Molecular Psychiatry最新文献

{"title":"Distinct and shared intrinsic resting-state functional networks in children with idiopathic autism spectrum disorder and fragile X syndrome","authors":"Dongyun Li, Danyong Feng, Chunchun Hu, Yuxin Tian, Allan L. Reiss, Randi J. Hagerman, Xiu Xu, Zhongwei Qiao, Rihui Li, Qiong Xu","doi":"10.1038/s41380-025-03112-y","DOIUrl":"https://doi.org/10.1038/s41380-025-03112-y","url":null,"abstract":"<p>Autism spectrum disorder (ASD) and fragile X syndrome (FXS) are behaviorally overlapped. However, little is known about the functional patterns underlying the cognitive and behavioral characteristics of FXS and ASD. The present study aimed to identify the distinct or/and shared functional networks in young children with FXS and idiopathic ASD. We recruited 150 children consecutively in a group with FXS, a group with idiopathic ASD, and a group with typically developing (TD) children. Resting-state functional magnetic resonance imaging (fMRI) and behavioral data were collected and genetic information was obtained in the FXS group. We compared functional connectivity (FC) among the three groups and found that both FXS and ASD showed significantly decreased FC among the default mode network (DMN), sensorimotor network (SMN), cerebellum network (CN), and visual network (VN) relative to TD. FXS specifically demonstrated decreased FC within DMN, while both FXS and ASD exhibited significantly decreased FC within the CN and also between the CN and DMN, SMN, VN, respectively. Aberrant topological alterations of CN were identified in children with FXS and ASD, while ASD group showed significantly lower segregation in regions that integrate sensory and visual information, and motor coordination function. Moreover, correlations between the severity of social affect and mean FC of various cerebral-cerebellum networks in FXS exhibited significantly distinct trends from those observed in ASD. In the FXS group, the topological measure at crus I of the cerebellum is found to be negatively associated with DNA methylation levels. These results were statistically robust and demonstrated the shared and distinct profiles of intrinsic functional networks in FXS and ASD, two phenotypically overlapping developmental disorders.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"108 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629665","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":"Targeting complement C3/C3aR pathway restores rejuvenation factor PF4 and mitigates neurocognitive impairments in age-related perioperative neurocognitive disorders","authors":"Jia-Li Wang, Cai-Hong Ye, Zhong-Fa Teng, Kai Zhou, Li-Li Pan, Man-Duo Ouyan, Zhi Zheng, Meng Lu, Shi-Lei Li, Jing Zhang, Pei-Chan Zheng, Jingjing Zhang, Hui Zhang, Mei-Hong Lin, Liang-Cheng Zhang, Shi-Shi Huang, Xiao-Ning Ren, Ning Zheng, Wen-Lin Wei, Zhenhuan Zhao, Shao-Bin Wang, Zhong-Meng Lai","doi":"10.1038/s41380-025-03103-z","DOIUrl":"https://doi.org/10.1038/s41380-025-03103-z","url":null,"abstract":"<p>Perioperative neurocognitive disorders (PND), including postoperative delirium (POD), delayed neurocognitive recovery (dNCR) and postoperative neurocognitive disorder (PNCD), affect up to 10% of surgical patients older than 60 years, and currently there are no effective therapies to prevent PND. The gut microbiota is linked to PND through the gut-brain axis, promoting neuroinflammation via activation and proliferation of microglia and astrocytes in the central nervous system (CNS). In this study, we show that perioperative use of ceftriaxone, a long-acting β-lactam antibiotic, can prevent the development of PND in elderly surgical patients. This effect is associated with reduced serum complement C3 levels and increased levels of platelet factor 4 (PF4). Using an aged mouse model of PND, we found that C3/C3aR axis mediated the interaction of astroglia and microglia during the early stages of neuroinflammation. Genetic ablation or pharmacological blockade of C3/C3aR signaling pathway suppressed neuroinflammation and attenuated cognitive declines in PND. The C3/C3aR axis is essential for surgery-induced platelet count and circulating PF4 declines, and mice supplemented with recombinant PF4 exhibited reduced neuroinflammation and improved cognitive function. Together, our findings revealed the new roles of the C3/C3aR signaling pathway in platelet dysfunction and neuroinflammation in age-related PND, and these results highlight new potential therapeutic strategies for PND.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"13 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629667","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 medial habenula neural circuit controlling anxiety-like behaviors in response to acute stress","authors":"Yao Wang, Xin-Yue Lv, Jiu-Ye Qiao, Mei-Hui Yue, Qian-Qian Yang, Si-Ran Wang, Han-Yun Kang, Hua-Li Yu, Xiao-Xiao He, Xiao-Juan Zhu, Zi-Xuan He","doi":"10.1038/s41380-025-03111-z","DOIUrl":"https://doi.org/10.1038/s41380-025-03111-z","url":null,"abstract":"<p>Anxiety is characterized by worried thoughts and an aversion to immediate threats. While the neural circuits underlying anxiety have been studied, the underlying circuit mechanisms remain largely unknown. Here, we report that the activity of tachykinin-expressing (Tac1) neurons in the medial habenula (MHb) is decreased and excitatory projections from these neurons are inhibited in response to acute stress in mice. Activation of interfascicular nucleus (IF)^GLUT→MHb^Tac1 projections ameliorates anxiety-like behaviors in stressed mice. Moreover, MHb^Tac1 neurons send excitatory projections to the lateral part of the interpeduncular nucleus (IPL), regulating the activity of Tac1-projecting IPL neurons and anxiety-like behaviors in stressed mice. In summary, these findings delineate the circuit involving Tac1 neurons in the MHb that mediates anxiety-like behaviors in response to acute stress in mice.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"2 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629666","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 and muscle chemistry in myalgic encephalitis/chronic fatigue syndrome (ME/CFS) and long COVID: a 7T magnetic resonance spectroscopy study","authors":"Beata R. Godlewska, Amy L. Sylvester, Uzay E. Emir, Ann L. Sharpley, William T. Clarke, Stephen R. Williams, Ana Jorge Gonçalves, Betty Raman, Ladislav Valkovič, Philip J. Cowen","doi":"10.1038/s41380-025-03108-8","DOIUrl":"https://doi.org/10.1038/s41380-025-03108-8","url":null,"abstract":"<p>Myalgic encephalitis/chronic fatigue syndrome (ME/CFS) is a common debilitating medical condition, whose main symptoms - fatigue, post-exertional malaise and cognitive dysfunction – are also present in many cases of long COVID. Magnetic resonance spectroscopy (MRS) allows the insight into their pathophysiology through exploration of a range of biochemicals putatively relevant to aetiological processes, in particular mitochondrial dysfunction and energy metabolism. 24 patients with ME/CFS, 25 patients with long COVID and 24 healthy controls (HC) underwent brain (pregenual and dorsal anterior cingulate cortex, respectively, pgACC and dACC) and calf muscle MRS scanning at 7 Tesla, followed by a computerised cognitive assessment. Compared to HC, ME/CFS patients had elevated levels of lactate in both pgACC and dACC, while long COVID patients had lowered levels of total choline in dACC. By contrast, skeletal muscle metabolites at rest did not significantly differ between the groups. The changes in lactate in ME/CFS are consistent with the presence of energetic stress and mitochondrial dysfunction. A reduction in total choline in long COVID is of interest in the context of the recently reported association between blood clots and ‘brain fog’, and earlier animal studies showing that choline might prevent intravascular coagulation. Importantly, differences in findings between ME/CFS and long COVID suggest that the underlying neurobiological mechanisms, while leading to similar clinical presentations, may differ. An important implication is that patients with ME/CFS and those with fatigue in the course of long COVID should not be studied as a single group, at least until the mechanisms are better understood.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"703 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144611238","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":"Epiphenomena in psychosis: how perinatal stressful events shape long-term outcomes","authors":"Clemente Garcia-Rizo, Byron K. Y. Bitanihirwe","doi":"10.1038/s41380-025-03096-9","DOIUrl":"https://doi.org/10.1038/s41380-025-03096-9","url":null,"abstract":"<p>Exposure to perinatal stress has been linked to the later emergence of mental health problems including neurodevelopmental disorders such as psychosis. Recent research highlights not only an increased risk of psychotic illness in offspring following perinatal maternal life events but also the future manifestation of diverse epiphenomena. These epiphenomena include metabolic disturbances, structural brain abnormalities, and cognitive impairment in addition to distinct psychopathological profiles involving motor and physical anomalies. Our aim here lies in discussing the different clinical features of psychosis as they emerge at onset and during the evolution of the disease—from a translational perspective—in terms of perinatal stressful experiences. A hypothetical model of metabolic manifestations that are present in adulthood stemming from perinatal events will be elaborated to provide a partial explanation of the increased morbidity and early mortality observed in patients who develop psychosis. This model will encompass aspects related to brain structural abnormalities, clinical psychopathological characteristics and the cognitive impairment typically observed in individuals with psychotic disorders. We also put forward a framework that encapsulates the ‘scars’ of perinatal stressful experiences associated with psychosis in terms of a public health agenda.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"92 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144603150","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":"Expanding the neurodevelopmental relevance of the SC–VTA pathway in autism spectrum disorder","authors":"Júlio César Claudino dos Santos","doi":"10.1038/s41380-025-03106-w","DOIUrl":"https://doi.org/10.1038/s41380-025-03106-w","url":null,"abstract":"<p>The study by Contestabile et al. presents compelling evidence for the involvement of the superior colliculus–ventral tegmental area (SC-VTA) pathway in the pathophysiology of social orienting deficits in autism spectrum disorder (ASD) [1]. Their translational approach bridges animal and human models, revealing a conserved circuit-level alteration that holds promise both as a biomarker and a therapeutic target.</p><p>The demonstration that reduced SC-VTA connectivity is associated with both behavioral and developmental outcomes in children with ASD invites us to reframe early social orienting as an emergent property of subcortical neuromodulatory circuits. From a developmental perspective, this pathway may serve as a mechanism for aligning attentional resources with socially salient cues. The superior colliculus, with its early maturation and multisensory integration capabilities [2, 3], may influence dopaminergic circuits supporting reinforcement learning and motivational salience [4]. However, it remains unclear whether SC-VTA dysconnectivity reflects a causal neurodevelopmental disruption or a compensatory response to atypical experience. Clarifying this distinction will be crucial.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"697 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144593912","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":"Opposing roles of microglial and macrophagic C3ar1 signaling in stress-induced synaptic and behavioral changes","authors":"Ashutosh Tripathi, Alona Bartosh, Dania Jose, Jocelyn Mata, Usama Hussein, Fernanda Laezza, Zhongming Zhao, Anilkumar Pillai","doi":"10.1038/s41380-025-03097-8","DOIUrl":"https://doi.org/10.1038/s41380-025-03097-8","url":null,"abstract":"<p>The social deficits following chronic stress conditions are linked to synaptic dysfunction in the brain. Complement system plays a critical role in synapse regulation. Although complement has been implicated in chronic stress-induced behavior deficits the cellular substrates and mechanisms underlying complement-mediated behavior changes under chronic stress conditions are not known. In the present study, we investigated the role of complement component 3a receptor (C3ar1) in microglia and monocytes/macrophages (Mo/MΦ) in chronic unpredictable stress (CUS)-induced synapse loss and behavior deficits in mice. We found that deletion of microglial C3ar1 attenuated stress-induced social behavior deficits and changes in neuroinflammatory as well as synaptic markers in the prefrontal cortex (PFC). RNA sequencing data revealed that microglial C3ar1 deletion attenuates CUS-mediated changes in the expression of immediate-early genes such as <i>Fos</i> and Nuclear Receptor Subfamily 4 Group A Member 1 (<i>Nr4a1</i>) in the PFC. In contrast, lack of C3ar1 in Mo/MΦ induced social behavior deficits. Together, these findings indicate opposite functions of C3ar1 signaling in microglia and Mo/MΦ under chronic stress conditions.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"149 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144603151","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":"Maternal stressors disrupt mouse placental proteome and fetal brain development in a sex-specific fashion through inflammation and oxidative stress","authors":"Chiara Musillo, Maria Antonietta Ajmone-Cat, Roberta De Simone, Roberta Tassinari, Francesca Maranghi, Sabrina Tait, Marianna Samà, Letizia Giona, Eleonora M. Pieroni, Roberta Alessi, Thorsten Henning, Daniela Weber, Rachel N. Lippert, Maria Elena Pisanu, Mattea Chirico, Egidio Iorio, Federica Fratini, Alessandra Berry, Francesca Cirulli","doi":"10.1038/s41380-025-03090-1","DOIUrl":"https://doi.org/10.1038/s41380-025-03090-1","url":null,"abstract":"<p>Adverse maternal conditions during pregnancy result in an increased risk for neuropsychiatric disorders in the offspring, although the underlying mechanisms are poorly understood. We have recently shown that two distinct insults, prenatal stress (PNS) or maternal high-fat diet (mHFD), increase inflammation and oxidative stress in the brain of adolescent female mice. Here, we sought to investigate the early mechanisms underlying such effects, focusing on the placenta and fetal brain, as well as the protective effects of the antioxidant N-acetyl-cysteine (NAC), in C57Bl6/N mice. We used a multi-disciplinary approach combining proteomic, metabolomic, lipidomic and histological analysis to characterize the structural and functional changes of the placenta; moreover, a targeted gene expression analysis was carried out in the brains of male and female fetuses to evaluate oxidative stress and inflammatory-related changes. Our data highlight comparable, but sex-specific, responses to the two maternal stressors, which target placenta and fetal brain, and are buffered by NAC administration. Placental function was specifically disrupted in males, with signaling pathways of cardio-metabolic risk emerging in this sex. By contrast, fetal brain was affected in females, with an increased expression of genes related to inflammation and oxidative stress. In conclusion, we provide evidence for an early origin of sex-dependent embedding of prenatal adverse experiences in different organs which might explain differential susceptibility to later disease trajectories.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"12 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144603769","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":"Interneuron migration defects during corticogenesis contribute to Dyrk1a haploinsufficiency syndrome pathogenesis","authors":"Maria Victoria Hinckelmann, Aline Dubos, Victorine Artot, Gabrielle Rudolf, Thu Lan Nguyen, Peggy Tilly, Valérie Nalesso, Maria del Mar Muniz Moreno, Marie-Christine Birling, Juliette D. Godin, Véronique Brault, Yann Herault","doi":"10.1038/s41380-025-03109-7","DOIUrl":"https://doi.org/10.1038/s41380-025-03109-7","url":null,"abstract":"<p>Interneuron development is a crucial step of brain corticogenesis. When affected it often leads to brain dysfunctions like epilepsy, intellectual disabilities and autism spectrum disorder. Such defects are observed in the <i>DYRK1A</i>-haploinsufficiency syndrome, caused by mutations in <i>DYRK1A</i>, and commonly associated to cortical excitatory/inhibitory imbalance. However, how this imbalance is established in this syndrome remains elusive. Here, using mouse models and live imaging, we demonstrate that <i>Dyrk1a</i> specifically regulates the development of the cortical GABAergic system. We show that, unlike projection excitatory neurons, interneuron tangential migration relies on <i>Dyrk1a</i> dosage and kinase activity. We further reveal that <i>Dyrk1a</i> regulates actomyosin cytoskeleton remodeling during interneuron migration. Interestingly, mice with heterozygous inactivation of <i>Dyrk1a</i> in interneurons exhibited decreased interneuron density together with behavioral defects and epileptic activity, recapitulating phenotypes observed in human patients. Altogether, these data highlight the critical role of <i>Dyrk1a</i> in the development of the GABAergic system and the pathophysiology of <i>DYRK1A</i>-haploinsufficiency syndrome.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"12 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144593917","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":"Alterations in miR-151a-3p of plasma-derived exosomes and associated multimodal neuroimaging patterns in major depressive disorder","authors":"Wenjia Liang, Lanwei Hou, Wenjun Wang, Bao Wang, Chenxi Sun, Yuan Zhang, Zhuoran Li, Rong Shi, Wenjuan Zhou, Yuchun Tang, Wei Wang, Lejin Yang, Shuwei Liu","doi":"10.1038/s41380-025-03102-0","DOIUrl":"https://doi.org/10.1038/s41380-025-03102-0","url":null,"abstract":"<p>Magnetic resonance imaging (MRI) has been recognized as a valuable tool for achieving ‘reification of clinical diagnosis’ of major depressive disorder (MDD). However, the reliability and validity of MRI results are often compromised by genetic, environmental, and clinical heterogeneity within test samples. Here, we combined MRI with other clinical findings using multimodal MRI fusion algorithm to construct a data-driven, bottom-up diagnostic approach. The covariation patterns between the multimodal MRI features and differential expression of exosomal microRNA (miRNA) were identified on a subset of 70 MDD patients and 71 healthy controls (HCs) (served as a training set) as classification features, whereas data from the other 45 MDD patients and 43 HCs served as a test set. Furthermore, longitudinal data from 28 MDD patients undergoing antidepressant treatment for six months were utilized to validate the identified biomarkers, and related signaling pathways were initially explored in depression-like mice. Plasma exosome-derived miR-151a-3p levels were found to be significantly lower in MDD patients compared to HCs and correlated with abnormal changes in functional MRI (fMRI) metrics in the anterior cingulate cortex (ACC), visual cortex, and default mode network, etc. Then, these multimodal MRI features associated with miR-151a-3p expression distinguished MDD patients from HCs with high classification accuracy of 92.05% in support vector machine (SVM) model, outperforming the diagnostic rate when only multimodal MRI features with intergroup differences were entered (70.45%). Furthermore, 10 out of 28 MDD patients exhibited a clinically significant response to the treatment (a reduction of over 50% in Hamilton Rating Scale for Depression (HAMD) score). The significant upregulation of plasma exosomal miR-151a-3p levels and changes of fMRI indicators were also observed in these 10 patients after treatment of six months. Animal experiments have shown that reducing the expression of miR-151-3p in ACC induces depression-like behaviors in mice, while elevating hsa-miR-151a-3p expression in ACC alleviates the depression-like behaviors of mice exposed to chronic unpredictable mild stress. Our study proposed an innovative diagnostic model of MDD by combining the plasma exosome-derived miR-151a-3p expression with its associated multimodal MRI patterns, potentially serving as a novel diagnostic tool.</p>","PeriodicalId":19008,"journal":{"name":"Molecular Psychiatry","volume":"10 1","pages":""},"PeriodicalIF":11.0,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586412","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}