HGG Advances最新文献_第5页

A phenome-wide association study of polygenic scores for selected childhood cancer: Results from the UK Biobank. 选定儿童癌症多基因评分的全表型关联研究：英国生物库的结果

IF 3.3

HGG Advances Pub Date : 2024-09-26 DOI: 10.1016/j.xhgg.2024.100356

Eun Mi Jung, Andrew R Raduski, Lauren J Mills, Logan G Spector

{"title":"A phenome-wide association study of polygenic scores for selected childhood cancer: Results from the UK Biobank.","authors":"Eun Mi Jung, Andrew R Raduski, Lauren J Mills, Logan G Spector","doi":"10.1016/j.xhgg.2024.100356","DOIUrl":"10.1016/j.xhgg.2024.100356","url":null,"abstract":"The aim of this study was to scan phenotypes in adulthood associated with polygenic risk scores (PRS) for childhood cancers with well-articulated genetic architectures-acute lymphoblastic leukemia (ALL), Ewing sarcoma, and neuroblastoma-to examine genetic pleiotropy. Furthermore, we aimed to determine which SNPs could drive associations. Per-SNP summary statistics were extracted for PRS calculation. Participants with white British ancestry were exclusively included for analyses. SNPs were queried from the UK Biobank genotype imputation data. Records from the cancer registry, death registry, and inpatient diagnoses were abstracted for phenome-wide scans. Firth logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) alongside corresponding p values, adjusting for age at recruitment and sex. A total of 244,332 unrelated white British participants were included. We observed a significant association between ALL-PRS and ALL (OR: 1.20e+24, 95% CI: 9.08e+14-1.60e+33). In addition, we observed a significant association between high-risk neuroblastoma PRS and nonrheumatic aortic valve disorders (OR: 43.9, 95% CI: 7.42-260). There were no significant phenotype associations with Ewing sarcoma and neuroblastoma PRS. Regarding individual SNPs, rs17607816 increased the risk of ALL (OR: 6.40, 95% CI: 3.26-12.57). For high-risk neuroblastoma, rs80059929 elevated the risk of atrioventricular block (OR: 3.04, 95% CI: 1.85-4.99). Our findings suggest that individuals with genetic susceptibility to ALL may face a lifelong risk for developing ALL, along with a genetic pleiotropic association between high-risk neuroblastoma and circulatory diseases.","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11538869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142355561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comparison of methods for building polygenic scores for diverse populations. 比较为不同人群建立多基因评分的方法。

IF 3.3

HGG Advances Pub Date : 2024-09-25 DOI: 10.1016/j.xhgg.2024.100355

Sophia Gunn, Xin Wang, Daniel C Posner, Kelly Cho, Jennifer E Huffman, Michael Gaziano, Peter W Wilson, Yan V Sun, Gina Peloso, Kathryn L Lunetta

{"title":"Comparison of methods for building polygenic scores for diverse populations.","authors":"Sophia Gunn, Xin Wang, Daniel C Posner, Kelly Cho, Jennifer E Huffman, Michael Gaziano, Peter W Wilson, Yan V Sun, Gina Peloso, Kathryn L Lunetta","doi":"10.1016/j.xhgg.2024.100355","DOIUrl":"10.1016/j.xhgg.2024.100355","url":null,"abstract":"Polygenic scores (PGSs) are a promising tool for estimating individual-level genetic risk of disease based on the results of genome-wide association studies (GWASs). However, their promise has yet to be fully realized because most currently available PGSs were built with genetic data from predominantly European-ancestry populations, and PGS performance declines when scores are applied to target populations different from the populations from which they were derived. Thus, there is a great need to improve PGS performance in currently under-studied populations. In this work we leverage data from two large and diverse cohorts the Million Veterans Program (MVP) and All of Us (AoU), providing us the unique opportunity to compare methods for building PGSs for multi-ancestry populations across multiple traits. We build PGSs for five continuous traits and five binary traits using both multi-ancestry and single-ancestry approaches with popular Bayesian PGS methods and both MVP META GWAS results and population-specific GWAS results from the respective African, European, and Hispanic MVP populations. We evaluate these scores in three AoU populations genetically similar to the respective African, Admixed American, and European 1000 Genomes Project superpopulations. Using correlation-based tests, we make formal comparisons of the PGS performance across the multiple AoU populations. We conclude that approaches that combine GWAS data from multiple populations produce PGSs that perform better than approaches that utilize smaller single-population GWAS results matched to the target population, and specifically that multi-ancestry scores built with PRS-CSx outperform the other approaches in the three AoU populations.","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11532986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142355562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differential inclusion of NEB exons 143 and 144 provides insight into NEB-related myopathy variant interpretation and disease manifestation. NEB 第 143 和 144 号外显子的不同包含方式为 NEB 相关肌病变异的解释和疾病表现提供了启示。

IF 3.3

HGG Advances Pub Date : 2024-09-23 DOI: 10.1016/j.xhgg.2024.100354

Sarah Silverstein, Rotem Orbach, Safoora Syeda, A Reghan Foley, Svetlana Gorokhova, Katherine G Meilleur, Meganne E Leach, Prech Uapinyoying, Katherine R Chao, Sandra Donkervoort, Carsten G Bönnemann

{"title":"Differential inclusion of NEB exons 143 and 144 provides insight into NEB-related myopathy variant interpretation and disease manifestation.","authors":"Sarah Silverstein, Rotem Orbach, Safoora Syeda, A Reghan Foley, Svetlana Gorokhova, Katherine G Meilleur, Meganne E Leach, Prech Uapinyoying, Katherine R Chao, Sandra Donkervoort, Carsten G Bönnemann","doi":"10.1016/j.xhgg.2024.100354","DOIUrl":"10.1016/j.xhgg.2024.100354","url":null,"abstract":"Biallelic pathogenic variants in the gene encoding nebulin (NEB) are a known cause of congenital myopathy. We present two brothers with congenital myopathy and compound heterozygous variants (NC_000002.12:g.151692086G>T; NM_001271208.2: c.2079C>A; p.(Cys693Ter) and NC_000002.12:g.151533439T>C; NM_001271208.2:c.21522+3A>G) in NEB. Transcriptomic sequencing on affected individual muscles revealed that the extended splice variant c.21522+3A>G causes exon 144 skipping. Nebulin isoforms containing exon 144 are known to be mutually exclusive with isoforms containing exon 143, and these isoforms are differentially expressed during development and in adult skeletal muscles. Affected individuals' MRI patterns of muscle involvement were compared with the known pattern of relative abundance of these two isoforms in muscle. We propose that the pattern of muscle involvement in these affected individuals better fits the distribution of exon 144-containing isoforms in muscle than with previously published MRI findings in NEB-related disease due to other variants. Our report introduces disease pathogenesis and manifestation as a result of alteration of isoform distributions in muscle.","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11525221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142355563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Response to Harding and Martinez. 对哈丁和马丁内斯的回应。

IF 3.3

HGG Advances Pub Date : 2024-07-18 Epub Date: 2024-05-14 DOI: 10.1016/j.xhgg.2024.100307

Dominique L Brooks, Kiran Musunuru, Xiao Wang

引用次数: 0

Targeted sequencing for hereditary breast and ovarian cancer in BRCA1/2-negative families reveals complex genetic architecture and phenocopies. 林奇纪念生物库中 BRCA1/2 阴性家族遗传性乳腺癌和卵巢癌的定向测序揭示了复杂的遗传结构和表型。

IF 3.3

HGG Advances Pub Date : 2024-07-18 Epub Date: 2024-05-10 DOI: 10.1016/j.xhgg.2024.100306

Jocelyn N Plowman, Evanjalina J Matoy, Lavanya V Uppala, Samantha B Draves, Cynthia J Watson, Bridget A Sefranek, Mark L Stacey, Samuel P Anderson, Michael A Belshan, Elizabeth E Blue, Chad D Huff, Yusi Fu, Holly A F Stessman

{"title":"Targeted sequencing for hereditary breast and ovarian cancer in BRCA1/2-negative families reveals complex genetic architecture and phenocopies.","authors":"Jocelyn N Plowman, Evanjalina J Matoy, Lavanya V Uppala, Samantha B Draves, Cynthia J Watson, Bridget A Sefranek, Mark L Stacey, Samuel P Anderson, Michael A Belshan, Elizabeth E Blue, Chad D Huff, Yusi Fu, Holly A F Stessman","doi":"10.1016/j.xhgg.2024.100306","DOIUrl":"10.1016/j.xhgg.2024.100306","url":null,"abstract":"Approximately 20% of breast cancer cases are attributed to increased family risk, yet variation in BRCA1/2 can only explain 20%-25% of cases. Historically, only single gene or single variant testing were common in at-risk family members, and further sequencing studies were rarely offered after negative results. In this study, we applied an efficient and inexpensive targeted sequencing approach to provide molecular diagnoses in 245 human samples representing 134 BRCA mutation-negative (BRCAX) hereditary breast and ovarian cancer (HBOC) families recruited from 1973 to 2019 by Dr. Henry Lynch. Sequencing identified 391 variants, which were functionally annotated and ranked based on their predicted clinical impact. Known pathogenic CHEK2 breast cancer variants were identified in five BRCAX families in this study. While BRCAX was an inclusion criterion for this study, we still identified a pathogenic BRCA2 variant (p.Met192ValfsTer13) in one family. A portion of BRCAX families could be explained by other hereditary cancer syndromes that increase HBOC risk: Li-Fraumeni syndrome (gene: TP53) and Lynch syndrome (gene: MSH6). Interestingly, many families carried additional variants of undetermined significance (VOUSs) that may further modify phenotypes of syndromic family members. Ten families carried more than one potential VOUS, suggesting the presence of complex multi-variant families. Overall, nine BRCAX HBOC families in our study may be explained by known likely pathogenic/pathogenic variants, and six families carried potential VOUSs, which require further functional testing. To address this, we developed a functional assay where we successfully re-classified one family's PMS2 VOUS as benign.","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11166883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140909245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A model organism pipeline provides insight into the clinical heterogeneity of TARS1 loss-of-function variants. 模型生物管道提供了对 TARS1 功能缺失变体临床异质性的深入了解。

IF 3.3

HGG Advances Pub Date : 2024-07-18 Epub Date: 2024-07-02 DOI: 10.1016/j.xhgg.2024.100324

Rebecca Meyer-Schuman, Allison R Cale, Jennifer A Pierluissi, Kira E Jonatzke, Young N Park, Guy M Lenk, Stephanie N Oprescu, Marina A Grachtchouk, Andrzej A Dlugosz, Asim A Beg, Miriam H Meisler, Anthony Antonellis

{"title":"A model organism pipeline provides insight into the clinical heterogeneity of TARS1 loss-of-function variants.","authors":"Rebecca Meyer-Schuman, Allison R Cale, Jennifer A Pierluissi, Kira E Jonatzke, Young N Park, Guy M Lenk, Stephanie N Oprescu, Marina A Grachtchouk, Andrzej A Dlugosz, Asim A Beg, Miriam H Meisler, Anthony Antonellis","doi":"10.1016/j.xhgg.2024.100324","DOIUrl":"10.1016/j.xhgg.2024.100324","url":null,"abstract":"Aminoacyl-tRNA synthetases (ARSs) are ubiquitously expressed, essential enzymes that complete the first step of protein translation: ligation of amino acids to cognate tRNAs. Genes encoding ARSs have been implicated in myriad dominant and recessive phenotypes, the latter often affecting multiple tissues but with frequent involvement of the central and peripheral nervous systems, liver, and lungs. Threonyl-tRNA synthetase (TARS1) encodes the enzyme that ligates threonine to tRNATHR in the cytoplasm. To date, TARS1 variants have been implicated in a recessive brittle hair phenotype. To better understand TARS1-related recessive phenotypes, we engineered three TARS1 missense variants at conserved residues and studied these variants in Saccharomyces cerevisiae and Caenorhabditis elegans models. This revealed two loss-of-function variants, including one hypomorphic allele (R433H). We next used R433H to study the effects of partial loss of TARS1 function in a compound heterozygous mouse model (R432H/null). This model presents with phenotypes reminiscent of patients with TARS1 variants and with distinct lung and skin defects. This study expands the potential clinical heterogeneity of TARS1-related recessive disease, which should guide future clinical and genetic evaluations of patient populations.","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11284558/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141493724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Trait selection strategy in multi-trait GWAS: Boosting SNP discoverability. 多性状 GWAS 中的性状选择策略：提高 SNPs 的可发现性。

IF 3.3

HGG Advances Pub Date : 2024-07-18 Epub Date: 2024-06-13 DOI: 10.1016/j.xhgg.2024.100319

Yuka Suzuki, Hervé Ménager, Bryan Brancotte, Raphaël Vernet, Cyril Nerin, Christophe Boetto, Antoine Auvergne, Christophe Linhard, Rachel Torchet, Pierre Lechat, Lucie Troubat, Michael H Cho, Emmanuelle Bouzigon, Hugues Aschard, Hanna Julienne

{"title":"Trait selection strategy in multi-trait GWAS: Boosting SNP discoverability.","authors":"Yuka Suzuki, Hervé Ménager, Bryan Brancotte, Raphaël Vernet, Cyril Nerin, Christophe Boetto, Antoine Auvergne, Christophe Linhard, Rachel Torchet, Pierre Lechat, Lucie Troubat, Michael H Cho, Emmanuelle Bouzigon, Hugues Aschard, Hanna Julienne","doi":"10.1016/j.xhgg.2024.100319","DOIUrl":"10.1016/j.xhgg.2024.100319","url":null,"abstract":"Since the first genome-wide association studies (GWASs), thousands of variant-trait associations have been discovered. However, comprehensively mapping the genetic determinant of complex traits through univariate testing can require prohibitive sample sizes. Multi-trait GWAS can circumvent this issue and improve statistical power by leveraging the joint genetic architecture of human phenotypes. Although many methodological hurdles of multi-trait testing have been solved, the strategy to select traits has been overlooked. In this study, we conducted multi-trait GWAS on approximately 20,000 combinations of 72 traits using an omnibus test as implemented in the Joint Analysis of Summary Statistics. We assessed which genetic features of the sets of traits analyzed were associated with an increased detection of variants compared with univariate screening. Several features of the set of traits, including the heritability, the number of traits, and the genetic correlation, drive the multi-trait test gain. Using these features jointly in predictive models captures a large fraction of the power gain of the multi-trait test (Pearson's r between the observed and predicted gain equals 0.43, p < 1.6 × 10-60). Applying an alternative multi-trait approach (Multi-Trait Analysis of GWAS), we identified similar features of interest, but with an overall 70% lower number of new associations. Finally, selecting sets based on our data-driven models systematically outperformed the common strategy of selecting clinically similar traits. This work provides a unique picture of the determinant of multi-trait GWAS statistical power and outlines practical strategies for multi-trait testing.","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11260573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141318512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Landscape of genomic structural variations in Indian population-based cohorts: Deeper insights into their prevalence and clinical relevance. 印度人群队列中的基因组结构变异景观：深入了解其流行率和临床相关性。

IF 3.3

HGG Advances Pub Date : 2024-07-18 Epub Date: 2024-03-23 DOI: 10.1016/j.xhgg.2024.100285

Krithika Subramanian, Mehak Chopra, Bratati Kahali

{"title":"Landscape of genomic structural variations in Indian population-based cohorts: Deeper insights into their prevalence and clinical relevance.","authors":"Krithika Subramanian, Mehak Chopra, Bratati Kahali","doi":"10.1016/j.xhgg.2024.100285","DOIUrl":"10.1016/j.xhgg.2024.100285","url":null,"abstract":"Structural variations (SV) are large (>50 base pairs) genomic rearrangements comprising deletions, duplications, insertions, inversions, and translocations. Studying SVs is important because they play active and critical roles in regulating gene expression, determining disease predispositions, and identifying population-specific differences among individuals of diverse ancestries. However, SV discoveries in the Indian population using whole-genome sequencing (WGS) have been limited. In this study, using short-read WGS having an average 42X depth of coverage, we identify and characterize 36,210 SVs from 529 individuals enrolled in population-based cohorts in India. These SVs include 24,574 deletions, 2,913 duplications, 8,710 insertions, and 13 inversions; 1.26% (456 out of 36,210) of the identified SVs can potentially impact the coding regions of genes. Furthermore, 56 of these SVs are highly intolerant to loss-of-function changes to the mapped genes, and five SVs impacting ADAMTS17, CCDC40, and RHCE are common in our study individuals. Seven rare SVs significantly impact dosage sensitivity of genes known to be associated with various clinical phenotypes. Most of the SVs in our study are rare and heterozygous. This fine-scale SV discovery in the underrepresented Indian population provides valuable insights that extend beyond Eurocentric human genetic studies.","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11007539/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140194674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

BRCA1 frameshift variants leading to extended incorrect protein C termini. BRCA1 易位变体导致蛋白质 C 端部延长不正确。

IF 3.3

HGG Advances Pub Date : 2024-07-18 Epub Date: 2024-04-25 DOI: 10.1016/j.xhgg.2024.100296

Thales C Nepomuceno, Tzeh Keong Foo, Marcy E Richardson, John Michael O Ranola, Jamie Weyandt, Matthew J Varga, Amaya Alarcon, Diana Gutierrez, Anna von Wachenfeldt, Daniel Eriksson, Raymond Kim, Susan Armel, Edwin Iversen, Fergus J Couch, Åke Borg, Bing Xia, Marcelo A Carvalho, Alvaro N A Monteiro

引用次数: 0

Critical reasoning on the co-expression module QTL in the dorsolateral prefrontal cortex. 背外侧前额叶皮层共表达模块 QTL 的批判性推理。

IF 3.3

HGG Advances Pub Date : 2024-07-18 Epub Date: 2024-05-21 DOI: 10.1016/j.xhgg.2024.100311

Alanna C Cote, Hannah E Young, Laura M Huckins

{"title":"Critical reasoning on the co-expression module QTL in the dorsolateral prefrontal cortex.","authors":"Alanna C Cote, Hannah E Young, Laura M Huckins","doi":"10.1016/j.xhgg.2024.100311","DOIUrl":"10.1016/j.xhgg.2024.100311","url":null,"abstract":"Expression quantitative trait locus (eQTL) analysis is a popular method of gaining insight into the function of regulatory variation. While cis-eQTL resources have been instrumental in linking genome-wide association study variants to gene function, complex trait heritability may be additionally mediated by other forms of gene regulation. Toward this end, novel eQTL methods leverage gene co-expression (module-QTL) to investigate joint regulation of gene modules by single genetic variants. Here we broadly define a \"module-QTL\" as the association of a genetic variant with a summary measure of gene co-expression. This approach aims to reduce the multiple testing burden of a trans-eQTL search through the consolidation of gene-based testing and provide biological context to eQTLs shared between genes. In this article we provide an in-depth examination of the co-expression module eQTL (module-QTL) through literature review, theoretical investigation, and real-data application of the module-QTL to three large prefrontal cortex genotype-RNA sequencing datasets. We find module-QTLs in our study that are disease associated and reproducible are not additionally informative beyond cis- or trans-eQTLs for module genes. Through comparison to prior studies, we highlight promises and limitations of the module-QTL across study designs and provide recommendations for further investigation of the module-QTL framework.","PeriodicalId":34530,"journal":{"name":"HGG Advances","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141076823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0