Genetics research最新文献

{"title":"Research Hotspots and Emerging Trends in Osteoporosis Epigenetics.","authors":"Maobin Zhou, Honglei Xiao, Ang Li, Hongze Chang, Xiaolong Yang, Feng Cai, Xiaodong Liu","doi":"10.1155/genr/7389868","DOIUrl":"10.1155/genr/7389868","url":null,"abstract":"<p><strong>Background: </strong>Osteoporosis (OP) and its associated complications have emerged as critical public health challenges worldwide, primarily due to the high rates of disability and mortality they cause. In terms of its complex pathogenesis, epigenetic mechanisms play significant roles. Against this backdrop, this study aims to clarify the current research trends and hotspots in OP.</p><p><strong>Methods: </strong>Literature was retrieved from the \"Web of Science,\" \"PubMed,\" and \"Scopus.\" Subsequently, publication counts, country distribution, regional collaborations, and keyword analyses were conducted by using the \"Bibliometrix\" and \"ggplot2\" packages in R Studio. For visualization analysis, institutional cooperation and keyword relationships were examined using \"CiteSpace\" and \"VOSviewer.\"</p><p><strong>Results: </strong>A total of 464 publications were included in this analysis. The five most frequently cited keywords were \"postmenopausal osteoporosis (PMOP),\" \"expression,\" \"mesenchymal stem-cells (MSCs),\" \"osteogenic differentiation,\" and \"differentiation.\" Keyword co-occurrence analysis further identified \"expression,\" \"PMOP,\" and \"MSCs\" as predominant research themes. Moving forward, the findings suggest that future research will focus on elucidating the role of miRNAs in the epigenetic mechanisms of OP and identifying potential therapeutic targets. Regarding global collaboration, China led in international partnerships, particularly with the United States.</p><p><strong>Conclusion: </strong>Epigenetic mechanisms constitute a core regulatory factor in OP, serving as the critical link between genetic predisposition and environmental influences. Emerging research emphasizes the combined analysis of epigenetics and metabolomics, artificial intelligence (AI)-based prediction of epigenetic regulatory networks, and gene editing therapies targeting epigenetic factors. Furthermore, therapeutic strategies-including gene therapy, stem cell-based interventions, and small-molecule targeted compounds-represent pivotal future directions for OP therapeutics.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e7389868"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13189465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971974","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":"Identification and Validation of Mitophagy-Related Biomarkers in Colorectal Cancer: An Integrated Analysis of Single-Cell Transcriptome and Mendelian Randomization.","authors":"Jingyi Zhao, Meng Kong, Sining Wang, Zhixin Cao, Xiangguo Tian","doi":"10.1155/genr/5579542","DOIUrl":"10.1155/genr/5579542","url":null,"abstract":"<p><p>Mitophagy is essential for cancer formation and invasion, but its role in colorectal cancer (CRC) remains unclear. We obtained sequencing data and mitophagy-related genes (MP-RGs) from public databases. Differential expression analysis and weighted gene coexpression network analysis (WGCNA) identified mitophagy-related differentially expressed genes (DE-MPGs). Mendelian randomization (MR) analysis identified candidate genes with genetically supported causal relevance to CRC. Biomarkers were identified using machine learning, receiver operating characteristic (ROC) analysis and expression studies. Single-cell RNA sequencing (scRNA-seq) analyzed biomarker expression profiles in various CRC cell types. Quantitative PCR (qPCR) validated biomarker expression in clinical CRC samples. 147 DE-MPGs were identified. MR analysis revealed seven genes with potential causal contributions to CRC susceptibility. Three genes, SGCE (IVW: OR = 1.00041, p = 0.011), ATP8B2 (IVW: OR = 0.99920, p = 0.042), and RANGAP1 (IVW: OR = 0.99861, p = 0.002), were selected as biomarkers. Immune microenvironment and checkpoint differences were observed between CRC and controls. Biomarker expression varied among cell types. qPCR showed decreased SGCE and ATP8B2 and increased RANGAP1 in CRC. SGCE, ATP8B2, and RANGAP1 can serve as mitophagy-related biomarkers with genetically supported causal relevance to CRC, providing new insights for CRC diagnosis and therapy.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e5579542"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13158581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868093","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":"Correction to \"STOML2 Alleviates Osteoarthritis by Regulating Mitochondrial Energy Metabolism and Oxidative Stress\".","authors":"","doi":"10.1155/genr/9865785","DOIUrl":"10.1155/genr/9865785","url":null,"abstract":"","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e9865785"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13462902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711964","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":"STOML2 Alleviates Osteoarthritis by Regulating Mitochondrial Energy Metabolism and Oxidative Stress.","authors":"Fei Xie, Kun Miao, Hao Wu, Xuejun Wu","doi":"10.1155/genr/9303825","DOIUrl":"10.1155/genr/9303825","url":null,"abstract":"<p><p>Osteoarthritis (OA) is associated with chondrocyte dysfunction and cartilage degeneration, but how mitochondrial homeostasis is maintained during OA progression remains incompletely understood. Here, we show that Stomatin-like protein 2 (STOML2) is downregulated in IL-1β-stimulated chondrocytes and in human OA cartilage. STOML2 depletion impairs oxidative phosphorylation, elevates mitochondrial reactive oxygen species, and promotes chondrocyte senescence and ferroptotic cell death. Mechanistically, STOML2 interacts with the mitochondrial Na⁺/Ca²⁺ exchanger (NCLX) to support mitochondrial Ca²⁺ efflux and metabolic stability. Restoring STOML2 enhances NCLX-dependent Ca²⁺ handling, mitigates mitochondrial Ca²⁺ overload and the glycolytic shift, and improves ATP production. In a rat OA model, intra-articular delivery of STOML2 attenuates cartilage degeneration and reduces inflammatory changes in the joint. Together, these findings identify a STOML2-NCLX axis that safeguards mitochondrial Ca²⁺ homeostasis and chondrocyte viability, suggesting STOML2 as a potential therapeutic target for OA.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e9303825"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13088865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698705","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":"A Novel Mutation of the FBN1 Gene in a Chinese Family With Marfan Syndrome and Unanticipated Discoveries of Family Members.","authors":"Hang Shi, Xuejian Han, Shukai Xing, Yuetong Zhao, Yanyan Wang, Mengtao Yun, Yang Lou, Xiaobo Cui, Baichun Wang, Xiangning Meng","doi":"10.1155/genr/7350256","DOIUrl":"10.1155/genr/7350256","url":null,"abstract":"<p><p>Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder caused by pathogenic variants in the FBN1 gene. Using whole-exome sequencing (WES) in a Chinese MFS family, we identified a novel heterozygous nonsense variant FBN1:c.1415dup;p.(Tyr472Ter), which cosegregates with the disease phenotype and results in protein truncation. Immunohistochemical analysis confirmed markedly reduced fibrillin-1 expression in the aortic wall of variant carriers, and this variant was classified as pathogenic. Unexpectedly, the proband's younger sister harbors three independent pathogenic variants responsible for MFS, familial hypercholesterolemia (FH), and oculopharyngeal muscular dystrophy (OPMD). Further transcript validation and functional assays demonstrated that the LDLR:c.1987+1G > A;p.Arg662_Gly663insAspLys splice-site mutation generates a stable in-frame insertion transcript, impairing protein structure and function. Supported by robust functional evidence and familial cosegregation, this LDLR variant was upgraded from a variant of uncertain significance to pathogenic. We provided formal genetic counseling, long-term clinical follow-up, and multidisciplinary surveillance to all affected family members, with particularly comprehensive management for the proband's sister. This study expands the mutational spectrum of FBN1, establishes functional evidence for the pathogenicity of the LDLR variant, and represents the first report of a pediatric individual carrying three coexisting pathogenic variants for rare diseases. Our findings provide critical insights for molecular diagnosis, genetic counseling, and clinical risk stratification in affected families.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e7350256"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13598443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024170","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":"Prognostic and Immunological Value of CTNNB1 in Pancreatic Adenocarcinoma: A Comprehensive NGS and Multicomponent Analysis.","authors":"ShuYan Liu, Yichen Wu, Hong Zhou, Ying Ding","doi":"10.1155/genr/8700258","DOIUrl":"10.1155/genr/8700258","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;To explore the prognostic value and immunomodulatory role of CTNNB1 in pancreatic ductal adenocarcinoma (PDAC), so as to provide evidence for the diagnosis and individualized treatment of PDAC.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Next-generation sequencing (NGS) was performed to detect 425 cancer-associated genes in PDAC specimens and matched normal pancreatic tissues. Integrative transcriptome analysis based on TCGA, GTEx, and multiple GEO datasets was conducted to identify the differential expression of CTNNB1 between PDAC and normal pancreatic tissues. The Human Protein Atlas (HPA, https://www.proteinatlas.org/) database was used to verify the protein expression and subcellular localization of CTNNB1 in normal pancreatic tissues and pancreatic ductal adenocarcinoma (PDAC) tissues. Single-cell RNA-sequencing and spatial transcriptomic data were further supplemented to delineate its cellular expression landscape. Forest plot, Kaplan-Meier survival analysis, and ROC curve analysis were applied to evaluate the correlations between CTNNB1 expression and prognostic and to verify its prognostic accuracy. The prognostic reliability was further validated using the independent cohort GSE57495. Immune cell infiltration and immune regulatory factors were quantified via TIMER, EPIC, MCPcounter, CIBERSORT, and xCell algorithms, and TMEscore was calculated to predict the responsiveness to immune checkpoint blockade (ICB). Pharmacogenomic datasets including GDSC1, GDSC2, PRISM, and CTRP were utilized to screen optimal candidate drugs for CTNNB1-high PDAC patients.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;CTNNB1 was significantly overexpressed in PDAC compared with normal pancreatic tissues. HPA immunohistochemistry confirmed CTNNB1 shifts from membranous to cytoplasmic localization in PDAC, indicating activated Wnt signaling and concordant dysregulation at mRNA and protein levels. CTNNB1 protein was mainly localized in malignant epithelial cells of PDAC, with elevated expression also observed in partial immune cell subsets by single-cell sequencing and spatial transcriptome assessment. Upregulated CTNNB1 was significantly linked to unfavorable clinical prognosis in PDAC. ROC analysis verified its good diagnostic efficiency for distinguishing PDAC from peritumoral tissues with favorable sensitivity and specificity. CTNNB1 expression was closely correlated with multiple immune biomarker molecules and ICB therapeutic efficacy; patients with low CTNNB1 expression tended to be more responsive to ICB treatment. Pharmacological prediction revealed that PDAC patients with high CTNNB1 expression exhibited enhanced sensitivity to clofibrate and several other small-molecule compounds.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;CTNNB1 may be remarkably effective as a suitable biomarker for the prognosis prediction of PDAC patients and is closely related to the tumor immune microenvironment. Such an association could provide novel thoughts for the therapy tacti","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e8700258"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555821/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911707","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":"Two Novel FBN2 Variants Causing Congenital Contractural Arachnodactyly.","authors":"Juan Zhao, Xiaolan Zhong, Lijun Du, Shaoqing Jiang, Ping Fang, Kexin Ruan, Sujian He, Guanghong Li, Hui Li, Haiming Yuan","doi":"10.1155/genr/8521542","DOIUrl":"10.1155/genr/8521542","url":null,"abstract":"<p><p>Congenital contractural arachnodactyly (CCA) is a rare, autosomal dominant connective tissue disease characterized by arachnodactyly, camptodactyly, multiple joint contractures, tall and slender habitus, crumpled ears, and scoliosis. It shares overlapping features with Marfan syndrome (MFS). This condition is caused by pathogenic variants in the fibrillin 2 (FBN2) gene. Currently, approximately 200 variants in FBN2 have been identified, with most of the variants located in the middle region of the gene (Exons 24-35). Here, we investigated the genetic etiology of CCA in two unrelated Chinese families. Whole-exome sequencing (WES) identified a novel in-frame deletion variant, NM_001999.4: c.4195_4209del, p.Trp1399_Gly1403del, in Exon 32 of FBN2 that was detected in all 3 affected patients but absent in 6 unaffected family members. The other novel missense variant in Exon 27 of FBN2 (c.3521G > A, p.Cys1174Tyr) was identified in an 8-month-old female patient who was diagnosed with CCA. This variant was verified to be inherited from her unaffected mother with low-level mosaicism. Our study expands the mutation spectrum of FBN2 and provides insights into the genotype-phenotype relationship in CCA as well as a foundation for its genetic diagnosis, counseling, and management.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e8521542"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13270415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257673","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":"Prenatal Evaluation of Genetic Abnormalities in Fetuses With Single Umbilical Artery: A Retrospective Cohort Study.","authors":"Yuqin Chen, Xiaoqing Wu, Meiying Cai, Linjuan Su, Xiaorui Xie, Hailong Huang, Rongzhao Zhang, Liangpu Xu","doi":"10.1155/genr/3827416","DOIUrl":"10.1155/genr/3827416","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the genetic factors associated with fetal single umbilical artery (SUA) and concomitant structural anomalies.</p><p><strong>Methods: </strong>A retrospective review was performed on the ultrasound characteristics of 375 SUA fetuses diagnosed by color Doppler ultrasound at Fujian Provincial Maternity and Children's Hospital from February 2010 to February 2022. Single-nucleotide polymorphism (SNP) array and karyotype analysis were performed to evaluate the relationship between chromosomal abnormalities and isolated/nonisolated SUA.</p><p><strong>Results: </strong>Most pregnant women were aged 25-35 years, and 210 were primigravida or nulliparous women with a history of miscarriage. Among 375 fetuses, 101 had isolated SUA (iSUA), 116 had SUA with additional abnormal ultrasound soft markers, and 158 had SUA with congenital structural malformations (predominantly cardiovascular and genitourinary). The chromosomal karyotype abnormality rate was 16.53%, significantly higher in the SUA with multiple system malformation group. SNP-array testing in 152 cases identified 11 cases of chromosome number abnormalities and 13 microdeletions or microduplications. Of the 131 cases with successful follow-up, 77 term live births, 49 elective terminations, 2 preterm births, and 3 deaths. All 29 cases in the SUA with multiple system malformation group were terminated.</p><p><strong>Conclusions: </strong>SUA was most common in pregnant women aged 25-35 and significantly higher in primigravidas and nulliparous women with a history of miscarriage. Female fetuses had a higher SUA incidence than males. Chromosomal abnormality rates increased with associated malformation number and occurred even in iSUA. SNP-array offers a higher resolution in detecting chromosomal microdeletions or microduplication syndromes compared to conventional karyotyping.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e3827416"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501011/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808330","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":"Correction to \"BRCA1 Exon 11 Mutations in Breast Cancer: A Study From Pakistan\".","authors":"","doi":"10.1155/genr/9873852","DOIUrl":"10.1155/genr/9873852","url":null,"abstract":"","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e9873852"},"PeriodicalIF":2.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147432573","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":"CDC20 Regulates the Progression of Clear Cell Renal Cell Carcinoma via the Wnt/β-Catenin Signaling Pathway.","authors":"YuHu Hao, Leizuo Zhao, Yanning Sun, Fan Peng, Tingting Xu, Wentao Deng, Qinghua Xia","doi":"10.1155/genr/1270981","DOIUrl":"10.1155/genr/1270981","url":null,"abstract":"<p><strong>Objective: </strong>To detect the expression level of cell division cycle 20 homolog (CDC20) in clear cell renal cell carcinoma (ccRCC) and to study the biological function of CDC20 in ccRCC.</p><p><strong>Methods: </strong>CDC20 expression levels and clinical significance of ccRCC were determined using the Cancer Genome Atlas (TCGA) database. We detected the expression level of CDC20 in ccRCC with the help of immunohistochemistry (IHC). The effect of CDC20 on the proliferation of renal cancer cells was investigated using EDU and CCK-8 proliferation assays. We used wound healing assays and Transwell assays to determine the effects of CDC20 on renal cancer cell migration and invasion and Wnt signaling pathway agonists in recovery experiments. The mechanism of CDC20 in ccRCC was detected using western blotting. Finally, the effect of CDC20 on renal cancer cells was verified in vivo in a nude mouse xenograft model.</p><p><strong>Results: </strong>Bioinformatics analysis found that CDC20 was upregulated in ccRCC, and its high expression was associated with poor prognosis in kidney renal cell carcinoma (KIRC) patients. In addition, we detected high expression of CDC20 in KIRC tissues, consistent with the results of bioinformatics analysis. Besides, knockdown of CDC20 can inhibit the biological functions of renal cancer cells. The recovery experiment proved that the biological function of the originally inhibited renal cancer cells was restored. In vivo, low expression of CDC20 can inhibit tumor growth.</p><p><strong>Conclusions: </strong>As CDC20 is highly expressed in KIRC tissues, it can be used as both a therapeutic target and a prognostic marker.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2026 1","pages":"e1270981"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13382150/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520223","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}