Journal of Human Genetics最新文献

{"title":"Implementation of comprehensive genome analysis in clinical sequencing at an academic institution","authors":"Naoko Saito-Sato, Masaki Tanaka, Junko Nomoto, Kanako Koike Fukushima, Masakazu Nishigaki, Shoji Tsuji","doi":"10.1038/s10038-026-01482-x","DOIUrl":"10.1038/s10038-026-01482-x","url":null,"abstract":"Given the increasing number of diseases for which causative genes have been identified, we are facing the need for implementing comprehensive genome sequence analysis as a molecular diagnostic system for patients with hereditary diseases in daily clinical practice. We established a laboratory-developed test (LDT) with the implementation of whole-exome sequence analysis (WES) as the clinical sequencing system at an academic institution. WES was conducted on 81 patients with suspected hereditary disorders referred from clinical departments in our hospital from 2021 to 2024. Target genes were selected on the basis of the clinical presentations of the patients and expanded when necessary. Additional analyses, including copy number and zygosity analyses, further improved the diagnostic accuracy. The overall diagnostic yield was 42.0%, excluding four patients with transthyretin cardiac amyloidosis confirmed as wild-type ATTR Amyloidosis (ATTRwt). High diagnostic yields were associated with the presence of family histories. Secondary findings were searched in 73 patients, and pathogenic or likely pathogenic variants were disclosed to three patients, leading to their subsequent clinical follow-up. Internal and external quality controls ensured analytical reliability. This study demonstrates that the implementation of LDT-based comprehensive genome analysis is highly useful in daily clinical practice, achieving a high diagnostic yield comparable to those in previous large-scale studies; furthermore, the clinical sequencing seamlessly harmonizes the research-level investigations, providing highly valuable results. Broader insurance coverage will be essential for expanding equitable access to the genetic tests based on comprehensive genome sequence analysis.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 9","pages":"587-594"},"PeriodicalIF":2.3,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s10038-026-01482-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gastrointestinal involvement in Ehlers–Danlos syndrome classical-like type 2 associated with a novel AEBP1 splice-site variant","authors":"Hikaru Nakahara, Tomomi Yamaguchi, Hiroaki Niitsu, Akiko Abe, Ryohei Hayashi, Shiro Oka, Koji Arihiro, Tomoki Kosho, Takao Hinoi","doi":"10.1038/s10038-026-01480-z","DOIUrl":"10.1038/s10038-026-01480-z","url":null,"abstract":"Ehlers-Danlos syndrome classical-like type 2 (clEDS2) is a rare autosomal recessive connective tissue disorder caused by biallelic loss-of-function variants in the gene encoding adipocyte enhancer-binding protein 1 (AEBP1). While cutaneous and skeletal manifestations are commonly observed, gastrointestinal complications, including bowel rupture, have been reported only rarely, and their histopathological basis remains poorly characterized. Here, we report findings of molecular investigations, gastrointestinal histopathological evaluation, and long-term clinical follow-up in the 16th reported patient with AEBP1-related clEDS2, complicated by spontaneous bowel perforation. A homozygous AEBP1 splice-site variant (NM_001129.5:c.1401-2 A > G) was identified by a custom next-generation sequencing–based panel analysis for hereditary connective tissue disorders. Transcript-level analysis by reverse transcription-polymerase chain reaction and Sanger sequencing demonstrated complete skipping of exon 12, resulting in a frameshift and predicted loss of function. Clinically, the patient experienced postoperative perforation in the sigmoid colon shortly after rectal cancer surgery, followed nearly 20 years later by spontaneous small intestinal perforation. Histopathological examination of the affected colonic tissue demonstrated mildly widened intermuscular spaces without other overt structural abnormalities. Notably, repeated upper and lower gastrointestinal endoscopic procedures were performed during long-term oncological surveillance without procedure-related bowel perforation. This observation could offer an opportunity to learn about gastrointestinal involvement in AEBP1-related clEDS2 and suggests that its gastrointestinal manifestations may differ in clinical context from those typically associated with vascular Ehlers-Danlos syndrome, warranting further investigation as additional cases are accumulated.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 9","pages":"571-577"},"PeriodicalIF":2.3,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s10038-026-01480-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148031653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HOXB13, a high-risk prostate cancer gene, also confers risk for breast cancer: novel variants of clinical significance, especially in hormone-positive patients","authors":"Filiz Ozen, Zeynep Yegin, Diyar Sayit","doi":"10.1038/s10038-026-01481-y","DOIUrl":"10.1038/s10038-026-01481-y","url":null,"abstract":"Germline mutations in high-risk genes, such as BRCA1 and BRCA2, are primarily responsible for inherited breast cancers, while mutations in moderate-risk genes also increase susceptibility. HOXB13 is established as a high-risk gene for prostate cancer (PCa), but few studies have explored its role in breast cancer. Here, we report, for the first time, novel HOXB13 variants identified in breast cancer patients, suggesting a potential association that warrants further investigation. This retrospective cohort study was conducted at the Medical Genetics Laboratory of Göztepe Prof. Dr. Süleyman Yalçın City Hospital, Turkey, between 2022 and 2025. A total of 4198 individuals who underwent hereditary cancer panel testing were screened. Targeted next-generation sequencing was performed using a Custom Hereditary Cancer (cHCS) panel on the Illumina NextSeq® platform. Raw sequencing data were analyzed using Dragen v3.6 and Sophia DDM pipelines. Among 4198 individuals, 1527 had a confirmed breast cancer diagnosis. Eleven patients harbored variants of uncertain significance (VUS) in HOXB13. Hormone-negative patients (n = 3) carried c.269del, c.766 T > C, and c.309_311del variants. Among hormone-positive patients (n = 8), two carried c.309_311del, one had c.404 G > A, and five carried c.728 A > G (p.K243R), the most frequent variant in this subgroup. The HOXB13 variant spectrum in the Turkish population differed from previously reported data. Novel HOXB13 variants, particularly c.728 A > G (p.K243R), may represent candidate variants of interest that require further validation before any clinical application. These findings highlight a potential association between HOXB13 variants and breast cancer, particularly in hormone receptor-positive patients, and emphasize the need for larger and functionally validated studies.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 9","pages":"565-570"},"PeriodicalIF":2.3,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s10038-026-01481-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148005430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transfer RNA-derived small RNAs: from biogenesis to regulatory roles in male reproductive system","authors":"Xiaodan Jiang, Xinliang Gu, Yang Li, Xiaojue Chen, Shaoqing Ju","doi":"10.1038/s10038-026-01478-7","DOIUrl":"10.1038/s10038-026-01478-7","url":null,"abstract":"With the advancement of next-generation sequencing technologies, transfer RNA (tRNA)-derived small RNAs (tsRNAs) have been progressively elucidated in their biogenesis and classification. tsRNAs are derived from precursor tRNAs (pre-tRNAs) or mature tRNAs and are classified into tRNA-derived fragments (tRFs) and tRNA-derived stress-induced RNAs (tiRNAs) based on their specific endonuclease cleavage sites and are functionally involved in diverse biological processes. tsRNAs are widely distributed within cells and are also present in the male reproductive system. Specifically, tRFs are the predominant tsRNA subspecies with established regulatory functions, whereas tiRNAs are less abundant and their roles remain less characterized. Notably, tsRNAs are particularly abundant in mature sperm, serving as vectors of paternal epigenetic inheritance. Multiple studies have shown that environmental factors and dietary modifications can significantly alter tsRNA profiles in the male reproductive system. Moreover, sperm tsRNAs regulate embryonic quality and are closely associated with male fertility. Collectively, these findings reveal the diverse roles of tsRNAs in male reproductive health and their potential as clinical biomarkers.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 9","pages":"547-555"},"PeriodicalIF":2.3,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanopore third-generation sequencing for the diagnosis of rare hemoglobinopathies in Southern China","authors":"Fen Lin, Shi-Xiong Yang, Yi-Yuan Ge, Ying Yang, Long-Xu Xie, Li-Ye Yang","doi":"10.1038/s10038-026-01477-8","DOIUrl":"10.1038/s10038-026-01477-8","url":null,"abstract":"Thalassemia, a genetically inherited hemoglobinopathy, represents a significant global health challenge with profound socioeconomic implications, particularly in endemic regions. The emergence of third-generation sequencing (TGS) technologies has revolutionized thalassemia research and diagnostic paradigms, offering unprecedented capabilities for comprehensive genetic characterization. Between 2021 and 2024, we conducted a comprehensive analysis of 536 clinically suspected thalassemia cases from southern China, conventional diagnostic methods and Nanopore TGS were performed simultaneously. Among the 536 subjects analyzed, TGS identified 332 cases harboring either common or rare variants, which included 160 cases with rare thalassemia variants, 50 cases with abnormal hemoglobin variants, and 122 cases carrying common α- or β-thalassemia mutations. --THAI and HKαα emerging as the most prevalent variants among rare thalassemia, followed by Chinese (Aγδβ)0 and α-Fusion gene. The predominant abnormal hemoglobin was Hb New York (HBB:c.341 T > A). We used TGS and discovered three rare variants that have not been identified by conventional diagnostic methods for thalassemia, the variants included two cases of α-globin chain 32.8 kb deletions and one case of β-globin chain 3.5 kb deletion. Hb G-Ferrara (HBB:c.174 C > A) and Hb Ethiopia (HBA2:c.421 T > C) were firstly identified in the Chinese population. Moreover, two novel α-globin variants: NC_000016.10:g.176260-176930del and HBA1:c.386 T > C were discovered in this study. This study expands the genetic landscape of hemoglobinopathies in Southern China by characterizing a comprehensive spectrum of rare variants. Our findings demonstrate the superior diagnostic capability of TGS in identifying rare thalassemia genotypes, suggesting its potential as a first-line molecular diagnostic tool for comprehensive hemoglobinopathy screening.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 9","pages":"557-564"},"PeriodicalIF":2.3,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Further delineation of the phenotype and genotype in a newly identified PAN2-related disorder","authors":"Erdem Kındış, Elif Eviz, Serdar Ceylaner","doi":"10.1038/s10038-026-01479-6","DOIUrl":"10.1038/s10038-026-01479-6","url":null,"abstract":"Regulation of mRNA decay is a critical mechanism for effective gene expression. Poly(A) tail length is directly associated with mRNA stability, and deadenylation, which shortens poly(A) tails, plays a central role in mRNA regulation. PAN2 encodes a key component of the deadenylation machinery. Recently, loss-of-function variants in PAN2 have been associated with neurodevelopmental delay and multiple congenital anomalies in seven patients from five unrelated families. Here, we report two siblings presenting with neurodevelopmental delay and multiple congenital anomalies consistent with previously described PAN2-related cases. Notably, both siblings also exhibited esophageal atresia (EA) and developmental dysplasia of the hip (DDH). Whole-exome sequencing (WES) in the older sibling identified a novel homozygous nonsense variant in PAN2, c.1432C>T (p.Arg478Ter). Segregation analysis confirmed homozygosity in the affected sibling, remaining family members were carrier. This study expands the genotypic spectrum of PAN2-related disorder and suggests additional clinical features contributing to this newly emerging disorder.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 10","pages":"677-681"},"PeriodicalIF":2.3,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147973018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Further delineation of KIDAR syndrome: Two new cases with novel variants, functional analysis of the variants and a comprehensive review","authors":"Şule Altıner, Ezgi Gökpınar İli, Ahmet Karer Yurtdaş, Okan Kurtçu, Neslihan Doğulu, Ayşe Öktem, Engin Köse, Fatma Tuba Eminoğlu, Behiye Tuğçe Yıldırım, Ayça Dilruba Aslanger, Gözde Yeşil Sayın, Halil Gürhan Karabulut","doi":"10.1038/s10038-026-01476-9","DOIUrl":"10.1038/s10038-026-01476-9","url":null,"abstract":"The syndrome known as KIDAR (keratitis, ichthyosis, deafness, autosomal recessive) is extremely rare. It is caused by biallelic mutations in AP1B1, encoding adaptor-related protein complex, beta-1 subunit. AP1 complex takes part in the formation of vesicles and the selection of cargo proteins in the trans-golgi network. It also contributes to vesicular transport of ATP7A and ATP7B. Accordingly, KIDAR has been defined as both an adaptinopathy and a copper metabolism disorder. Eleven cases have been reported to date. We report two new KIDAR cases with novel splice site variants—c.1796+1 G > T and c.1796+1 G > C—in AP1B1 (NM_001127.4) gene. Functional analysis of the first variant revealed that this mutation disrupts the normal splicing process, resulting in the creation of a cryptic donor site 150 base pairs downstream of the canonical donor site which introduces a premature stop codon into the transcript. We also present a review of previously reported KIDAR cases and genetic disorders involving altering copper metabolism and highlight our patients’ new clinical features, which may broaden the recognized phenotype. A detailed study of these cases may contribute to the ongoing genetic and clinical characterization of KIDAR syndrome.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 8","pages":"513-520"},"PeriodicalIF":2.3,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13400296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of polygenic risk scores for type 2 diabetes with metabolic measures in Pacific Islanders from Guam and Saipan","authors":"Maria J. Ramirez-Luzuriaga, Saied Safabakhsh, Rasol Salehi, Sayuko Kobes, Tanisha F. Aflague, Jenny Duenas Sarmiento, Joanne E. Curran, Robert G. Nelson, Jeffrey M. Curtis, Carol D. Moffett, Wen-Chi Hsueh, Robert L. Hanson","doi":"10.1038/s10038-026-01474-x","DOIUrl":"10.1038/s10038-026-01474-x","url":null,"abstract":"Several polygenic risk scores (PRSs) for type 2 diabetes (T2D) have been derived from genome-wide association studies (GWASs), but Pacific populations have generally not been represented in these GWASs. The aim of this study was to examine the association of PRS for T2D with diabetes and clinical measures in Pacific Islander populations from Guam and Saipan. We analyzed seven constructions of PRSs in 1990 participants in a GWAS from a community-based cross-sectional study of diabetes. Associations of T2D PRS with diabetes, maximum body mass index (BMI), fasting glucose, and HbA1c were examined with adjustment for age, sex, and the first four genetic principal components (PCs) from the GWAS (to account for population stratification). Insulin resistance/secretion measures were also analyzed in 989 participants without diabetes. All seven PRSs were strongly associated with T2D (p < 5 × 10−9 for each); a 1-SD increase in the PRS was associated with 39–81% increase in the odds of T2D (i.e., standardized odds ratio [OR] ranging 1.39–1.81) adjusting for age, sex, and PCs. We also found that a 1-SD increase in the PRS was associated with 0.30–0.46 mmol/L higher fasting glucose, and with 2.68–4.63 mmol/mol higher HbA1c adjusting for age, sex, and PCs. We found no associations of PRSs with maximum BMI or insulin measures. All seven of the T2D polygenic risk scores evaluated associated significantly and strongly with diabetes, fasting glucose and HbA1c. These analyses suggest that T2D polygenic scores, as currently derived, have a certain degree of transferability to individuals from Pacific populations.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 8","pages":"493-500"},"PeriodicalIF":2.3,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13400312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and structural characterisation of a novel mutation in the CNKSR2 gene associated with Houge-Type X-Linked Intellectual Developmental Disorder","authors":"Anil Kumar, Ajay Kumar, Chandraniv Dey, Arvinder Wander, Sudip Chakraborty, Anjana Munshi","doi":"10.1038/s10038-026-01475-w","DOIUrl":"10.1038/s10038-026-01475-w","url":null,"abstract":"Neurological disorders with overlapping phenotypes pose significant diagnostic challenges, especially the ones that occur on account of rare genetic variants. We hereby report a case of a 16-year-old male with clinical symptoms of severe intellectual disability, excessive appetite, an elongated face with decreased body weight (<-2 SD) and microcephaly (<-3 SD). Behavioral manifestations like attention deficit, hyperactivity, and impulsivity were also observed in the patient. The Exome sequencing of affected child revealed a novel frameshift insertion in the CNKSR2 gene, or connector enhancer of kinase suppressor of Ras 2, which is located on the X chromosome. In consensus with the phenotypes of the patient, this novel variant has an association with Houge type of X-linked intellectual developmental disorder. This is the first case reporting a pathogenic frameshift insertion in CNKSR2 (c.2489dup: p. Arg831Glufs *21) gene that encodes a protein that plays a significant role in neuronal proliferation, migration, and differentiation. The integrative molecular dynamics simulation analyses revealed substantial differences in the structural dynamics and stability between the wild-type protein and its mutant form, resulting in a more rigid protein due to the presence of the mutation. This finding broadens the mutation spectrum of CNKSR2 and the importance of exploring mutations in this gene in association with Intellectual developmental disorders. Early detection of such pathogenic variants in associated genes not only helps with clinical diagnosis and management but also has the potential to avert the birth of another affected individual in the family.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 8","pages":"501-512"},"PeriodicalIF":2.3,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SMN1 mutation spectrum and functional analysis of novel SMN1 variants in a Chinese spinal muscular atrophy cohort","authors":"Gui-He Li, Li-Wen Wu, Jing Li, Sen-Wei Dong, Jing-Mei Hong, Ying-Xuan Xie, Yu-Hao Sun, Jin He, Ning Wang, Wan-Jin Chen, Hai-Zhu Chen","doi":"10.1038/s10038-026-01473-y","DOIUrl":"10.1038/s10038-026-01473-y","url":null,"abstract":"Spinal muscular atrophy is the most common fatal neurogenetic disorder in infancy and early childhood, caused by insufficient expression of SMN protein due to mutations in the survival motor neuron 1 (SMN1) gene. In this study, we describe the SMN1 mutation spectrum in our SMA cohort and the clinical characteristics of 30 patients with SMN1 compound heterozygous mutations. We find the c.22_23insA hotspot mutation has a founder effect, and identify 6 novel SMN1 variants and verify the pathogenicity of these variants at molecular levels. This study proposes that SMA newborn screening should integrate RT-PCR, MLPA, and long-read sequencing to prevent missed diagnoses of compound heterozygous mutations. Furthermore, in the era of therapeutics, new clinical classification methods based on genetic characteristics are worthy of further exploration.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 8","pages":"535-540"},"PeriodicalIF":2.3,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}