Psychiatric Genetics最新文献

{"title":"Shared genetic architecture between autism spectrum disorder, loneliness, and social isolation reveals novel genetic loci.","authors":"Sigrun Hope, Aihua Lin, Linn Rodevand, Saira Jameela Hübenette, Daniel S Quintana, Ida E Sønderby, Weiqiu Cheng, Oleksandr Frei, Shahram Bahrami, Guy F L Hindley, Anett Kaale, Alexey A Shadrin, Kevin S O'Connell, Nadine Parker, Srdjan Djurovic, Terje Nærland, Ole A Andreassen","doi":"10.1097/YPG.0000000000000406","DOIUrl":"10.1097/YPG.0000000000000406","url":null,"abstract":"<p><strong>Objective: </strong>Deficits in social communication and social interaction are core features of autism spectrum disorder (ASD), and studies suggest that loneliness and social isolation are common. ASD has a strong genetic basis, but the genetic architecture and overlap with social phenotypes are not clear.</p><p><strong>Methods: </strong>We analyzed summary statistics from genome-wide association studies on ASD (46 350), loneliness (452 302), and social isolation (288 950), using linkage disequilibrium score regression, local analysis of covariant annotation (LAVA), bivariate causal mixture model (MiXeR), and the conditional/conjunctional false discovery rate (cond/conjFDR).</p><p><strong>Results: </strong>For ASD and social isolation, we found nonsignificant global genetic correlation ( rg = 0.02, P  = 0.8), but LAVA identified 72 genomic regions with bidirectional correlations, and MiXeR estimated that 8.7 k of 13.1 k variants (81%) were shared, of which 53% had concordant effect directions. For ASD and loneliness, we found a positive genetic correlation ( rg = 0.26, P  = 2e-10), LAVA identified 80 genomic regions with bidirectional genetic correlations, and MiXeR suggested that at least 3.8 k variants were shared. We identified nine specific shared genetic loci between ASD and loneliness and eight between ASD and social isolation (conjFDR < 0.05). Of these, 12 loci were novel for ASD. Genes mapped to these loci are involved in γ-aminobutyric acid (GABA), glutamate, calcium, and stress hormone signaling, cerebral glucose transport, TAU-accumulation, and immune function.</p><p><strong>Conclusion: </strong>We found extensive overlap in genetic architecture between ASD, loneliness, and social isolation, with bidirectional effects. By leveraging data for ASD and social traits, we identified 12 novel ASD related genetic loci implicating several genes, thereby elucidating potential pathways underlying their shared genetic architecture.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":" ","pages":"13-25"},"PeriodicalIF":1.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12834293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145565125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dissecting the genetic interaction between breast cancer risk and schizophrenia: evidence from crosstrait genome-wide analysis.","authors":"Min Zhang, Yongli Wu, Yujie Qin","doi":"10.1097/YPG.0000000000000410","DOIUrl":"10.1097/YPG.0000000000000410","url":null,"abstract":"<p><strong>Background: </strong>Epidemiological evidence suggests a link between schizophrenia (SCZ) and increased breast cancer (BC) risk, but the genetic mechanisms remain unclear. Exploring their shared genetic susceptibility may help reveal the basis of this comorbidity.</p><p><strong>Methods: </strong>This study was conducted utilizing genome-wide association study (GWAS) data for SCZ and BC, employing a multitiered genetic analytical framework to systematically assess the genetic association patterns between these two conditions. Initially, linkage disequilibrium score regression and high-dimensional likelihood modeling were applied to quantitatively evaluate genome-wide genetic correlations, while localized variant association analysis was performed to detect regional genetic association signals within specific genomic loci. Subsequently, conditional/conjunctional false discovery rate (condFDR/conjFDR) methodologies were implemented to uncover the shared genetic architecture underlying both traits. Ultimately, conjFDR was integrated with multitrait analysis of GWAS (MTAG) strategies to further identify and validate potentially overlapping genetic variant loci.</p><p><strong>Results: </strong>The analysis revealed significantly positive genome-wide genetic correlations between SCZ and BC, as well as among various BC subtypes. Regional genetic structure analysis identified numerous chromosomal loci exhibiting shared genetic signals. The condFDR/conjFDR models provided additional confirmation of the genetic overlap between the two traits. Through the combined application of conjFDR and MTAG, a collection of shared genetic loci with plausible biological relevance was identified and substantiated, including BATXN7, FOXP1, EMB, LINC00536, ZNF365, MAPT, STXBP4 , and GATAD2A .</p><p><strong>Conclusion: </strong>The findings elucidated genetic associations between SCZ and BC and identified critical shared genetic contributors, thereby offering molecular evidence for the investigation of comorbidity mechanisms and potential intervention strategies.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":" ","pages":"32-41"},"PeriodicalIF":1.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145744166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What do European clinical guidelines say about genetic testing for people with neuropsychiatric disorders? A scoping review.","authors":"Izemnur Arican, Marte van der Horst, Nicholas Bass, Janneke R Zinkstok","doi":"10.1097/YPG.0000000000000407","DOIUrl":"10.1097/YPG.0000000000000407","url":null,"abstract":"<p><p>Genomic medicine has progressed rapidly, and many high-risk genetic variants for neuropsychiatric disorders have now been identified. However, clinical genetic testing is rarely utilized in psychiatric settings. This scoping review examined European clinical practice guidelines (CPGs) for genetic testing in neuropsychiatric disorders to map recommendations and identify gaps. Seventeen CPGs published since 2010 met the inclusion criteria. There was a wide variation in scope, quality, and conditions covered. Seven CPGs addressed autism spectrum disorder, generally recommending testing when additional features such as intellectual disability or dysmorphology were present. One CPG covered the investigation of intellectual disability, advising Fragile X testing, chromosomal microarray, and whole-genome sequencing. Most CPGs (11/17), related to dementia, advising testing with very early onset and/or an indicative family history. Overall, European CPGs for genetic testing in psychiatry vary significantly, contributing to clinician uncertainty. Harmonizing evidence-based CPGs is crucial to advance the integration of genetic testing in psychiatric practice.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":" ","pages":"1-12"},"PeriodicalIF":1.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12834271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic predisposition and the role of homocysteine in a female with late diagnosis of autism.","authors":"George Zografakis, Katerina Papanikolaou, Niki Pehlivanidi, Ioannis Malogiannis, Eleni Giannoulis, Efthymia Pavlou, Efrosyni Nomikou, Artemios Pehlivanidis","doi":"10.1097/YPG.0000000000000408","DOIUrl":"https://doi.org/10.1097/YPG.0000000000000408","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social interaction and communication, as well as restricted and repetitive behaviors. Although ASD often manifests during early childhood, many individuals are diagnosed later in life due to difficulties in meeting increasing social demands. Early diagnosis and personalized treatment are crucial in lifetime ASD symptom trajectories. We report the case of a 27-year-old woman diagnosed with ASD in adulthood, in correlation with elevated homocysteine (Hcy) levels due to homozygosity for the MTHFR C677T polymorphism, whose symptoms deteriorated, possibly related to dietary changes. Following Hcy blood levels normalization, autistic symptoms of social interaction improved. This case highlights a potential relationship between environmental factors, such as dietary changes, and the late diagnosis of ASD, supporting the theory that interaction between environment and genetics, possibly, plays a role in ASD development.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neonatal genetic screening in Changsha: a multicenter study and preliminary findings.","authors":"Jun He, Jingjing Zhang, Shuanglin Xiang, Xing Fan","doi":"10.1097/YPG.0000000000000403","DOIUrl":"10.1097/YPG.0000000000000403","url":null,"abstract":"<p><strong>Background: </strong>Newborn screening (NBS) is a public health service aimed at identifying infants with severe genetic disorders. Genetic testing is now commonly used for secondary or confirmatory testing after a positive result in some NBS programs. Recently, next-generation sequencing (NGS) has emerged as a robust tool that enables large panels of genes to be scanned together rapidly. Rapid advances in NGS emphasize the potential for genomic sequencing to improve NBS programs. Neonatal genetic screening represents a critical advancement within contemporary NBS frameworks, integrating NGS to enhance disease detection sensitivity and specificity.</p><p><strong>Materials and methods: </strong>This study, conducted through multicenter collaboration in Changsha, screened 2019 neonatal samples for 75 common genetic disorders involving 135 pathogenic genes. The aim was to explore the incidence and mutation spectrum of these disorders in the Chinese population and to propose an optimized screening model.</p><p><strong>Results: </strong>The results showed a positive detection rate of 0.74% and a carrier rate of 31.50%.</p><p><strong>Conclusion: </strong>This study provides valuable data for refining neonatal genetic screening protocols in China.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":" ","pages":"166-170"},"PeriodicalIF":1.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145392426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polygenic risks and cardiovascular treatment effects in severe mental illness.","authors":"Kai Yao, Alexandra Burton, Samira Heinkel, David Osborn, Nick Bass, Andrew McQuillin","doi":"10.1097/YPG.0000000000000401","DOIUrl":"10.1097/YPG.0000000000000401","url":null,"abstract":"<p><strong>Objective: </strong>Patients with severe mental illness (SMI) experience increased cardiovascular risks, leading to reduced life expectancy. Polygenic risk scores (PRS) prediction is promising for assessing cardiovascular risks. This study evaluated the predictive utility of cardiovascular PRS and the impact from risk-reducing interventions among patients with SMI.</p><p><strong>Methods: </strong>Using samples from the PRIMROSE programme, involving longitudinal cardiovascular interventions within primary care, we calculated seven cardiovascular and two psychiatric (bipolar/schizophrenia) PRS to predict seven corresponding cardiovascular measures [total cholesterol/high-density lipoprotein cholesterol/low-density lipoprotein cholesterol (LDL)/triglyceride/systolic blood pressure/diastolic blood pressure/BMI] assessed at baseline and 12-month follow-up. We applied multiple linear regression models at the two time points and explored the interactions between cardiovascular and psychiatric PRS on these treatment outcomes.</p><p><strong>Results: </strong>At baseline, most cardiovascular PRS were associated with the respective measures, except LDL. At follow-up, the participants showed significant improvements in total cholesterol and systolic blood pressure measures; however, these two PRS's prediction effects attenuated toward the null. LDL measures became negatively associated with bipolar PRS posttreatment, though no significant interaction effects were found. Participants in the highest bipolar PRS quartile group had 0.58 mmol/L lower LDL measures than the lowest quartile group at follow-up. These results were robust to potential power reduction, participants' age, sex, prescribed medications, smoking habits, alcohol consumption, and physical activity.</p><p><strong>Conclusion: </strong>Our findings underscore the dynamic interplay between genetic risks and treatment effects on cardiovascular outcomes in SMI and warrant careful PRS assessment timing. While the clinical utility of PRS is still evolving, future research should explore different disorders' subtype-specific genetic interactions with interventions.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":" ","pages":"143-153"},"PeriodicalIF":1.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12588646/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145392518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between symptom severity, glutamate levels, and N-methyl-D-aspartate receptor target microRNA expression in patients with panic disorder.","authors":"Tuba Tuğ Altunöz, Nazan Dolapoğlu, Özgür Baykan, Hilmi Bolat, Ayla Solmaz Avcikurt, Tunay Karlidere","doi":"10.1097/YPG.0000000000000402","DOIUrl":"https://doi.org/10.1097/YPG.0000000000000402","url":null,"abstract":"<p><strong>Background: </strong>Glutamate, an excitatory neurotransmitter in the central nervous system, plays a role in neurodevelopment, learning, and memory. It is thought to interact with the GABAergic system in the development of panic symptoms; however, the relationship between blood glutamate levels and panic disorder severity remains unclear. While research on miRNAs is increasing, studies on their role in panic disorder are limited. This study aimed to evaluate blood glutamate levels and the expression of miR-138-2-3p, which affects glutamate receptors, in panic disorder.</p><p><strong>Methods: </strong>The study included 46 panic disorder patients and 46 healthy controls. All participants completed sociodemographic, Panic Disorder Severity Scale (PDSS), Anxiety Sensitivity Index-3 (ASI-3), and Somatosensory Exaggeration Scale (SSAS) forms. Peripheral venous blood was collected for genetic and biochemical analysis. MicroRNA expression was assessed by real-time PCR, and glutamate levels were measured using ELISA.</p><p><strong>Results: </strong>Patients with panic disorder exhibited significantly lower plasma glutamate levels compared with healthy controls, with median values (25-75% percentiles) of 96.7 nmol/ml (51.39-133.62) versus 209 nmol/ml (95.6-521.9, P < 0.001). Moreover, glutamate levels were negatively associated with symptom severity as measured by the PDSS, ASI-3, and SSAS. In parallel, miR-138-2-3p expression was significantly reduced in patients relative to controls, with median ratios (25-75% percentiles) of 0.27 (0.14-0.57) versus 0.48 (0.23-0.98, P = 0.034), corresponding to a 1.77-fold higher expression in controls.</p><p><strong>Conclusion: </strong>Altered miR-138-2-3p expression and reduced peripheral glutamate levels may contribute to the pathophysiology and clinical severity of panic disorder.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":"35 6","pages":"171-176"},"PeriodicalIF":1.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145452627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bidirectional genetic overlap between mood swings and irritable bowel syndrome.","authors":"Qinghua Luo, Jiawen Wang, Mingwei An, Leichang Zhang, Chen Wang","doi":"10.1097/YPG.0000000000000405","DOIUrl":"10.1097/YPG.0000000000000405","url":null,"abstract":"<p><strong>Background: </strong>Mood swings and irritable bowel syndrome (IBS) are closely related. However, the reason for the clinical concurrence of this phenomenon is unknown, and maybe it is because the two share genetic underpinnings.</p><p><strong>Methods: </strong>Genome-wide association studies (GWAS) of mood swings and IBS data were used for the study. Genetic correlation was assessed using the linkage disequilibrium score regression (LDSC), genetic covariance analyzer (GNOVA), and SUPERGNOVA method. Two-sample Mendelian randomization (TwoSampleMR) was used to explore the causal relationship between the two conditions. The conditional/conjoint false discovery rate (cond/conjFDR) was used for genetic overlap analysis. Finally, LDSC applied to specific expression gene analysis was performed to identify tissues associated with the two conditions.</p><p><strong>Results: </strong>At the genomic level, mood swings and IBS have global and local genetic correlations. Analysis of the two traits by Mendelian randomization revealed a bidirectional causal relationship. We identified 21 genetic risk loci (concFDR < 0.05) shared by mood swings and IBS, which acted in the same direction on the two traits. Additionally, mood swings and IBS shared 11 sites in the brain tissues as origins.</p><p><strong>Conclusion: </strong>The present study suggests the existence of polygenic overlap between mood swings and IBS and provides novel insights into the genetic underpinnings and mechanisms of comorbidities occurring in these two conditions.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":"35 6","pages":"154-165"},"PeriodicalIF":1.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145452610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bidirectional genetic overlap between mood swings and irritable bowel syndrome.","authors":"Qinghua Luo, Jiawen Wang, Mingwei An, Leichang Zhang, Chen Wang","doi":"10.1097/YPG.0000000000000405","DOIUrl":"https://doi.org/10.1097/YPG.0000000000000405","url":null,"abstract":"<p><strong>Background: </strong>Mood swings and irritable bowel syndrome (IBS) are closely related. However, the reason for the clinical concurrence of this phenomenon is unknown, and maybe it is because the two share genetic underpinnings.</p><p><strong>Methods: </strong>Genome-wide association studies (GWAS) of mood swings and IBS data were used for the study. Genetic correlation was assessed using the linkage disequilibrium score regression (LDSC), genetic covariance analyzer (GNOVA), and SUPERGNOVA method. Two-sample Mendelian randomization (TwoSampleMR) was used to explore the causal relationship between the two conditions. The conditional/conjoint false discovery rate (cond/conjFDR) was used for genetic overlap analysis. Finally, LDSC applied to specific expression gene analysis was performed to identify tissues associated with the two conditions.</p><p><strong>Results: </strong>At the genomic level, mood swings and IBS have global and local genetic correlations. Analysis of the two traits by Mendelian randomization revealed a bidirectional causal relationship. We identified 21 genetic risk loci (concFDR < 0.05) shared by mood swings and IBS, which acted in the same direction on the two traits. Additionally, mood swings and IBS shared 11 sites in the brain tissues as origins.</p><p><strong>Conclusion: </strong>The present study suggests the existence of polygenic overlap between mood swings and IBS and provides novel insights into the genetic underpinnings and mechanisms of comorbidities occurring in these two conditions.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145452587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The DNA methyltransferase complex conundrum: novel DNA methyltransferase 1 mutation in an Indian patient with dementia and sensory neural hearing loss on a background of long-standing psychosis.","authors":"Mude Jeevan Naik, Pannaga Prasad Ganapathi, Manik Inder Singh Sethi, Guru S Gowda, Satish Suhas, Karthick Navin, John P John, Ravi Yadav, Meera Purushottam, Sanjeev Jain, Venkata Senthil Kumar Reddi","doi":"10.1097/YPG.0000000000000397","DOIUrl":"10.1097/YPG.0000000000000397","url":null,"abstract":"<p><p>Epigenetic alterations, like DNA methylation, are increasingly recognised as integral to the development of both neurological and psychiatric disorders. Mutations in the DNA methyltransferase 1 ( DNMT1 ) gene have also been linked to specific neurodegenerative syndromes. Despite these advances, when and how these alterations influence disease expression remains to be understood. This report highlights a novel heterozygous missense mutation in exon 30 of the DNMT1 gene that was detected in a middle-aged lady who presented with early-onset dementia on a background of long-standing psychosis with depression and neuroleptic sensitivity. This case expands the phenotypic spectrum associated with DNMT1 mutations and highlights the potential value of genetic testing in evaluating atypical neuropsychiatric presentations. The phenotypic complexity highlights the critical need for further research to elucidate the mechanistic links between DNMT1 mutations and neuropsychiatric disease, paving the way for targeted therapeutic interventions.</p>","PeriodicalId":20734,"journal":{"name":"Psychiatric Genetics","volume":" ","pages":"136-141"},"PeriodicalIF":1.4,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144592038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}