American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics最新文献

{"title":"The Multifaceted Etiology of Mental Disorders With a Focus on Trace Elements, a Review of Recent Literature.","authors":"Maria Francesca Astorino, Marco Calabrò, Carmenrita Infortuna, Maria Rosaria Anna Muscatello, Silvana Briuglia, Nicola Cicero, Chiara Fabbri, Alessandro Serretti, Concetta Crisafulli","doi":"10.1002/ajmg.b.33045","DOIUrl":"https://doi.org/10.1002/ajmg.b.33045","url":null,"abstract":"<p><p>Mental disorders are a significant global public health concern, affecting nearly one in eight individuals worldwide. This review investigates the multifaceted etiology of mental disorders-specifically major depressive disorder (MDD), schizophrenia (SCZ), and bipolar disorder (BD)-through genetic, neurobiological, and environmental perspectives, with a particular emphasis on the role of trace elements (TrEs). TrEs such as zinc, magnesium, copper, iron, and selenium are essential micronutrients that influence several central nervous system functions, including enzymatic activity, neurotransmitter synthesis, and synaptic plasticity. Both deficiencies and excesses of these elements have been linked to psychiatric disorders. This study explores the associations between TrEs, psychiatric symptoms, and biological pathways due to the Research Domain Criteria (RDoC) framework. We discuss clinical evidence and genetic studies to evaluate possible correlations between TrEs and key RDoC endophenotypes. By elucidating these connections, this review focuses on the potential and current limitations of TrEs in mental health.</p>","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33045"},"PeriodicalIF":0.0,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Equitable Collaboration Between LMIC and HIC Researchers, Part I: A Preliminary Framework for Capacity Building in Psychiatric Genetics Research.","authors":"Brenda Cabrera-Mendoza, Margit Burmeister, Marcella Rietschel, David Crepaz-Keay, Yatan Pal Singh Balhara, Soraya Seedat, Victoria Marshe, Sian Hemmings, Roseann Peterson, Ruchika Kaushik, Biju Viswanath, Reeteka Sud, Partha Haldar, Mandy Johnstone, Anish V Cherian, Todd Lencz, Janneke Zinkstok, Renato Polimanti, Daniel J Mueller, Gabriel Lázaro-Muñoz, Chunyu Liu, Nurnberger John, Humberto Nicolini, Consuelo Walss-Bass, Marcos Santoro, Sujata Satapathy, Chittaranjan Behera, Anna R Docherty","doi":"10.1002/ajmg.b.33042","DOIUrl":"https://doi.org/10.1002/ajmg.b.33042","url":null,"abstract":"<p><p>International collaborations between high-income countries (HICs) and low- and middle-income countries (LMICs) have become increasingly essential in advancing global health, particularly within psychiatric research. These partnerships not only accelerate scientific discovery and enhance public health, but they also bring to light significant challenges in equity and fairness. Specifically, research partnerships often suffer from imbalances, such as \"helicopter\" research approaches or the exploitation and marginalization of LMIC researchers. Here, we present a consensus report by members of the International Society for Psychiatric Genetics, outlining key considerations and strategies for planning, implementing, and disseminating equitable collaborative research. Throughout the collaboration process, we identified both challenges and opportunities and provided recommendations to maximize the benefits of these partnerships. Among our considerations, we emphasize that Equitable Collaboration must begin with comprehensive stakeholder engagement, fostering a participatory environment that includes local communities, governments, and institutions from both HICs and LMICs. Among the potential challenges we identify are differences in ethical research and data-sharing frameworks across countries, inequalities in research resources and infrastructure, and reduced visibility of research conducted in LMICs. These factors can significantly impact research outcomes and their applicability. In conclusion, while global collaboration in psychiatric genetics presents complex challenges, it also offers substantial opportunities for impactful research and improved global mental health.</p>","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33042"},"PeriodicalIF":0.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144602719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improving Machine Learning Prediction of ADHD Using Gene Set Polygenic Risk Scores and Risk Scores From Genetically Correlated Phenotypes.","authors":"Eric J Barnett, Yanli Zhang-James, Stephen V Faraone","doi":"10.1002/ajmg.b.33043","DOIUrl":"https://doi.org/10.1002/ajmg.b.33043","url":null,"abstract":"<p><p>Polygenic risk scores (PRSs), which sum the effects of SNPs throughout the genome to measure risk afforded by common genetic variants, have improved our ability to estimate disorder risk for Attention-Deficit/Hyperactivity Disorder (ADHD) but the accuracy of risk prediction is rarely investigated. In a study of 10,887 participants across nine cohorts, we performed gene set analysis of GWAS data to select gene sets associated with ADHD within a training subset. For each gene set, we generated gene set polygenic risk scores (gsPRSs), which sum the effects of SNPs for each selected gene set. We created gsPRS for ADHD and for phenotypes that are genetically correlated with ADHD. These gsPRS were added to the standard PRS as input to machine learning models predicting ADHD. On the test subset, a random forest (RF) model using PRSs from ADHD and genetically correlated phenotypes and an optimized group of 20 gsPRS had an area under the receiving operating characteristic curve (AUC) of 0.72 (95% CI: 0.70-0.74). This AUC was a statistically significant improvement over logistic regression models and RF models using only PRS from ADHD and genetically correlated phenotypes. Summing risk at the gene set level and incorporating genetic risk from disorders with high genetic correlations with ADHD improved the accuracy of predicting ADHD. Learning curves suggest that additional improvements would be expected with larger study sizes. Our study suggests that better accounting of genetic risk and the genetic context of allelic differences results in more predictive models.</p>","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33043"},"PeriodicalIF":0.0,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144593700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptional Patterns of Functional Connectivity Associated With Somatic Symptoms in Major Depressive Disorder.","authors":"Shiying Wang, Chengfeng Chen, Jiang Wang, Runhua Wang, Fuqiang Mao, Bin Zhang","doi":"10.1002/ajmg.b.33041","DOIUrl":"https://doi.org/10.1002/ajmg.b.33041","url":null,"abstract":"<p><p>Somatic symptoms are common in major depressive disorder (MDD), but their neurobiological and gene expression mechanisms are not yet well understood. To address this gap, we analyzed a multicenter magnetic resonance imaging dataset comprising 417 MDD patients. First, we conducted a correlation analysis between functional connectivity (FC) and somatic symptoms. Next, gene expression data from the Allen Human Brain Atlas were integrated with FC using partial least squares regression. Finally, functional enrichment analysis identified biological processes, molecular functions, and cellular components associated with the genes linked to FC. Our findings revealed that FC between the medial cerebellum and several cortical regions, including the occipital, temporal, parietal, and mid-insular cortices, was positively associated with somatic symptom severity. Similarly, FC between the parietal cortex and regions such as the anterior prefrontal cortex, ventral frontal cortex, temporal cortex, and precuneus also showed positive associations with somatic symptom severity. Moreover, connectome-transcriptome correlation analysis revealed that the expression of 1120 genes was spatially correlated with FC, and these genes were primarily enriched in synapses and ion channels. Our results indicated that gene expression variations in synaptic translation and ion channels may affect FC associated with somatic symptoms.</p>","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33041"},"PeriodicalIF":0.0,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Psychiatric Symptoms and Neuropsychological Findings in an Extremely Rare Case of 47,XXY Presenting With a Female Phenotype due to Deletion of the SRY Gene.","authors":"Lucas Giraldelli, Arthur Tolentino, Felipe Mendonça Rocha Barros, Liliane Smaniotto, Carolina Tessler, Luiz Fernando Longuim Pegoraro, Andrea Trevas Maciel Guerra, Claudio E M Banzato","doi":"10.1002/ajmg.b.33039","DOIUrl":"https://doi.org/10.1002/ajmg.b.33039","url":null,"abstract":"","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33039"},"PeriodicalIF":0.0,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of SLC39A8.p.(Ala391Thr) in Schizophrenia Symptom Severity and Cognitive Ability: Cross-Sectional Studies of Schizophrenia and the General UK Population.","authors":"Sophie E Smart, Sophie E Legge, Eilidh Fenner, Antonio F Pardiñas, Grace Woolway, Amy J Lynham, Valentina Escott-Price, Jeremy Hall, Lawrence Wilkinson, Peter Holmans, Michael C O'Donovan, Michael J Owen, James T R Walters","doi":"10.1002/ajmg.b.33037","DOIUrl":"10.1002/ajmg.b.33037","url":null,"abstract":"<p><p>The missense SNP NC_000004.12:g.102267552C>T (also known as SLC39A8.p.(Ala391Thr), rs13107325) in SLC39A8 encodes a zinc transporter. This SNP has been linked to schizophrenia and is the likely causal variant for one of the genome-wide association loci associated with the disorder. Using regression analyses, we tested whether the schizophrenia-risk allele at p.(Ala391Thr) was associated with schizophrenia-related phenotypes, including positive, negative, and disorganized symptoms, cognitive ability, educational attainment, and age of psychosis onset, within three schizophrenia cohorts (combined N = 1232) and, with equivalent phenotypes, in a sample of population controls (UK Biobank, N = 355,069). We also used the population controls to test for associations with rare protein-truncating and deleterious missense variants within SLC39A8. Within the schizophrenia cohorts, after correction for multiple testing, p.(Ala391Thr) was not significantly associated with any schizophrenia-related phenotypes. In the unaffected participants from the UK Biobank, the schizophrenia-risk allele at p.(Ala391Thr) was associated with significantly poorer cognitive ability and fluid intelligence, a lower probability of obtaining GCSEs or a degree-level qualification, and fewer years in education. There was no association between p.(Ala391Thr) and self-reported psychotic experiences in this cohort. Rare variants in SLC39A8 were nominally associated with poorer cognitive ability, but these associations did not survive correction for multiple testing. The schizophrenia-risk allele was associated with poorer cognitive ability, but not psychotic experiences, in a volunteer sample drawn from the general population. We found no evidence that p.(Ala391Thr) was associated with symptom severity in schizophrenia. To understand the impact of rare variants in SLC39A8 on cognitive impairment, larger independent samples are required.</p>","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33037"},"PeriodicalIF":0.0,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144328324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetics of Response to ECT, TMS, Ketamine and Esketamine.","authors":"Clio E Franklin, Murat Altinay, Kala Bailey, Mahendra T Bhati, Brent R Carr, Susan K Conroy, Khurshid Khurshid, William M McDonald, Brian J Mickey, James W Murrough, Sean M Nestor, Thomas Nickl-Jockschat, Irving M Reti, Gerard Sanacora, Nicholas T Trapp, Biju Viswanath, Jesse H Wright, Peter P Zandi, James B Potash","doi":"10.1002/ajmg.b.33038","DOIUrl":"10.1002/ajmg.b.33038","url":null,"abstract":"<p><p>Treatment-resistant mood disorders are often managed with intensive interventions that include electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS), ketamine, and esketamine, but the role of genetics in clinical response to those interventions is yet to be clearly determined. Here, we review the current literature on the genetics of response to these treatment modalities. To date, the limited number of studies done to investigate genetic predictors of treatment response have primarily focused on single variants in candidate genes, and none of these have been consistently reproducible. The majority of candidate gene studies examine the effect of variants in the COMT and BDNF genes on treatment response. There are a limited number of genome-wide association studies (GWAS) looking at treatment response, though they are almost all underpowered, with only one study including a sample size > 1000. As a result, there have been few single nucleotide polymorphisms (SNPs) found to be associated with treatment response at a statistically significant level, all in genes other than COMT and BDNF. The challenge is now to generate data from a large group of patients undergoing these therapies in order to more robustly assess the genetic factors affecting treatment response. This will not only help establish genetic predictors of response, but also potentially develop differential predictors of response to available treatments, which could provide clinicians with critical information to aid in deciding which treatment modality to recommend for treatment-resistant depression. We are currently pursuing such a strategy in our 50-site worldwide Gen-ECT-ic consortium.</p>","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33038"},"PeriodicalIF":0.0,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12230785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144319089","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":"Genome Sequencing Uncovers Additional Findings in Phelan-McDermid Syndrome.","authors":"Rachel Gore Moses, Morgan Similuk, Alexandra Hehn, Rylee Duncan, Margaret Pekar, Eliza Gordon-Lipkin, Maria T Acosta, Deena Zeltser, Nadjalisse Reynolds-Lallement, Latha Soorya, Mustafa Sahin, Tess Levy, Alexander Kolevzon, Joseph D Buxbaum, Elizabeth Berry-Kravis, Craig M Powell, Jonathan A Bernstein, Mari Tokita, Bryce A Seifert, Rajarshi Ghosh, Magdalena A Walkiewicz, Audrey Thurm","doi":"10.1002/ajmg.b.33036","DOIUrl":"10.1002/ajmg.b.33036","url":null,"abstract":"<p><p>Phelan-McDermid syndrome (PMS) is a genetic condition caused by deletions of chromosome 22q13.3 or pathogenic variants in the SHANK3 gene. Neurologic features typically include intellectual disability, autism spectrum disorder, hypotonia, and absent speech, though there is considerable variability even among individuals with the same molecular cause. This prospective study aimed to explore the utility of genome sequencing to identify additional molecular diagnoses that may contribute to variability in a cohort of patients with PMS. Twenty probands diagnosed with PMS (60% with a 22q13 deletion, 40% with a SHANK3 variant) underwent trio or duo genome sequencing and chromosomal microarray. This analysis identified a second molecular finding associated with a neurological condition in 3/20 participants. Molecular diagnoses related to neurological phenotypes included: (1) spinal muscular atrophy, lower extremity-predominant, 2A, autosomal dominant (SMALED2A), (2) spastic paraplegia 7, and (3) 16p11.2 deletion syndrome. Five additional new molecular diagnoses were associated with a clinically actionable secondary or incidental finding. This exploratory study provides early evidence for the potential utility of expanded sequencing among individuals with PMS, even for those without phenotypic features outside of the expected range.</p>","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33036"},"PeriodicalIF":0.0,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144304338","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":"Genome-Wide Insights and Polygenic Risk Scores in Common Epilepsies: A Narrative Review.","authors":"Mario Mastrangelo, Simona Petrucci, Giuliana Lentini, Marco Fabiani, Maria Piane, Francesco Pisani","doi":"10.1002/ajmg.b.33040","DOIUrl":"https://doi.org/10.1002/ajmg.b.33040","url":null,"abstract":"<p><p>The research of single gene-related disorders or pathogenic copy-number variations (CNVs) has given a significant impetus to the shift from a diagnostic work-up focused on epileptic syndromes to genomic approaches in individuals with severe pediatric-onset epilepsies and in developmental and epileptic encephalopathies. Genome-wide association studies (GWAS) have identified various loci of susceptibility for common epilepsies and highlighted a strong predisposing role of common variants in several genes involved in well-known monogenic diseases. The largest GWAS identified eight major loci with stronger genome-wide significance for epilepsy, regardless the underlying epileptic syndrome: 2q24.3, 2p16.1, 4p15.1, 7q21.11, 8p23.1, 9q21.13, 10q24.32, 16q12.1, 2p16.1 and 2q24.3 occurred more frequently in patients with genetic generalized epilepsies. Loci 4p12, 8q23.1 and 16p11.2 achieved a high genome-wide significance for Juvenile Myoclonic Epilepsy. Childhood Absence Epilepsy was significantly genome-wide associated with 2p16.1 and 2q22.3. The loci 3q25.31, 6q22.31 and 2q24.3 were significantly associated with non-acquired focal epilepsies. Polygenic risk scores (PRS) are used to quantify the cumulative effects of several common genetic variants in a single score, each of which individually contributes minimally to disease susceptibility. The impact of PRS on clinical practice might be relevant for epilepsy risk prediction in groups of patients at high risk of developing epilepsy in the near future. Elevated PRS values have been observed in genetic generalized epilepsies particularly in familial forms, females, and patients with previous seizure events. Among comorbidities associated with epilepsy, depression, psychosis, and attention-deficit/hyperactivity disorder (ADHD) showed significantly elevated PRS.</p>","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33040"},"PeriodicalIF":0.0,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144288115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic Analysis of Trichotillomania.","authors":"Matthew W Halvorsen, Melanie E Garrett, Michael L Cuccaro, Allison E Ashley-Koch, James J Crowley","doi":"10.1002/ajmg.b.33035","DOIUrl":"10.1002/ajmg.b.33035","url":null,"abstract":"<p><p>Trichotillomania (TTM) is a psychiatric condition in which people feel an overwhelming urge to pull out their hair, resulting in noticeable hair loss and significant distress. Twin and family studies suggest that TTM is at least partly genetic, but no genome-wide analyses have been completed. To fill the gap in this field, we have conducted a case-control study of genotype array data from 101 European ancestry TTM cases and 488 ancestry-matched unaffected controls. TTM cases were ascertained in the United States through web-based recruitment, patient support groups, and conferences organized by the Trichotillomania Learning Center. Following clinical confirmation of a TTM diagnosis, patients completed self-report assessments of frequency and duration of hair pulling, other psychiatric symptoms, and family history. Unaffected controls were also ascertained in the United States and were matched to cases by ancestry. In the first formal genome-wide association study of TTM, we did not identify any common variants with a genome-wide significant (p < 5 × 10^-8) association level with case status. We found that cases carry a higher load of common polygenic risk for psychiatric disorders (p = 0.008). We also detected copy number variants previously associated with neuropsychiatric disorders (specifically, deletions in NRXN1, CSMD1, and 15q11.2). These results further support genetics' role in the etiology of TTM and suggest that larger studies are likely to identify risk variation and, ultimately, specific risk genes associated with the condition.</p>","PeriodicalId":520553,"journal":{"name":"American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics","volume":" ","pages":"e33035"},"PeriodicalIF":0.0,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144288116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}