Mammalian Genome最新文献

{"title":"Alternative splicing dynamics in pig tissues under soybean oil supplementation.","authors":"Fernanda Nery Ciconello, Bruna Pereira Martins da Silva, Milena Lucia Cornejo, Vivian Vezzoni de Almeida, James Eugene Koltes, Aline Silva Mello Cesar","doi":"10.1007/s00335-026-10279-4","DOIUrl":"10.1007/s00335-026-10279-4","url":null,"abstract":"<p><p>Lipid metabolism in pigs is a relevant model for understanding human metabolic regulation due to physiological similarities between the species. Alternative splicing (AS) generates transcript variants that can modulate metabolic pathways in the brain, liver, and skeletal muscle. This study aimed to identify and characterize AS events to explore the dynamics of AS under supplementation of soybean oil in these three tissues. We performed RNA sequencing in 36 pigs fed a soybean-corn diet supplemented with 1.5% or 3.0% soybean oil, using brain, liver, and muscle tissues. Expression matrices and structural annotation were generated for SUPPA analyses. Seven classes of splicing events were identified for each tissue, and only candidate genes exhibiting the highest differential proportion of spliced-in (DPSI) values were considered. Events were detected in both coding regions and 5' UTRs, indicating potential functional consequences. Differential splicing was present in FRMPD1 for brain, G6PC3 for liver, and MED1 and FBXL20 for muscle. These findings suggest that AS may regulate lipid metabolism and that coordinated splicing responses across tissues could also influence the metabolic adaptation and growth performance.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149194686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and validation of a high density SNP array for indigenous Indian pigs.","authors":"Karan Veer Singh, Upasna Sharma, Reena Arora, Sonika Ahlawat, Ramesh Kumar Vijh, N H Mohan","doi":"10.1007/s00335-026-10280-x","DOIUrl":"10.1007/s00335-026-10280-x","url":null,"abstract":"<p><p>The present study describes the design and development of a high density SNP array for indigenous Indian pigs. Using whole-genome resequencing of eight populations, over 61 million variants were discovered and filtered to produce a final panel of 635,974 high quality bi-allelic SNPs with genome-wide coverage. The technical performance of the customized array was validated by genotyping 96 samples from a diverse set of porcine breeds. The genotyping results identified 553,289 markers as Poly High Resolution, while only 0.819% were Mono High Resolution. Average call rate was 99.636% and 91.121% or 579,504 markers were best and recommended. The array effectively captured population-level diversity and resolved genetic structure among Indian pigs. An in silico evaluation using SNPs of the customized array extracted from whole genome sequences distinguished both indigenous and global pig breeds. The developed customized high density SNP array offers substantial opportunities for advancing pig genomics in India. It provides a powerful platform with improved precision for population genetics and admixture analysis in porcine populations.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative bioinformatics and machine learning reveal hub genes and immune signatures bridging type 2 diabetes mellitus, fracture susceptibility, and osteoblast differentiation dysfunction.","authors":"Shulong Sun, Qian Chen, Hua Li, Yujing Cao, Ji Li","doi":"10.1007/s00335-026-10276-7","DOIUrl":"10.1007/s00335-026-10276-7","url":null,"abstract":"<p><p>To investigate the causal relationship between type 2 diabetes mellitus (T2DM) and fracture and identify molecular targets linking T2DM to impaired osteogenesis, we performed two-sample Mendelian randomization (MR) using large-scale GWAS data, followed by integrated bioinformatic and machine learning analyses of T2DM-, fracture-, and osteoblast differentiation-related datasets. Hub genes were identified through WGCNA, differential expression analysis, PPI network analysis, and multiple machine learning algorithms, and further evaluated by GSEA, cross-dataset validation, and immune cell infiltration analysis. In vitro validation was performed in MC3T3-E1 preosteoblasts cultured under normal-glucose, high-glucose, and osmotic-control conditions using Alizarin Red S staining, qRT-PCR, and Western blotting. MR analysis confirmed a positive causal effect of T2DM on fracture risk without evidence of horizontal pleiotropy. A total of 280 overlapping genes were identified, mainly enriched in extracellular matrix organization, ossification, bone remodeling, osteogenic differentiation, and pathways related to the cell cycle and AGE-RAGE signaling. PLK1, CCNA2, and CHEK1 were identified as hub genes and were associated with cell cycle regulation. Cross-dataset validation confirmed their upregulation in T2DM patients, while immune infiltration analysis indicated a predominance of neutrophils. High-glucose exposure markedly impaired osteogenic mineralization in MC3T3-E1 cells and dysregulated PLK1, CCNA2, and CHEK1 expression at both the mRNA and protein levels. Collectively, T2DM may increase fracture risk and impair bone regeneration through dysregulated cell cycle and AGE-RAGE signaling, with PLK1, CCNA2, and CHEK1 representing potential therapeutic targets.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149039615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.","authors":"Danielle Brister, Mariana Zarate-Mendez, Denisa Hathazi, Rita Horvath","doi":"10.1007/s00335-026-10278-5","DOIUrl":"10.1007/s00335-026-10278-5","url":null,"abstract":"<p><p>Mitochondria are essential organelles responsible for cellular energy production and the regulation of key metabolic and signalling pathways. Their function depends on the coordinated expression of both mitochondrial and nuclear genomes, and mitochondrial dysfunction leads to a diverse group of mitochondrial diseases. The nervous system is particularly vulnerable to mitochondrial dysfunction due to the high energetic demands and complex morphology of neurons. Neurons rely heavily on mitochondrial ATP production to support processes such as synaptic transmission, axonal transport, and calcium homeostasis, which are tightly regulated by mitochondrial dynamics, intracellular trafficking, and quality control mechanisms. In mitochondrial diseases, impairment of these processes contributes to a range of neurological manifestations, including epilepsy, stroke-like episodes, Leigh syndrome, ataxia, and peripheral neuropathy. Despite the ubiquitous presence of mitochondria, neuronal vulnerability varies between distinct neuronal populations, reflecting differences in neuronal morphology and metabolic demands. This review summarises key mechanisms underlying neuronal susceptibility in mitochondrial disease and highlights how defects in mitochondrial bioenergetics, dynamics, and transport contribute to characteristic neurological phenotypes. Understanding these mechanisms may provide insights into tissue-specific vulnerability and identify potential therapeutic targets to treat mitochondrial diseases and other neurodegenerative disorders associated with mitochondrial mechanisms.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP38 promotes breast cancer immune evasion and malignant progression by deubiquitinating and stabilizing PD-L1.","authors":"Dongqin Liu, Zijun Yang, Chunrun Qi, Wanqing Jin, Weiwei Shao","doi":"10.1007/s00335-026-10277-6","DOIUrl":"10.1007/s00335-026-10277-6","url":null,"abstract":"<p><p>Breast cancer (BC) represents the most common malignancy among women worldwide. Immune evasion serves as a critical factor for treatment resistance and recurrence metastasis. For USP38, a member within deubiquitinating enzyme family, its expression pattern, biological function, and regulatory mechanism on tumor immune microenvironment in BC lacked systematic investigation. TIMER and UALCAN databases were used to analyze USP38 expression profile. Forty pairs BC tissue and cell lines were collected for validation. Knockdown/overexpression models were constructed. CCK-8, Transwell, co-immunoprecipitation, ubiquitination analysis, CD8 + T cell co-culture, and in vivo tumor‑bearing experiments were employed to explore function and mechanism. USP38 was highly expressed in BC tissues and cells. USP38 knockdown inhibited proliferation, migration, and invasion. Mechanistically, USP38 directly bound PD-L1 and removed its ubiquitination modification, enhancing PD-L1 stability. USP38 knockdown activated CD8 + T cell function, promoted IFN-γ and granzyme B secretion, and enhanced anti-tumor immunity. In vivo USP38 knockdown suppressed tumor growth, whereas PD-L1 overexpression reversed this effect. USP38 stabilizes PD-L1 through deubiquitination, inhibits CD8 + T cell-mediated anti-tumor immunity, and promotes immune evasion and malignant progression in BC.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic analysis of breed composition and population structure in Montana composite cattle.","authors":"Caroline Assis Almeida, Rafael Espigolan, Rachel Santos Bueno Carvalho, Elisângela Chicaroni de Mattos, Victor Breno Pedrosa, Gabriela Giacomini, Fernando Baldi, José Bento Sterman Ferraz","doi":"10.1007/s00335-026-10275-8","DOIUrl":"10.1007/s00335-026-10275-8","url":null,"abstract":"<p><p>The Montana composite was developed in Brazil from crosses between Bos indicus and Bos taurus and structured into four biological types: Zebu (N), adapted taurine (A), British taurine (B), and continental taurine (C). This study aimed to characterize the genetic diversity and population structure of the Montana composite using genomic data through principal component analysis (PCA), admixture analysis, and Wright's F_ST statistic. The PCA revealed a clear separation between Bos indicus and Bos taurus groups, with Montana animals distributed in an intermediate position. The first two principal components explained 69.48% and 3.45% of the total variation, respectively. Supervised admixture estimates indicated a predominance of taurine contribution, with type A accounting for 34.47%, 52.64%, and 51.71% at K = 4, 9, and 11, respectively. Increasing the ancestry resolution refined the contribution of individual founder breeds without changing the overall predominance of taurine ancestry. Comparisons between breed proportions obtained from pedigree and genomic data revealed significant differences, for most biological types and ancestry models (P < 0.001), indicating that realized breed composition deviates from theoretical expectations. Estimates of genetic differentiation confirmed greater divergence between Zebu and taurine groups, as well as reduced distances among populations sharing common ancestry. Specific relationships were identified between the composite and some of its founder breeds, particularly Belmont Red, Senepol, and Tuli. Overall, the results demonstrate that the Montana composite has a complex genomic structure, with genomic ancestry varying according to the resolution adopted and differing from pedigree-based expectations.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550078/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148906633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic convergence of diabetes and prostate cancer: from dysglycemia to tumor microenvironment reprogramming.","authors":"Anirban Goutam Mukherjee, Ankit Kumar Bharti, Deepthi Maria Mathew, Abilash Valsala Gopalakrishnan, S Nishu","doi":"10.1007/s00335-026-10274-9","DOIUrl":"10.1007/s00335-026-10274-9","url":null,"abstract":"<p><p>The relationship between diabetes mellitus and prostate cancer (PC) represents one of the most intriguing paradoxes in cancer epidemiology, with diabetic individuals exhibiting a reduced incidence of PC yet poorer prognosis following diagnosis. This apparent contradiction underscores the need for an integrated understanding of how systemic metabolic dysfunction influences prostate carcinogenesis and disease progression. The present review critically synthesizes contemporary epidemiological, mechanistic, and translational evidence to establish metabolic convergence as a unifying framework linking diabetes-associated metabolic abnormalities with PC biology. Current evidence indicates that chronic dysglycemia, hyperinsulinemia, insulin resistance, and endocrine perturbations orchestrate interconnected intracellular signaling networks involving PI3K-AKT-mTOR, AMPK, AGE-RAGE signaling, oxidative stress, mitochondrial dysfunction, and epigenetic reprogramming, collectively driving metabolic adaptation and tumor evolution. Beyond tumor-intrinsic mechanisms, diabetes profoundly remodels the prostate tumor microenvironment through alterations in stromal metabolism, cancer-associated fibroblast activation, adipocyte-tumor crosstalk, extracellular matrix (ECM) remodeling, hypoxic adaptation, and vascular dysfunction, while simultaneously promoting immunometabolic reprogramming characterized by macrophage polarization, T-cell dysfunction, immune checkpoint activation, and immune evasion. The review further examines the bidirectional interactions between antidiabetic therapies and PC treatment, critically evaluating the translational potential of metformin and emerging glucose-lowering agents within the context of precision metabolic therapeutics. Finally, future directions encompassing biomarker-guided patient stratification, longitudinal metabolic profiling, multi-omics integration, artificial intelligence, and clinically relevant mechanistic validation are discussed as essential components of next-generation precision oncology. Collectively, this review reframes diabetes as an active metabolic determinant of PC rather than a coincidental comorbidity and highlights metabolism-centered precision strategies as promising avenues for improving risk stratification, therapeutic decision-making, and clinical outcomes in diabetes-associated PC.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning identifies ac4C-related prognostic signature and TUBA1C as therapeutic target in COAD.","authors":"Baizhi Zhai, Yuxiang Fan, Heng Ma, Xiaowei Xia, Yi Zhao, Jia Lu, Zhihong Zhang, Yi Wang, Bo Wu, Xia Yuan, Zhihui Yu","doi":"10.1007/s00335-026-10267-8","DOIUrl":"10.1007/s00335-026-10267-8","url":null,"abstract":"<p><p>To explore the role of N4-acetylcytidine (ac4C)-related genes (acRGs) in colon adenocarcinoma (COAD) and identify reliable prognostic biomarkers and potential therapeutic targets. Multi-source transcriptomic datasets (TCGA-COAD, GSE39582, GSE17536) and single-cell RNA-seq data were analyzed. Ten machine learning algorithms were integrated to construct an acRG-based prognostic signature (acRGBS). Immune microenvironment (TME) and genomic profiling were performed, with in vitro functional experiments validating TUBA1C's role. acRGBS, comprising four hub genes (SARAF, CDC42SE2, TSPYL2, TUBA1C), effectively stratified COAD patients into high- and low-risk groups with distinct survival outcomes and was an independent prognostic factor. High-risk patients exhibited increased genomic instability and immunosuppressive TME, while low-risk patients had favorable immunotherapy response. TUBA1C was overexpressed in COAD cells, and its knockdown inhibited proliferation/migration and induced apoptosis. The acRGBS is a robust prognostic tool for COAD, and TUBA1C serves as a candidate therapeutic target, providing new insights for personalized COAD management.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation of miR-141/200c conditional knockout mice from knockout-first, reporter-tagged parent and functional validation of the floxed allele.","authors":"Sanjeev Kumar Yadav, Rashmi Srivastava, Mary-Katherine Cormier, Katie Lowther, Siu-Pok Yee, Rajkumar Verma","doi":"10.1007/s00335-026-10271-y","DOIUrl":"10.1007/s00335-026-10271-y","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) of the miR-200 family-specifically miR-141 and miR-200c-regulate neurogenesis, differentiation, and epithelial-mesenchymal transitions in development. Dysregulation of these miRNAs is associated with several diseases including cancer and stroke. The Mirc13tm1Mtm/Mmjax mouse line, which targets the miR-141/200c cluster, was originally generated and described by Park et al. 2012 as a knockout-first, reporter-tagged insertion with conditional potential (conditional-ready) mouse line. Harnessing its full potential requires a two-step breeding process: breeding with FLP mice to excise the lacZ/neo cassette, then breeding with Cre to delete the floxed miRNA cluster (Park et al. 2012). However, many studies either bypassed removal of the lacZ/Neo cassettes and treated the mouse line as Mirc13 knockouts or bred directly with Cre mouse lines, which could lead to unpredictable recombination and genotypes. Here we show that retention of the lacZ/Neo cassette is associated with reduced expression of the neighboring genes Ptpn6, Phb2 and Atn1 in the olfactory bulb, and that these genes are expressed normally once the cassette is excised. We therefore recommend a validated two-step FLPo-then-Cre breeding plan for this line, together with case-by-case allele validation for other knockout-first, reporter-tagged mouse lines.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long non-coding RNAs link DNA methylation to immune regulatory networks in bovine subclinical mastitis.","authors":"Shraddha Dwivedi, Amit Kumar, Ujjwal Kumar De, Anuj Chauhan, Shivani Khanna, Amritanshu Upadhyay, Diksha Upreti, Bablu Kumar, Girish Kumar Jha, Subodh Kumar","doi":"10.1007/s00335-026-10273-w","DOIUrl":"10.1007/s00335-026-10273-w","url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) are emerging as important regulators of inflammatory and immune signaling, yet their contribution to bovine subclinical mastitis remains poorly defined. Here, we characterized the lncRNA expression landscape associated with disease in milk somatic cells of healthy and subclinical mastitic Vrindavani cattle. We identified 11,403 high-confidence lncRNAs, of which 104 were differentially expressed in subclinical mastitis (adjusted P < 0.05; |log2FC| ≥ 1), with the vast majority upregulated in mastitic samples. Predicted cis- and trans-associated target analyses identified 637 non-redundant genes, and KEGG analysis identified 8 significantly enriched cis-associated pathways and 152 significantly enriched trans-associated pathways (adjusted P < 0.05), predominantly enriched for immune and inflammation-related pathways. These findings prioritized a subset of mastitis-associated lncRNAs for subsequent methylation and interaction-network analyses. A subset of these lncRNAs further overlapped differentially methylated regions (DMRs), suggesting a potential association between lncRNA expression changes and DNA methylation alterations. Integration of lncRNA-miRNA and miRNA-mRNA interactions identified lncRNA-miRNA-mRNA interaction networks involving DMR-associated lncRNAs. Among the prioritized candidates, MSTRG.28878.1 showed overlap with a hypomethylated promoter-associated DMR, increased expression, and multiple connections within the predicted interaction network. Together, these findings identify candidate lncRNAs, methylation-associated loci, and predicted molecular interactions associated with bovine subclinical mastitis and provide a resource for future functional investigation of candidate non-coding RNA-associated mechanisms in disease.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148881019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}