BMC Medical Genomics最新文献

{"title":"A genome-wide association study of methamphetamine use among people with HIV.","authors":"A Venkataraman, T Jia, S A Ruderman, C B Haas, R M Nance, L S Mixson, K H Mayer, M S Saag, G Chander, R D Moore, J Jacobson, S Napravnik, K Christopolous, W J Lee, B M Whitney, I Peter, H M Crane, J A C Delaney, S Lindström","doi":"10.1186/s12920-025-02105-8","DOIUrl":"10.1186/s12920-025-02105-8","url":null,"abstract":"<p><strong>Background: </strong>Amphetamine-like stimulants are the most used psychostimulants in the world; methamphetamine use is the most prevalent in people with HIV. Prolonged methamphetamine use can cause lasting damage to the heart, gut, and brain, as well as auditory hallucinations and paranoid thinking. However, relatively little is known about methamphetamine use and its genetic contributors.</p><p><strong>Methods: </strong>Using genetic information from the Centers for AIDS Research Network of Integrated Clinical Systems (CNICS) cohort, we conducted a multi-ancestry genome-wide association study (GWAS) of methamphetamine use among people with HIV (n = 1,196 reported ever use, n = 4,750 reported never use).</p><p><strong>Results: </strong>No single nucleotide polymorphism was statistically associated with methamphetamine use at the genome-wide level (p < 5 * 10^-8) in our study. Further, we did not replicate previously suggested genetic variants from other studies (all p > 0.05 in our analysis).</p><p><strong>Discussion: </strong>Our study suggests that there is no single strong genetic contributor to lifetime use of methamphetamine in people with HIV enrolled in CNICS. Larger studies with more refined outcome assessment are warranted to further understand the contribution of genetics to methamphetamine use and use disorder. Investigation into social and environmental contributors to methamphetamine use are similarly necessary.</p>","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"46"},"PeriodicalIF":2.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Experience of copy number variation sequencing applied in spontaneous abortion.","authors":"Yi-Fang Dai, Xiao-Qing Wu, Hai-Long Huang, Shu-Qiong He, Dan-Hua Guo, Ying Li, Na Lin, Liang-Pu Xu","doi":"10.1186/s12920-025-02118-3","DOIUrl":"https://doi.org/10.1186/s12920-025-02118-3","url":null,"abstract":"","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"45"},"PeriodicalIF":2.1,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ARMC5 mutations in primary bilateral macronodular adrenal hyperplasia: a family case report.","authors":"Yikai Wang, Weibing Shuang","doi":"10.1186/s12920-025-02112-9","DOIUrl":"10.1186/s12920-025-02112-9","url":null,"abstract":"<p><strong>Background: </strong>Primary bilateral macronodular adrenal hyperplasia (PBMAH) is a rare cause of overt Cushing's syndrome (CS), which usually manifests as bilateral macronodular adrenal nodules and varying levels of cortisol secretion. Previous studies have shown that ARMC5 play a huge role in the occurrence of PBMAH, which may be inherited to family members and lead to more severe clinical symptoms. ARMC5 variants may be associated with meningiomas, which is also illustrated by our report.</p><p><strong>Case presentation: </strong>This is a 41-year-old male patient with high blood pressure for 10 years and multiple adrenal nodules on both sides. In addition, the patient also suffered from pituitary microadenoma and meningioma. According to the patient's clinical manifestations, laboratory tests, imaging examinations, and the results of whole exon gene testing, we diagnosed the patient with PBMAH. The patient underwent a posterior laparoscopic nephrectomy of the left adrenal gland. Pathology reported a left macronodular adrenal hyperplasia, multifocal, 2 cm to 3 cm in diameter. Molecular analysis of DNA extracted from the patient's peripheral blood revealed an ARMC5 heterozygous mutation, which was classified as likely pathogenic.</p><p><strong>Conclusion: </strong>Screening of family members of PBMAH patients with ARMC5 germline mutations and active monitoring of family members carrying ARMC5 variants are recommended.</p>","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"44"},"PeriodicalIF":2.1,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of CYP19 gene SNPs (rs7176005 and rs6493497) with polycystic ovary syndrome susceptibility in Northern Chinese women.","authors":"Ya-Li Hao, Chun-Miao Liu, Na Wang, Rong-Miao Zhou, Ya-Nan Wei, Xiao-Shuang Bai, Xi Huang","doi":"10.1186/s12920-025-02115-6","DOIUrl":"https://doi.org/10.1186/s12920-025-02115-6","url":null,"abstract":"<p><strong>Purpose: </strong>The objective of this study was to elucidate the relationship between two single nucleotide polymorphisms (SNPs) rs7176005 and rs6493497 in CYP19 gene and the risk of polycystic ovary syndrome (PCOS) in Northern Chinese women.</p><p><strong>Methods: </strong>In this case-control study, a total of 340 women with PCOS and 340 matched healthy controls were recruited. Polymerase chain reaction ligase detection reaction (PCR-LDR) method was used to investigate two SNPs (rs7176005 and rs6493497) in the 5'-flanking region of CYP19 gene exon 1.</p><p><strong>Results: </strong>We observed a significant association of rs7176005 and rs6493497 with reduced risk of PCOS. Compared with CC genotype, a significant association of CT genotype (p = 0.019), TT genotype (p < 0.001) and combined CT + TT genotype (p < 0.001) with reduced risk of PCOS was observed. The result of linkage disequilibrium analysis showed that these two SNPs are in complete linkage disequilibrium (r² = 1). For rs7176005 SNP, compared with CC genotype, CT, TT and CT + TT genotypes reduced the risk of PCOS. The age, BMI-adjusted OR were 0.650 (95% CI = 0.460-0.917), 0.158 (95% CI = 0.066-0.376) and 0.545(95% CI = 0.391-0.759), respectively.</p><p><strong>Conclusions: </strong>These findings highlight a significant association between CYP19 gene polymorphisms and PCOS susceptibility, implying potential protective effects of T and A alleles. Of course, the major limitation of this study is the sample size of the case-control study. Larger cohort studies are needed to confirm these findings and investigate the underlying causes.</p>","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"43"},"PeriodicalIF":2.1,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling a novel FBN1 variant in Marfan syndrome with dilated aortic root manifestation.","authors":"Amirreza Sabahizadeh, Amir Askarinejad, Saranaz Seyed AliAkbar, Mahdieh Soveizi, Golnaz Houshmand, Hojjat Mortezaeian, Amin Elahifar, Majid Maleki, Samira Kalayinia","doi":"10.1186/s12920-025-02111-w","DOIUrl":"10.1186/s12920-025-02111-w","url":null,"abstract":"<p><strong>Background: </strong>Marfan syndrome (MFS) is a genetic disorder affecting connective tissue, with variable incidence rates. A significant portion of cases stems from novel genetic variants, while others inherit it from affected parents.</p><p><strong>Objective: </strong>This study focuses on identifying the genetic cause of MFS in a specific family, using whole-exome sequencing (WES).</p><p><strong>Methods: </strong>A 15-year-old male with confirmed MFS was examined, showing symptoms of palpitations and severe mitral valve regurgitation. WES was performed, followed by confirmation with Sanger sequencing. Variants were assessed for pathogenicity using bioinformatics tools and the American College of Medical Genetics and Genomics (ACMG) guidelines.</p><p><strong>Results: </strong>One potentially novel pathogenic variant was found in exon 14 of the FBN1 gene: c.1676delCinsAAT, p.Ala559GlufsTer21. In silico analysis suggested a deleterious impact on protein structure and function, supporting their pathogenic classification.</p><p><strong>Conclusion: </strong>The identification of this novel variant highlights the importance of the FBN1 gene in MFS, especially its cardiovascular manifestations. Early intervention can improve patient outcomes, while ongoing research holds promise for further advancements in treatment for Marfan syndrome.</p>","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"42"},"PeriodicalIF":2.1,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of a novel non-coding deletion in Allan-Herndon-Dudley syndrome by long-read HiFi genome sequencing.","authors":"Jihoon G Yoon, Seungbok Lee, Soojin Park, Se Song Jang, Jaeso Cho, Man Jin Kim, Soo Yeon Kim, Woo Joong Kim, Jin Sook Lee, Jong-Hee Chae","doi":"10.1186/s12920-024-02058-4","DOIUrl":"10.1186/s12920-024-02058-4","url":null,"abstract":"<p><strong>Background: </strong>Allan-Herndon-Dudley syndrome (AHDS) is an X-linked disorder caused by pathogenic variants in the SLC16A2 gene. Although most reported variants are found in protein-coding regions or adjacent junctions, structural variations (SVs) within non-coding regions have not been previously reported.</p><p><strong>Methods: </strong>We investigated two male siblings with severe neurodevelopmental disorders and spasticity, who had remained undiagnosed for over a decade and were negative from exome sequencing, utilizing long-read HiFi genome sequencing. We conducted a comprehensive analysis including short-tandem repeats (STRs) and SVs to identify the genetic cause in this familial case.</p><p><strong>Results: </strong>While coding variant and STR analyses yielded negative results, SV analysis revealed a novel hemizygous deletion in intron 1 of the SLC16A2 gene (chrX:74,460,691 - 74,463,566; 2,876 bp), inherited from their carrier mother and shared by the siblings. Determination of the breakpoints indicates that the deletion probably resulted from Alu/Alu-mediated rearrangements between homologous AluY pairs. The deleted region is predicted to include multiple transcription factor binding sites, such as Stat2, Zic1, Zic2, and FOXD3, which are crucial for the neurodevelopmental process, as well as a regulatory element including an eQTL (rs1263181) that is implicated in the tissue-specific regulation of SLC16A2 expression, notably in skeletal muscle and thyroid tissues.</p><p><strong>Conclusions: </strong>This report, to our knowledge, is the first to describe a non-coding deletion associated with AHDS, demonstrating the potential utility of long-read sequencing for undiagnosed patients. Although interpreting variants in non-coding regions remains challenging, our study highlights this region as a high priority for future investigation and functional studies.</p>","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"41"},"PeriodicalIF":2.1,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: whole exome sequencing revealed variants in four genes underlying X-linked intellectual disability in four Iranian families: novel deleterious variants and clinical features with the review of literature.","authors":"Atefeh Mir, Yongjun Song, Hane Lee, Hossein Khanahmad, Erfan Khorram, Jafar Nasiri, Mohammad Amin Tabatabaiefar","doi":"10.1186/s12920-025-02100-z","DOIUrl":"10.1186/s12920-025-02100-z","url":null,"abstract":"","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"40"},"PeriodicalIF":2.1,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11866631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP2 reversed cisplatin resistance through p53-mediated ferroptosis in NSCLC.","authors":"Yanmei Gong, Ruichao Li, Rui Zhang, Li Jia","doi":"10.1186/s12920-025-02108-5","DOIUrl":"10.1186/s12920-025-02108-5","url":null,"abstract":"<p><strong>Background: </strong>It has demonstrated the indispensable role of ferroptosis in conferring cisplatin resistance in non-small cell lung cancer (NSCLC), as well as the involvement of ubiquitin-specific protease (USP) in regulating ferroptosis. This paper aspired to the mechanism of USP2 and ferroptosis on NSCLC cisplatin resistance.</p><p><strong>Methods: </strong>Ubiquitin-specific protease mRNA expression, was detected through RT-qPCR. In vitro functional assays assessed the effects of USP2 overexpression on DDP resistance, cell proliferation capability, and ferroptosis markers in A549/DDP and H1299/DDP cells. Ubiquitination assays evaluated the ubiquitination levels of p53 following USP2 overexpression. Co-immunoprecipitation (Co-IP) assays confirmed the binding relationship between USP2 and p53. In vivo experiments in mice explored the specific role of the USP2-p53 axis in a xenograft tumor model.</p><p><strong>Results: </strong>USP2 expression was suppressed in cisplatin-resistant NSCLC cells. USP2 overexpression inhibited cell viability in cisplatin-resistant cells. Among the ferroptosis markers, the results showed that USP2 overexpression promoted LDH release, Fe²⁺ level, MDA and Lipid ROS, while inhibited GPX4 activity and GSH levels. The WB results revealed that USP2 overexpression inhibited GPX4, SLC7A11 and cytoplasm p53 protein expression, while promoted the nucleus p53 protein expression. Moreover, USP2 directly bound to p53 and USP2 overexpression stabilized p53 protein by suppressing its ubiquitination. In vivo experiments further suggest that the USP2-p53 pathway plays a crucial role in regulating cisplatin sensitivity in A549/DDP cells.</p><p><strong>Conclusion: </strong>USP2 acted on the K305R site of p53, which resulted in its deubiquitination. This cellular process could modulate cisplatin resistance through ferroptosis in NSCLC. This study could provide a potential therapeutic target to NSCLC.</p>","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"39"},"PeriodicalIF":2.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11866681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting RECQL4 in hepatocellular carcinoma: from prognosis to therapeutic potential.","authors":"Yingchen Li, Linan Yin, Bowen Liu, Yan Liu, Dongfeng He, Xuesong Liu, Ruibao Liu","doi":"10.1186/s12920-025-02107-6","DOIUrl":"10.1186/s12920-025-02107-6","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study is to assess the clinical utility of RecQ Like Helicase 4 (RECQL4) as a prognostic marker in hepatocellular carcinoma (HCC) and investigate its associations with various biological processes, angiogenesis-related factors, immune cell infiltration, immune checkpoints, and drug sensitivity.</p><p><strong>Methods: </strong>RECQL4 expression was analyzed across a range of cancer types utilizing data from the TCGA database. Disparities in RECQL4 expression levels between normal and malignant tissues were evaluated, alongside an analysis of progression-free interval (PFI), disease-specific survival (DSS), and overall survival (OS) curves. Exploration of pertinent pathways, immune cell infiltration, single-cell RNA-seq data, and drug sensitivity was conducted employing The Cancer Genome Atlas (TCGA) and Tumor Immune Single-Cell Hub (TISCH) databases. Furthermore, validation of in-silico results was validated through qPCR, Western blotting, CCK-8 assay, EdU assay, clonogenic assay, wound-healing assay, and transwell assay.</p><p><strong>Results: </strong>In HCC, RECQL4 was highly expressed and associated with poorer prognosis (p < 0.05). It positively correlated with pathways related to MYC targets, DNA replication, PI3K/AKT/mTOR signaling, DNA repair mechanisms, and the G2/M checkpoint (R > 0.24, p < 0.001). RECQL4 also showed significant correlations with angiogenesis-related genes, including PTK2 (R > 0.4, p < 0.05), suggesting a potential role in angiogenesis regulation. Immune analysis indicated that RECQL4 was associated with immune cell types such as T helper 2 cells, NK CD56bright cells, and follicular helper T cells, suggesting a positive relationship with their infiltration. High RECQL4 expression was also linked to increased sensitivity to drugs including Sorafenib, 5-Fluorouracil, Cisplatin, and Doxorubicin. Cellular experiments showed that RECQL4 expression at the mRNA and protein levels were significantly higher in HCC cell lines Hep3B and Huh7 compared to the normal liver cell line MHA. Moreover, RECQL4 knockdown resulted in reduced proliferation and migration in HCC cell lines (p < 0.05).</p><p><strong>Conclusions: </strong>RECQL4 shows promise as a biomarker for predicting recurrence and survival in HCC and may affect angiogenesis regulation. Its expression also appears to impact sensitivity to drugs such as Sorafenib, 5-Fluorouracil, Cisplatin, and Doxorubicin. Furthermore, silencing RECQL4 significantly inhibits HCC cell line proliferation and migration.</p>","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"38"},"PeriodicalIF":2.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11863661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143498644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"m6A regulator-based molecular classification and hub genes associated with immune infiltration characteristics and clinical outcomes in diffuse gliomas.","authors":"Jie Lu, Siyu Chen, Wanming Hu, Ke Sai, Depei Li, Pingping Jiang","doi":"10.1186/s12920-025-02104-9","DOIUrl":"10.1186/s12920-025-02104-9","url":null,"abstract":"<p><strong>Background: </strong>m6A methylation modification is a new regulatory mechanism involved in tumorigenesis and tumor-immunity interaction. However, its impact on glioma immune microenvironment and clinical outcomes remains unclear.</p><p><strong>Methods: </strong>Comprehensive expression profiles of 18 m6A regulators were used to identify molecular subtypes exhibiting distinct m6A modification patterns in 1673 glioma samples sourced from public datasets. A multi-genes signature was constructed for predicting clinical outcomes and response to immunotherapy in glioma patients. Immunohistochemistry and cellular experiments were performed for validation.</p><p><strong>Results: </strong>Two m6A subtypes of gliomas were identified. The m6A-low-risk subtype was characterized by paucity of immune infiltrates; While the m6A-high-risk subtype had higher abundances of multiple immune cells including lymphocyte and macrophage as well as increased expression of PD-L1, corresponding to an immunosuppressive phenotype. The m6A-high-risk subtype had poorer survival than the m6A-low-risk subtype in both the glioblastoma and lower grade gliomas cohorts. Eight m6A-related hub genes of high prognostic significances were identified and selected for developing a scoring signature termed as m6Ascore. Elevated m6Ascore indicated worse survival for glioma patients under standard care, but showed enhanced response to immunotherapy. Moreover, we demonstrated that overexpression of FTO, a m6A demethylase, inhibited the expressions of m6A-related hub genes (PTX3, SPAG4), impaired glioma cell viability and reduced macrophage chemotaxis.</p><p><strong>Conclusion: </strong>This work develops an immune- and clinical-relevant m6A subtyping and a scoring model, which enhances our understanding of the role of m6A modification in regulating immune infiltration microenvironment in gliomas and helps to identify patients who are more likely to benefit from immunotherapy.</p>","PeriodicalId":8915,"journal":{"name":"BMC Medical Genomics","volume":"18 1","pages":"37"},"PeriodicalIF":2.1,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11853526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}