Human Gene最新文献

{"title":"Corrigendum to ‘Dysregulated of the FAM138E and CLRN1-AS1 lncRNAs could be diagnosis biomarkers in colorectal cancer’ <Human Gene 39 (2024) 201249>","authors":"Zahra Karimi ,&nbsp;Nastaran Asghari Moghaddam ,&nbsp;Maryam Yousefi ,&nbsp;Mohammad Abdolvand ,&nbsp;Atefeh Zamani ,&nbsp;Nasrin Fatahi Dolatabadi ,&nbsp;Maryam Peymani","doi":"10.1016/j.humgen.2025.201496","DOIUrl":"10.1016/j.humgen.2025.201496","url":null,"abstract":"","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201496"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145568668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomic meta-analysis of sarcoidosis peripheral blood using STARGEO identifies immune signatures and potential biomarkers","authors":"Maya Hammonds ,&nbsp;Sarah Voskamp ,&nbsp;Martha Londoni ,&nbsp;Peter Wearden ,&nbsp;Jennifer Nelson","doi":"10.1016/j.humgen.2025.201460","DOIUrl":"10.1016/j.humgen.2025.201460","url":null,"abstract":"<div><div>Over 90 % of sarcoidosis patients have pulmonary and mediastinal involvement, and late-stage disease may necessitate heart or lung transplantation. This study investigated the molecular mechanisms underlying sarcoidosis, a complex inflammatory disease, by analyzing differential gene expression patterns in peripheral blood samples. The Search Tag Analyze Resource for NCBI's Gene Expression Omnibus (STARGEO) platform was utilized to identify 218 sarcoidosis and 271 non-sarcoidosis peripheral blood samples. iPathwayGuide identified 639 genes with significant differential expression between sarcoidosis and control samples. The most upregulated genes were FCGR1CP, FCGR1B, PANDAR, DEFA1B, ANKRD22, and CARD17. Upstream regulators showing significant activation included IRF9, STAT2, IFNβ1, IFNG, and IRF7, which are largely involved in inflammatory responses. The top differentially expressed pathways were NOD-like receptor signaling, HSV-1 infection, Influenza A, COVID-19, and the intestinal immune network for IgA production. Differentially expressed genes and pathways play a large role in the immune system's response and regulation. These findings support the known involvement of specific immune responses in the pathogenesis of sarcoidosis. Notably, pathways upregulated in the immune response against several common viruses are also activated in sarcoidosis. The identified differentially expressed genes may serve as potential therapeutic targets, warranting further investigation.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201460"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144887347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of a novel m6A reader CSTF2 amplification and overexpression in head and neck cancer development","authors":"Paramasivam Arumugam ,&nbsp;Chandra Pandi ,&nbsp;Vijayashree Priyadharsini Jayaseelan","doi":"10.1016/j.humgen.2025.201473","DOIUrl":"10.1016/j.humgen.2025.201473","url":null,"abstract":"<div><h3>Objective</h3><div>This study examines the oncogenic role of cleavage stimulation factor subunit 2 (CSTF2), a newly identified N6-methyladenosine (m6A)-binding protein in the pathogenesis of head and neck squamous cell carcinoma (HNSCC). We also explored its amplification-driven overexpression, its prognostic significance, and its mechanistic contributions to tumor aggressiveness.</div></div><div><h3>Method</h3><div>A dataset of patients with HNSCC was used from the Cancer Genome Atlas (TCGA), which included information on clinical characteristics. Moreover, mRNA and protein expression data of CSTF2 were obtained from the Human Protein Atlas (HPA) database. Additionally, <em>CSTF2</em> mRNA levels were validated in an independent cohort of HNSCC patient tissues and cell lines using real-time PCR. The prognostic significance of <em>CSTF2</em> was evaluated using Kaplan-Meier survival plots. Additionally, protein-protein interaction networks of CSTF2 were established using the GeneMANIA database, and functional enrichment analysis was performed with Metascape.</div></div><div><h3>Result</h3><div>The study demonstrated that the <em>CSTF2</em> gene was significantly amplified, which correlated with elevated mRNA expression. Moreover, independent cohort analysis confirmed that <em>CSTF2</em> was overexpressed in HNSCC tissues and cell lines compared to non-tumorous tissues and normal cells. In addition, protein levels were markedly higher in HNSCC tissues, and elevated <em>CSTF2</em> mRNA expression was associated with poorer overall survival. Functional enrichment analysis showed that CSTF2 is involved in regulating oncogenic processes and the progression of HNSCC.</div></div><div><h3>Conclusion</h3><div>These data indicate that the <em>CSTF2</em> gene is amplified and overexpressed in HNSCC, indicating that this gene could be a significant prognostic marker and a potential therapeutic target for HNSCC.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201473"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145044157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-507 and miR-665 as central MicroRNA regulators in the ceRNA network of adrenocortical carcinoma: A systems biology approach","authors":"Javad Omidi","doi":"10.1016/j.humgen.2025.201498","DOIUrl":"10.1016/j.humgen.2025.201498","url":null,"abstract":"<div><div>MicroRNAs (miRNAs) are key regulators of post-transcriptional gene expression and have been increasingly implicated in the pathogenesis of rare malignancies such as adrenocortical carcinoma (ACC). Here, a systems biology approach was employed to construct and analyze context-specific competing endogenous RNA (ceRNA) networks using transcriptomic profiles from ACC tumors (TCGA) and normal adrenal tissues obtained from both GTEx 2025 and miRNATissueAtlas 2025 datasets, leveraging a novel integrative analytical framework specifically developed in this study. Comparative network topology revealed extensive regulatory rewiring in tumors, with miR-507 and miR-665 emerging as tumor-specific central miRNAs. While miR-507 was significantly upregulated and associated with favorable patient survival, miR-665 was downregulated and displayed radiation-sensitive expression dynamics. Target gene prediction and correlation analyses identified distinct sets of oncogenic and tumor-suppressive genes regulated by each miRNA. Functional enrichment and PPI network analysis indicated that miR-507 targets are strongly enriched in cell cycle, mitotic checkpoint, and chromosomal stability pathways, whereas miR-665 influences more context-dependent immune and signaling mechanisms. These findings support the prognostic and therapeutic potential of miR-507 in ACC and suggest a radiotherapy-modulated regulatory role for miR-665. This study demonstrates the power of multi-source transcriptomic integration for discovering functional miRNA hubs in rare endocrine cancers.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201498"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145362204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin-synthesized silver nanoparticles modulate inflammatory and thyroid-related gene expression in pubertal rats exposed to chlorpyrifos","authors":"Mohammad Hossein Gorji Dizabadi ,&nbsp;Maryam Rezaei ,&nbsp;Tahereh Farkhondeh ,&nbsp;Saeed Samargahndian ,&nbsp;Zahra Khademi ,&nbsp;Atena Mansouri","doi":"10.1016/j.humgen.2025.201503","DOIUrl":"10.1016/j.humgen.2025.201503","url":null,"abstract":"<div><h3>Introduction</h3><div>Green synthesis is a preferred method for producing silver nanoparticles (Ag-NPs). In addition to its advantages for industrial and biomedical applications, it also represents a promising research field. This study aimed to evaluate the effects of chlorpyrifos (CPF) on thyroid hormone levels and the expression of inflammatory factors while highlighting the therapeutic potential of curcumin-synthesized silver nanoparticles (CUR-Ag-NPs) in mitigating CPF-induced thyroid damage.</div></div><div><h3>Materials and methods</h3><div>Six groups of rats were studied: control, CPF (5 mg/kg), CUR-AgNPs 40 μg/kg, CUR-AgNPs 80 μg/kg, CPF+ CUR-AgNPs 40, μg/kg, and CPF+ CUR-AgNPs 80 μg/kg. Treatments were administered daily for 30 days. At the end of the study, the rats were anesthetized with ketamine (50 mg/kg), and xylazine, (10 mg/kg). Blood was collected for serum analysis of thyroid hormone levels and thyroid gland tissue was preserved in RNAlater to the evaluation of inflammation markers.</div></div><div><h3>Results</h3><div>CPF exposure increased the expression of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and nitric oxide synthase 2 (NOS2). Co-administration of CUR-AgNPs significantly reduced the expression of these genes. CPF also disrupted thyroid hormone secretion, while CUR-AgNPs treatment in CPF-exposed rats nearly restored thyroid function.</div></div><div><h3>Conclusion</h3><div>These findings suggest that CUR-AgNPs can attenuate CPF-induced thyroid toxicity, offering potential therapeutic value.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201503"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145415608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated in silico and experimental analysis identifies MAGE-A3, TRIM28, and HLA-A as immunomodulatory targets in lung cancer","authors":"Gaurang Telang ,&nbsp;Smriti Mishra ,&nbsp;Anurag Sureshbabu ,&nbsp;Sagar Barage ,&nbsp;A.W. Santhosh Kumar ,&nbsp;Rajshri Singh","doi":"10.1016/j.humgen.2025.201492","DOIUrl":"10.1016/j.humgen.2025.201492","url":null,"abstract":"<div><div>MAGEA3, a cancer-testis antigen selectively expressed in tumors, has been widely explored as a target for cancer immunotherapy, yet its broader immunoregulatory function in the lung tumor microenvironment remains insufficiently characterized. In this study, we conducted an integrative in silico analysis using transcriptomic data from TCGA-LUSC to delineate the expression landscape, immune contexture, and molecular interactions of MAGEA3. Protein–protein interaction networks constructed via STRING and ranked through CytoHubba identified TRIM28 and HLA-A as key co-regulatory molecules, implicating MAGEA3 in transcriptional repression and antigen presentation. TIMER2.0 deconvolution revealed cell-type–specific associations, including differential relationships with CD8⁺ T cells, dendritic cells, and macrophages. Gene-wise survival modeling in TCGA-LUSC indicated MAGEA3 and MAGEA6 associate with reduced overall survival, whereas TRIM28 showed a borderline protective trend. Experimental validation via RT-qPCR in A549 cells confirmed detectable expression of MAGEA3, TRIM28, and HLA-A, reinforcing the computational predictions and highlighting potential cross-histological relevance. Collectively, these findings position MAGEA3 within immunomodulatory circuits of lung cancer and support its consideration in multimodal immunotherapeutic paradigms.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"46 ","pages":"Article 201492"},"PeriodicalIF":0.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145219618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic identification of molecular biomarkers and drug candidates targeting MAPK3 in multiple sclerosis","authors":"Bilal Khan,&nbsp;Ruqia Sartaj,&nbsp;Muhammad Rahiyab,&nbsp;Syed Shujait Ali,&nbsp;Zahid Hussain,&nbsp;Ishaq Khan,&nbsp;Arshad Iqbal","doi":"10.1016/j.humgen.2025.201436","DOIUrl":"10.1016/j.humgen.2025.201436","url":null,"abstract":"<div><div>Multiple sclerosis (MS) exists as a persistent autoimmune illness affecting the central nervous system because it produces demyelination and injures axons, besides causing CNS neuroinflammation. Research advances into MS pathophysiology have not solved the complexity of treating this condition. The research examined both vital MS-related molecular biomarkers as well as therapeutic possibilities through computational methods. GEO2R analyzed the gene expression dataset <span><span>GSE17393</span><svg><path></path></svg></span>, which reported that MS patients had differentially expressed genes than healthy controls. The biological processes involved in MS became clearer with the help of functional enrichment analyses, which contained both GO and KEGG pathway analysis. The STRING database enabled the construction of a PPI network, followed by hub gene identification through the CytoHubba application. The study revealed MAPK3 as the most influential hub gene essential for MS pathophysiological processes. Scientists used the Robetta server to forecast MAPK3's 3D structure, which they then optimized in Galaxy Refine before carrying out structural quality tests. Lab simulation using PyRx showed that potential medications such as Hypericin, Yibeissine, and Physalin F effectively bind with the MAPK3 protein. Among the compounds, Hypericin achieved the best binding affinity of −10.7 kcal/mol toward MAPK3, as Yibeissine and Physalin F reached −10.0 kcal/mol binding levels. MD simulations tested the stability of all MAPK3-ligand complex structures. The combination of ADME testing demonstrated that Yibeissine possessed ideal drug absorption features with strong blood-brain barrier penetration alongside good gastrointestinal absorption, yet Hypericin showed poor oral availability. The ProTox-II analysis revealed that the substance Hypericin presented major risks for mutation and cancer development, although Physalin F significantly damaged the human immune system. Current research indicates MAPK3 inhibition represents a promising treatment approach for MS, since Yibeissine stands out as the best drug candidate because it possesses an ideal ADME profile and low toxicity risks.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"45 ","pages":"Article 201436"},"PeriodicalIF":0.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144299018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of lithium treatment during pregnancy on miR124 gene expression of offspring rats","authors":"Zeynab Askari ,&nbsp;Parisa Hasanein ,&nbsp;Alishir Haidari ,&nbsp;Seyed Mohsen Saleh ,&nbsp;Saeedeh Askarian","doi":"10.1016/j.humgen.2025.201429","DOIUrl":"10.1016/j.humgen.2025.201429","url":null,"abstract":"<div><div>Lithium, recognized as a mood stabilizer, is widely used in the treatment of bipolar disorder. Discontinuation of this medication during pregnancy can have serious consequences, leading to severe mood fluctuations such as mania or depression in the mother. Despite the advantage effects of lithium, its molecular impacts on neonates are still under investigation. The aim of this study is to examine the expression levels of the miR-124 gene in the offspring of rats whose mothers were exposed to lithium during pregnancy. In this experimental study, female rat received a daily dose of 30 mg/kg of lithium carbonate through their drinking water. The offsprings were divided into control and experimental groups and were maintained until the age of two months. The hippocampus and serum from the offspring were isolated for the analysis of target gene expression. Total RNA was extracted and cDNA was synthesized. The expression of miR-124 was estimated using qRT-PCR, using the ddCt and Pfaffl methods, and compared with the control group. The expression of miR-124 decreased in the hippocampal tissue of neonates whose mothers received lithium during pregnancy, while an increase in miR-124 expression was observed in serum samples. No significant distinction between the two evaluation methods was observed, even though the Pfaffl method claimed greater precision. The increase in miR-124 expression in serum and its decrease in hippocampal tissue may demonstrate complex changes in gene expression regulation and physiological responses, during stress, inflammation or metabolic changes. Concurrent analysis of gene expression in both tissue and serum could provide valuable insights into disease status and the body's biological responses, enabling scientists to gain a better understanding of the treatment process.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"45 ","pages":"Article 201429"},"PeriodicalIF":0.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A case of Cockayne syndrome with two novel mutations in the ERCC6 gene: Expanding the phenotypic and genetic spectrum","authors":"Xinyao Wang,&nbsp;Lingzhao Min,&nbsp;Jia Wei,&nbsp;Xiaoqiang Wang","doi":"10.1016/j.humgen.2025.201420","DOIUrl":"10.1016/j.humgen.2025.201420","url":null,"abstract":"<div><div>A one-year-old East Asian boy presented with significant growth and developmental delays, including microcephaly, poor motor development, and feeding difficulties. He also exhibited poor visual and auditory tracking, along with occasional vomiting and skin vulnerability to sun exposure. Cranial CT revealed cortical dysplasia and a septum pellucidum cyst. Whole exome sequencing identified three heterozygous mutations in the ERCC6(Excision repair cross-complementation group 6) gene: two novel mutations (c.1557G &gt; A and c.1821 + 1del) inherited from the father and mother, respectively, and a third mutation (c.1820 A &gt; T) with uncertain pathogenicity, also inherited from the mother. The genetic findings led to a diagnosis of Cockayne syndrome, contributing to the expanding knowledge of the ERCC6 gene mutation spectrum and aiding in the clinical diagnosis and genetic counseling for the family. This case underscores the importance of accurate genetic diagnosis in managing prognosis and providing counseling for high-risk families.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"45 ","pages":"Article 201420"},"PeriodicalIF":0.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Superoxide dismutase gene expression and promoter methylation as biomarkers for type 2 diabetes mellitus","authors":"Ashwin Kumar Shukla ,&nbsp;Komal Awasthi ,&nbsp;Kauser Usman ,&nbsp;Monisha Banerjee","doi":"10.1016/j.humgen.2025.201427","DOIUrl":"10.1016/j.humgen.2025.201427","url":null,"abstract":"<div><h3>Background</h3><div>Type 2 diabetes mellitus (T2DM) is associated with oxidative stress and altered gene expression, particularly the antioxidant defense genes named as <em>SOD1</em> and <em>SOD2</em>. These enzymes serve a significant function in mitigating oxidative damage, and their regulation may be significantly influenced by epigenetic modifications, including DNA methylation.</div></div><div><h3>Objective</h3><div>This study aimed to investigate the promoter methylation status and expression levels of <em>SOD1</em> and <em>SOD2</em> genes in T2DM patients compared to healthy controls, to explore their potential as molecular biomarkers for T2DM.</div></div><div><h3>Methodology</h3><div>A total of 84 T2DM patients and 60 healthy controls were enrolled. Methylation-specific PCR (MSP) was applied to investigate the promoter methylation status of <em>SOD1</em> and <em>SOD2</em> genes, while real-time PCR was utilized to evaluate the expression levels of these genes in whole blood samples. Statistical analyses were performed to compare results between the T2DM group and the control group.</div></div><div><h3>Results</h3><div>The study revealed significant downregulation of both <em>SOD1</em> and <em>SOD2</em> gene expression in T2DM patients compared to controls, with <em>p</em>-values of 0.001 for both genes. Methylation analysis indicated increased promoter methylation of <em>SOD2</em> in T2DM subjects, whereas <em>SOD1</em> did not show any significant difference in the methylation status.</div></div><div><h3>Conclusion</h3><div>Our findings highlighted the critical role of reduced <em>SOD1</em> and <em>SOD2</em> expression in oxidative stress associated with T2DM. Although <em>SOD2</em> downregulation was observed, the lack of significant differences in methylation frequency between patients and controls indicated that it may not serve as a definitive biomarker by itself. Therefore, the potential influence of methylation on <em>SOD2</em> transcription warrants further investigation. Understanding these mechanisms could lead to novel therapeutic strategies targeting oxidative stress in diabetes management and at the same time improve our knowledge regarding the role of epigenetic factors in metabolic diseases.</div></div>","PeriodicalId":29686,"journal":{"name":"Human Gene","volume":"45 ","pages":"Article 201427"},"PeriodicalIF":0.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144170316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}