Biological Psychiatry最新文献

{"title":"PTSD is Associated with Advanced Epigenetic Age in 43,155 US Military Veterans.","authors":"Erika J Wolf, Rui Zhang, Xiang Zhao, Mark W Logue, Brendan M Despard, Phillip Ma, Meghan Wilkinson, Kelsey N Serier, Adam X Maihofer, Kelly M Harrington, J Michael Gaziano, Alexandre C Pereira, Mark W Miller","doi":"10.1016/j.biopsych.2026.10.032","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.10.032","url":null,"abstract":"<p><strong>Background: </strong>Posttraumatic stress disorder (PTSD) has been associated with advanced biological age in DNA methylation data, but results have been inconsistent. This study evaluated PTSD in association with epigenetic age in the largest cohort to date (by ∼20 fold).</p><p><strong>Methods: </strong>Participants were 43,155 US Veterans (92.96% male) enrolled in the VA's Million Veteran Program, with VA electronic health record (EHR), self-report PTSD severity (n = 21,999), and DNA methylation and genotype data. PTSD diagnoses predated the blood draw for obtaining DNA by ≥ one year.</p><p><strong>Results: </strong>PTSD diagnosis and symptom severity were associated with age-adjusted metrics of epigenetic age (\"age residuals\") per the Horvath, Hannum, PhenoAge, GrimAge, and DunedinPACE algorithms after multiple testing adjustment. PTSD severity showed the most consistent associations with epigenetic age residuals, ranging from up to ∼7 months (Horvath) to ∼2 years (GrimAge) advanced age and up to 16 days faster pace per year (DunedinPACE). The relationships between PTSD severity and GrimAge, PhenoAge, and DunedinPACE residuals were stronger among younger vs. older Veterans. PTSD was associated with all epigenetic age residuals in the European ancestry subgroup (n = 26,630), but fewer significant associations emerged in the African ancestry participants (n = 11,119). Associations were similar across male and female Veterans.</p><p><strong>Conclusions: </strong>PTSD was associated with advanced epigenetic aging in the largest study to date to evaluate this question. Effects were generally small in magnitude, though meaningful when considering the personal and healthcare system impact of advanced aging in the large population of VA users with PTSD.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149369889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune-Microbiome Crosstalk in the Developmental Origins of Neurodevelopmental Disorders.","authors":"Elizabeth C Plunk, Hannah Hazzard, Evan Bordt, Serena Banu Gumusoglu","doi":"10.1016/j.biopsych.2026.10.029","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.10.029","url":null,"abstract":"<p><p>Neurodevelopmental disorders (NDDs) arise from genetic and environmental factors converging across development, from embryogenesis through adulthood. Two systems central to brain development, the immune system and the microbiome, are incompletely formed at birth. Development of these immune and microbiome systems is shaped by factors transferred across prenatal and postnatal maternal-offspring interfaces including the placenta, birth canal, and breast. Despite literature linking each system independently to NDD risk, these fields have largely proceeded in parallel, rarely interrogating their interactions. This siloed approach constrains mechanistic understanding and progress. Here, we present evidence that the immune system and microbiome are interacting, not independent, influences on neurodevelopmental programming. Preclinical evidence from germ-free, antibiotic depletion, and maternal immune activation models demonstrates that perturbation of either system alters the other; human cohort evidence remains largely associational. Across each maternal-offspring interface, immune and microbial signals converge on the developing brain, acting on peripheral and neuroimmune populations. Microglia emerge as a recurring cellular mediator. Resolving mechanisms of NDD risk requires experimental designs that treat immune and microbial variables as interactive and that span prenatal through postnatal development. The field must move beyond disciplinary silos to integrate these systems across the full neurodevelopmental time course they jointly shape.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149317571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-dependent structural brain aging in medication-free major depressive disorder: A multi-site analysis from COORDINATE-MDD consortium.","authors":"Bhanu Sharma, Pedro L Ballester, Luciano Minuzzi, Wenyi Xiao, Mathilde Antoniades, Dhivya Srinivasan, Guray Erus, Jose A Garcia, Yong Fan, Danilo Arnone, Stephen R Arnott, Taolin Chen, Ki Sueng Choi, Katharine Dunlop, Cherise Chin Fatt, Rachel D Woodham, Beata R Godlewska, Stefanie Hassel, Keith Ho, Andrew M McIntosh, Kun Qin, Susan Rotzinger, Matthew D Sacchet, Jonathan Savitz, Haochang Shou, Ashish Singh, Vibe G Frokjaer, Melanie Ganz, Aleks Stolicyn, Irina Strigo, Duygu Tosun, Dongtao Wei, Ian M Anderson, W Edward Craighead, J F William Deakin, Boadie W Dunlop, Rebecca Elliott, Qiyong Gong, Ian H Gotlib, Catherine J Harmer, Sidney H Kennedy, Gitte M Knudsen, Helen S Mayberg, Martin P Paulus, Jiang Qiu, Madhukar H Trivedi, Heather C Whalley, Chao-Gan Yan, Allan H Young, Christos Davatzikos, Cynthia H Y Fu, Benicio N Frey","doi":"10.1016/j.biopsych.2026.10.028","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.10.028","url":null,"abstract":"<p><strong>Background: </strong>Major depressive disorder (MDD) is associated with altered brain structure and accelerated brain aging. However, previous studies have been limited by clinical samples with mixed medication status and multiple mood states, modest sample sizes, underrepresentation of older adults with MDD, and/or reliance on summary-level data.</p><p><strong>Methods: </strong>Harmonized T1-weighted MRI from MDD (n = 645), all medication-free and in a current depressive episode, and matched healthy controls (n = 645), segmented into 145 regional volumes, from 11 sites in COORDINATE-MDD consortium. Brain age gap (BAG) was estimated cross-sectionally using gradient boosting regression with nested cross-validation. Group differences in BAG (and age-corrected BAG [cBAG]) were examined across age strata. Regional contributions were evaluated using SHAP values.</p><p><strong>Results: </strong>MDD was associated with significantly elevated cBAG compared with healthy controls (mean difference + 2.0 years [95% CI 1.251, 2.774], Cohen's d -0.289 [95% CI -0.399, -0.179]). Age-stratified analyses showed no differences before mid-30s, with progressively larger gaps thereafter, reaching +6.8 years in MDD aged 55 and older in unadjusted analyses (4.3 years after accounting for site). cBAG differed across neuroanatomical phenotypes previously identified using COORDINATE-MDD data. Key contributing regions included lateral and medial prefrontal regions, middle temporal gyrus, putamen, supplementary motor cortex, central operculum, and cerebellum.</p><p><strong>Conclusions: </strong>Structural brain aging in MDD is age-dependent and most pronounced in a neuroanatomical phenotype associated with poorer key clinical outcomes. The findings are consistent with, but do not establish, neuroprogression models of MDD and demonstrate that cBAG is not a uniform feature of MDD, being more strongly expressed in a specifically clinically vulnerable disease phenotype.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149317569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Dynamic Model of Amygdala Circuits in Threat and Reward: Implications for Affective Disorders.","authors":"Yi Zhu, Shi-Ze Xie, Chun-Yue Li, Jia-Xue Hu, Xiao-Ming Li","doi":"10.1016/j.biopsych.2026.10.030","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.10.030","url":null,"abstract":"<p><p>Animals must continuously evaluate their surroundings and select adaptive responses to survive in ever-changing environments. Central to this capacity is the assignment of importance to environmental cues, which guides motivated behavior toward rewarding opportunities and away from potential threats. Here we propose a theoretical framework, a dynamic motivational model based on threat and reward imminence, in which motivational states evolve continuously as a function of imminence rather than shifting between discrete stages. Within this framework, three interacting dimensions define the stimulus relevance of an environmental cue: salience, valence, and value. We leverage the amygdala as a substrate to illustrate the circuit mechanisms underlying importance assignment and examine how stimulus imminence drives motivational state transitions to promote adaptive behavior. Applied to affective disorders, it reframes amygdala dysfunction as projection- and circuit-specific stress adaptation rather than uniform regional hyperactivity, providing a common language for comparing major depressive disorder, anxiety disorders, post-traumatic stress disorder, and substance use disorders. By integrating animal circuit studies with human neuroimaging and clinical evidence, this framework positions amygdala-centered networks as candidate biomarkers for biologically informed subtyping and targets for personalized treatment in depression and related affective disorders.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149317568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harmonization of transdiagnostic psychiatric phenotypes across a large multi-site study reveals high burden of neuropsychiatric multimorbidity in 16p11.2 and 22q11.2 copy number variant carriers.","authors":"Danielle Baribeau, Vincent-Raphaël Bourque, Ania M Fiksinski, Cora M Taylor, Angela Abril, Jessica Hall, Raquel E Gur, Marianne B M van den Bree, Therese van Amelsvoort, Ann Swillen, Sébastien Jacquemont, Anne S Bassett, Jonathan Sebat, Scott M Myers, Samuel J R A Chawner, Joanne L Doherty, Kosha Ruparel, Scott Troyan, Donna M McDonald-McGinn, Carrie E Bearden, Jacob A S Vorstman","doi":"10.1016/j.biopsych.2026.09.031","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.09.031","url":null,"abstract":"<p><strong>Background: </strong>Modern psychiatric research is increasingly collaborative, but significant differences in recruitment and assessment methods across cohorts present major methodological challenges when integrating data.</p><p><strong>Methods: </strong>The Core Psychiatric Phenotype Summary (C2PS) tool was developed to harmonize data on psychiatric/neurodevelopmental diagnoses and subthreshold symptoms from multiple sources. Demonstrating its reliability, and breadth and depth, we report findings in the largest cohort to date of individuals with reciprocal copy number variants (CNVs) at 22q11.2 or 16p11.2, collected across 14 international sites in the Genes to Mental Health (G2MH) Network.</p><p><strong>Results: </strong>Neuropsychiatric phenotypes were harmonized for 1,325 G2MH participants (22qdel: n=752, 22qdup: 219, 16pdel: 227, 16pdup: 127, median age 16.0 years [IQR 11.0, 27.0], 52% female). Inter-rater reliability indicated fair-to-excellent agreement across C2PS domains (Light's Kappa: 0.48 to 1). Completion was feasible, with an average of 4% missingness (range 1% to 13%). Multimorbidity (> 2 disorders) affected 57%, with a median of 3 (IQR: 2 to 5) disorders per individual. Of those without any neuropsychiatric diagnosis (n= 244, 18%), subthreshold symptoms were common (82% in >1 domain, 57% > 2 domains). Higher multimorbidity was associated with lower adaptive functioning on the Vineland Adaptative Behavior Scales [-5.5 points per additional impacted domain (95% CI: -7.5, -3.6; p=5x10^-8].</p><p><strong>Conclusions: </strong>The C2PS is a pragmatic and reliable tool to harmonize heterogeneous neuropsychiatric phenotypic data for large multi-national studies. Observations in 1,325 individuals with CNVs at 16p11.2 or 22q11.2 reveal variant-specific psychiatric profiles, emphasize burden and impact of psychiatric multimorbidity, and provide insights beyond categorical diagnoses.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149317570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex Chromosome Aneuploidies and the Brain: from Neurodevelopmental Risk to Fundamental Biology.","authors":"Adam Pavlinek, Shanlee Davis, Andrés Ingason, Siena Mollerstuen, Elizabeth Levitis, Marcela Legue, Srishti Rau, Siyuan Liu, Thomas Werge, Nicole Tartaglia, Armin Raznahan","doi":"10.1016/j.biopsych.2026.10.021","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.10.021","url":null,"abstract":"<p><p>Sex chromosome aneuploidies (SCAs) are collectively common (∼1/400 individuals) conditions that involve loss or gain of one or more X- or Y- chromosomes. A recent surge in SCA research has highlighted their underappreciated penetrance for multiple neuropsychiatric outcomes - motivating this integrative review across the latest epidemiological, behavioral, neuroimaging, and genomic studies. SCAs show a high penetrance-for-prevelance across multiple psychiatric diagnoses, which often exceeds that of better recognized genetic risk factors, and includes substantial symptom burden below diagnostic thresholds. Some clinical outcomes show differential sensitivity to X- vs. Y-chromosome changes. SCAs exert large effects on global brain size, and also reconfigure regional brain anatomy, with strikingly correlated regional effects of X- and Y-chromosome dosage variation. Genomic studies nominate X-Y gametologs as highly dosage sensitive genes that may shape wider SCA effects on autosomal gene expression. These insights advance clinical and mechanistic understanding of SCAs as: impactful genetic disorders in their own right; genetics-first models for broader psychiatry; and, a window onto potential sex chromosome dosage effects in the general population. Major future growth areas in SCA clinical research include: the much-needed founding of new clinical research networks and registries in close partnership with families; studies of early development in prenatally diagnosed children; in vitro cellular models of effects in human neural tissue; and greater translational focus on sources of variability in patient outcomes. The new and emerging work reviewed herein underlines the need for greater recognition and focus on SCAs in psychiatry and related disciplines.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149294186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trends in Autism Spectrum Disorder Cumulative Incidence and Incidence Density: A Systematic Review.","authors":"Young Shin Kim, Yoon Jae Cho, Yuji Choi, Bennett Leventhal","doi":"10.1016/j.biopsych.2026.10.022","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.10.022","url":null,"abstract":"<p><strong>Background: </strong>Claims of an \"autism epidemic\" imply a true increase in ASD occurrence and changing underlying risk yet largely rely on rising prevalence estimates rather than incidence. Both measures are influenced by diagnostic practices, service access, documentation, and ascertainment; prevalence is additionally affected by service-related migration. Incidence studies follow a defined population previously not identified, to examine outcomes over a specified period and study area; incidence is more likely to capture temporal changes in underlying risk. We systematically reviewed autism incidence studies across differing methodological designs.</p><p><strong>Methods: </strong>Following PRISMA 2020 guidelines, we identified population-based studies reporting ASD or Autistic Disorder incidence in individuals under 18 years. Studies were classified as Category A (birth-defined cohorts with definable risk periods) or Category B (dynamic population annual incidence density). Due to heterogeneity, incidence estimates were compared narratively.</p><p><strong>Results: </strong>Twenty-seven studies met inclusion criteria (14 Category A; 13 Category B). While ASD incidence increased, patterns varied by incidence framework, diagnostic definition, risk period, and ascertainment comprehensiveness (population coverage and detection of undiagnosed cases). High-comprehensiveness birth cohort studies tended to show inconsistent patterns and lower male-to-female ratios, whereas studies with moderate or low comprehensiveness often showed consistent increases. Increases were stronger for broader ASD category.</p><p><strong>Conclusions: </strong>ASD incidence increased in dynamic, administratively defined study populations with moderate or low ascertainment comprehensiveness. In contrast, birth-defined cohorts with fixed risk periods and high ascertainment comprehensiveness showed inconsistent patterns. Overall, the available data do not provide compelling evidence of a true increase in ASD occurrence-an \"autism epidemic.\"</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149294235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basics of Ultrasound for Transcranial Therapeutics Purposes.","authors":"Mark Schafer, Tasneem Arsiwala, Benjamin Pless, Manish Ranjan, Geoffrey Adams, Jacob Elliott, Victor Finomore, Aniruddha Bhagwat, Ali Rezai","doi":"10.1016/j.biopsych.2026.10.020","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.10.020","url":null,"abstract":"<p><p>Transcranial focused ultrasound therapy emerged as a uniquely versatile modality for non-invasive neuromodulation for the treatment of a range of neurological conditions and neuropsychiatric disorders. This work is intended to provide practitioners with fundamental background information directly relevant to the current application in this field, allowing them to critically interpret the literature and understand the technical and methodological considerations that underlie device operation, treatment planning and study parameter evaluation.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149294060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clarifying neurobehavioral associations between early-life stress and episodic memory development.","authors":"Jordan C Foster, Felicia A Hardi, Taylor J Keding, Lucinda M Sisk, Sumedha Mishra, Elizabeth V Goldfarb, Dylan G Gee","doi":"10.1016/j.biopsych.2026.10.023","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.10.023","url":null,"abstract":"","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149294220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain systems supporting the narrative self and psychopathology.","authors":"Trevor Steward, Sarah M Tashjian, Po-Han Kung, Kim L Felmingham, Luke Ney, Christopher G Davey, Ben J Harrison","doi":"10.1016/j.biopsych.2026.10.026","DOIUrl":"https://doi.org/10.1016/j.biopsych.2026.10.026","url":null,"abstract":"<p><p>Disturbances in the narrative self are implicated across psychiatric disorders, with abnormalities in the neural systems supporting its generation and regulation constituting a transdiagnostic risk factor for mental illness. This review highlights how alterations in these brain systems underlie prevalent clinical features, including diminished, rigid, and sustained negative beliefs within the narrative self. The narrative self is framed as a higher-order construct that emerges from multiple systems, with reward, punishment, and motivational signals biasing which experiences are encoded as self-defining and which self-beliefs are reinforced over time. We discuss recent evidence demonstrating how the narrative self is supported by distributed brain networks in which subcortical inputs from the basal forebrain, habenula and mediodorsal thalamus modulate default mode network activity, with the salience, frontoparietal, cingulo-opercular, and hippocampal-parahippocampal networks regulating how self-beliefs are established or updated. Adolescence is emphasized as a developmental period uniquely vulnerable to disturbances in the formation of a coherent, flexible narrative self, wherein asynchronous subcortical and cortical development and pubertal changes interact to confer risk for diminished and rigid self-beliefs. Belief-updating tasks, hierarchical computational models, and ecological momentary assessment are proposed as approaches to quantify how self-beliefs form and shift across time, linking neural signatures of the narrative self to momentary variability. We propose that treating the narrative self as a primary level of explanation for psychopathology positions it as a testable target for future neuroimaging research, providing a clearer bridge from self-referential cognition to interventions in daily life.</p>","PeriodicalId":8918,"journal":{"name":"Biological Psychiatry","volume":" ","pages":""},"PeriodicalIF":10.3,"publicationDate":"2026-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149294082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}