Nature genetics最新文献

{"title":"A multi-tissue single-cell expression atlas in cattle","authors":"Bo Han, Houcheng Li, Weijie Zheng, Qi Zhang, Ao Chen, Senlin Zhu, Tao Shi, Fei Wang, Dong Zou, Yu Song, Wen Ye, Aixia Du, Yihan Fu, Minghui Jia, Zhonghao Bai, Zhixiang Yuan, Wansheng Liu, Wenbin Tuo, Jayne C. Hope, David E. MacHugh, John F. O’Grady, Ole Madsen, Goutam Sahana, Yonglun Luo, Lin Lin, Congjun Li, Zexi Cai, Bingjie Li, Jinming Huang, Lin Liu, Zhang Zhang, Zhu Ma, Yali Hou, George E. Liu, Yu Jiang, Hui-zeng Sun, Lingzhao Fang, Dongxiao Sun","doi":"10.1038/s41588-025-02329-5","DOIUrl":"https://doi.org/10.1038/s41588-025-02329-5","url":null,"abstract":"<p>Systematic characterization of the molecular states of cells in livestock tissues is essential for understanding the cellular and genetic mechanisms underlying economically and ecologically important physiological traits. Here, as part of the Farm Animal Genotype-Tissue Expression (FarmGTEx) project, we describe a comprehensive reference map including 1,793,854 cells from 59 bovine tissues in calves and adult cattle, spanning both sexes, which reveals intra-tissue and inter-tissue cellular heterogeneity in gene expression, transcription factor regulation and intercellular communication. Integrative analysis with genetic variants that underpin bovine monogenic and complex traits uncovers cell types of relevance, such as spermatocytes, responsible for sperm motility and excitatory neurons for milk fat yield. Comparative analysis reveals similarities in gene expression between cattle and humans, allowing for the detection of relevant cell types to study human complex phenotypes. This Cattle Cell Atlas will serve as a key resource for cattle genetics and genomics, selective breeding and comparative biology.</p>","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"24 1","pages":""},"PeriodicalIF":30.8,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144995748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation influences human centromere positioning and function","authors":"Catalina Salinas-Luypaert, Danilo Dubocanin, Rosa Jooyoung Lee, Lorena Andrade Ruiz, Riccardo Gamba, Marine Grison, Leonid Velikovsky, Annapaola Angrisani, Andrea Scelfo, Yuan Xu, Marie Dumont, Viviana Barra, Therese Wilhelm, Guillaume Velasco, Marialucrezia Losito, René Wardenaar, Claire Francastel, Floris Foijer, Geert J. P. L. Kops, Karen H. Miga, Nicolas Altemose, Daniele Fachinetti","doi":"10.1038/s41588-025-02324-w","DOIUrl":"https://doi.org/10.1038/s41588-025-02324-w","url":null,"abstract":"<p>Maintaining the epigenetic identity of centromeres is essential to prevent genome instability. Centromeres are epigenetically defined by the histone H3 variant CENP-A. Prior work in human centromeres has shown that CENP-A is associated with regions of hypomethylated DNA located within large arrays of hypermethylated repeats, but the functional importance of these DNA methylation (DNAme) patterns remains poorly understood. To address this, we developed tools to perturb centromeric DNAme, revealing that it causally influences CENP-A positioning. We show that rapid loss of methylation results in increased binding of centromeric proteins and alterations in centromere architecture, leading to aneuploidy and reduced cell viability. We also demonstrate that gradual centromeric DNA demethylation prompts a process of cellular adaptation. Altogether, we find that DNAme causally influences CENP-A localization and centromere function, offering mechanistic insights into pathological alterations of centromeric DNAme.</p>","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"33 1","pages":""},"PeriodicalIF":30.8,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144987450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chromatin dynamics of a large-sized genome provides insights into polyphenism and X0 dosage compensation of locusts","authors":"Qing Liu,&nbsp;Feng Jiang,&nbsp;Ran Li,&nbsp;Shanlin Liu,&nbsp;Wenjing Fang,&nbsp;Xiao Li,&nbsp;Ting Hu,&nbsp;Lianyun Feng,&nbsp;Jie Zhang,&nbsp;Zhikang Liu,&nbsp;Jing He,&nbsp;Wei Guo,&nbsp;Xianhui Wang,&nbsp;Zongyi Sun,&nbsp;Jingjing Li,&nbsp;Yunan Gao,&nbsp;Jiacheng Yi,&nbsp;Qiye Li,&nbsp;Xiaoxiao Wang,&nbsp;Liya Wei,&nbsp;Le Kang","doi":"10.1038/s41588-025-02330-y","DOIUrl":"10.1038/s41588-025-02330-y","url":null,"abstract":"Locusts are characterized by a large genome size, polyphenism and an X0 sex determination system. Here we generated chromosome-level genomes for both desert and migratory locusts, as well as a comprehensive chromatin map for the latter. We found that genome enlargement is associated with an increased number of enhancers in expanded intronic regions. To explore the function of expanded enhancers, we identified a distal enhancer that contributes to behavioral differences between solitary and gregarious locusts. In the X0 sex system, H4K16ac enrichment and H4K20me1 depletion maintain balanced X-linked expression in male soma. Notably, the distance-dependent H4K16ac enrichment diminishes gradually in intergenic regions, revealing a special dosage compensation mechanism in large genomes. Furthermore, the distance-dependent H4K16ac results in a lag in the evolution of dosage compensation for the X-linked genes translocated recently from autosomes. Therefore, expanded intronic and intergenic regions shape a distinct chromatin regulation landscape in large genomes. Chromosome-level genome assemblies of migratory and desert locusts, coupled with epigenomic profiling of migratory locusts, reveal chromatin dynamics underlying polyphenism and X-linked dosage compensation following autosomal gene translocation.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2264-2275"},"PeriodicalIF":29.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02330-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144923927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inactivation of β-1,3-glucan synthase-like 5 confers broad-spectrum resistance to Plasmodiophora brassicae pathotypes in cruciferous plants","authors":"Yupo Wu,&nbsp;Chuanji Zhao,&nbsp;Yi Zhang,&nbsp;Cuicui Shen,&nbsp;Yuanyuan Zhang,&nbsp;Xiong Zhang,&nbsp;Lixia Gao,&nbsp;Lingyi Zeng,&nbsp;Qinglin Ke,&nbsp;Li Qin,&nbsp;Fan Liu,&nbsp;Junyan Huang,&nbsp;Li Ren,&nbsp;Yueying Liu,&nbsp;Hongtao Cheng,&nbsp;Chaobo Tong,&nbsp;Qiong Hu,&nbsp;Xiaohui Cheng,&nbsp;Yangdou Wei,&nbsp;Shengyi Liu,&nbsp;Lijiang Liu","doi":"10.1038/s41588-025-02306-y","DOIUrl":"10.1038/s41588-025-02306-y","url":null,"abstract":"Clubroot disease, caused by the obligate intracellular rhizarian protist Plasmodiophora brassicae, is devastating to cruciferous crops worldwide. Widespread field P. brassicae pathotypes frequently overcome the pathotype-specific resistance of modern varieties, posing a challenge for durable control of this disease. Here a genome-wide association study of 3 years of data comprising field clubroot phenotyping of 244 genome-resequenced Brassica napus accessions identified a strong association of β-1,3-glucan synthase-like 5 (GSL5) with clubroot susceptibility. GSL5 was evolutionarily conserved, and inactivation of GSL5 by genome editing in Arabidopsis, B. napus, Brassica rapa and Brassica oleracea conferred broad-spectrum, high-level resistance to P. brassicae pathotypes without yield penalties in B. napus. GSL5 inactivation derepressed the jasmonic acid-mediated immunity during P. brassicae secondary infection, and this immune repression was possibly reinforced through stabilization of GSL5 by a P. brassicae effector, facilitating clubroot susceptibility. Our study provides durable resistance resources for cruciferous clubroot disease control and insights into plant resistance against intracellular eukaryotic phytopathogens. This study implicates GSL5 inactivation in high, broad-spectrum resistance to the clubroot pathogen Plasmodiophora brassicae in Arabidopsis thaliana, Brassica napus, Brassica oleracea and Brassica rapa.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2302-2312"},"PeriodicalIF":29.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02306-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144923928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The future of polygenic risk scores in direct-to-consumer genomics","authors":"Yuhao Sun,&nbsp;John Vines,&nbsp;Albert Tenesa","doi":"10.1038/s41588-025-02313-z","DOIUrl":"10.1038/s41588-025-02313-z","url":null,"abstract":"","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2077-2078"},"PeriodicalIF":29.0,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144910969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Telomere attrition becomes an instrument for clonal selection in aging hematopoiesis and leukemogenesis","authors":"Matthew A. McLoughlin,&nbsp;Sruthi Cheloor Kovilakam,&nbsp;William G. Dunn,&nbsp;Muxin Gu,&nbsp;Jake Tobin,&nbsp;Yash Pershad,&nbsp;Nicholas Williams,&nbsp;Daniel Leongamornlert,&nbsp;Kevin Dawson,&nbsp;Laura Bond,&nbsp;Ludovica Marando,&nbsp;Sean Wen,&nbsp;Rachael Wilson,&nbsp;Giampiero Valenzano,&nbsp;Vasiliki Symeonidou,&nbsp;Justyna Rak,&nbsp;Aristi Damaskou,&nbsp;Malgorzata Gozdecka,&nbsp;Xiaoxuan Liu,&nbsp;Clea Barcena,&nbsp;Josep Nomdedeu,&nbsp;Paul Costeas,&nbsp;Ioannis D. Dimitriou,&nbsp;Edoardo Fiorillo,&nbsp;Valeria Orrù,&nbsp;Jose Guilherme de Almeida,&nbsp;Thomas McKerrell,&nbsp;Matthew Cullen,&nbsp;Irina Mohorianu,&nbsp;Theodora Foukaneli,&nbsp;Alan J. Warren,&nbsp;Chi Wong,&nbsp;George Follows,&nbsp;Anna L. Godfrey,&nbsp;Emma Gudgin,&nbsp;Francesco Cucca,&nbsp;Eoin McKinney,&nbsp;E. Joanna Baxter,&nbsp;Moritz Gerstung,&nbsp;Jonathan Mitchell,&nbsp;Daniel Wiseman,&nbsp;Alexander G. Bick,&nbsp;Margarete Fabre,&nbsp;Pedro M. Quiros,&nbsp;Jyoti Nangalia,&nbsp;Siddhartha Kar,&nbsp;George S. Vassiliou","doi":"10.1038/s41588-025-02296-x","DOIUrl":"10.1038/s41588-025-02296-x","url":null,"abstract":"The mechanisms through which mutations in splicing factor genes drive clonal hematopoiesis (CH) and myeloid malignancies, and their close association with advanced age, remain poorly understood. Here we show that telomere maintenance plays an important role in this phenomenon. First, by studying 454,098 UK Biobank participants, we find that, unlike most CH subtypes, splicing-factor-mutant CH is more common in those with shorter genetically predicted telomeres, as is CH with mutations in PPM1D and the TERT gene promoter. We go on to show that telomere attrition becomes an instrument for clonal selection in advanced age, with splicing factor mutations ‘rescuing’ HSCs from critical telomere shortening. Our findings expose the lifelong influence of telomere maintenance on hematopoiesis and identify a potential shared mechanism through which different splicing factor mutations drive leukemogenesis. Understanding the mechanistic basis of these observations can open new therapeutic avenues against splicing-factor-mutant CH and hematological or other cancers. This study explores the relationship between telomere length and clonal hematopoiesis. Splicing factor and PPM1D gene mutations are more frequent in people with genetically predicted shorter telomere lengths, suggesting that these mutations protect against the consequences of telomere attrition.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2215-2225"},"PeriodicalIF":29.0,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02296-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144910970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mystery of tamoxifen-associated uterine cancer uncovered","authors":"","doi":"10.1038/s41588-025-02316-w","DOIUrl":"10.1038/s41588-025-02316-w","url":null,"abstract":"Tamoxifen is an essential drug in breast cancer therapy. Unlike prevailing models of therapy-related tumorigenesis, tamoxifen acts by directly activating the PI3K pathway, bypassing the need for mutations in one of the most common driver genes in sporadic uterine cancer. These findings open avenues for investigating similar mechanisms in other drugs.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2084-2085"},"PeriodicalIF":29.0,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144906067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cross-biobank generalizability and accuracy of electronic health record-based predictors compared to polygenic scores","authors":"Kira E. Detrois,&nbsp;Tuomo Hartonen,&nbsp;Maris Teder-Laving,&nbsp;Bradley Jermy,&nbsp;Kristi Läll,&nbsp;Zhiyu Yang,&nbsp;Estonian Biobank research team,&nbsp;FinnGen,&nbsp;Reedik Mägi,&nbsp;Samuli Ripatti,&nbsp;Andrea Ganna","doi":"10.1038/s41588-025-02298-9","DOIUrl":"10.1038/s41588-025-02298-9","url":null,"abstract":"Electronic health record (EHR)-based phenotype risk scores (PheRS) leverage individuals’ health trajectories to estimate disease risk, similar to how polygenic scores (PGS) use genetic information. While PGS generalizability has been studied, less is known about PheRS generalizability across healthcare systems and whether PheRS are complementary to PGS. We trained elastic-net-based PheRS to predict the onset of 13 common diseases for 845,929 individuals (age = 32–70 years) from three biobank-based studies in Finland (FinnGen), the UK (UKB) and Estonia (EstB). All PheRS were statistically significantly associated with the diseases of interest and most generalized well without retraining when applied to other studies. PheRS and PGS were only moderately correlated and models including both predictors improved onset prediction compared to PGS alone for 8 of 13 diseases. Our results indicate that EHR-based risk scores can transfer well between EHRs, capture largely independent information from PGS, and provide additive benefits for disease risk prediction. Comparison of electronic health record-based phenotype risk scores (PheRS) and polygenic scores (PGS) across 13 common diseases and three biobank-based studies indicates that PheRS and PGS may provide additive benefits for risk prediction.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2136-2145"},"PeriodicalIF":29.0,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02298-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144906068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Author Correction: Alterations of the CIB2 calcium- and integrin-binding protein cause Usher syndrome type 1J and nonsyndromic deafness DFNB48","authors":"Saima Riazuddin,&nbsp;Inna A. Belyantseva,&nbsp;Arnaud P. J. Giese,&nbsp;Kwanghyuk Lee,&nbsp;Artur A. Indzhykulian,&nbsp;Sri Pratima Nandamuri,&nbsp;Rizwan Yousaf,&nbsp;Ghanshyam P. Sinha,&nbsp;Sue Lee,&nbsp;David Terrell,&nbsp;Rashmi S. Hegde,&nbsp;Rana A. Ali,&nbsp;Saima Anwar,&nbsp;Paula B. Andrade-Elizondo,&nbsp;Asli Sirmaci,&nbsp;Leslie V. Parise,&nbsp;Sulman Basit,&nbsp;Abdul Wali,&nbsp;Muhammad Ayub,&nbsp;Muhammad Ansar,&nbsp;Wasim Ahmad,&nbsp;Shaheen N. Khan,&nbsp;Javed Akram,&nbsp;Mustafa Tekin,&nbsp;Sheikh Riazuddin,&nbsp;Tiffany Cook,&nbsp;Elke K. Buschbeck,&nbsp;Gregory I. Frolenkov,&nbsp;Suzanne M. Leal,&nbsp;Thomas B. Friedman,&nbsp;Zubair M. Ahmed","doi":"10.1038/s41588-025-02332-w","DOIUrl":"10.1038/s41588-025-02332-w","url":null,"abstract":"","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2340-2342"},"PeriodicalIF":29.0,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02332-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ERG-driven prostate cancer initiation is cell-context dependent and requires KMT2A and DOT1L","authors":"Weiran Feng,&nbsp;Erik Ladewig,&nbsp;Matthew Lange,&nbsp;Nazifa Salsabeel,&nbsp;Huiyong Zhao,&nbsp;Young Sun Lee,&nbsp;Anuradha Gopalan,&nbsp;Hanzhi Luo,&nbsp;Wenfei Kang,&nbsp;Ning Fan,&nbsp;Eric Rosiek,&nbsp;Elisa de Stanchina,&nbsp;Yu Chen,&nbsp;Brett S. Carver,&nbsp;Christina S. Leslie,&nbsp;Charles L. Sawyers","doi":"10.1038/s41588-025-02289-w","DOIUrl":"10.1038/s41588-025-02289-w","url":null,"abstract":"Despite the high prevalence of ERG transcription factor translocations in prostate cancer, the mechanism of tumorigenicity remains poorly understood. Using lineage tracing, we find the tumor-initiating activity of ERG resides in a subpopulation of murine basal cells that coexpress luminal genes (BasalLum) and not in the larger population of ERG+ luminal cells. Upon ERG activation, BasalLum cells give rise to highly proliferative intermediate (IM) cells with stem-like features that coexpress basal, luminal, hillock and club marker genes, before transitioning to Krt8+ luminal cells. Transcriptomic analysis of ERG+ human prostate cancers confirms the presence of rare ERG+ BasalLum cells, as well as IM cells whose presence is associated with a worse prognosis. Single-cell analysis revealed a chromatin state in ERG+ IM cells enriched for STAT3 transcription factor binding sites and elevated expression of the KMT2A/MLL1 and DOT1L, all three of which are essential for ERG-driven tumorigenicity in vivo. In addition to providing translational opportunities, this work illustrates how single-cell approaches combined with lineage tracing can identify cancer vulnerabilities not evident from bulk analysis. Lineage tracing in mice identifies a subpopulation of basal cells that express Tmprss2 and Nkx3 as the origin of ERG-driven prostate cancer. Upon expansion, these cells show an enrichment for STAT3 chromatin binding and elevated expression of KMT2A and DOT1L as dependencies for ERG oncogenicity.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 9","pages":"2177-2191"},"PeriodicalIF":29.0,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02289-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}