367357","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":"Dynamics of an SEIRV endemic model: effects of reinfection.","authors":"Aditya Khan, Lin Wang, Juxin Liu, Momiao Xiong","doi":"10.1080/17513758.2026.2713881","DOIUrl":"https://doi.org/10.1080/17513758.2026.2713881","url":null,"abstract":"<p><p>The threshold interpretation of <math><msub><mi>R</mi><mn>0</mn></msub></math> can fail to describe elimination in epidemic models with imperfect vaccination and reinfection. We study an SEIRV model in which vaccinated individuals remain partially susceptible and recovered individuals may be reinfected. The main novelty is an explicit threshold account of how reinfection can sustain endemic equilibria even when the vaccinated-population reproduction number satisfies <math><mrow><msub><mi>R</mi><mn>0</mn></msub><mo><</mo><mn>1</mn></mrow></math>. We derive the disease-free equilibrium, <math><msub><mi>R</mi><mn>0</mn></msub></math>, and a sufficient condition for convergence to the disease-free state, showing why local disease-free stability and global elimination are distinct. We reduce the endemic-equilibrium problem to a scalar equation and identify a reinfection threshold <math><msubsup><mi>β</mi><mn>2</mn><mo>∗</mo></msubsup></math> determining the local direction of bifurcation at <math><mrow><msub><mi>R</mi><mn>0</mn></msub><mo>=</mo><mn>1</mn></mrow></math>. When <math><mrow><msub><mi>β</mi><mn>2</mn></msub><mo>></mo><msubsup><mi>β</mi><mn>2</mn><mo>∗</mo></msubsup></mrow></math>, we prove a lower critical threshold <math><mrow><msubsup><mi>R</mi><mn>0</mn><mi>C</mi></msubsup><mo><</mo><mn>1</mn></mrow></math> separating elimination from subcritical endemic persistence. We also give an efficient-vaccine approximation and general numerical algorithm for computing <math><msubsup><mi>R</mi><mn>0</mn><mi>C</mi></msubsup></math>. Simulations using an illustrative Omicron-era parameterisation show how these thresholds organise the model dynamics.</p>","PeriodicalId":48809,"journal":{"name":"Journal of Biological Dynamics","volume":"20 1","pages":"2713881"},"PeriodicalIF":2.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148698048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}