NPJ Genomic Medicine最新文献

{"title":"Landscape of copy number variants in Spanish people with dementia.","authors":"Itziar de Rojas, Pablo García-González, Clàudia Olivé, Raquel Puerta, Laura Montrreal, Montserrat Alegret, Oscar Sotolongo-Grau, Amanda Cano, Marta Marquié, Sergi Valero, Miguel Calero, Alberto Rábano, Ana Belén Pastor, Teodoro Del Ser, Inés Quintela, Juan Macías, Anaïs Corma-Gómez, Juan A Pineda, Emilio Franco-Macías, Dolores Buiza-Rueda, María Bernal Sánchez-Arjona, Jose Luis Royo, Silvia Mendoza, Carmen Lage, Carmen Antúnez, Arturo Corbatón-Anchuelo, María Teresa Martínez-Larrad, Mónica Diez-Fairen, Ignacio Alvarez, Raquel Huerto Vilas, Alfonso Arias Pastor, Manuel Menéndez-González, Carmen Martínez Rodríguez, Irene Rosas Allende, Sebastián García-Madrona, Ana Frank-García, Angel Martín-Montes, Miquel Baquero, Jordi Pérez-Tur, María J Bullido, Guillermo Garcia-Ribas, Victoria Álvarez, Gerard Piñol-Ripoll, Pau Pastor, Eloy Rodriguez-Rodriguez, Jose María García-Alberca, Pablo Mir, Luis M Real, Miguel Medina, María Eugenia Sáez, Ángel Carracedo, Michael T Heneka, Lluís Tàrraga, Mercè Boada, Pascual Sánchez-Juan, M Victoria Fernández, Sven J van der Lee, Agustín Ruiz","doi":"10.1038/s41525-026-00589-6","DOIUrl":"https://doi.org/10.1038/s41525-026-00589-6","url":null,"abstract":"<p><p>Recent studies suggest that copy number variants (CNVs) may contribute to the missing heritability of complex diseases such as Alzheimer's disease (AD) and related dementias (ADRD). We performed a CNV analysis using genotyping data (Axiom 815 K Spanish biobank array) from the GR@ACE/DEGESCO dementia dataset (n = 20,067) of the Spanish population. Applying PennCNV and extensive quality control, 8275 controls and 7818 dementia cases were selected for gene-level case/control associations. We identified 43,833 CNVs with deletions (47%) and duplications (53%). No genome-wide significant associations were found, but nominal associations were observed in PKP3-SIGIRR and FBRSL1 loci. CNVs in 2970 genes were exclusive to dementia cases and enriched in vascular-related pathways. Notable findings included 14q11.2 duplication and VPS13B deletions in ADRD cases, the latter confirmed by optical genome mapping. Our findings suggest potential novel genes associated with ADRD in the Spanish population. However, the limited resolution of array-based technologies in detecting CNVs warrants further investigation.</p>","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic evaluation of long-read and short-read sequencing in neurological disorders diagnosis: a direct comparison study of 310 patients.","authors":"Dream Lok Sze Chan, Helen Ying Fung Tam, Amy Hin Yan Tong, Wei Ma, Chak Sing Lau, Ho Ming Luk, Shirley Yin Yu Pang, Shirley Sze Wing Cheng, Yuan Gao, Lai Ting Leung, Denis Long Him Yeung, Claudia Ching Yan Chung, Steve Tsz Fung Chan, Shirley Pik Ying Hue, Anson Man Chun Xi, Dicky Or, Steve Cheuk Yiu Yeung, Jamie Sui Lam Kwok, Nattily Sum Yin Tai, Carol Ching Fun Lau, Wai Lap Wong, Raven Yan Wah Lee, Janice Kai Ning Wong, Hong Kong Genome Project, Annie Tsz Wai Chu, Brian Hon Yin Chung","doi":"10.1038/s41525-026-00593-w","DOIUrl":"10.1038/s41525-026-00593-w","url":null,"abstract":"<p><p>Genetic neurological disorders are highly heterogeneous, and many are driven by complex variants that challenge short‑read genome sequencing (srGS). Long‑read genome sequencing (lrGS) has recently shown promise, but head‑to‑head evaluations are limited. A direct comparison study of srGS and lrGS was performed for 310 families with undiagnosed neurological disorders from the Hong Kong Genome Project to assess their diagnostic performance, technical capabilities and costing. Genome sequencing showed an overall diagnostic yield of 22.6% (n = 70/310, 77 variants). lrGS and srGS showed comparable variant detection rates at 92.2% (n = 71/77) and 96.1% (n = 74/77), respectively. lrGS solely confirmed three repeat expansions with phased methylation data and enhanced accuracy in two complex structural variants. srGS detected six variants in homopolymeric regions that were missed by lrGS. Costing analysis revealed a comparable unit cost per sample for srGS and lrGS with USD1,545.97 and USD1,580.00, respectively. This study demonstrated that srGS excels in detecting variants near homopolymers while lrGS offers better resolution for complex variants and enables the simultaneous analysis of methylation and phasing. Although lrGS is not yet capable of fully replacing srGS, we anticipate that the continued technical improvement would position lrGS as the first‑tier genomic test for neurological disorders.</p>","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GANomics: bridging legacy and modern transcriptomic platforms for clinical applications.","authors":"Leihong Wu, Hadi Salman, Weida Tong","doi":"10.1038/s41525-026-00585-w","DOIUrl":"10.1038/s41525-026-00585-w","url":null,"abstract":"<p><p>The evolution of transcriptomic technologies requires effective translation between legacy and modern platforms to fully leverage historical data. We present GANomics, a generative adversarial network (GAN) framework that enables bidirectional translation between microarray and RNA-seq data using a small number of samples profiled by both technologies. By integrating paired and unpaired samples through a pair-aware feedback loss, GANomics enforces one-to-one transcript mappings while preserving global gene expression distributions. Applied to a neuroblastoma cohort (n = 498; 10,042 genes) and benchmarked against six alternative methods, GANomics achieved high per-sample correlations ( > 0.96) between real and synthetic data with as few as ten paired profiles. With fifty paired profiles, it accurately recapitulated differential expression, maintained pathway-level rankings, and enabled a cross-platform classifier to transfer comparable to real data. Consistent performance across five additional benchmark datasets confirmed its robustness. By bridging legacy and contemporary transcriptomic data while retaining biological consistency, GANomics facilitates scalable data integration for biomarker reuse and the expansion of transcriptomic resources in clinical applications.</p>","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148284008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BCL2 promoter region mutations are an independent marker of BCL2 level in lymphoid malignancies.","authors":"Daniel Kuznicki, Paulina Galka-Marciniak, Malwina Suszynska, Piotr Kozlowski","doi":"10.1038/s41525-026-00590-z","DOIUrl":"10.1038/s41525-026-00590-z","url":null,"abstract":"","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":"11 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13279811/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148278134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dyskeratosis Congenita with Pigmentary Mosaicism and Hematopoietic Trisomy 9 in a Female Associated with a de novo DKC1 Variant and Markedly Skewed X Chromosome Inactivation.","authors":"Benilde García-de-Teresa, Tianna Zhao, Consuelo Salas-Labadía, Moisés Fiesco-Roa, Weiyin Zhou, Silvia Sánchez, Ulises Juárez-Figueroa, Bertha Molina, Leda Torres, Raymond Caylor, Difei Wang, Chad A Highfill, Maryam Rafati, Jia Liu, Logan P Zeigler, Angélica Monsivais, Esther Lieberman, María de la Luz Orozco-Covarrubias, Mauricio Rojas, Burak Altintas, Neelam Giri, Kristine M Jones, Komal Jain, Lisa J McReynolds, Belynda Hicks, Sara Frías, Sharon A Savage","doi":"10.1038/s41525-026-00587-8","DOIUrl":"10.1038/s41525-026-00587-8","url":null,"abstract":"<p><p>Pathogenic germline variants (PGVs) in dyskerin pseudouridine synthase 1 (DKC1) cause X-linked recessive dyskeratosis congenita (DC), a telomere biology disorder. Females with heterozygous DKC1 PGVs rarely exhibit DC phenotypes due to favorable X chromosome inactivation (XCI). We report a female with classic DC, pigmentary mosaicism and bone marrow failure associated with a novel de novo DKC1 variant (c.190 G > C, p.Val64Leu) with reduced expression of DKC1 and TERC along with downregulated signatures associated with aberrant telomere biology and ribosome function. Markedly skewed XCI was detected with expression of the mutated allele in skin fibroblasts and wild-type DKC1 expression in the bone marrow. We hypothesize that selective pressure in the bone marrow favored wild type expressing cells which acquired a trisomy 9 but were unable to resume normal hematopoiesis. This study demonstrates DKC1 c. 190 G > C as a likely PGV causing classic DC and highlights the molecular and clinical complexities associated with skewed XCI.</p>","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13594237/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148211881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two cases of mosaic germline SVA insertions in SMARCB1: implications for rhabdoid tumour predisposition diagnosis.","authors":"Laura Raiti, Kyoko E Yuki, Lise Cinq-Mars, Edward J Higginbotham, Vilma Navickiene, Yisu Li, Zhuozhi Wang, Bhooma Thiruv, Tristan Charlinski, Bailey Gallinger, Rosemarie E Venier, Annie Huang, Avram Denburg, Kathy Chun, Anita Villani","doi":"10.1038/s41525-026-00584-x","DOIUrl":"10.1038/s41525-026-00584-x","url":null,"abstract":"<p><p>Rhabdoid tumour predisposition syndrome (RTPS) is a highly penetrant cancer predisposition syndrome caused by germline variants in SMARCB1 or less frequently in SMARCA4. Genetic testing for this syndrome involves sequence and deletion/duplication analysis of these two genes. Standard clinical testing is limited in detecting structural variants. Here we describe two patients who tested negative on standard clinical germline panel testing for RTPS but were each found to have a mosaic germline insertion of an SVA (SINE-VNTR-Alu) element in the SMARCB1 gene by more advanced comprehensive genomic analysis. These two cases demonstrate the importance of structural variants and broader genomic sequencing for individuals suspected of having an underlying germline cancer predisposition syndrome, such as RTPS.</p>","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148176433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted reflex RNA sequencing for enhanced variant classification on exome and genome sequencing improves patient outcomes.","authors":"Xiaonan Zhao, Robert Rigobello, Morgan Driver, Sydney Lau, Mei Ling Chong, Jason Chibuk, Hongzheng Dai, Wilson C W Wu, Christina Peroutka, Laura Famularo, Alexander Y Kim, Bailey Hummel, Sarah Dugan, Tinsley Douglas, Linyan Meng, Fan Xia, Christine M Eng","doi":"10.1038/s41525-026-00571-2","DOIUrl":"10.1038/s41525-026-00571-2","url":null,"abstract":"<p><p>RNA sequencing (RNA-seq) has been utilized to provide functional evidence regarding the impact of splicing variants. This study explores the utility of targeted reflex RNA-seq to inform classification of predicted splicing variants identified through clinical exome sequencing (ES) and genome sequencing (GS). A retrospective analysis was conducted on consecutive ES/GS cases completed at a single center in which targeted reflex RNA-seq was performed following identification of eligible variants. There were 131 cases (4.1%) that had at least one RNA-seq eligible variant reported, with eight of these cases having two unique eligible variants. Of the 139 eligible variants, 125 were classified as variants of uncertain significance (VUS). Sixty-four cases had targeted reflex RNA-seq completed with 27 cases having at least one variant reclassified (42.2%). After reclassification, 23 cases had positive results, and two cases had a likely diagnosis of an autosomal recessive condition. Clinical outcomes data regarding positive RNA-seq cases showed that 71% (10/14) had clinical management changes and 43% (6/14) had treatment changes. Incorporation of targeted reflex RNA-seq analysis into the diagnostic pipeline of rare diseases enhances variant classification and resolves uncertainty regarding predicted splice variants, leading to an estimated 1.6% increase in diagnostic yield of clinical ES/GS.</p>","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13562735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148176422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of MYH6 Variants in atrial cardiomyopathy: insights from clinical observations and zebrafish models.","authors":"Yike Zhang, Qing Wang, Xiangao Ji, Zhou Xu, Jingzhe Hao, Yue Zhu, Jia Song, Hongwu Chen, Zhiyong Zhang, Chang Cui, Minglong Chen","doi":"10.1038/s41525-026-00586-9","DOIUrl":"10.1038/s41525-026-00586-9","url":null,"abstract":"<p><p>Atrial cardiomyopathy, which often comes with underlying genetic defects, has been recognized as a possible substrate of atrial fibrillation. MYH6 encodes α-myosin heavy chain (α-MHC), predominantly expressed in the atria and pivotal in sarcomere organization and muscle contraction. Genetic investigation in patients with a family history of atrial cardiomyopathy identified three probands carrying MYH6 variants (D629N, V893M, A1327T). However, the role of MYH6 in atrial diseases has not been fully elucidated, and the genetic cause of atrial cardiomyopathy needs further investigation. Here, we employed CRISPR/Cas9 to generate myh6 knockout zebrafish, assessing cardiac abnormalities in structural, electrical, and gene expression levels through diverse methodologies. Our findings revealed that myh6 defects in zebrafish impaired atrial and ventricular function and disordered sarcomere, which underscores the pivotal role of MYH6 in maintaining atrial function and development. Transcriptomic sequencing also identified 1318 differentially expressed genes enriched in muscle development, calcium ion homeostasis, and sarcomere pathways. The association between MYH6 dysfunction and atrial cardiomyopathy highlights the role of sarcomeric abnormalities in atrial remodeling, a process implicated in atrial fibrillation.</p>","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13542202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148157366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the contribution of rare variants to congenital heart disease through a large-scale case-control exome study.","authors":"Enrique Audain, Anna Wilsdon, Gregor Dombrowsky, Alejandro Sifrim, Jeroen Breckpot, Yasset Perez-Riverol, Siobhan Loughna, Allan Daly, Pavlos Antoniou, Philipp Hofmann, Amilcar Perez-Riverol, Anne-Karin Kahlert, Ulrike Bauer, Thomas Pickardt, Sabine Klaassen, Felix Berger, Ingo Daehnert, Sven Dittrich, Brigitte Stiller, Hashim Abdul-Khaliq, Frances Bu'lock, Anselm Uebing, Hans-Heiner Kramer, Vivek Iyer, Lars Allan Larsen, J David Brook, Marc-Phillip Hitz","doi":"10.1038/s41525-026-00582-z","DOIUrl":"10.1038/s41525-026-00582-z","url":null,"abstract":"<p><p>Several studies have demonstrated the value of large-scale human exome and genome data analysis to maximise gene discovery in rare diseases. Using this approach, we have analysed the exomes of 4747 cases and 52,881 controls to identify genes which confer a substantial risk of congenital heart disease (CHD). We identified both rare loss-of-function and missense coding variants in 14 genes, which reached genome-wide significance at FDR 5%. Ten genes have been associated with CHD, whereas four genes (PBX1, KAT6B, SHOX2, HCAR1) have not been reported as genome-wide significant so far. We highlight distinct genetic contributions to syndromic and non-syndromic CHD by independently analysing probands from these two groups. In addition, by integrative analysis of exome data with single-cell transcriptomics data from human embryonic hearts, we identified cardiac-specific cells, such as neural crest cells and endothelial cells, as well as putative biological processes underlying the pathogenesis of CHD. In summary, our findings strengthen the association of known CHD genes and have identified additional novel disease genes contributing to the aetiology of CHD.</p>","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":"11 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13230774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expanding the phenotypic spectrum of FGF12-epilepsy-does prompt precision therapy affect outcomes?","authors":"Leo Arkush, Kristina Karandasheva, Frédérique Ouellet, Alissa M D'Gama, Beth Rosen Sheidley, Nicole S Y Liang, Vann Chau, Gregory Costain, Lacey Smith, Anoushka Alwis, Christin Eltze, Annapurna Poduri, Felice D'Arco, Josh Adams, Kristen Lee, Jaspal Singh, Alexander P Y Brown, Arjuna Nagendran, Ben Pode-Shakked, Michal Tzadok, Bruria Ben Zeev, Amy McTague","doi":"10.1038/s41525-026-00581-0","DOIUrl":"10.1038/s41525-026-00581-0","url":null,"abstract":"<p><p>Fibroblast growth factor-12 (FGF12) variants have been associated with developmental and epileptic encephalopathy (DEE) with evidence of modulation of voltage-gated sodium channels Na_v1.2 and Na_v1.6. We aim to expand the phenotypic spectrum of FGF12-related epilepsy with emphasis on precision therapy. We describe 12 patients: eight with neonatal onset seizures with the recurrent p.Arg52His (c.155 G > A) variant, two with a previously unreported p.Glu153Gly (c.458 A > G) variant, one with a p.Gly50Ser (c.148 G > A) variant, and one with a de novo whole-gene duplication. Atypical absence seizures were present in 5/12 patients. Brain MRI was normal in 10/12; one patient's MRIs showed progressive cerebellar atrophy, and one patient's MRI showed a hemispheric infarct. 8 patients promptly started on sodium channel blockers became seizure-free with good developmental outcomes while 4 developed DEE. In summary, we expand the phenotypic spectrum of FGF12-related epilepsy and discuss the role of early precision therapy in developmental and epilepsy outcomes.</p>","PeriodicalId":19273,"journal":{"name":"NPJ Genomic Medicine","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13385693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148016544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}