American journal of human genetics最新文献

{"title":"Polymorphic CGG repeats in gene regulation and disease.","authors":"Yijing Zhao, Dale Annear, Emily G Allen, R Frank Kooy, David L Nelson, Peng Jin","doi":"10.1016/j.ajhg.2026.05.001","DOIUrl":"10.1016/j.ajhg.2026.05.001","url":null,"abstract":"<p><p>Polymorphic CGG repeats, present at thousands of loci across the human genome, represent a distinctive class of regulatory DNA elements with dual roles in gene regulation and disease. Once regarded primarily as pathogenic triggers, CGG repeats are now recognized as modulators of transcription, chromatin state, and RNA metabolism. When expanded beyond normal thresholds, these repeats can drive neurodevelopmental and neurodegenerative disorders through transcriptional silencing, RNA toxicity, and repeat-associated non-AUG (RAN) translation. Recent advances in long-read sequencing have enabled comprehensive mapping of CGG repeat diversity, uncovering novel expansion loci and complex methylation and structural patterns underlying multiple human disorders. Together, these discoveries highlight CGG repeats as dynamic elements shaping gene expression, genome stability, and disease susceptibility. Emerging evidence further links CGG repeat expansions to non-neurological phenotypes, including cardiomyopathy, broadening their clinical significance. This review summarizes current understanding of CGG repeat polymorphisms in gene regulation and their mechanistic roles in disease, emphasizing both convergent and distinct pathogenic pathways across CGG expansion disorders.</p>","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":" ","pages":"1131-1158"},"PeriodicalIF":7.7,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13277698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148004332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Meta-analysis across six global biobanks identifies recessive coding associations with complex traits and diseases.","authors":"Frederik H Lassen, Georgios Kalantzis, Andrea Eoli, Barney Hill, Kyuto Sonehara, Shinichi Namba, Isaac Wade, Sam Hodgson, Wei Zhou, Benjamin M Neale, Konrad J Karczewski, Yukinori Okada, David A van Heel, Sarah Finer, Cecilia M Lindgren, Henrike O Heyne, Hilary C Martin, Duncan S Palmer","doi":"10.1016/j.ajhg.2026.04.005","DOIUrl":"10.1016/j.ajhg.2026.04.005","url":null,"abstract":"<p><p>Rare bi-allelic variation is a major contributor to human disease risk, yet its effects are difficult to study at scale in population cohorts owing to the limited number of individuals with putatively deleterious bi-allelic genotypes and the challenges of accurately phasing low-frequency variants. Here, we present recessive, gene-based analyses of rare and low-frequency variants in up to 948,690 exome- or whole-genome-sequenced individuals across six biobanks with linked electronic health records. Through statistical phasing, we inferred putatively damaging compound-heterozygous genotypes, increasing the number of bi-allelic damaging genotypes by 19%. Restricting to predicted loss-of-function (pLoF) variants, we identified 5,563 genes harboring bi-allelic genotypes, a 19.8% increase in putative knockouts. We then considered all low-frequency variants (minor allele frequency [MAF] <5%) and performed gene-based recessive association testing using putatively damaging bi-allelic genotypes, identifying 58 significant associations (false discovery rate [FDR] ≤1% or p_rec≤7.5 × 10^-7) after meta-analysis and Cauchy combination of nonsynonymous annotations. Comparing recessive and additive models, we found 17 instances where recessive effects were more pronounced, including several previously unreported associations, such as HBB with heart failure (p_rec = 2.6 × 10^-14; p_add = 0.98), LECT2 with height (p_rec = 3.7 × 10^-14; p_add = 4.1 × 10^-10), and ENSG00000267561 with height (p_rec = 2.9 × 10^-9; p_add = 0.37). This study demonstrates the potential of federated approaches to study the effects of rare bi-allelic variation.</p>","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":" ","pages":"1330-1346"},"PeriodicalIF":7.7,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13277689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Putting polygenic scores in context: How intersectional factors affect relative and absolute genetic risk.","authors":"Mihael Cudic, Justin D Tubbs, Tian Ge, Jordan W Smoller","doi":"10.1016/j.ajhg.2026.03.013","DOIUrl":"10.1016/j.ajhg.2026.03.013","url":null,"abstract":"<p><p>The clinical utility of polygenic scores (PGSs) is known to vary when training and test samples differ in ancestry, with recent work suggesting that sociodemographic differences can also impact PGS performance. However, the impact of belonging to multiple intersecting contexts on genetic risk remains understudied. We analyzed lifetime disease odds ratio (OR) and absolute risk (AR) estimates in high-PGS individuals across 106 two-way intersections of sociodemographic factors (sex, age, alcohol intake, smoking, income, and deprivation). Seven diseases were assessed: atrial fibrillation, coronary artery disease, type 2 diabetes, hypercholesterolemia, asthma, obesity, and major depression. Primary analyses were performed in the UK Biobank (UKB; n = 375,054, British-European-like ancestry), with replication in All of Us (AoU; n = 36,552, African-like ancestry and n = 99,477, European-like ancestry). ORs varied significantly across contexts, with greater variation observed across intersectional contexts. On average, the maximal OR varied across two-way contexts by 56%. AR deviations were more moderate after adjusting for context prevalence but still showed intersectional effects. For example, high-PGS, low-income individuals had an average 1.0 percentage-point drop in estimated AR across phenotypes using a context-aware vs. context-unaware PGS, while those additionally reporting low alcohol intake had a 3.1-point lower AR estimate for major depression in the UKB. Results were generally consistent across datasets, with strongest replication in European-like AoU samples. Our findings show that intersectional contexts can have a sizable impact on genetic risk effect estimates. Future clinical applications may need to incorporate these contextual effects to improve accuracy and fairness for individual-specific genetic risk assessment.</p>","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":" ","pages":"966-977"},"PeriodicalIF":7.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147687693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Specifications of the ACMG/AMP variant curation guidelines for the analysis of germline ATM sequence variants.","authors":"Marcy E Richardson, Megan Holdren, Terra Brannan, Miguel de la Hoya, Amanda B Spurdle, Sean V Tavtigian, Colin C Young, Lauren Zec, Susan Hiraki, Michael J Anderson, Logan C Walker, Shannon McNulty, Clare Turnbull, Marc Tischkowitz, Katherine Schon, Thomas Slavin, William D Foulkes, Melissa Cline, Alvaro N Monteiro, Tina Pesaran, Fergus J Couch","doi":"10.1016/j.ajhg.2026.03.016","DOIUrl":"10.1016/j.ajhg.2026.03.016","url":null,"abstract":"","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":" ","pages":"1123"},"PeriodicalIF":7.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13262645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147525317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bi-allelic ATG12 variants impair autophagy and cause a neurodevelopmental disorder.","authors":"James Lambton, Shotaro Asano, Yuxiang Huang, Fumi Suomi, Tomoya Eguchi, Cassidy Petree, Kevin Huang, Magali Prigent, Aliza Imam, Thomas J McCorvie, Daniel Warren, Emma Hobson, Helen McCullagh, Doriana Misceo, Anna Bjerre, Marie F Smeland, Claus Klingenberg, Eirik Frengen, Swati Naik, Gavin Ryan, Annapurna Sudarsanam, Katherine Foster, Pradeep Vasudevan, Rajib Samanta, Fatima Rahman, Shazia Maqbool, Vrajesh Udani, Stephanie Efthymiou, Henry Houlden, Robert McFarland, Jack J Collier, Reza Maroofian, Wyatt W Yue, Gaurav K Varshney, Daniel J Klionsky, Renaud Legouis, Thomas G McWilliams, Noboru Mizushima, Monika Oláhová, Charlotte L Alston, Robert W Taylor","doi":"10.1016/j.ajhg.2026.03.002","DOIUrl":"10.1016/j.ajhg.2026.03.002","url":null,"abstract":"<p><p>Autophagy is an essential developmental and homeostatic process, defined by the endolysosomal degradation of intracellular components and pathogens. Dysfunctional autophagy is implicated in complex human disease, yet reports of congenital autophagy disorders were considered exceedingly rare until the recent report of several unrelated families with bi-allelic variants in the core autophagy effector ATG7, complementing the report of two individuals harboring ATG5 variants. We now report six affected individuals from five families with bi-allelic ATG12 variants with complex neurological phenotypes overlapping those seen in individuals with pathogenic variants in ATG5 and ATG7: developmental delay, intellectual disability, congenital ataxia, hypotonia, and seizures with cerebellar vermis hypoplasia evident on neuroradiological imaging. Structural modeling implicated a potential disruption of the ATG12-ATG5-ATG16N-ATG3 complex. Biochemical analyses of primary fibroblasts confirmed the loss of stable ATG12-ATG5 conjugate in one family and altered autophagic flux in one unrelated family. The HaloTag processing assay in HeLa cells demonstrated a decrease in ATG12-ATG5 conjugate and reduced autophagic flux in response to starvation. Complementation studies demonstrated that equivalent missense atg12 variants were unable to fully recover the biochemical defect in atg12-null yeast, with microscopy analysis demonstrating a reduced delivery of autophagy substrates to the yeast's degradative compartment. Zebrafish studies confirmed that Atg12 is required for normal growth, brain development, and neural function. Collectively, our findings underscore the pivotal role of autophagy in maintaining human neural integrity, emphasize an emerging group of congenital autophagy disorders, and expand our understanding of adaptive homeostasis in human health and disease.</p>","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":" ","pages":"1090-1107"},"PeriodicalIF":7.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13277686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147525335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Specifications of the ACMG/AMP variant curation guidelines for the analysis of germline PALB2 sequence variants.","authors":"Marcy E Richardson, Megan F H Bishop, Megan A Holdren, Miguel de la Hoya, Amanda B Spurdle, Sean V Tavtigian, Terra Brannan, Colin C Young, Lauren Zec, Susan Hiraki, Clare Turnbull, Marc Tischkowitz, Kara A Bernstein, Jean-Yves Masson, Shannon M McNulty, Tina Pesaran, Alvaro N Monteiro, Logan C Walker, William D Foulkes, Fergus J Couch","doi":"10.1016/j.ajhg.2026.03.015","DOIUrl":"10.1016/j.ajhg.2026.03.015","url":null,"abstract":"","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":" ","pages":"1122"},"PeriodicalIF":7.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13262694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147525339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of sex on the immune system explored at the single-cell level.","authors":"Seyhan Yazar, Jose Alquicira-Hernandez, Kristof Wing, Anne Senabouth, Stacey Andersen, Kirsten A Fairfax, Alex W Hewitt, Joseph E Powell, Sara Ballouz","doi":"10.1016/j.ajhg.2026.04.003","DOIUrl":"10.1016/j.ajhg.2026.04.003","url":null,"abstract":"<p><p>Sex has a key role in disease susceptibility (in particular, autoimmunity). Sex differences in the immune system originate from genes and their interactions with both intrinsic and extrinsic factors. However, the cellular-level factors influencing sexual dimorphism are not fully understood. We thus examined immune sex differences at single-cell resolution to dissect the genetic impacts. Female-biased sex-differentially expressed genes (sex-DEGs) in multiple immune cells were involved in tumor necrosis factor alpha (TNF-α) signaling, whereas male DEGs were enriched for ribosomal-related functions. While cis-expression trait quantitative loci (eQTLs) were less common on sex chromosomes, we identified over 1,000 sex-specific eQTLs and 51 sex-interacting eQTLs on autosomes. When we examined the effect of genetic control on sex-DEGs, we found genetic variants affecting the female-biased expression of FCGR3A in natural killer (NK) cells (rs2099684) and ITGB2 in monocytes (rs760462), both of which are associated with systemic lupus erythematosus. Our work reveals biases masked in bulk analyses and highlights sexually dimorphic genes and pathways at baseline.</p>","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":"113 5","pages":"1006-1023"},"PeriodicalIF":7.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13277697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sensitivity of HiFi long-read genome sequencing for difficult-to-detect pathogenic variants when applied to real-world clinical laboratory samples.","authors":"Joseph M Devaney,Jessica X Chong,Patricia C Lopes,Jessica Noya,April S Berlyoung,Shamila Yusuff,Solomon Lynch,Rhonda Brandon,Kathleen S Hruska,Lucas Lochovsky,Julianna Spangler,Kirsty McWalter,Keith Nykamp,Sarah R Poll,Andrew B Stergachis,John Greally,Paul Kruszka,Egor Dolzhenko,Xiao Chen,Alexander V Robertson,William J Rowell,Juniper A Lake,Andrew Carroll,Robert Kueffner,Michael A Eberle,Flavia M Facio,Michael J Bamshad,Britt Johnson","doi":"10.1016/j.ajhg.2026.04.001","DOIUrl":"https://doi.org/10.1016/j.ajhg.2026.04.001","url":null,"abstract":"Leveraging new sequencing and omic technologies to enhance the detection of pathogenic variants in known disease genes is a key step toward increasing the likelihood of a precise genetic diagnosis for affected individuals. Short-read sequencing is widely used in clinical laboratories for multi-gene panels and exome and genome sequencing, but this technology has inherent limitations in detecting certain classes of genetic variation. As a result, diagnostic laboratories continue to offer complementary assays, often used sequentially, reducing efficiency and speed in providing a diagnosis. We applied PacBio long-read genome sequencing (HiFi) to samples from 191 probands previously tested with short-read sequencing alone and/or other diagnostic technologies and enriched for pathogenic variants difficult to detect (VDDs). HiFi's pipeline automatically detected 479 of 481 (99.6%) disease-causing variants, many of which were called in samples not optimized for long-read genome sequencing (such as buccal samples or low-molecular-weight DNA). The two variants not automatically detected were a mosaic trisomy 18 (23% mosaicism) and a 5,594-bp mosaic deletion (13% mosaicism). However, other mosaic variants were detected, indicating that HiFi at ∼30× genome coverage is sensitive to the degree of mosaicism. Of 481 variants, 49 were suspected based on the clinical report but not confirmed molecularly prior to HiFi. Our findings demonstrate that HiFi sequencing detects a wide range of VDDs in real-world clinical laboratory samples, highlighting a key advantage of HiFi as a potential first-tier test over the myriad of complementary technologies currently used to detect VDDs.","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":"4 1","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147754560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benchmarking genetic birth prevalence estimates against newborn screening data.","authors":"Michael C Sierant,Nicholas Knoblauch,Evan Witt,Daniel Gaffney,Sara L Pulit,Arthur Wuster","doi":"10.1016/j.ajhg.2026.04.002","DOIUrl":"https://doi.org/10.1016/j.ajhg.2026.04.002","url":null,"abstract":"Accurate prevalence estimates for rare congenital conditions are critical for understanding disease epidemiology and enabling drug development. They inform public health investment, identify communities with high disease burden or underdiagnosis, and highlight unmet clinical need. Large biobanks have enabled genetics-based models to estimate disease prevalence. Autosomal-recessive (AR) diseases are particularly suited to this approach, as birth prevalence can be inferred from pathogenic allele frequency in unaffected populations; however, this approach has not been validated against real-world clinical datasets at scale. Newborn screening (NBS), which tests for neonatal diseases using quantitative diagnostic methods, provides a uniquely robust comparator for birth prevalence with low ascertainment bias, large sample size, and low diagnostic variability. With the objective of benchmarking a commonly used approach for determining disease prevalence, we applied a genetic model to estimate birth prevalence for 28 AR diseases from NBS panels and compared them with reported birth prevalence from 23 million newborns in the United States. We found that concordance between the genetic estimate and NBS was impacted by the source of allele frequency estimates, ancestry-matching methodology, and pathogenic variant inclusion criteria. Incorporating these refinements, we demonstrate that a genetics-first approach can provide first-order estimates of AR disease birth prevalence for 25 of 28 NBS diseases (89%). However, we note a general underestimate of the genetic prevalence, suggesting that identifying additional sources of pathogenicity would improve concordance with NBS. Further, we assessed the impact of epidemiological and genetic variables, highlighting diseases where genetic prevalence estimates may not be accurate.","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":"136 1","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147743876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Defining a tandem repeat catalog and variation clusters for genome-wide analyses and population databases.","authors":"Ben Weisburd,Egor Dolzhenko,Mark F Bennett,Matt C Danzi,Isaac R L Xu,Hope Tanudisastro,Bida Gu,Adam English,Laurel Hiatt,Tom Mokveld,Guilherme De Sena Brandine,Readman Chiu,Nehir Edibe Kurtas,Helyaneh Ziaei Jam,Harrison Brand,Indhu-Shree Rajan-Babu,Melanie Bahlo,Mark J P Chaisson,Stephan Züchner,Melissa Gymrek,Harriet Dashnow,Michael A Eberle,Heidi L Rehm","doi":"10.1016/j.ajhg.2026.03.020","DOIUrl":"https://doi.org/10.1016/j.ajhg.2026.03.020","url":null,"abstract":"Tandem repeat (TR) catalogs are important components of repeat genotyping studies because they define the genomic coordinates and expected motifs of all TR loci being analyzed. In recent years, genome-wide studies have used catalogs ranging in size from fewer than 200,000 to over 7 million loci. These catalogs differed not only in which loci were included but often also in their definitions of TR locus boundaries and motifs. Now, with multiple groups developing public databases of TR variation in large population cohorts, there is a risk that the use of divergent repeat catalogs will lead to confusion, fragmentation, and incompatibility across resources. Here, we compare existing TR catalogs and discuss desirable features of a comprehensive genome-wide catalog. We then present a new, richly annotated catalog designed for genome-wide analyses and population datasets based on short-read or long-read samples. Additionally, using an algorithm that leverages long-read HiFi sequencing data, our catalog stratifies TRs into (1) isolated repeats suitable for repeat copy-number analysis and (2) variation clusters where TRs are embedded within wider polymorphic regions best studied through sequence-level analysis. We share the TR catalog, variation clusters, and annotations through the TRExplorer portal in order to support both the initial selection of TR loci for inclusion in an analysis and the subsequent interpretation of results.","PeriodicalId":7659,"journal":{"name":"American journal of human genetics","volume":"18 1","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147735341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}