Journal of Human Genetics最新文献

{"title":"Osteoporosis genetic risk prediction using bone mineral density polygenic scores in Japanese: TMM CommCohort study.","authors":"Yayoi Otsuka-Yamasaki, Yoichi Sutoh, Tsuyoshi Hachiya, Motoki Nakao, Shiori Minabe, Shohei Komaki, Hideki Ohmomo, Makoto Sasaki, Atsushi Shimizu","doi":"10.1038/s10038-026-01498-3","DOIUrl":"https://doi.org/10.1038/s10038-026-01498-3","url":null,"abstract":"<p><p>Osteoporosis and fractures are major health concerns. We developed and validated a polygenic score (PGS) for quantitative ultrasound (QUS)-defined osteoporosis risk in Japanese individuals using heel QUS-derived T-scores. Genome-wide association study summary statistics from up to 10,794 participants in the Tohoku Medical Megabank Community-Based Cohort identified genome-wide significant loci, including MBL2, TMEM135, and WNT16. PGS models were constructed and evaluated using independent datasets for model selection (n = 1419) and validation (n = 8711). Adding the PGS to age and sex yielded only modest improvements in discrimination, whereas PGS quintiles supported genetic risk stratification. Compared with the intermediate group, individuals in the lowest PGS quintile had higher odds of the outcome (1.22, 95% confidence interval [CI]: 1.07-1.40), whereas those in the highest quintile had lower odds (0.85, 95% CI: 0.74-0.98). During prospective follow-up (mean 3.5 years), a similar gradient was observed, with higher incidence rate ratios in the lowest quintile (1.42, 95% CI: 1.17-1.73) and lower incidence rate ratios in the highest quintile (0.70, 95% CI: 0.54-0.89). No statistically significant interaction between age and PGS was observed, and age-T-score regression analyses showed no differences in age-related T-score decline across genetic risk groups. However, analyses in young adults (20-44 years) and extrapolation to age 20 suggested lower bone status around peak bone mass in individuals at high genetic risk for QUS-defined osteoporosis. These findings suggest that a Japanese-specific PGS may help identify individuals at elevated genetic risk earlier in adulthood.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912559","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":"Broadening the Okur-Chung syndrome phenotype: adult-onset metabolic features and a contiguous 20p13 deletion in a Turkish multicenter cohort.","authors":"Çağrı Doğan, Alper Gezdirici, Hatice Özışık, Samim Özen, Ayça Aykut, Asude Durmaz, Elif Yılmaz Güleç, Mukaddes Feyza Baltacı, Eyyüp Üçtepe, Serdar Ceylaner, Mustafa Tarık Alay, İrem Kalay, Kübra Ateş, Mehmet Burak Mutlu","doi":"10.1038/s10038-026-01514-6","DOIUrl":"https://doi.org/10.1038/s10038-026-01514-6","url":null,"abstract":"<p><p>Okur-Chung neurodevelopmental syndrome (OCNDS; OMIM #617062) is an ultra-rare autosomal dominant disorder caused by heterozygous CSNK2A1 variants encoding CK2α; although the CSNK2A1 Foundation registry lists more than 350 diagnosed individuals worldwide, individual-level phenotypic data have been published for far fewer, and reports from Türkiye remain scarce. We retrospectively studied nine unrelated Turkish probands (4 F/5 M; 11 months to 23 years) from nine medical genetics centers across four geographic regions of Türkiye, diagnosed by exome sequencing (ES; n = 8) or chromosomal microarray (n = 1). A PRISMA 2020-compliant systematic review (inception-April 2026) provided an individual-level comparator pooled with our cohort (n = 61). Six distinct CSNK2A1 alterations were identified: the recurrent p.(Lys198Arg) p + 1 loop hotspot in 4/9 probands (44.4%); novel/rare p.(Arg195Gln) and p.(Asp156His) missense changes; two nonsense variants (p.(Tyr182Ter), p.(Arg333Ter)); and one ~537 kb heterozygous 20p13 contiguous deletion (arr[GRCh37] 20p13(61568_598427)x1). This proband also represents 20p13 deletion syndrome; previously reported cases of that entity were compared with our cohort. Core OCNDS features (developmental delay, intellectual disability, hypotonia, dysmorphism, behavioral disturbance) occurred at frequencies comparable to those in the pooled literature. Adult-onset obesity with type 2 diabetes (2/9) and hypogonadism (2/9), both essentially unreported in the predominantly pediatric pooled literature, were observed in two adolescent/young-adult males (one with p.(Lys198Arg), one with the 20p13 deletion). This series consolidates Lys198 as a recurrent hotspot across ethnically diverse cohorts, extends the structural-variant spectrum with the first Turkish CSNK2A1 contiguous-gene deletion, and supports adult-onset metabolic-reproductive complications as under-recognized OCNDS features. Systematic adolescent and adult metabolic-endocrine surveillance is recommended regardless of variant class.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148906327","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":"Beyond in silico prediction: multi-omics to identify a pathogenic deep intronic HNRNPK variant in Au-Kline syndrome.","authors":"Z Kowalzyk, J Porrmann, P Y B Au, S Choufani, R Weksberg, K Hackmann, A Kübler, A Kögler, N S Lewis, A Köhler, J Wagner, M Bermudez, C Hübner, J Schallner, R Jauss, C Vogelberg, B Mayer, N Di Donato, E Schröck, D Le Duc, A Jahn","doi":"10.1038/s10038-026-01511-9","DOIUrl":"https://doi.org/10.1038/s10038-026-01511-9","url":null,"abstract":"<p><p>Pathogenic variants in HNRNPK are associated with autosomal dominant Au-Kline syndrome (AKS, Au-Kline-Okamoto syndrome, OMIM #616580). This syndrome is characterized by developmental delay and intellectual disability, hypotonia, and distinctive facial features. Despite the use of whole-genome sequencing (WGS) as a powerful diagnostic tool, we nearly dismissed a novel intronic variant (NM_031263.4(HNRNPK):c.214-55 T > A) affecting HNRNPK splicing and function. Although commonly used bioinformatic splice prediction tools, including SpliceAI and PDIVAS, yielded inconclusive results, Face2Gene analysis indicated a high phenotypic similarity to AKS. Characteristic facial features described by Choufani et al. [1] supported the clinical diagnosis of AKS. Subsequent functional studies demonstrated aberrant splicing with intron retention, and DNA methylation profiling revealed a positive HNRNPK-specific episignature. These insights and the de novo status support an evaluation as likely pathogenic. This case report supports the relevance of facial analysis and comprehensive variant validation strategies, particularly for deep intronic variants with ambiguous in silico splicing predictions.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892023","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":"Biallelic nonsense variants in GAS8 associated with asthenoteratozoospermia and PCD-like symptoms.","authors":"Mingjia Zhao, Shuyu Guo, Lanxi Ran, Yue Meng, Yijia Zhao, Jing Wang, Binbin Wang","doi":"10.1038/s10038-026-01512-8","DOIUrl":"https://doi.org/10.1038/s10038-026-01512-8","url":null,"abstract":"<p><p>We report a 28-year-old infertile male presenting with markedly reduced progressive sperm motility and severe morphological abnormalities (normal morphology rate: 1%), accompanied by primary ciliary dyskinesia (PCD)-like symptoms, including chronic rhinitis, adolescent nasal polypectomy, and persistent rhinorrhea. Transmission electron microscopy (TEM) revealed ultrastructural defects involving the sperm head, nucleus, and flagellar axoneme. Whole-exome sequencing (WES) identified two novel compound heterozygous nonsense variants in the GAS8 gene: c.280 G > T (p.Glu94Ter) and c.382 C > T (p.Gln128Ter). Based on these findings, testicular sperm aspiration (TESA) combined with intracytoplasmic sperm injection (ICSI) was performed, resulting in a biochemical pregnancy. This case expands the mutational and phenotypic spectrum of GAS8 and provides additional clinical evidence relevant to genetic diagnosis, genetic counseling, and assisted reproductive management of male infertility accompanied by PCD-like symptoms.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890753","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":"THE1 repeats: Ancient endogenous retroviruses rampaging behind sarcoid myopathy.","authors":"Aritoshi Iida, Shunsuke Funaguma, Ichizo Nishino","doi":"10.1038/s10038-026-01510-w","DOIUrl":"10.1038/s10038-026-01510-w","url":null,"abstract":"<p><p>Transposon-like human element (THE1) repeats are classified as part of the ERVL (endogenous retrovirus-like) -MaLR family and were previously thought to be remnants derived from retroviral infections in the germ cells of ancient primates. At present, at least 60,561 THE1 repeats have been mapped in the human genome, and they are divided into four subfamilies: THE1A, THE1B, THE1C, and THE1D. Although these repeats are largely silenced in somatic cells through multiple mechanisms, some of them are known to influence gene functions and genomic structures, particularly under disease conditions. Recently, we happened to identify the CIR1 driven from THE1B in the individuals with sarcoid myopathy (SM), which is characterized by the non-caseating granulomatous inflammation recognized in skeletal muscles biopsy. Retrotrans-genomics based on the COFFEE method showed that various THE1B fusion transcripts (THE1B/FTs) and retrotransposon-associated genomic dynamics in muscle of SM, including (1) splicing of THE1B to neighborhood exons, (2) expression of THE1B associated long noncoding RNAs in the intergenic regions, (3) ectopic expression of tissue specific transcripts driven by THE1B in SM, and (4) identification of a read through transcript, SIRPB1-SIRPD. Seven of eight THE1B/FTs downregulated by tofacitinib in cutaneous sarcoidosis were confined to the granuloma associated macrophage in sarcoidosis. The remaining transcript, SMFT4 exhibited stronger expression in mesenchymal stem cells. In addition, ectopic co-expression of canonical and LINE1 and THE1A-exonizing IL23R transcripts were identified in SM. This directory of THE1B/FTs in SM may serve as a fundamental molecular basis for understanding the pathogenesis of sarcoidosis.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148887522","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":"Cross-biobank comparison of ASCVD heritability and genetic correlation.","authors":"Hari B Acharya, Samuel S Gidding, Matthew T Oetjens, Alexander S F Berry","doi":"10.1038/s10038-026-01508-4","DOIUrl":"https://doi.org/10.1038/s10038-026-01508-4","url":null,"abstract":"<p><p>Estimates of SNP-based heritability for atherosclerotic cardiovascular disease (ASCVD) vary widely across populations, complicating interpretation of genetic architecture. We compared SNP-based heritability and cross-cohort genetic correlation for ASCVD and its nested subphenotypes, coronary events (CE) and myocardial infarction (MI), across Geisinger's MyCode, the UK Biobank, and the NIH's All of Us using GWAS summary statistics and LD score regression. Heritability estimates differed significantly across cohorts, with consistently higher values in the UK Biobank and higher heritability for more narrowly defined phenotypes (MI) relative to broader ASCVD definitions. In contrast, genetic correlations between cohorts were uniformly high for all phenotypes, with confidence intervals spanning 1.0. These results suggest substantial sharing of common variant genetic effects across biobanks and indicate that cross-cohort differences in SNP-based heritability may primarily reflect differences in ASCVD ascertainment and phenotype capture rather than underlying genetic architecture.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148850886","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":"Systematic genotype-phenotype mapping and transcriptomic analyses highlight SEMA6A as a candidate for neuronal migration defects in 5q22-q23 deletions.","authors":"Kengo Kora, Takeshi Yoshida, Atsuko Ikegawa, Kiyohiro Kim, Shu Hamada, Toshiro Maihara, Takahito Wada","doi":"10.1038/s10038-026-01507-5","DOIUrl":"https://doi.org/10.1038/s10038-026-01507-5","url":null,"abstract":"<p><p>Interstitial deletions of the long arm of chromosome 5 (5q) are rare and associated with variable neurodevelopmental features. While proximal deletions involving APC are well-characterized, the genetic basis of structural brain malformations in this region remains poorly defined. Here, we report a pediatric patient with a 14.5 Mb interstitial deletion at 5q22.3-q23.3 who presented with global developmental delay, congenital heart defects, and bilateral periventricular nodular heterotopia. To identify candidate genes that may contribute to structural brain malformations in this interval, we conducted a systematic genotype-phenotype analysis of 64 cases compiled from the literature and the DECIPHER database. Structural brain malformations were identified in four cases. Of these, two involved developmental brain abnormalities with potential relevance to neuronal migration: periventricular nodular heterotopia in our proband and cerebellar vermis hypoplasia in a reference case carrying a focal ~452 kb deletion in which SEMA6A was the only haploinsufficiency-intolerant gene. This convergence pointed to SEMA6A as a candidate contributor to migration-related brain abnormalities. We further examined the relationship between SEMA6A and FLNA, an established disease gene for periventricular nodular heterotopia. Protein-protein interaction analysis revealed that SEMA6A and FLNA are connected within a network through Rho/Rac signaling effectors. Furthermore, re-analysis of human fetal cortex single-cell RNA sequencing data demonstrated that SEMA6A and FLNA are significantly co-expressed in apical radial glia and newborn excitatory neurons. These findings suggest that SEMA6A is a candidate contributor to neuronal migration defects in 5q22.3-q23.3 deletions, likely exhibiting incomplete penetrance.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839984","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":"Identification and characterisation of a novel homozygous KDM5A variant associated with severe axial hypotonia, seizures, and cardiac anomalies.","authors":"Serdar Bozlak, Cuneyd Yavas, Yusuf Seflekci, Tunay Dogan, Yunus Emre Arvas","doi":"10.1038/s10038-026-01506-6","DOIUrl":"https://doi.org/10.1038/s10038-026-01506-6","url":null,"abstract":"<p><p>KDM5A is a critical chromatin-modifying enzyme with lysine-specific demethylase activity and is highly expressed in brain tissues. Biallelic pathogenic variants in KDM5A are linked to KDM5A-related neurodevelopmental disorders, a rare disorder involving significant cognitive and motor impairments. We conducted a clinical and genetic evaluation of a patient with severe neurodevelopmental delay. Exome sequencing was performed to identify the genetic aetiology, followed by quantitative expression analysis to assess the functional impact of the identified variant on KDM5A mRNA levels. A novel homozygous KDM5A c.2836 C > T p.(Gln946Ter) variant was identified in the proband. Quantitative analysis showed a reduction in KDM5A expression. However, this decrease was not statistically significant. The patients displayed neuromotor developmental delay, severe axial hypotonia, absence of head control and mild upper-extremity spasticity. Additional findings included a history of seizures, facial dysmorphism and congenital heart disease. These findings expand the known clinical spectrum of El Hayek-Chahrour neurodevelopmental disorder (OMIM #620820), specifically highlighting severe motor impairment and complex cardiac involvement, including major aortopulmonary collateral artery, as previously undescribed features of this condition. The non-significant decrease in expression suggests that pathogenicity may arise from altered protein function rather than transcript depletion. Our findings underscore the importance of exome sequencing in delineating phenotypic variability in rare neurodevelopmental syndromes.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148794154","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":"Clinical significance of miRNAs and exosomal miRNAs in non-small cell lung cancer: diagnostic, prognostic, and therapeutic perspectives.","authors":"Imteyaz Ahmad Khan, Surabhi Gupta, Jagdish Prasad Meena","doi":"10.1038/s10038-026-01505-7","DOIUrl":"https://doi.org/10.1038/s10038-026-01505-7","url":null,"abstract":"<p><p>Lung cancer is the most frequently diagnosed malignancy and the leading cause of cancer-related mortality worldwide, with approximately 85% of cases classified as non-small cell lung cancer (NSCLC). Despite significant advances in diagnostic techniques and therapeutic strategies, including immunotherapy and targeted therapies, the prognosis of lung cancer remains poor, with an overall 5-year survival rate of approximately 22%. MicroRNAs (miRNAs) are small, single-stranded, non-coding RNA molecules that regulate gene expression at the post-transcriptional level and play critical roles in key biological processes, such as proliferation, apoptosis, migration, and invasion. miRNAs can function as oncogenes (oncomiRs) or tumor suppressors (TS-miRs), and their dysregulation is frequently observed in various malignancies, including NSCLC. Owing to their remarkable stability in serum and plasma, miRNAs have emerged as promising non-invasive biomarkers for the diagnosis and prognosis of NSCLC. In particular, exosomal miRNAs are encapsulated within a lipid bilayer that protects them from enzymatic degradation, thereby further enhancing their utility as liquid biopsy components and as potential biomarkers and therapeutic targets. Moreover, a single miRNA can regulate multiple target genes, highlighting their promise as therapeutic targets. This review summarizes the diagnostic, prognostic, predictive, and therapeutic potential of tissue-derived, circulating, and exosomal miRNAs in NSCLC and discusses the major challenges limiting the clinical translation of miRNA-based biomarkers and therapeutics.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148794157","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":"Clinical features of four unrelated Japanese patients with autosomal recessive spinocerebellar ataxia type 32.","authors":"Hiromi Fukuda, Hiroshi Doi, Shunsuke Ogata, Eriko Koshimizu, Kohei Hamanaka, Satoko Miyatake, Yuichi Higashiyama, Yosuke Kudo, Rumiko Kato, Takamasa Nukui, Kazuki Yamada, Shinichi Shirai, Ichiro Yabe, Naomichi Matsumoto, Fumiaki Tanaka","doi":"10.1038/s10038-026-01504-8","DOIUrl":"https://doi.org/10.1038/s10038-026-01504-8","url":null,"abstract":"<p><p>Peroxiredoxin 3 (PRDX3) encodes a mitochondrially localized antioxidant enzyme. Biallelic pathogenic variants in PRDX3 cause autosomal recessive spinocerebellar ataxia type 32 (SCAR32), a rare form of spinocerebellar ataxia. We report four unrelated Japanese patients with SCAR32 identified among 411 ataxia cases negative for repeat expansion disorders. Age at onset was 9-30 years, with a predominantly pure cerebellar phenotype; one patient had autoimmune comorbidities. MRI showed cerebellar atrophy and T2 hyperintensity in dentate nuclei in all patients, and three had cerebellar cortical T2 hyperintensity, a potentially representative feature of SCAR32. Genetic analysis identified one homozygous and three compound heterozygous PRDX3 nonsense variants: the previously reported p.Arg207* in all patients, p.Arg170* in two, and novel p.Gln50* in one. The relatively high p.Arg207* allele frequency in East Asians and the 0.97% prevalence in our undiagnosed ataxia cohort support SCAR32 as an important cause of early-onset autosomal recessive cerebellar ataxia in Japan.</p>","PeriodicalId":16077,"journal":{"name":"Journal of Human Genetics","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148794181","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}