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Human Genome Variation最新文献

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National Center Biobank Network. 国家中心生物银行网络。
IF 1.5
Human Genome Variation Pub Date : 2022-11-04 DOI: 10.1038/s41439-022-00217-6
Yosuke Omae, Yu-Ichi Goto, Katsushi Tokunaga
{"title":"National Center Biobank Network.","authors":"Yosuke Omae,&nbsp;Yu-Ichi Goto,&nbsp;Katsushi Tokunaga","doi":"10.1038/s41439-022-00217-6","DOIUrl":"https://doi.org/10.1038/s41439-022-00217-6","url":null,"abstract":"<p><p>There are six national centers (6NCs) for advanced and specialized medicine in Japan that conduct basic and clinical research on major diseases that have a substantial impact on national health. Disease-specific bioresources and information collected by each NC are stored in a separate biobank. The National Center Biobank Network (NCBN) was established in 2011 and coordinates the biobanks and researchers of the 6NCs via an open-access database (Catalogue Database: http://www2.ncbiobank.org/Index_en ) as an efficient means of providing registered biological resources and data for use in research communities. The NCBN resources are characterized by their high-quality and rich medical information and are available for life science research and for the development of novel testing methodologies (biomarkers), new treatments, and drugs for future health care in the scope of personalized medicine through a deeper understanding of disease pathogenesis. Here, we explain the activities of the NCBN and the characteristics of the NCBN Catalogue Database.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9636156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10513150","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: 2
An MSH6 germline pathogenic variant p.Gly162Ter associated with Lynch syndrome. 与Lynch综合征相关的MSH6种系致病变异p.Gly162Ter。
IF 1.5
Human Genome Variation Pub Date : 2022-10-26 DOI: 10.1038/s41439-022-00216-7
Olga A Vostrukhina, Elena D Mirlina, Darya N Khmelkova, Galina M Butrovich, Alexandra D Shakhmatova, Yury V Kil, Yliya L Polyatskin, Anna S Artemyeva, Alexey V Gulyaev, Valery N Verbenko
{"title":"An MSH6 germline pathogenic variant p.Gly162Ter associated with Lynch syndrome.","authors":"Olga A Vostrukhina,&nbsp;Elena D Mirlina,&nbsp;Darya N Khmelkova,&nbsp;Galina M Butrovich,&nbsp;Alexandra D Shakhmatova,&nbsp;Yury V Kil,&nbsp;Yliya L Polyatskin,&nbsp;Anna S Artemyeva,&nbsp;Alexey V Gulyaev,&nbsp;Valery N Verbenko","doi":"10.1038/s41439-022-00216-7","DOIUrl":"https://doi.org/10.1038/s41439-022-00216-7","url":null,"abstract":"<p><p>We identified a three-generation Russian family with Lynch syndrome with a novel germline variant of the MSH6 gene. An 84-year-old female was diagnosed with endometrial adenocarcinoma at the age of 49 years. Her son was diagnosed with colorectal tubular adenoma at the age of 32 years. A germline nonsense variant (c.484 G > T:p.Gly162Ter) in exon 3 of the MSH6 gene was revealed by whole-exome sequencing. Sanger sequencing confirmed the cosegregation of the MSH6 nonsense variant in family members.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9605995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10498470","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: 1
Cloud service checklist for academic communities and customization for genome medical research. 学术界的云服务清单和基因组医学研究的定制。
IF 1.5
Human Genome Variation Pub Date : 2022-10-17 DOI: 10.1038/s41439-022-00214-9
Kumiko Kobayashi, Hiroshi Yoshida, Tomoya Tanjo, Kento Aida
{"title":"Cloud service checklist for academic communities and customization for genome medical research.","authors":"Kumiko Kobayashi,&nbsp;Hiroshi Yoshida,&nbsp;Tomoya Tanjo,&nbsp;Kento Aida","doi":"10.1038/s41439-022-00214-9","DOIUrl":"https://doi.org/10.1038/s41439-022-00214-9","url":null,"abstract":"<p><p>In this paper, we present a cloud service checklist designed to help IT administrators or researchers in academic organizations select the most suitable cloud services. This checklist, which comprises items that we believe IT administrators or researchers in academic organizations should consider when they adopt cloud services, comprehensively covers the issues related to a variety of cloud services, including security, functionality, performance, and law. In response to the increasing demands for storage and computing resources in genome medical science communities, various guidelines for using resources operated by external organizations, such as cloud services, have been published by different academic funding agencies and the Japanese government. However, it is sometimes difficult to identify the checklist items that satisfy the genome medical science community's guidelines, and some of these requirements are not included in the existing checklists. This issue provided our motivation for creating a cloud service checklist customized for genome medical research communities. The resulting customized checklist is designed to help researchers easily find information about the cloud services that satisfy the guidelines in genome medical science communities. Additionally, we explore whether many cloud service providers satisfy the requirements or checklist items in the cloud service checklist for genome medical research by evaluating their survey responses.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9574824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10556442","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 Japanese patient with neonatal biotin-responsive basal ganglia disease. 日本新生儿生物素反应性基底神经节病1例。
IF 1.5
Human Genome Variation Pub Date : 2022-09-29 DOI: 10.1038/s41439-022-00210-z
Mizuki Kobayashi, Yuichi Suzuki, Maki Nodera, Ayako Matsunaga, Masakazu Kohda, Yasushi Okazaki, Kei Murayama, Takanori Yamagata, Hitoshi Osaka
{"title":"A Japanese patient with neonatal biotin-responsive basal ganglia disease.","authors":"Mizuki Kobayashi,&nbsp;Yuichi Suzuki,&nbsp;Maki Nodera,&nbsp;Ayako Matsunaga,&nbsp;Masakazu Kohda,&nbsp;Yasushi Okazaki,&nbsp;Kei Murayama,&nbsp;Takanori Yamagata,&nbsp;Hitoshi Osaka","doi":"10.1038/s41439-022-00210-z","DOIUrl":"https://doi.org/10.1038/s41439-022-00210-z","url":null,"abstract":"<p><p>Biotin-responsive basal ganglia disease (BBGD) with SLC19A3 mutation was first reported in 1998, and over 30 mutations have been reported. We report a neonatal BBGD case with sudden-onset feeding difficulty and impaired consciousness. Encephalopathy resolved after the initiation of biotin and thiamine treatment. Genetic testing revealed a novel heterozygous mutation [c.384_387del, p.Tyr128fs];[c.265 A > C, p.Ser89Arg] in SLC19A3. Early treatment for BBGD is essential, especially with onset in the neonatal or early infancy period.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9522647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10512609","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: 1
Pathological variants in genes associated with disorders of sex development and central causes of hypogonadism in a whole-genome reference panel of 8380 Japanese individuals. 在8380名日本人的全基因组参考小组中，与性发育障碍和性腺功能减退的主要原因相关的基因病理变异。
IF 1.5
Human Genome Variation Pub Date : 2022-09-28 DOI: 10.1038/s41439-022-00213-w
Naomi Shiga, Yumi Yamaguchi-Kabata, Saori Igeta, Jun Yasuda, Shu Tadaka, Takamichi Minato, Zen Watanabe, Junko Kanno, Gen Tamiya, Nobuo Fuse, Kengo Kinoshita, Shigeo Kure, Akiko Kondo, Masahito Tachibana, Masayuki Yamamoto, Nobuo Yaegashi, Junichi Sugawara
{"title":"Pathological variants in genes associated with disorders of sex development and central causes of hypogonadism in a whole-genome reference panel of 8380 Japanese individuals.","authors":"Naomi Shiga,&nbsp;Yumi Yamaguchi-Kabata,&nbsp;Saori Igeta,&nbsp;Jun Yasuda,&nbsp;Shu Tadaka,&nbsp;Takamichi Minato,&nbsp;Zen Watanabe,&nbsp;Junko Kanno,&nbsp;Gen Tamiya,&nbsp;Nobuo Fuse,&nbsp;Kengo Kinoshita,&nbsp;Shigeo Kure,&nbsp;Akiko Kondo,&nbsp;Masahito Tachibana,&nbsp;Masayuki Yamamoto,&nbsp;Nobuo Yaegashi,&nbsp;Junichi Sugawara","doi":"10.1038/s41439-022-00213-w","DOIUrl":"https://doi.org/10.1038/s41439-022-00213-w","url":null,"abstract":"<p><p>Disorders of sex development (DSD) comprises a congenital condition in which chromosomal, gonadal, or anatomical sex development is atypical. In this study, we screened for pathogenic variants in 32 genes associated with DSDs and central causes of hypogonadism (CHG) in a whole-genome reference panel including 8380 Japanese individuals constructed by Tohoku Medical Megabank Organization. Candidate pathogenic (P) or likely pathogenic (LP) variants were extracted from the ClinVar, InterVar, and Human Gene Mutation databases. Ninety-one candidate pathological variants were found in 25 genes; 28 novel candidate variants were identified. Nearly 1 in 40 (either ClinVar or InterVar P or LP) to 157 (both ClinVar and InterVar P or LP) individuals were found to be carriers of recessive DSD and CHG alleles. In these data, genes implicated in gonadal dysfunction did not show loss-of-function variants, with a relatively high tendency of intolerance for haploinsufficiency based on pLI and Episcore, both of which can be used for estimating haploinsufficiency. We report the types and frequencies of causative variants for DSD and CHG in the general Japanese population. This study furthers our understanding of the genetic causes and helps to refine genetic counseling of DSD and CHG.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9519586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10516916","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
The ATRX splicing variant c.21-1G>A is asymptomatic. ATRX剪接变异体c.21-1G>A无症状。
IF 1.5
Human Genome Variation Pub Date : 2022-09-14 DOI: 10.1038/s41439-022-00212-x
Karin Kojima, Takahito Wada, Hiroko Shimbo, Takahiro Ikeda, Eriko F Jimbo, Hirotomo Saitsu, Naomichi Matsumoto, Takanori Yamagata
{"title":"The ATRX splicing variant c.21-1G>A is asymptomatic.","authors":"Karin Kojima,&nbsp;Takahito Wada,&nbsp;Hiroko Shimbo,&nbsp;Takahiro Ikeda,&nbsp;Eriko F Jimbo,&nbsp;Hirotomo Saitsu,&nbsp;Naomichi Matsumoto,&nbsp;Takanori Yamagata","doi":"10.1038/s41439-022-00212-x","DOIUrl":"https://doi.org/10.1038/s41439-022-00212-x","url":null,"abstract":"<p><p>The ATRX variant c.21-1G>A was detected by an exome analysis of a patient with Cockayne syndrome without alpha thalassemia X-linked intellectual disability syndrome (ATR-XS). In addition, variants in ERCC6 were detected. ATRX c.21-1G>A is localized at the splicing acceptor site of intron 1. This splicing event, NM_000489.6: c.21_133del p.S7Rfs*1, induces exon 2 deletion and early termination. The start codon in exon 3 of ATRX is presumed to produce a slightly shorter but functional ATRX protein.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9474544/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10491073","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
Maternal uniparental disomy of chromosome 7 underlying argininosuccinic aciduria and Silver-Russell syndrome. 精氨酸琥珀酸尿和银罗素综合征的7号染色体单亲二体。
IF 1.5
Human Genome Variation Pub Date : 2022-09-12 DOI: 10.1038/s41439-022-00211-y
Atsushi Hattori, Torayuki Okuyama, Tetsumin So, Motomichi Kosuga, Keiko Ichimoto, Kei Murayama, Masayo Kagami, Maki Fukami, Yasuyuki Fukuhara
{"title":"Maternal uniparental disomy of chromosome 7 underlying argininosuccinic aciduria and Silver-Russell syndrome.","authors":"Atsushi Hattori,&nbsp;Torayuki Okuyama,&nbsp;Tetsumin So,&nbsp;Motomichi Kosuga,&nbsp;Keiko Ichimoto,&nbsp;Kei Murayama,&nbsp;Masayo Kagami,&nbsp;Maki Fukami,&nbsp;Yasuyuki Fukuhara","doi":"10.1038/s41439-022-00211-y","DOIUrl":"https://doi.org/10.1038/s41439-022-00211-y","url":null,"abstract":"<p><p>We describe a patient presenting with argininosuccinic aciduria and Silver-Russell syndrome (SRS). SRS was caused by maternal uniparental disomy of chromosome 7 (UPD(7)mat). UPD(7)mat also unmasked a maternally inherited splicing variant in ASL on chromosome 7, leading to the onset of argininosuccinic aciduria. The phenotype of the present case was more severe than that of a previous case, demonstrating a phenotypic variation in the combination of argininosuccinic aciduria and SRS.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9468177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10512103","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: 1
A genomic deletion encompassing CRYBB2-CRYBB2P1 is responsible for autosomal recessive congenital cataracts. 包含CRYBB2-CRYBB2P1的基因组缺失是常染色体隐性遗传性先天性白内障的原因。
IF 1.5
Human Genome Variation Pub Date : 2022-09-08 DOI: 10.1038/s41439-022-00208-7
Bushra Irum, Firoz Kabir, Nadav Shoshany, Shahid Y Khan, Bushra Rauf, Muhammad Asif Naeem, Tanveer A Qaiser, Sheikh Riazuddin, J Fielding Hejtmancik, S Amer Riazuddin
{"title":"A genomic deletion encompassing CRYBB2-CRYBB2P1 is responsible for autosomal recessive congenital cataracts.","authors":"Bushra Irum,&nbsp;Firoz Kabir,&nbsp;Nadav Shoshany,&nbsp;Shahid Y Khan,&nbsp;Bushra Rauf,&nbsp;Muhammad Asif Naeem,&nbsp;Tanveer A Qaiser,&nbsp;Sheikh Riazuddin,&nbsp;J Fielding Hejtmancik,&nbsp;S Amer Riazuddin","doi":"10.1038/s41439-022-00208-7","DOIUrl":"https://doi.org/10.1038/s41439-022-00208-7","url":null,"abstract":"<p><p>Here we report a consanguineous Pakistani family with multiple affected individuals with autosomal recessive congenital cataract (arCC). Exclusion analysis established linkage to chromosome 22q, and Sanger sequencing coupled with PCR-based chromosome walking identified a large homozygous genomic deletion. Our data suggest that this deletion leads to CRYBB2-CRYBB2P1 fusion, consisting of exons 1-5 of CRYBB2 and exon 6 of CRYBB2P1, the latter of which harbors the c.463 C > T (p.Gln155*) mutation, and is responsible for arCC.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9458725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9073828","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 novel COL4A5 splicing variant causing X-linked Alport syndrome: A case report. 一种新的COL4A5剪接变异导致x连锁Alport综合征:1例报告。
IF 1.5
Human Genome Variation Pub Date : 2022-08-31 DOI: 10.1038/s41439-022-00209-6
Naonori Kumagai, Yuji Matsumoto, Tomomi Kondoh, Yohei Ikezumi
{"title":"A novel COL4A5 splicing variant causing X-linked Alport syndrome: A case report.","authors":"Naonori Kumagai,&nbsp;Yuji Matsumoto,&nbsp;Tomomi Kondoh,&nbsp;Yohei Ikezumi","doi":"10.1038/s41439-022-00209-6","DOIUrl":"https://doi.org/10.1038/s41439-022-00209-6","url":null,"abstract":"<p><p>Alport syndrome is a hereditary disorder characterized by renal impairment, hearing loss, and ocular symptoms and is caused by COL4A3, COL4A4, and COL4A5 mutations. Here, we report the case of 3-year-old boy with isolated hematuria detected in routine preventative urinary screening conducted in 3-year-old children. He carried a novel variant, NM_033380.3:c. 1032 + 1 G > A, which caused a splicing abnormality in COL4A5. He was diagnosed with X-linked Alport syndrome.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9433376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10497419","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 Japanese family with dystonia due to a pathogenic variant in SGCE. 一个日本家族因SGCE致病性变异而出现肌张力障碍。
IF 1.5
Human Genome Variation Pub Date : 2022-08-22 DOI: 10.1038/s41439-022-00207-8
Takuya Morikawa, Shiroh Miura, Luoming Fan, Emina Watanabe, Ryuta Fujioka, Hiromichi Motooka, Shingo Yasumoto, Yusuke Uchiyama, Hiroki Shibata
{"title":"A Japanese family with dystonia due to a pathogenic variant in SGCE.","authors":"Takuya Morikawa,&nbsp;Shiroh Miura,&nbsp;Luoming Fan,&nbsp;Emina Watanabe,&nbsp;Ryuta Fujioka,&nbsp;Hiromichi Motooka,&nbsp;Shingo Yasumoto,&nbsp;Yusuke Uchiyama,&nbsp;Hiroki Shibata","doi":"10.1038/s41439-022-00207-8","DOIUrl":"https://doi.org/10.1038/s41439-022-00207-8","url":null,"abstract":"<p><p>Dystonia (DYT) is a heterogeneous neurological disorder, and there are many types of DYT depending on the responsible genes. DYT11 is an autosomal dominant DYT caused by functional variants in the SGCE gene. We examined a Japanese patient with myoclonic dystonia. By using exome analysis, we identified a rare variant in the SGCE gene, NM_003919.3: c.304C > T [Arg102*], in this patient. Therefore, this patient has been molecularly diagnosed with DYT11. By Sanger sequencing, we confirmed that this variant was paternally inherited in this patient. By allele-specific PCR, we confirmed that the maternally inherited normal allele of SGCE was silenced, and only the paternally inherited variant allele was expressed in this patient. Despite the pathogenicity, identical variants have been recurrently reported in eight independent families from different ethnicities, suggesting recurrent mutations at this mutational hotspot in SGCE.</p>","PeriodicalId":36861,"journal":{"name":"Human Genome Variation","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2022-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9395531/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9073808","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
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