American Journal of Medical Genetics Part A最新文献_第8页

Investigating TNNC1 gene inheritance and clinical outcomes through a comprehensive familial study. 通过一项全面的家族研究调查 TNNC1 基因遗传和临床结果。

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-09-09 DOI: 10.1002/ajmg.a.63838

Constantinos Patsalis, Skevi Kyriakou, Michaella Georgiadou, Lygia Ioannou, Louisa Constantinou, Valando Soteriou, Antonis Jossif, Paola Evangelidou, Carolina Sismani, Elena Kypri, Marios Ioannides, George Koumbaris

{"title":"Investigating TNNC1 gene inheritance and clinical outcomes through a comprehensive familial study.","authors":"Constantinos Patsalis, Skevi Kyriakou, Michaella Georgiadou, Lygia Ioannou, Louisa Constantinou, Valando Soteriou, Antonis Jossif, Paola Evangelidou, Carolina Sismani, Elena Kypri, Marios Ioannides, George Koumbaris","doi":"10.1002/ajmg.a.63838","DOIUrl":"https://doi.org/10.1002/ajmg.a.63838","url":null,"abstract":"Hypertrophic cardiomyopathy (HCM) and restrictive cardiomyopathy (RCM) have significant phenotypic overlap and a similar genetic background, both caused mainly by variants in sarcomeric genes. HCM is the most common cardiomyopathy, while RCM is a rare and often underdiagnosed heart condition, with a poor prognosis. This study focuses on a large family with four infants diagnosed with fatal RCM associated with biventricular hypertrophy. Affected infants were found to be homozygous for NM_003280.3(TNNC1):c.23C>T(p.Ala8Val) variant. Interestingly, this variant resulted in a low penetrance and mild form of hypertrophic cardiomyopathy (HCM) in relatives carrying a single copy of the variant. Overall, this study underscores the complex nature of genetic inheritance in cardiomyopathies and the wide range of clinical presentations they can exhibit. This emphasizes the vital role of genetic testing in providing essential insights crucial for diagnosis, prognosis, early intervention, and the development of potential treatment strategies.","PeriodicalId":7507,"journal":{"name":"American Journal of Medical Genetics Part A","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

A Comparison of Clinical and Radiological Presentations of Sporadic and Tuberous Sclerosis Complex-Associated Lymphangioleiomyomatosis. 散发性和结节性硬化症复合体相关淋巴管瘤病的临床和放射学表现比较。

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-09-07 DOI: 10.1002/ajmg.a.63871

Taylor E Savage, Kennedy R Geenen, Melissa C Price, Souheil Y El-Chemaly, Elizabeth P Henske, Amita Sharma, Elizabeth A Thiele

{"title":"A Comparison of Clinical and Radiological Presentations of Sporadic and Tuberous Sclerosis Complex-Associated Lymphangioleiomyomatosis.","authors":"Taylor E Savage, Kennedy R Geenen, Melissa C Price, Souheil Y El-Chemaly, Elizabeth P Henske, Amita Sharma, Elizabeth A Thiele","doi":"10.1002/ajmg.a.63871","DOIUrl":"https://doi.org/10.1002/ajmg.a.63871","url":null,"abstract":"This research aims to compare and assess the clinical and radiological presentations of tuberous sclerosis complex (TSC)-associated lymphangioleiomyomatosis (LAM) and sporadic LAM. A retrospective medical record review was conducted for 90 patients with confirmed LAM diagnoses. Radiologists who were blinded to the LAM type evaluated CT images of the chest and abdomen for the presence of four CT phenotypes: multiple sclerotic bone lesions (SBLs), multifocal micronodular pneumocyte hyperplasia (MMPH), hepatic fat-containing lesions, and cardiac fat-containing lesions. Statistical analyses were then completed to analyze the differences between TSC-LAM and sporadic LAM. Sporadic LAM patients reported a greater number of clinical symptoms at the time of diagnosis than TSC-LAM patients. All four CT phenotypes were present among the TSC-LAM patient population, whereas hepatic fat containing lesions were the only phenotype present in sporadic LAM patients evaluated in this study. The clinical and radiological presentations of sporadic LAM and TSC-LAM differ significantly, suggesting that the diagnostic criteria for sporadic LAM and/or TSC itself could be adapted accordingly. However, the similarities in the presentation of the LAM types are also important to note as these trends inform theories surrounding the potential underlying pathogenic mechanisms of sporadic LAM.","PeriodicalId":7507,"journal":{"name":"American Journal of Medical Genetics Part A","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142144939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Two novel compound heterozygous HOXB1 variants in congenital facial palsy: A case report and a brief review of the literature. 先天性面瘫中的两种新型复合杂合子 HOXB1 变异：病例报告和文献综述。

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-09-05 DOI: 10.1002/ajmg.a.63848

Chiara Brugnoli, Susanna Rizzi, Carlo Alberto Cesaroni, Carlotta Spagnoli, Giovanna Pregnolato, Stefano Giuseppe Caraffi, Manuela Napoli, Rosario Pascarella, Roberta Zuntini, Francesca Peluso, Livia Garavelli, Eleonora Chiarotto, Alberta Leon, Daniele Frattini, Carlo Fusco

{"title":"Two novel compound heterozygous HOXB1 variants in congenital facial palsy: A case report and a brief review of the literature.","authors":"Chiara Brugnoli, Susanna Rizzi, Carlo Alberto Cesaroni, Carlotta Spagnoli, Giovanna Pregnolato, Stefano Giuseppe Caraffi, Manuela Napoli, Rosario Pascarella, Roberta Zuntini, Francesca Peluso, Livia Garavelli, Eleonora Chiarotto, Alberta Leon, Daniele Frattini, Carlo Fusco","doi":"10.1002/ajmg.a.63848","DOIUrl":"https://doi.org/10.1002/ajmg.a.63848","url":null,"abstract":"Hereditary congenital facial palsy (HCFP) is a medical condition caused by dysfunction of the seventh cranial nerve. HCFP is characterized by feeding difficulties and dysmorphic features in the orofacial region. In some cases hearing loss, strabismus, limb malformations, and musculoskeletal defects may be associated. There are three types of HCFP: HCFP3 (OMIM 614744) results from autosomal recessive pathogenic variants in the HOXB1 gene, while HCFP1 and 2 (OMIM 601471, 604185) are autosomal dominant, genetically less defined conditions. We report on a case of congenital bilateral facial palsy due to two novel compound heterozygous variants in the HOXB1 gene, found by exome sequencing (ES), in a child with facial nerve axonal neuropathy without evidence of nerve hypoplasia on neuroimaging. The results of this report suggest that in individuals with congenital facial paralysis and preserved ocular motor skills, with or without facial nerve hypoplasia and with confirmed facial nerve axonal neuropathy, HOXB1 variants and therefore a diagnosis of HCFP3 should be primarily considered.","PeriodicalId":7507,"journal":{"name":"American Journal of Medical Genetics Part A","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

WDR44 Loss-of-Function Promoter Deletion in a Male Newborn With a Ciliopathy Phenotype. 一名男性新生儿纤毛症表型中的 WDR44 功能缺失启动子缺失。

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-09-05 DOI: 10.1002/ajmg.a.63861

Tam P Sneddon, Kelly L Gilmore, Mai Xiong, Karen E Weck, Bradford C Powell, Neeta L Vora

引用次数: 0

Expanding MNS1 Heterotaxy Phenotype. 扩大 MNS1 异位表型。

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-09-05 DOI: 10.1002/ajmg.a.63862

Julien Maraval, Andrée Delahaye-Duriez, Caroline Racine, Ange-Line Bruel, Anne-Sophie Denommé-Pichon, Léa Gaudillat, Christel Thauvin-Robinet, Marie Lucain, Véronique Satre, Charles Coutton, Jean-Madelaine de Sainte Agathe, Boris Keren, Laurence Faivre

{"title":"Expanding MNS1 Heterotaxy Phenotype.","authors":"Julien Maraval, Andrée Delahaye-Duriez, Caroline Racine, Ange-Line Bruel, Anne-Sophie Denommé-Pichon, Léa Gaudillat, Christel Thauvin-Robinet, Marie Lucain, Véronique Satre, Charles Coutton, Jean-Madelaine de Sainte Agathe, Boris Keren, Laurence Faivre","doi":"10.1002/ajmg.a.63862","DOIUrl":"https://doi.org/10.1002/ajmg.a.63862","url":null,"abstract":"MNS1 (meiosis-specific nuclear structural protein-1 gene) encodes a structural protein implicated in motile ciliary function and sperm flagella assembly. To date, two different homozygous MNS1 variants have been associated with autosomal recessive visceral heterotaxy (MIM#618948). A French individual was identified with compound heterozygous variants in the MNS1 gene. A collaborative call was proposed via GeneMatcher to describe new cases with this rare syndrome, leading to the identification of another family. The first patient was a female presenting complete situs inversus and unusual symptoms, including severe myopia and dental agenesis of 10 permanent teeth. She was found to carry compound heterozygous frameshift and nonsense variants in MNS1. The second and third patients were sibling fetuses with homozygous in-frame deletion variants in MNS1 and homozygous missense variants in GLDN. Autopsies revealed a complex prenatal malformation syndrome. We add here new cases with the ultra-rare MNS1-related disorder and provide a review of all published individuals.","PeriodicalId":7507,"journal":{"name":"American Journal of Medical Genetics Part A","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 Contributions to Lower Urinary Tract Dysfunction. 下尿路功能障碍的遗传因素

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-09-04 DOI: 10.1002/ajmg.a.63859

Lilian R Hiltebeitel, Steve Seltzsam, Chunyan Wang, Ted Lee, Leah Bolsius, Mohamed Shalaby, Sherif El Desoky, Jameela A Kari, Shirlee Shril, Friedhelm Hildebrandt, Nina Mann

{"title":"Genetic Contributions to Lower Urinary Tract Dysfunction.","authors":"Lilian R Hiltebeitel, Steve Seltzsam, Chunyan Wang, Ted Lee, Leah Bolsius, Mohamed Shalaby, Sherif El Desoky, Jameela A Kari, Shirlee Shril, Friedhelm Hildebrandt, Nina Mann","doi":"10.1002/ajmg.a.63859","DOIUrl":"https://doi.org/10.1002/ajmg.a.63859","url":null,"abstract":"Lower urinary tract dysfunction (LUTD) can manifest as a spectrum of voiding symptoms in childhood, including urinary urgency, frequency, hesitancy, and incontinence. In severe cases, it can lead to frequent urinary tract infections, hydronephrosis, kidney scarring, and chronic kidney disease. Non-neurogenic neurogenic bladder (NNNB) is a diagnosis of exclusion in which children develop discoordination between the detrusor smooth muscle and external urethral sphincter in the absence of neurological or obstructive lesions, resulting in severe LUTD. Historically, such disorders of voiding were thought to result from behavioral maladaptation. However, it is now increasingly recognized that some individuals may have an underlying genetic etiology for their symptoms. Here, we performed exome sequencing for five probands with NNNB or other forms of severe LUTD, and we identified two individuals with monogenic etiologies for their symptoms. One individual had a homozygous exon 9 deletion in HPSE2 and another had a homozygous single amino acid deletion (p.Gly167del) in ARL6. We performed PCR experiments to identify the breakpoints of the HPSE2 exon 9 deletion and implicate microhomology-mediated end joining as a potential mechanism by which the deletion arose. These findings suggest that genetic testing should be considered for children with severe LUTD.","PeriodicalId":7507,"journal":{"name":"American Journal of Medical Genetics Part A","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142124552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Bridging the Diagnostic Gap for Hypermobile Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorders: Evidence of a Common Extracellular Matrix Fragmentation Pattern in Patient Plasma as a Potential Biomarker. 弥合高移动性埃勒斯-丹洛斯综合征和高移动性谱系障碍的诊断差距：患者血浆中共同的细胞外基质碎裂模式作为潜在生物标志物的证据。

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-09-03 DOI: 10.1002/ajmg.a.63857

Marco Ritelli, Nicola Chiarelli, Valeria Cinquina, Valeria Bertini, Silvia Piantoni, Alessia Caproli, Silvia Ebe Lucia Della Pinna, Franco Franceschini, Guido Zarattini, Woodrow Gandy, Marina Venturini, Nicoletta Zoppi, Marina Colombi

{"title":"Bridging the Diagnostic Gap for Hypermobile Ehlers-Danlos Syndrome and Hypermobility Spectrum Disorders: Evidence of a Common Extracellular Matrix Fragmentation Pattern in Patient Plasma as a Potential Biomarker.","authors":"Marco Ritelli, Nicola Chiarelli, Valeria Cinquina, Valeria Bertini, Silvia Piantoni, Alessia Caproli, Silvia Ebe Lucia Della Pinna, Franco Franceschini, Guido Zarattini, Woodrow Gandy, Marina Venturini, Nicoletta Zoppi, Marina Colombi","doi":"10.1002/ajmg.a.63857","DOIUrl":"https://doi.org/10.1002/ajmg.a.63857","url":null,"abstract":"Diagnosing hypermobile Ehlers-Danlos syndrome (hEDS) and hypermobility spectrum disorders (HSD), common overlapping multisystemic conditions featuring symptomatic joint hypermobility, is challenging due to lack of established causes and diagnostic tools. Currently, the 2017 diagnostic criteria for hEDS are used, with non-qualifying cases classified as HSD, although the distinction remains debated. We previously showed extracellular matrix (ECM) disorganization in both hEDS and HSD dermal fibroblasts involving fibronectin (FN), type I collagen (COLLI), and tenascin (TN), with matrix metalloproteinase-generated fragments in conditioned media. Here, we investigated these fragments in patient plasma using Western blotting across diverse cohorts, including patients with hEDS, HSD, classical EDS (cEDS), vascular EDS (vEDS), rheumatoid arthritis (RA), psoriatic arthritis (PsA), and osteoarthritis (OA), and healthy donors, uncovering distinctive patterns. Notably, hEDS/HSD displayed a shared FN and COLLI fragment signature, supporting their classification as a single disorder and prompting reconsideration of the hEDS criteria. Our results hold the promise for the first blood test for diagnosing hEDS/HSD, present insights into the pathomechanisms, and open the door for therapeutic trials focused on restoring ECM homeostasis using an objective marker. Additionally, our findings offer potential biomarkers also for OA, RA, and PsA, advancing diagnostic and therapeutic strategies in these prevalent joint diseases.","PeriodicalId":7507,"journal":{"name":"American Journal of Medical Genetics Part A","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Bilateral Perisylvian Polymicrogyria, Intellectual Disability and Nephronophthisis Associated With Compound Heterozygous Pathogenic Variants in the CEP83 Gene. 与 CEP83 基因复合杂合子致病性变异有关的双侧脐周多畸形、智力障碍和肾炎。

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-09-01 DOI: 10.1002/ajmg.a.63863

Elena Parrini, Simona Balestrini, Domenico Rutigliano, Maria Luisa Ricci, Davide Mei, Renzo Guerrini

{"title":"Bilateral Perisylvian Polymicrogyria, Intellectual Disability and Nephronophthisis Associated With Compound Heterozygous Pathogenic Variants in the CEP83 Gene.","authors":"Elena Parrini, Simona Balestrini, Domenico Rutigliano, Maria Luisa Ricci, Davide Mei, Renzo Guerrini","doi":"10.1002/ajmg.a.63863","DOIUrl":"https://doi.org/10.1002/ajmg.a.63863","url":null,"abstract":"The centrosomal protein 83 (CEP83) is a centriolar protein involved in primary cilium assembly, an early and critical step in ciliogenesis. Bi-allelic pathogenic variants in the CEP83 gene have been associated with infantile nephronophthisis and, in a few patients, retinitis pigmentosa. We describe a 5-year-old boy with bilateral perisylvian polymicrogyria, intellectual disability, and nephronophthisis in whom, using exome sequencing, we identified the c.1052T>G p.(Leu351*) stopgain variant inherited from the father and the c.2024T>C p.(Leu675Pro) missense variant inherited from the mother, in a compound heterozygous pattern. Polymicrogyria or, in general, malformations of cortical development had not been previously observed in patients with pathogenic CEP83 variants. However, defects in CEP83 can affect the formation and function of cilia or centrosomal structures, resulting in a polymicrogyric pattern overlapping with that associated with pathogenic variants affecting other genes coding for centrosomal components. This observation expands the spectrum of phenotypes associated with the CEP83 gene and adds it to the list of genes associated with bilateral perisylvian polymicrogyria.","PeriodicalId":7507,"journal":{"name":"American Journal of Medical Genetics Part A","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Intrafamilial Phenotypic Variability in SYNE1-Related Disorder. SYNE1相关疾病的同卵双生表型变异。

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-08-30 DOI: 10.1002/ajmg.a.63858

Heather Pekeles, Kenneth A Myers

引用次数: 0

MED12 Loss-of-Function Variants as a Cause of Congenital Diaphragmatic Hernia in Females With Hardikar Syndrome and Nonspecific Intellectual Disability. MED12功能缺失变异是哈迪卡综合征和非特异性智力障碍女性先天性膈疝的病因之一。

IF 1.7 4区生物学

American Journal of Medical Genetics Part A Pub Date : 2024-08-30 DOI: 10.1002/ajmg.a.63868

Eric C Kao, Elizabeth A Mizerik, Carlos A Bacino, Hongzheng Dai, Liesbeth Vossaert, Daryl A Scott

{"title":"MED12 Loss-of-Function Variants as a Cause of Congenital Diaphragmatic Hernia in Females With Hardikar Syndrome and Nonspecific Intellectual Disability.","authors":"Eric C Kao, Elizabeth A Mizerik, Carlos A Bacino, Hongzheng Dai, Liesbeth Vossaert, Daryl A Scott","doi":"10.1002/ajmg.a.63868","DOIUrl":"https://doi.org/10.1002/ajmg.a.63868","url":null,"abstract":"Mediator complex subunit 12 (MED12) is required for the assembly of the kinase module of Mediator, a regulatory complex that controls the formation of the RNA polymerase II-mediated preinitiation complex. MED12-related disorders display unique gender-specific genotype-phenotype associations and include X-linked recessive Opitz-Kaveggia syndrome, Lujan-Fryns syndrome, Ohdo syndrome, and nonspecific intellectual disability in males predominantly carrying missense variants, and X-linked dominant Hardikar syndrome and nonspecific intellectual disability in females known to predominantly carry de novo nonsense/frameshift and nonsense/missense variants, respectively. MED12 was previously identified as a low-penetrance candidate gene for non-isolated congenital diaphragmatic hernia (CDH+). At the time, however, there was insufficient evidence to confirm this association. In a clinical database search, we identified 18 individuals who were molecularly diagnosed with MED12-related disorders by exome or genome sequencing, including eight missense, four frameshift, two nonsense, and one splice variant. Nine of these variants have not been previously reported. Two females with nonspecific intellectual disability were found to carry a de novo frameshift variant, indicating that potentially truncating variants causing nonspecific intellectual disability are not limited to nonsense variants. Notably, CDH was reported in three out of seven females with Hardikar syndrome or nonspecific intellectual disability but was not reported in males with MED12-related disorders. These results suggest that pathogenic MED12 variants are a cause of CDH+ in females with Hardikar syndrome and nonspecific intellectual disability.","PeriodicalId":7507,"journal":{"name":"American Journal of Medical Genetics Part A","volume":null,"pages":null},"PeriodicalIF":1.7,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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