Global Medical Genetics最新文献

{"title":"Exploring Health Care Disparities in Genetic Testing and Research for Hereditary Cardiomyopathy: Current State and Future Perspectives.","authors":"Helen Huang, Jay Verma, Valerie Mok, Hareesha R Bharadwaj, Maen M Alrawashdeh, Adarsh Aratikatla, Sourav Sudan, Suprateeka Talukder, Minatoullah Habaka, Gary Tse, Mainak Bardhan","doi":"10.1055/s-0044-1779469","DOIUrl":"10.1055/s-0044-1779469","url":null,"abstract":"<p><p><b>Background</b>  Hereditary cardiomyopathies are commonly occurring myocardial conditions affecting heart structure and function with a genetic or familial association, but the etiology is often unknown. Cardiomyopathies are linked to significant mortality, requiring robust risk stratification with genetic testing and early diagnosis. <b>Hypothesis</b>  We hypothesized that health care disparities exist in genetic testing for hereditary cardiomyopathies within clinical practice and research studies. <b>Methods</b>  In a narrative fashion, we conducted a literature search with online databases such as PubMed/MEDLINE, Google Scholar, EMBASE, and Science Direct on papers related to hereditary cardiomyopathies. A comprehensive analysis of findings from articles in English on disparities in diagnostics and treatment was grouped into four categories. <b>Results</b>  Racial and ethnic disparities in research study enrollment and health care delivery favor White populations and higher socioeconomic status, resulting in differences in the development and implementation of effective genetic screening. Such disparities have shown to be detrimental, as minorities often suffer from disease progression to heart failure and sudden cardiac death. Barriers related to clinical genetic testing included insurance-related issues and health illiteracy. The underrepresentation of minority populations extends to research methodologies, as testing in ethnic minorities resulted in a significantly lower detection rate and diagnostic yield, as well as a higher likelihood of misclassification of variants. <b>Conclusions</b>  Prioritizing minority-based participatory research programs and screening protocols can address systemic disparities. Diversifying research studies can improve risk stratification strategies and impact clinical practice.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"11 1","pages":"36-47"},"PeriodicalIF":1.2,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10834107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139673198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Multifaceted Role of Oxytocinergic System and <i>OXTR</i> Gene.","authors":"Rakibul Hasan","doi":"10.1055/s-0044-1779039","DOIUrl":"10.1055/s-0044-1779039","url":null,"abstract":"<p><p>The article explores the multifaceted role of the neuropeptide oxytocin in human behavior and its connection to the oxytocin receptor ( <i>OXTR</i> ) gene. Oxytocin, produced in specific brain nuclei, is implicated in emotional, social, and maternal behaviors, stress reduction, uterine contraction during childbirth, and lactation. The <i>OXTR</i> gene, located on chromosome 3, encodes oxytocin receptors found in various body parts, including critical brain regions associated with social behaviors. The article delves into studies on rodents, revealing correlations between <i>OXTR</i> gene expression and pair bonding in the prefrontal cortex and social behavior regulation in the amygdala. The discussion extends to the impact of oxytocin on social support-seeking behavior, focusing on a specific genetic variation, rs53576. The article explores how this genetic variation influences empathy, stress reactivity, and susceptibility to disorders such as autism and social anxiety. Furthermore, the article examines structural and functional changes in the brain associated with <i>OXTR</i> gene variations. It discusses the role of DNA methylation in influencing oxytocin receptor availability, affecting social perception and responsiveness to negative stimuli. The article also highlights the oxytocinergic system's involvement in disorders such as autism and social anxiety, emphasizing the interplay between genetics and environmental factors. The article also touches on the potential therapeutic use of exogenous oxytocin in mitigating symptoms associated with these disorders. In summary, the article underscores the intricate relationship between oxytocin, the <i>OXTR</i> gene, and diverse aspects of human behavior, providing insights into social bonding, perception, and the development of behavioral disorders.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"11 1","pages":"29-33"},"PeriodicalIF":1.7,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10796195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139492416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"On the Pentapeptide as the Measurement Unit in Immunology.","authors":"Darja Kanduc","doi":"10.1055/s-0044-1779041","DOIUrl":"10.1055/s-0044-1779041","url":null,"abstract":"<p><p>This communication concerns a crucial query in immunology, that is, the dimension of an epitope. The issue has essential implications in vaccine formulations.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"11 1","pages":"34-35"},"PeriodicalIF":1.7,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10796194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139492413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Variants of CEP152 in a Case of Compound-Heterozygous Inheritance of Epilepsy.","authors":"Weiran Li, Xiaowei Lu, Jianbo Shu, Yingzi Cai, Dong Li, Chunquan Cai","doi":"10.1055/s-0043-1777807","DOIUrl":"10.1055/s-0043-1777807","url":null,"abstract":"<p><p><b>Introduction</b>   <i>CEP152</i> encodes protein Cep152, which associates with centrosome function. The lack of Cep152 can cause centrosome duplication to fail. <i>CEP152</i> mutates, causing several diseases such as Seckel syndrome-5 and primary microencephaly-9. <b>Methods</b>  In this study, we reported a patient diagnosed with epilepsy in Tianjin Children's Hospital. We performed clinical examination and laboratory test, and whole-exome sequencing was performed for the proband's and his parents' peripheral blood. The suspected compound-heterozygous variant in the <i>CEP152</i> gene was verified by Sanger sequencing and quantitative real-time polymerase chain reaction technology. <b>Results</b>  We discovered three variants-two of them from <i>CEP152</i> and one from <i>HPD</i> . The result showed the variants in <i>CEP152</i> only. The patient presented with seizures frequently. Sanger sequencing showed two novel variants in <i>CEP152</i> are in exon26 (NM_014985.3 c.3968C > A p.Ser1323*) and in exon16 (NM_014985.3 c.2034_2036del p.Tyr678*). <b>Conclusions</b>  We reported a novel compound-heterozygous variant in the <i>CEP152</i> gene in this study. Most of the phenotypes are Seckel syndrome and primary microencephaly, and the novel variant may cause an atypical phenotype that is epilepsy.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"11 1","pages":"20-24"},"PeriodicalIF":1.7,"publicationDate":"2024-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10791487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139479541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Pair of Compound Heterozygous <i>IARS2</i> Variants Manifesting West Syndrome and Electrolyte Disorders in a Chinese Patient.","authors":"Feiyu Zhou, Gui Yi, Xiangyu Liu, Wenchao Sheng, Jianbo Shu, Dong Li, Chunquan Cai","doi":"10.1055/s-0043-1778091","DOIUrl":"10.1055/s-0043-1778091","url":null,"abstract":"<p><p><b>Background</b>  Aminoacyl-tRNA synthetases (ARSs) are evolutionarily conserved enzymes that ensure the accuracy of the translation process. Isoleucyl-tRNA synthetase 2 ( <i>IARS2</i> ) gene is a type of ARS that encodes mitochondrial isoleucine-tRNA synthetase. Pathogenic variants in the <i>IARS2</i> gene are associated with mitochondrial disease which involves several patients presenting broad clinical phenotypes. These clinical phenotypes include West syndrome, Leigh syndrome, and Cataract, growth hormone deficiency, sensory neuropathy, sensorineural hearing loss, and skeletal dysplasia syndrome. Only 29 cases have been reported worldwide. The patient manifested recurrent convulsions, and specific clinical manifestations included electrolyte disorders and recurrent infections. <b>Methods</b>  Whole-exome sequencing was performed on the child with West syndrome. Three-dimensional structure reconstruction and thermodynamic stability prediction were performed to further analyze the relationship between variation and phenotype. <b>Conclusion</b>  This study further expands the clinical spectrum of <i>IARS2</i> pathogenic variants. The case summaries help raise clinical awareness of <i>IARS2</i> -associated disease and reduce misdiagnosis. <b>Result</b>  In this report, a 13-month-old girl was diagnosed with West syndrome and Leigh syndrome for 7 months. Compound heterozygous variants in the IARS2 gene (NM_018060.4), c.2450G>A (Arg817His) and copy number variation (NC_000001. 11: g. (220267549_220284289) del), were detected by WES. This study further expands the clinical spectrum of IARS2 pathogenic variants. The case summaries help raise clinical awareness of IARS2-associated disease and reduce misdiagnosis.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"11 1","pages":"25-28"},"PeriodicalIF":1.7,"publicationDate":"2024-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10791488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139479535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Two Variants c.2697A > C and c.3305A > C in USP7 by Analysis of Whole-Exome Sequencing in Chinese Patients with Hao-Fountain Syndrome.","authors":"Mei Sun, Qing Li, Ying Zhang, Yingzi Cai, Yan Dong, Jianbo Shu, Dong Li, Chunquan Cai","doi":"10.1055/s-0043-1778089","DOIUrl":"10.1055/s-0043-1778089","url":null,"abstract":"<p><p><b>Background</b>  Variants of ubiquitin-specific protease 7 ( <i>USP7</i> ) gene in humans are associated with a neurodevelopmental disorder-Hao-Fountain syndrome, its core symptoms including developmental delay, intellectual disability, and speech delay. Other variable symptoms can affect multiple systems. In present study, we report two patients with core features from two unrelated consanguineous families originating from the Tianjin Children's Hospital. <b>Methods and Results</b>  Genomic DNA was extracted from the peripheral blood samples collected from the probands with their family members and whole-exome sequencing (WES) was used to detect the pathogenic genes in the probands. Suspected variants were subsequently validated by Sanger sequencing. In family 1, WES revealed that the proband carried the de novo variant c.2697A > C (p.Leu899Phe) in <i>USP7</i> (NM_003470.3). In family 2, WES identified the variant c.3305A > C (p.Asn1102Thr) in <i>USP7</i> (NM_003470.3) from the proband. <b>Conclusion</b>  We reported two cases of Hao-Fountain syndrome caused by novel <i>USP7</i> variants. In addition, we report the first case of mosaicism with a <i>USP7</i> variant in Chinese family. Our findings demonstrate the importance of WES in diagnosis of genetic diseases and expands the <i>USP7</i> variants spectrum in Hao-Fountain syndrome. Moreover, we summarize the cases caused by <i>USP7</i> variants in the literature. Our study can provide a vital reference for the diagnosis of future cases.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"11 1","pages":"13-19"},"PeriodicalIF":1.7,"publicationDate":"2024-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10791489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139479538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Orchestration of Genetic Alterations in <i>PSEN1</i> and <i>PSEN2</i> Genes in Development of Alzheimer's Disease through Computational Analysis.","authors":"Asif Mir, Zainab Kamran, Wajid Iqbal","doi":"10.1055/s-0043-1777849","DOIUrl":"10.1055/s-0043-1777849","url":null,"abstract":"<p><p>Dementia is a syndrome that can cause a number of progressive illnesses that affect memory, thinking, and ability to perform everyday tasks. Alzheimer's disease (AD) is the most common cause of dementia and represents a major public health problem. AD is a progressive disease, where in early stages there is mild memory loss and in late-stage patient loses the ability to carry on a conversation. AD (for which there is no exact cause and cure known so far) is the sixth leading cause of deaths in the United States. Every 68 second someone develops AD. This study focuses on protein structure modeling of genes presenilin 1 and 2 ( <i>PSEN1</i> and <i>PSEN2</i> ) and their mutated forms (Asn141Tyr found in Chinese family, Gly34Ser identified in a Japanese patient, and Arg62Cys & Val214Leu identified in the Korean patients). It also involves wild and mutant type comparison, protein interaction studies, docking and phylogenetic history based on representative ortholog species and also sheds insight into the comparative evolutionary rates of coding sequence across various orthologs. This study gives a time and cost-effective analysis of genes ( <i>PSEN1</i> and <i>PSEN2</i> ) underlying AD and genetic alterations that drive development and causes of disease.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"11 1","pages":"1-12"},"PeriodicalIF":1.7,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10777486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139425683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative Analysis of <i>PAIP2B</i> to Identify a Novel Biomarker for Pancreatic Ductal Adenocarcinoma.","authors":"Yaoxian Xiang, Li Wang, Yurong Cheng, Huanjuan An, Chan Zhang, Jing Wang, Yingying Tong, Dong Yan","doi":"10.1055/s-0043-1777789","DOIUrl":"10.1055/s-0043-1777789","url":null,"abstract":"<p><p>The aim of the study was to evaluate the potential diagnostic and prognostic value of gene, Poly A-Binding Protein Interacting Protein 2B ( <i>PAIP2B</i> ) in pancreatic cancer. We used the gene expression data and clinical information of pancreatic adenocarcinoma patients from The Cancer Genome Atlas database and Gene Expression Omnibus database to analyze the expression of <i>PAIP2B</i> in pancreatic cancer samples, and validated the expression of <i>PAIP2B</i> in tumor tissue, using bioinformatics technology to explore the prognostic value of <i>PAIP2B</i> and its possible biological function. A significantly lower level of <i>PAIP2B</i> was observed in pancreatic cancer patients than in controls, and validated by immunohistochemistry. <i>PAIP2B</i> reduced the proliferation and invasion of cancer cells and had a significantly high expression in early stage. Patients with lower levels of <i>PAIP2B</i> had a significantly shorter median survival time than those with higher levels. DNA demethylation played an important role in <i>PAIP2B</i> expression. In addition, <i>PAIP2B</i> expression was significantly associated with the tumor-infiltrating immune cells, especially T cells CD8, T cells CD4 memory resting, macrophages M0, and dendritic cells resting. Our study also found that <i>PAIP2B</i> regulated miRNA function leading to disease progression in pancreatic cancer patients. Our study explored the potential value of <i>PAIP2B</i> as a biological link between prognosis and pancreatic cancer, and provided reference for the follow-up study on the role of <i>PAIP2B</i> in pancreatic cancer.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"10 4","pages":"388-394"},"PeriodicalIF":1.7,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10730282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138811013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Severe Unilateral Microtia with Aural Atresia, Hair White Patch, Stereotypes in a Young Boy with De novo 16p13.11 Deletion: Reasons for a New Genotype-Phenotype Correlation.","authors":"Piero Pavone, Xena Giada Pappalardo, Claudia Parano, Enrico Parano, Antonio Corsello, Martino Ruggieri, Giovanni Cacciaguerra, Raffaele Falsaperla","doi":"10.1055/s-0043-1777362","DOIUrl":"10.1055/s-0043-1777362","url":null,"abstract":"<p><p><b>Background</b>  Microtia is an uncommon congenital malformation ranging from mild anatomic structural abnormalities to partial or complete absence of the ear leading to hearing impairment. Congenital microtia may present as a single malformation (isolated microtia) or sometimes associated with other congenital anomalies involving various organs. Microtia has been classified in three degrees according to the complexity of the auricular malformation and to anotia referred to the total absence of the ear. Genetic role in causing auricular malformation has been widely demonstrated, and genotype-phenotype correlation has been reported in cases of syndromic microtia. <b>Case Presentation</b>  We report here a young patient with a third degree of scale classification and aural atresia. The patient showed unspecific facial dysmorphism, speech delay, precocious teething, hair white patch, and stereotypic anomalous movements. Genetic analysis displayed a de novo 16p13.11 deletion. <b>Conclusion</b>  Microtia with aural atresia is an uncommon and severe birth defect, which affects functional and esthetic aspects, often associated with other malformations. As traumatic this disorder may be for the parents, the microtia and aural atresia are treatable, thanks to the improving and evolving surgical techniques. Based on the genetic analysis and the clinical features observed in the present case, a genotype-phenotype correlation has been proposed.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"10 4","pages":"370-375"},"PeriodicalIF":1.7,"publicationDate":"2023-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10695706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138488672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study on Screening Core Biomarkers of Noise and Drug-Induced Hearing Loss Based on Transcriptomics.","authors":"Xin Qiu, Qing-Qing Jiang, Wei-Wei Guo, Ning Yu, Shi-Ming Yang","doi":"10.1055/s-0043-1777069","DOIUrl":"10.1055/s-0043-1777069","url":null,"abstract":"<p><p><b>Background</b>  Noise and drug-induced hearing loss (HL) is becoming more and more serious, but the integration and analysis based on transcriptomics and proteomics are lacking. On the one hand, this study aims to integrate existing public transcriptomic data on noise and gentamicin-induced HL. On the other hand, the study aims to establish the gentamicin and noise-induced HL model of guinea pigs, then to perform the transcriptomic and proteomic analyses. Through comprehensive analysis of the above data, we aim to screen, predict, and preliminarily verify biomarkers closely related to HL. <b>Material and Methods</b>  We screened the Gene Expression Omnibus database to obtain transcriptome data expression profiles of HL caused by noise and gentamicin, then constructed the guinea pig HL model and perform the transcriptomic and proteomic analyses. Differential expression and enrichment analysis were performed on public and self-sequenced data, and common differentially expressed genes (DEGs) and signaling pathways were obtained. Finally, we used proteomic data to screen for common differential proteins and validate common differential expression genes for HL. <b>Results</b>  By integrating the public data set with self-constructed model data set, we eventually obtained two core biomarkers of HL, which were RSAD2 and matrix metalloproteinase-3 (MMP3). Their main function is to regulate the development of sense organ in the inner ear and they are mainly involved in mitogen-activated protein kinase and phosphoinositol-3 kinase/protein kinase B signaling pathways. Finally, by integrating the proteomic data of the self-constructed model, we also found differential expression of MMP3 protein. This also preliminarily and partially verified the above-mentioned core biomarkers. <b>Conclusion and Significance</b>  In this study, public database and transcriptomic data of self-constructed model were integrated, and we screened out two core genes and various signal pathways of HL through differential analysis, enrichment analysis, and other analysis methods. Then, we preliminarily validated the MMP3 by proteomic analysis of self-constructed model. This study pointed out the direction for further laboratory verification of key biomarkers of HL, which is of great significance for revealing the core pathogenic mechanism of HL.</p>","PeriodicalId":40142,"journal":{"name":"Global Medical Genetics","volume":"10 4","pages":"357-369"},"PeriodicalIF":1.7,"publicationDate":"2023-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10695707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138488673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}