Journal of Human Genetics最新文献_第9页

Rebuttal Letter: Response to Albert Min-Shan Ko, Hung-Pin Tu and Ying-Chin Ko, “Genetic insights into the origin, admixture, and migration of the early Austronesian peoples” 反驳函：回应柯敏山、杜鸿彬、柯颖钦，“早期南岛人的起源、混合及迁移之遗传学见解”。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-12-17 DOI: 10.1038/s10038-025-01420-3

Hirofumi Matsumura, Hsiao-Chun Hung, Peter Bellwood

引用次数: 0

Commentary on the Austronesian peoples have nothing to do with the so-called “two-layer” model 对南岛人的评论与所谓的“两层”模型无关。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-12-17 DOI: 10.1038/s10038-025-01440-z

Albert Min-Shan Ko, Hung-Pin Tu, Ying-Chin Ko

引用次数: 0

Genome and transcriptome-wide association studies identify multiple novel loci for dementia with grain in Japanese 基因组和全转录组关联研究确定了日本谷物痴呆的多个新位点。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-12-17 DOI: 10.1038/s10038-025-01438-7

Risa Mitsumori, Kouichi Ozaki, Yuko Saito, Daichi Shigemizu, Atsushi Iwata, Shigeo Murayama, Masahiro Akishita, Tomio Arai, Shumpei Niida, Kenji Toba

{"title":"Genome and transcriptome-wide association studies identify multiple novel loci for dementia with grain in Japanese","authors":"Risa Mitsumori, Kouichi Ozaki, Yuko Saito, Daichi Shigemizu, Atsushi Iwata, Shigeo Murayama, Masahiro Akishita, Tomio Arai, Shumpei Niida, Kenji Toba","doi":"10.1038/s10038-025-01438-7","DOIUrl":"10.1038/s10038-025-01438-7","url":null,"abstract":"Argyrophilic grain (AG) is a common neurodegenerative accumulation of 4 repeat tau in dendritic spine. Dementia with grain (DG) is defined as AGs with a sole pathological basis for cognitive decline. As with other multifactorial diseases, DG could result from interactions of environmental and genetic factors. However, the genetic basis of DG is largely unknown. To clarify the genetic architecture of DG pathogenesis, we conducted a genome-wide association study (GWAS) with 214 DG cases versus 12,405 controls. We have identified a candidate locus associated with the risk of DG, the SVIL locus on chromosome 10, with genome-wide significance (rs11595141, P = 4.86 $$times$$ 10–8) in the GWAS. Transcriptome-wide association analysis using summary statistics for DG-GWAS identified DAPK2 (PTWAS = 3.68 $$times$$ 10–5) as a novel candidate causal gene for DG pathogenesis in the brain frontal cortex. The genetic association analysis for the APOE locus revealed that the APOE allele did not affect DG pathogenesis. We also identified new variants in the MAPT encoding tau protein that could potentially affect DG pathology. This is the first GWAS for DG, and our genetic findings provide biological and clinical insights into the pathogenesis of DG.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 5","pages":"301-308"},"PeriodicalIF":2.5,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s10038-025-01438-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145768258","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}

引用次数: 0

TMEM53 as an outer nuclear membrane regulator of cranial and tubular bone formation in craniotubular dysplasia TMEM53作为颅小管发育不良患者颅小管骨形成的外核膜调节剂。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-12-17 DOI: 10.1038/s10038-025-01443-w

Kaitao Ren, Yiyang Fu, Jinhui Zhu, Wanqi Liu, Yuxin Han, Shuying Zhang, Xiaorui Zhang, Mingyue Chen, Congcong Xia, Kexin Sun, Dan Xiao, Yuan Liu, Lin Wang, Rong Qiang, Chisa Shukunami, Katta M. Girisha, Shiro Ikegawa, Long Guo

{"title":"TMEM53 as an outer nuclear membrane regulator of cranial and tubular bone formation in craniotubular dysplasia","authors":"Kaitao Ren, Yiyang Fu, Jinhui Zhu, Wanqi Liu, Yuxin Han, Shuying Zhang, Xiaorui Zhang, Mingyue Chen, Congcong Xia, Kexin Sun, Dan Xiao, Yuan Liu, Lin Wang, Rong Qiang, Chisa Shukunami, Katta M. Girisha, Shiro Ikegawa, Long Guo","doi":"10.1038/s10038-025-01443-w","DOIUrl":"10.1038/s10038-025-01443-w","url":null,"abstract":"Transmembrane protein 53 (TMEM53) is an outer nuclear membrane protein that plays a crucial role in maintaining skeletal homeostasis. Pathogenic variants in TMEM53 have been identified as the genetic cause of craniotubular dysplasia, Ikegawa type (CTDI), a rare form of sclerosing bone dysplasia characterized by skull hyperostosis, cranial deformities, and increased bone density. To date, the causal association of bi-allelic pathogenic variants of TMEM53 in CTDI has been identified in 14 patients from eight unrelated families. Mechanistically, TMEM53 negatively regulates BMP–SMAD signaling by restricting the nuclear import of phosphorylated SMAD1/5/9, thereby modulating osteoblast differentiation and bone formation. This review summarizes the current understanding of TMEM53 function and the consequences of its deficiency. We aim to clarify genotype-phenotype correlations, outline therapeutic prospects for CTDI, and explore the distinct mechanisms underlying cranial and tubular bone formation.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 5","pages":"319-325"},"PeriodicalIF":2.5,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145774724","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}

引用次数: 0

Polygenic and single-locus selection on BMI during Polynesian expansion 波利尼西亚扩张时期BMI的多基因和单位点选择。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-12-15 DOI: 10.1038/s10038-025-01441-y

Hanako Miwa, Mariko Isshiki, Izumi Naka, Ryosuke Kimura, Tsukasa Inaoka, Yasuhiro Matsumura, Jun Ohashi

{"title":"Polygenic and single-locus selection on BMI during Polynesian expansion","authors":"Hanako Miwa, Mariko Isshiki, Izumi Naka, Ryosuke Kimura, Tsukasa Inaoka, Yasuhiro Matsumura, Jun Ohashi","doi":"10.1038/s10038-025-01441-y","DOIUrl":"10.1038/s10038-025-01441-y","url":null,"abstract":"The ‘thrifty’ variant hypothesis, which posits that certain genetic adaptations promoting efficient energy storage during periods of food scarcity, has been invoked to explain the high prevalence of obesity in modern human populations. Although several candidate variants have been proposed, the timing and effects of these variants on body mass index (BMI) in specific populations remain poorly understood. In this study, we performed whole-genome sequencing of 22 Tongan individuals. A previous study identified the rs373863828-A variant in the CREBRF gene as a target of positive selection in Samoans based on iHS analysis. Here, we replicated this signal in Tongans, confirming that this variant has been subject to adaptive pressures more broadly across Polynesian populations. Using the CLUES program, we inferred the allele frequency trajectory of rs373863828-A in Tongans, revealing a marked increase over the past ~100 generations that temporally aligns with the period of Polynesian maritime expansion. The trajectory of the Polygenic Score (PS) showed an increase in the PS for BMI in ancestors of Tongans between 150 and 50 generations ago, followed by a recent decline. Analysis of polarized trait integrated haplotype scores detected significant polygenic selection favoring lower BMI in recent generations. Our findings suggest that the CREBRF variant underwent strong positive selection during oceanic dispersal, while numerous modest-effect variants collectively contributed to adaptation to food-limited environments during long sea voyages. More recently, however, selection pressures may have shifted toward lower BMI, indicating a potential evolutionary mismatch between past adaptations and modern environments.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 5","pages":"293-300"},"PeriodicalIF":2.5,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s10038-025-01441-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145763141","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}

引用次数: 0

Galactose mutarotase deficiency as the galactosemia type IV. 半乳糖变性酶缺乏症称为半乳糖血症IV型。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-12-15 DOI: 10.1038/s10038-025-01439-6

Yoichi Wada, Yu Aihara, Yasuko Mikami-Saito, Tomohisa Suzuki, Ryoji Fujiki, Osamu Ohara, Atsuo Kikuchi, Shigeo Kure

{"title":"Galactose mutarotase deficiency as the galactosemia type IV.","authors":"Yoichi Wada, Yu Aihara, Yasuko Mikami-Saito, Tomohisa Suzuki, Ryoji Fujiki, Osamu Ohara, Atsuo Kikuchi, Shigeo Kure","doi":"10.1038/s10038-025-01439-6","DOIUrl":"https://doi.org/10.1038/s10038-025-01439-6","url":null,"abstract":"<p><p>Galactose, a monosaccharide, plays diverse biological roles in energy production, especially in the glycolysis and glycosylation of proteins and lipids. Galactose metabolism is mediated by the Leloir pathway, which comprises four key enzymes. Following lactose hydrolysis, galactose mutarotase (GALM) catalyzes the anomerization of β-D-galactose to α-D-galactose, providing a substrate for the downstream pathway. In 2019, GALM deficiency was defined as the fourth type of galactosemia. Affected individuals may develop cataracts similar to those observed in individuals with galactokinase deficiency, disrupting the subsequent steps in the Leloir pathway. However, cataracts generally occur less frequently and tend to be milder in patients with GALM deficiency, likely because of the partial compensation provided by spontaneous galactose mutarotation in aqueous solutions. Because lactose, the primary dietary source of galactose, is the predominant carbohydrate consumed until weaning, the timely initiation of lactose restriction can prevent or even reverse cataract formation. To date, other complications or adverse events, including those in heterozygous carriers of GALM variants, have not been clearly demonstrated. This review aims to synthesize current knowledge and findings of GALM deficiency on molecular mechanisms, clinical presentation, diagnostic approaches, carrier risk, and dietary management, with particular emphasis on cataract prevention and reversibility through early lactose restriction. By consolidating available evidence, we propose future research directions, with broader implications for newborn screening programs, clinical decision-making, and a deeper understanding of galactose metabolism.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145763178","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}

引用次数: 0

Genetic characterization of a Chinese cohort of suspected pediatric NF1 patients: a large-scale study using optimized whole-exome sequencing 中国疑似儿童NF1患者队列的遗传特征：一项使用优化全外显子组测序的大规模研究。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-12-10 DOI: 10.1038/s10038-025-01433-y

Kaiyu Wang, Miao Jing, Jun Mao, Manli Wang, Yuxiang Lin, Mei Peng, Fang Zheng, Li Zhang, Quanze He

{"title":"Genetic characterization of a Chinese cohort of suspected pediatric NF1 patients: a large-scale study using optimized whole-exome sequencing","authors":"Kaiyu Wang, Miao Jing, Jun Mao, Manli Wang, Yuxiang Lin, Mei Peng, Fang Zheng, Li Zhang, Quanze He","doi":"10.1038/s10038-025-01433-y","DOIUrl":"10.1038/s10038-025-01433-y","url":null,"abstract":"Neurofibromatosis type 1 (NF1) is a common autosomal dominant disorder with broad clinical variability, making diagnosis in pediatric patients particularly challenging due to age-dependent penetrance and variable expressivity. In this study, we analyzed 536 unrelated Chinese children with clinical suspicion of NF1 using optimized whole-exome sequencing (WES) enhanced by targeted probe enrichment and exon-level copy number variation (CNV) analysis to investigate the molecular etiology and mutation spectrum. Pathogenic or likely pathogenic variants were identified in 288 patients (53.7%), including 271 with variants in the NF1 gene. These consisted of 197 distinct small sequence variants (SNVs) and 25 CNVs, of which 19 were large multigenic deletions, and 6 were intragenic. Notably, 62 of the NF1 SNVs were novel. The incorporation of exon-level CNV analysis and probe enrichment improved the diagnostic yield by 9.2% and 2.2%, respectively. Seven patients were found to have dual diagnoses involving NF1 and other genetic disorders, including six novel combinations. In addition, 17 were diagnosed with non-NF1 conditions such as RASopathies and cancer predisposition syndromes. Our findings highlight the value of optimized WES strategies in improving diagnostic accuracy and yield, particularly for pediatric patients with atypical clinical presentations. This study represents one of the most comprehensive assessments of NF1 molecular diagnostics in a Chinese pediatric population.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 5","pages":"283-291"},"PeriodicalIF":2.5,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145724016","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}

引用次数: 0

Respiratory complex I deficiency caused by a novel multi-exonic PUS1 deletion 由一种新的多外显子PUS1缺失引起的呼吸复合体I缺陷。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-12-08 DOI: 10.1038/s10038-025-01437-8

Jun-Hui Yuan, Yujiro Higuchi, Masahiro Ando, Akihiro Hashiguchi, Yuji Okamoto, Yu Hiramatsu, Akiko Yoshimura, Kento Kodama, Yusuke Sakiyama, Jun Mitsui, Shoji Tsuji, Hiroshi Takashima

{"title":"Respiratory complex I deficiency caused by a novel multi-exonic PUS1 deletion","authors":"Jun-Hui Yuan, Yujiro Higuchi, Masahiro Ando, Akihiro Hashiguchi, Yuji Okamoto, Yu Hiramatsu, Akiko Yoshimura, Kento Kodama, Yusuke Sakiyama, Jun Mitsui, Shoji Tsuji, Hiroshi Takashima","doi":"10.1038/s10038-025-01437-8","DOIUrl":"10.1038/s10038-025-01437-8","url":null,"abstract":"Myopathy, lactic acidosis, and sideroblastic anemia type 1 (MLASA1) is an extremely rare mitochondrial disorder caused by biallelic pathogenic variants in PUS1, which encodes a mitochondrial tRNA pseudouridine synthase essential for mitochondrial protein synthesis. We describe two affected siblings presenting with progressive myopathy, lactic acidosis, sideroblastic anemia, short stature, developmental delay, and mild cognitive impairment. Depth-based copy number variation analysis of whole-exome sequencing data revealed a novel homozygous multi-exonic deletion in PUS1. The deletion breakpoints were defined by Sanger sequencing as a 9964 bp deletion spanning part of intron 3 through exons 4–6 and extending into the 3′ untranslated region, resulting in complete loss of the C-terminal coding region. Skeletal muscle histology demonstrated ragged red fibers, whereas immunohistochemistry showed a selective and near-complete loss of NDUFB8, indicating impaired assembly of respiratory chain complex I. A systematic review of previously reported MLASA1 cases revealed marked clinical heterogeneity, including frequent developmental delay, dysmorphic features, and multi-organ involvement. These findings expand the genotypic and phenotypic landscape of MLASA1 and highlight the diagnostic value of copy number variation analysis in unresolved mitochondrial disorders. The impairment of complex I underscores the particular vulnerability of translation-dependent respiratory chain components in PUS1-related diseases.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 5","pages":"275-282"},"PeriodicalIF":2.5,"publicationDate":"2025-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145708039","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}

引用次数: 0

Functional analysis of AKT1 knockout in fibrosarcoma cells using CRISPR/Cas9 technology 利用CRISPR/Cas9技术分析纤维肉瘤细胞中AKT1基因敲除的功能。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-11-26 DOI: 10.1038/s10038-025-01436-9

So-Hee Kim, Moon-Moo Kim

{"title":"Functional analysis of AKT1 knockout in fibrosarcoma cells using CRISPR/Cas9 technology","authors":"So-Hee Kim, Moon-Moo Kim","doi":"10.1038/s10038-025-01436-9","DOIUrl":"10.1038/s10038-025-01436-9","url":null,"abstract":"AKT1 (Protein Kinase B alpha) is a serine/threonine kinase that plays a pivotal role in regulating various cellular processes. To elucidate the role of the AKT1 gene in signaling pathways, this study generated AKT1 knockout (KO) HT-1080 cells using the CRISPR/Cas9 system. Gene-editing efficiency was validated through Sanger DNA sequencing and insertion/deletion (InDel) analysis. Quantitative real-time PCR and Western blot analyses were performed to evaluate the expression levels of AKT1 mRNA and protein, as well as to examine the expression of AKT1 downstream effectors: mTOR, BCL-2, and FOXO1. The AKT1 single-guide RNA sequence was successfully cloned into the CRISPR/Cas9 vector, leading to the establishment of AKT1 KO cells. InDel analysis identified eight editing types, with two dominant populations. The expression levels of AKT1 mRNA and protein were significantly reduced in the KO cells. The expression levels of mTOR, BCL-2, and FOXO1 were significantly altered in the KO cells compared to normal cells. These findings highlight the impact of AKT1 disruption on signaling pathways and provide fundamental insights into the regulatory role of the AKT1 gene.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 5","pages":"309-313"},"PeriodicalIF":2.5,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145634415","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}

引用次数: 0

Loss-of-function variant of SLC27A3 causes mitochondrial dysfunction and a metabolic neurodevelopmental disorder via impaired fatty acid transport SLC27A3的功能缺失变体通过受损的脂肪酸运输导致线粒体功能障碍和代谢性神经发育障碍。

IF 2.5 3区生物学

Journal of Human Genetics Pub Date : 2025-11-25 DOI: 10.1038/s10038-025-01435-w

S. Rehan Ahmad, Nazim Nasir, Anupriya Kumari, Atiq Ul Hassan

{"title":"Loss-of-function variant of SLC27A3 causes mitochondrial dysfunction and a metabolic neurodevelopmental disorder via impaired fatty acid transport","authors":"S. Rehan Ahmad, Nazim Nasir, Anupriya Kumari, Atiq Ul Hassan","doi":"10.1038/s10038-025-01435-w","DOIUrl":"10.1038/s10038-025-01435-w","url":null,"abstract":"Inborn errors of metabolism (IEMs) lead to early-onset neurodegenerative disorders often caused by mitochondrial dysfunction. In this study, we identified a homozygous frameshift mutation (c.283dupG; p.Cys65LeufsTer13) in SLC27A3, identified through exome sequencing in a 2-month-old female proband presenting with developmental regression, hypotonia, seizure, feeding difficulty, and bilateral putaminal lesions on brain magnetic resonance imaging (MRI). The mutation results in a truncated, non-functional protein and complete loss of SLC27A3 expression in proband-derived fibroblasts. Results show the absence of SLC27A3 and aberrant mitochondrial morphology with clumped networks. Metabolic profiling showed elevated acyl-carnitine levels in the cytosol of proband cells, indicative of disrupted fatty acid oxidation. Additionally, mitochondrial respiratory chain activity was significantly reduced, and flow cytometry revealed increased cell death in mutant cells compared to controls. Protein-protein interaction analysis revealed SLC27A3 networks linked to fatty acid metabolism, ER-associated degradation (ERAD), and ion transport. GO enrichment demonstrated strong associations with transporter activity, protein homeostasis, and ER-mitochondrial membrane networks. Regional expression profiling showed high SLC27A3 transcript levels in the basal ganglia, correlating with the observed neuropathology. These findings position SLC27A3 as a critical lipid transporter involved in neuronal energy metabolism and proteostasis, and implicate its loss in mitochondrial encephalopathy. This study expands the genotypic and phenotypic spectrum of metabolic neurodevelopmental disorders and highlights the importance of fatty acid transport proteins in mitochondrial health and brain development. Our findings propose SLC27A3 as a novel candidate gene for early-onset mitochondrial disorders.","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":"71 5","pages":"265-273"},"PeriodicalIF":2.5,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145604538","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}

引用次数: 0