Translational Psychiatry最新文献

{"title":"Temporal imprecision and its dynamics in schizophrenia.","authors":"Stephan Lechner, Ming H Hsieh, Yi-Ting Lin, Chih-Min Liu, I-Fei Chen, Chen-Chung Liu, Yi-Ling Chien, Tzung-Jeng Hwang, Hai-Gwo Hwu, Georg Northoff","doi":"10.1038/s41398-025-03510-4","DOIUrl":"10.1038/s41398-025-03510-4","url":null,"abstract":"<p><p>Schizophrenia is a complex mental disorder whose pathophysiological mechanisms remain yet unclear. Various lines of evidence converge on a temporal disorder with temporal imprecision occurring in the millisecond range of the ongoing phase cycles. However, the intertrial phase coherence (ITPC) often used to index such temporal imprecision in EEG, is by itself not able to capture temporal irregularities in the range of around 10 milliseconds. This is due to its static calculation with the averaging over trials. To obtain a more dynamic measures in the millisecond range, we introduce 1. The precision index (PI) as temporally more precise measure, and 2. a novel more dynamic method to calculate the ITPC in temporally resolved way, i.e., dITPC. We show that schizophrenia subjects show decreased PI during deviant tones in an auditory oddball task which shows strong but not one to one correlation with the ITPC. Moreover, we demonstrate that schizophrenia subjects showed higher latencies and frequencies over the course of time in the dITPC. Finally, employing multiple regression models, we show that the latency of the dITPC, as calculated dynamically across both standard and deviant tones, predicts the PI deficits in the deviant tones. Together, our findings demonstrate temporal alterations in the phase dynamics of schizophrenia with temporal irregularities in the dynamic background predicting temporal imprecision in the lower millisecond range in the more cognitive foreground.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"279"},"PeriodicalIF":6.2,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12350930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144849178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of the COVID-19 pandemic on neurobiological functioning in adolescents.","authors":"Justin P Yuan, Lauren R Borchers, Yoonji Lee, Jessica L Buthmann, Saché M Coury, Julian Joachimsthaler, Emma L Jaeger, Tiffany C Ho, Ian H Gotlib","doi":"10.1038/s41398-025-03485-2","DOIUrl":"10.1038/s41398-025-03485-2","url":null,"abstract":"<p><p>The COVID-19 pandemic and its associated lockdowns were an unprecedented source of stress, with striking adverse effects on adolescents' mental health but relatively unknown effects on important aspects of neurobiological functioning. Using data from 154 adolescents (age M ± SD = 16.2 ± 1.1 years; range = 13.9-19.4) drawn from an ongoing longitudinal study and assessed either before or after the pandemic, we compared the pre-pandemic and post-pandemic groups on three key stress-sensitive biological systems: the hypothalamic-pituitary-adrenal (HPA) axis, immune response, and neural responses to affective stimuli. We found that compared to those assessed before the pandemic, adolescents assessed post-lockdown had significantly lower total cortisol production, elevated levels of systemic inflammation, and reduced neural activation in the prefrontal cortex during affective processing (pseudo-F(1,3250) = 7.43, p = 0.006). These findings suggest that, for adolescents, the experience of the pandemic was associated with significant disruptions in multiple biological systems that are sensitive to stress that might have enduring adverse developmental effects.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"276"},"PeriodicalIF":6.2,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12343994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144837904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of AdipoR1 in the hippocampus impairs synaptic function and structure and causes depression-like behavior.","authors":"Peilin Zhu, Yanmin Luo, Yue Li, Jing Tang, Li Liu, Yuhui Deng, Jing Li, Lin Jiang, Wenyu Yang, Qian Xiao, Shun Wang, Yuning Zhou, Fenglei Chao, Lei Zhang, Chunni Zhou, Yong Tang, Xin Liang","doi":"10.1038/s41398-025-03495-0","DOIUrl":"10.1038/s41398-025-03495-0","url":null,"abstract":"<p><p>Previous studies have indicated that impaired synaptic plasticity is a main pathological alteration in depression. However, the mechanism underlying this pathological change has not been clarified. Adiponectin, an adipokine, crosses the blood‒brain barrier to function in specific brain regions. Previous studies have suggested that the downregulation of adiponectin signaling is involved in the occurrence of depression. The adiponectin receptors (AdipoRs) AdipoR1 and AdipoR2, which serve as the main receptors for adiponectin in the central nervous system, mediate the downstream biological effects of this compound, which has been reported to have positive effects on synaptic plasticity. However, it is not clear whether alterations in adiponectin/AdipoR signaling are associated with impaired synaptic plasticity in depression. Therefore, the aim of this study was to investigate whether changes in the adiponectin/AdipoR pathway in the hippocampus during depression are involved in the regulation of synaptic plasticity damage. We detected reduced plasma concentrations of adiponectin and lower expression levels of AdipoR1 but not AdipoR2 in the hippocampi of mice exposed to chronic unpredictable stress. An adeno-associated virus was subsequently used to knockdown hippocampal AdipoR1 to further verify the effects of decreased expression levels of this receptor on depressive-like behaviors and hippocampal synaptic plasticity. We found that the mice in which hippocampal AdipoR1 was knocked down presented with anhedonia and passive stress-coping behaviors as well as a decreased number of dendritic spines and density of excitatory and inhibitory synapses. Our results suggest that the downregulation of AdipoR1 expression might be an important factor that causes impaired synaptic plasticity in depression. These results may provide new insights into the pathogenesis of depression and new therapeutic targets for treating this disease.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"277"},"PeriodicalIF":6.2,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12344148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144837903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent developments in omics studies and artificial intelligence in depression and suicide.","authors":"Qingzhong Wang, Yogesh Dwivedi","doi":"10.1038/s41398-025-03497-y","DOIUrl":"10.1038/s41398-025-03497-y","url":null,"abstract":"<p><p>Major depressive disorder (MDD) is the most prevalent and severe form of mental illness and is significantly linked to suicide. At present, addressing the treatment and prevention of depression and suicide poses significant challenges, largely due to the remaining uncertainties surrounding their pathogenesis. Thus, there is an urgent need to find new molecular pathways, as well as effective biomarkers and drug targets, to provide effective diagnosis, prognosis, and treatments for depression and suicide. Recent advancements in high-throughput sequencing technology and whole-genome analysis have enabled the collection of extensive omics data from blood samples, human autopsy brain tissue, and various animal models. This data captures significant molecular-level changes, including alterations in gene transcripts, epigenomes, and proteins, effectively reflecting the biological state of the disease. This review provides a systematic overview of advancements in transcriptomics, non-coding RNA, and AI related to depression and suicide. It discusses new research approaches, such as spatial transcriptomics, addresses challenges connected to various research materials and methodologies, and proposes avenues for future studies.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"275"},"PeriodicalIF":6.2,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339732/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the potential of hypothalamic deep brain stimulation for obesity: Impacts on memory, neuroplasticity and brain metabolism in the Zucker rat.","authors":"Marta Casquero-Veiga, Meritxell Llorca-Torralba, Clara Bueno-Fernandez, Diego Romero-Miguel, Nicolás Lamanna-Rama, Christine Winter, Esther Berrocoso, Juan Nacher, Manuel Desco, Mª Luisa Soto-Montenegro","doi":"10.1038/s41398-025-03478-1","DOIUrl":"10.1038/s41398-025-03478-1","url":null,"abstract":"<p><p>The lateral hypothalamus (LH) plays a key role in regulating energy balance and appetite, making it a potential target for deep brain stimulation (DBS) in treatment-resistant obesity. In this study, we evaluated the short and long-term in vivo effects of continuous LH-DBS over 15 days in a genetic model of obesity: the Zucker rat. We examined changes in body weight, brain glucose metabolism (via positron emission tomography, PET), and memory performance, along with ex vivo neuroplasticity in different hippocampal layers one month post-treatment. Contrary to expectations, continuous LH-DBS did not reduce the weight gain or food intake. While stimulated rats exhibited hippocampal hypermetabolism and enhanced synaptogenesis, these changes did not translate into cognitive improvements. Interestingly, long-term memory benefits were observed in all animals that underwent surgery, regardless of whether they received stimulation. In conclusion, our results do not support continuous LH-DBS as an effective treatment to reduce body weight in cases of obesity with genetic leptin resistance. However, the hippocampal modulation induced by continuous LH-DBS shows potential for addressing cognitive impairments associated with leptin resistance. These findings suggest that alternative DBS protocols may help restore hippocampal function, warranting further investigation.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"273"},"PeriodicalIF":6.2,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12335527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive behavioral characterization and impaired hippocampal synaptic transmission in R1117X Shank3 mutant mice.","authors":"Jingyao Gao, Shumin Wu, Jingxuan Yang, Tong Ye, Jie Yang, Wenhua Shen, Xingwang Chen, Li Huang, Ruiqi Pang, Ping Lin, Jiahe Lin, Yi Zhou, Wei Wang, Tao Tan","doi":"10.1038/s41398-025-03505-1","DOIUrl":"10.1038/s41398-025-03505-1","url":null,"abstract":"<p><p>Mutations in the Shank3 gene are strongly associated with various neurodevelopmental disorders, particularly autism spectrum disorder (ASD). The R1117X mutation, which results in truncated SHANK3 protein, has been implicated in dysfunctions in the striatum and cortex. However, its effects on hippocampal function remain poorly understood. In this study, we performed a comprehensive behavioral and synaptic analysis of homozygous R1117X Shank3 mutant mice. These mice exhibited deficits in sensory gating, motor coordination, and pain perception, alongside severe anxiety in novel environment. Additionally, they showed significant impairments in learning and memory, as well as abnormal spontaneous fine motor behaviors. Histological analysis revealed morphological changes in the hippocampus, which were coupled with deficits in synaptic transmission and plasticity. Notably, we observed a downregulation of glutamatergic receptors in the hippocampus, particularly NMDA receptor subtypes. Taken together, these findings demonstrate that the homozygous R1117X Shank3 mutant mouse represents a valuable model for investigating schizophrenia associated with intellectual disability. The altered hippocampal morphology, impaired synaptic function, and deficits in learning and memory observed in this model provide new insights into the underlying mechanisms of Shank3-related neurodevelopmental disorders.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"274"},"PeriodicalIF":6.2,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12335487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Entorhinal cortex layer III Adgrl2 expression controls topographical circuit connectivity required for sequence learning.","authors":"Jordan D Donohue, Crisylle Blanton, Anna Chen, Amna Ahmad, Elizabeth D Liu, Lisette Saab, Rajbir Kaur, Woojin Yang, Garret R Anderson","doi":"10.1038/s41398-025-03490-5","DOIUrl":"10.1038/s41398-025-03490-5","url":null,"abstract":"<p><p>The entorhinal cortex and hippocampus are interconnected brain regions required for episodic learning and memory. For this functional encoding, correct assembly of specific synaptic connections across this circuit is critical during development. To guide the connection specificity between neurons, a multitude of circuit building molecular components are required, including the latrophilin family of adhesion G protein-coupled receptors (Lphn1-3; gene symbols Adgrl1-3). Within this genetic family, Adgrl2 exhibits a unique topographical and cell-type specific expression patterning in the entorhinal cortex and hippocampus that mirrors connectivity. To investigate the role of Adgrl2 in a cell-type specific fashion for this circuit, we here created a transgenic mouse (Adgrl2^fl/fl;pOxr1-Cre) with targeted and selective Adgrl2 deletion in medial entorhinal cortex layer III neurons (MECIII). Using these mice, we find two major input/output circuitry pathways to be topographically shifted with Adgrl2 deletion in MECIII neurons. These neural connectivity impacts include MECIII axon projections to contralateral MEC layer I, and presubiculum axons to ipsilateral MEC layer III. To test the behavioral consequences of these circuitry alterations, we investigated varying entorhinal cortex dependent behaviors, revealing selective deficits in spatial-temporal sequence learning. Taken together, this study demonstrates that Adgrl2 expression in MECIII neurons is necessary for the accurate assembly of MEC topographical circuits that support episodic learning.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"272"},"PeriodicalIF":6.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144804879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alterations of NoGo P300 ERP in schizophrenia in social setting: a hyperscanning study.","authors":"Máté Fullajtár, Brigitta Kakuszi, István Bitter, Pál Czobor","doi":"10.1038/s41398-025-03481-6","DOIUrl":"10.1038/s41398-025-03481-6","url":null,"abstract":"<p><p>Although patients with schizophrenia exhibit profound deficits in social cognition, studies into the neurobiological background of these deficits examined individuals in isolation, in single-person settings. We investigated the neurobiological basis of social cognitive deficits in a social setting, applying a novel approach using EEG-hyperscanning. Eighty subjects were included in the analyses, 49 healthy controls (HC) and 31 patients with schizophrenia. We recorded high-density EEG from pairs of participants, where one (the observer) watched their own screen while the other (the actor) actively performed a Go/NoGo task. The task was administered twice, with the participants switching roles. We focused on investigating the P300 event-related potential from the observer condition. The PANSS scale was used to characterize psychopathology. The Reading the Mind in the Eyes Test and the d-prime index were applied to characterize mentalization and signal detection ability. We found that patients with schizophrenia showed significant P300 reduction compared to the HC group at the first task exposure. They, however, exhibited augmented P300 with the repeated exposure, while HCs manifested a decrease. More severe positive symptoms were associated with larger P300 at both task-exposures. Moreover, poorer mentalization and signal detection performance were associated with decreased P300. Our findings provide evidence that P300 alterations in schizophrenia can be detected in social setting. The opposite changes in the two groups may be due to disparate reasons: habituation in HCs, whereas the alterations in patients may result from various factors, including deficient habituation and an aberrant processing of stimulus salience in a social setting.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"270"},"PeriodicalIF":6.2,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12331909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144800296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal valproic acid on the basis of gestational diabetes also induces autistic behavior and disrupts myelination and oligodendroglial maturation slightly in offspring.","authors":"Maolin Li, Zhifei Qiao, Jizheng Li, Hongli Zhou, Dong Huang, Yan Cai, Xiaolong Li, Zuo Zhang, Jianyun Zhou, Jiyin Zhou","doi":"10.1038/s41398-025-03450-z","DOIUrl":"10.1038/s41398-025-03450-z","url":null,"abstract":"<p><strong>Introduction: </strong>Gestational diabetes mellitus (GDM) and prenatal exposure to valproic acid (VPA) are both constitute risk factors for autism in progeny. Notably, dysmyelination in the corpus callosum serves as a prominent element connecting GDM and autism in the white matter lesions.</p><p><strong>Objective: </strong>The cumulative effects of GDM and prenatal VPA on both autistic behavior and dysmyelination in progeny have been investigated in this study.</p><p><strong>Methods: </strong>In vivo, female mice exhibiting leptin receptor deficiencies and maintained on a high-fat diet were utilized to create GDM models, to which prenatal VPA was administered. In vitro, oligodendrocyte precursor cells (OPCs) were treated with VPA in the high-fat and high-glucose culture.</p><p><strong>Results: </strong>The offspring subjected to both GDM and prenatal VPA demonstrated comparable declines in social interaction, myelination, and OPC maturation, akin to those exclusively exposed to VPA. Remarkably, the application of clemastine facilitated remyelination, ameliorated autistic behaviors, and promoted the progression of OPCs. Furthermore, the compromised myelination and OPC maturation instigated by the combination of GDM and prenatal VPA were found to be less severe compared to those precipitated by VPA alone. This differential impact can be attributed to the opposing influences of GDM and VPA on gamma-aminobutyric acid receptor activation in OPCs, extracellular regulated protein kinases (ERK) phosphorylation in OPCs, and the modulation of histone deacetylase 3 and dual specificity phosphatase 5 expression.</p><p><strong>Conclusions: </strong>we delineate the antagonistic effects of GDM and prenatal VPA on ERK phosphorylation in fetal OPCs, consequently altering their proliferation and differentiation, thereby culminating in milder dysmyelination and autistic behaviors.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"271"},"PeriodicalIF":6.2,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12332004/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144800297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic neural network modulation associated with rumination in major depressive disorder: a prospective observational comparative analysis of cognitive behavioral therapy and pharmacotherapy.","authors":"Nariko Katayama, Kazushi Shinagawa, Jinichi Hirano, Yuki Kobayashi, Atsuo Nakagawa, Satoshi Umeda, Kei Kamiya, Miyuki Tajima, Mizuki Amano, Waka Nogami, Sakae Ihara, Sachiko Noda, Yuri Terasawa, Toshiaki Kikuchi, Masaru Mimura, Hiroyuki Uchida","doi":"10.1038/s41398-025-03489-y","DOIUrl":"10.1038/s41398-025-03489-y","url":null,"abstract":"<p><p>Cognitive behavioral therapy (CBT) and pharmacotherapy are primary treatments for major depressive disorder (MDD). However, their differential effects on the neural networks associated with rumination, or repetitive negative thinking, remain poorly understood. This study included 135 participants, whose rumination severity was measured using the rumination response scale (RRS) and whose resting brain activity was measured using functional magnetic resonance imaging (fMRI) at baseline and after 16 weeks. MDD patients received either standard CBT based on Beck's manual (n = 28) or pharmacotherapy (n = 32). Using a hidden Markov model, we observed that MDD patients exhibited increased activity in the default mode network (DMN) and decreased occupancies in the sensorimotor and central executive networks (CEN). The DMN occurrence rate correlated positively with rumination severity. CBT, while not specifically designed to target rumination, reduced DMN occurrence rate and facilitated transitions toward a CEN-dominant brain state as part of broader therapeutic effects. Pharmacotherapy shifted DMN activity to the posterior region of the brain. These findings suggest that CBT and pharmacotherapy modulate brain network dynamics related to rumination through distinct therapeutic pathways.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"15 1","pages":"267"},"PeriodicalIF":6.2,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12325608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144790056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}