Progress in Neurobiology最新文献

{"title":"Stress-induced heme metabolic disorder in peripheral B cells contributes to depressive-like behaviors in male mice","authors":"Yuye Yin ,&nbsp;Bin Li ,&nbsp;Longfei Du ,&nbsp;Shusheng Wu","doi":"10.1016/j.pneurobio.2025.102800","DOIUrl":"10.1016/j.pneurobio.2025.102800","url":null,"abstract":"<div><div>Major depressive disorder (MDD) is a common and burdensome psychiatric illness with high rates of recurrence. Most of the current therapeutic drugs for depression mainly achieve their antidepressant effect by tuning the landscape of neurotransmitters in the central nervous system (CNS). However, almost half of patients with MDD cannot fully benefit from these available treatments. Consequently, it is urgent to find novel therapeutic targets for the treatment of MDD. Peripheral B lymphocytes have been reported as a major contributor to the occurrence of stress-induced depression. However, the pathological role and underlying regulatory mechanism of peripheral B cells in MDD have not been well established. Here, we show that peripheral B cells are significantly infiltrated into the CNS of male mice after exposure to chronic unpredictable mild stress (CUMS). Adoptive transfer of B cells from CUMS mice into B-cell-deficient male mice could significantly induce higher severity depressive symptoms than adoptive transfer of B cells from control mice. The lack of B cells protects male mice from CUMS-induced neuroinflammation and depressive-like behaviors. Interestingly, the pathological B cells in CUMS mice are characterized by increased heme biosynthesis, whereas its inhibition can ameliorate depressive-like behaviors in B-cell-deficient mice that received pathological B cells from CUMS mice. Our findings suggest a critical role of the heme biosynthesis in B cells for contributing to the pathogenesis of depression and indicate that these pathological B cells featuring high heme may be a promising immune target for the development of precision medicine approaches in MDD.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"251 ","pages":"Article 102800"},"PeriodicalIF":6.7,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144335892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential susceptibility to repeated social stress induces synaptic plasticity impairment and cognitive deficit in the 5xFAD mouse model","authors":"Eun-Jeong Yang ,&nbsp;Md Al Rahim ,&nbsp;Sibilla Masieri ,&nbsp;Giulio Maria Pasinetti","doi":"10.1016/j.pneurobio.2025.102797","DOIUrl":"10.1016/j.pneurobio.2025.102797","url":null,"abstract":"<div><div>Stress-related disorders including depression are common comorbidities in Alzheimer's Disease (AD). In AD, heightened stress reactivity may contribute to an increased risk of cognitive dysfunction. This study aimed to investigate the differential responses of wild-type (WT) and 5xFAD mice, a model of AD, to repeated social defeat stress (RSDS) and explore the molecular mechanisms associated with stress susceptibility. Both WT and 5xFAD mice exhibited susceptibility to initial exposure to RSDS, with a greater proportion of stress-susceptible (Sus) individuals observed in 5xFAD mice compared to WT mice. In presymptomatic 5xFAD mice repeatedly exposed to RSDS, cognitive impairment was evident through a lower discrimination index in the NOR test compared to controls. To investigate the effects of RSDS on peripheral immune responses, we performed CyTOF analysis, revealing a significant increase in CD8 + and CD4 + memory T cells exclusively in the peripheral blood of 5xFAD-Sus mice. To further explore the molecular mechanisms underlying RSDS in the brain, RNA sequencing revealed distinct patterns of differentially expressed genes associated with inflammatory pathways in stress-Sus mice. Specifically, 5xFAD-Sus mice exhibited dysregulation in immune-related pathways, while WT-Sus mice displayed alterations in pathways related to cell adhesion and cytoskeletal organization. In addition, when comparing 5xFAD-Sus to 5xFAD-resilience mice, significant disruptions in synaptic plasticity pathways were observed in 5xFAD-Sus mice, and these changes were accompanied by cognitive impairment. These findings suggest that increased stress susceptibility in 5xFAD is linked to distinct peripheral immune dysregulation, potentially contributing to synaptic plasticity impairments and cognitive dysfunction in the early stages of AD.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"251 ","pages":"Article 102797"},"PeriodicalIF":6.7,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond neurons: How does dopamine signaling impact astrocytic functions and pathophysiology?","authors":"Giulia Favetta ,&nbsp;Luigi Bubacco","doi":"10.1016/j.pneurobio.2025.102798","DOIUrl":"10.1016/j.pneurobio.2025.102798","url":null,"abstract":"<div><div>Astrocytes, the most abundant glial cells in the central nervous system (CNS), are critical regulators of brain homeostasis and play an active role in synaptic signaling and plasticity. While dopamine, a key catecholamine neurotransmitter, has been traditionally associated with neuronal functions, emerging evidence highlights its significant impact on astrocytic physiology. This review explores how astrocytes contribute to dopaminergic signaling and the implications of this interaction in both physiological and pathological contexts. Specifically, we examined astrocytic dopamine receptor expression, signaling mechanisms, and region-specific effects on neuroinflammation, synaptic regulation, and neurotrophic factor secretion. Notably, astrocytic dopamine receptor activation plays dual inflammatory roles, modulating both anti- and pro- inflammatory responses depending on the receptor subtype and pathological environment. Furthermore, dopamine-evoked gliotransmitter release and neurotrophin secretion highlight the role of astrocytes in astrocyte-to-neuron communication, which impacts synaptic plasticity and neuronal survival. Dysfunction of astrocytic dopaminergic signaling has been implicated in neurodegenerative diseases such as Parkinson’s disease, where dopamine depletion drives reactive astrogliosis, altered glutamate homeostasis, and inflammatory responses. These findings underscore the complexity of astrocytic responses to dopamine and their potential as targets in conditions characterized by dysregulation of dopaminergic signaling. By highlighting recent advancements in understanding dopamine-astrocyte interactions, this review aims to provide insights into the broader roles of astrocytes in dopaminergic systems and their therapeutic potential in CNS disorders.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"251 ","pages":"Article 102798"},"PeriodicalIF":6.7,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The low-density lipoprotein receptor-related protein-1 (LRP1) in Schwann cells controls mitochondria homeostasis in peripheral nerves","authors":"Stefano Martellucci ,&nbsp;Melissa Heredia ,&nbsp;Zixuan Wang ,&nbsp;Thomas Whisenant ,&nbsp;Dudley K. Strickland ,&nbsp;Richard Sanchez ,&nbsp;Takahito Arai ,&nbsp;Morgan Zhang ,&nbsp;Haoming Wang ,&nbsp;Zhiting Gong ,&nbsp;Kesava Asam ,&nbsp;Brad E. Aouizerat ,&nbsp;Gulcin Pekkurnaz ,&nbsp;Yi Ye ,&nbsp;Wendy M. Campana","doi":"10.1016/j.pneurobio.2025.102796","DOIUrl":"10.1016/j.pneurobio.2025.102796","url":null,"abstract":"<div><div>Following peripheral nerve injury, Schwann cell (SC) survival is imperative for successful nerve regeneration. The low-density lipoprotein receptor-related protein-1 (LRP1) has been identified as a pro-survival SC plasma membrane signaling receptor, however, the responsible mechanisms underlying SC homeostasis remain incompletely understood. Herein, we establish that LRP1 largely manages mitochondrial dynamics and bioenergetics in SCs by limiting mitochondria fission, maintaining healthy mitochondria membrane potentials, and reducing lactate production associated with peripheral sensitization. When SC LRP1 is suppressed, inner-mitochondria-linked pathways in peripheral nerve proteome are dramatically altered, and cristae integrity in unmyelinated C-fibers is compromised. SC LRP1 protected sensory neurons from mitochondrial dysfunction and modulated mitochondria-related biological pathways in the DRG transcriptome. Conditional deletion of LRP1 in SCs induces pain-related behaviors in mice without nerve injury. Results point to a significant role for LRP1 in SC mitochondrial homeostasis and advance our understanding of the sensory neuron response to alterations in SC bioenergetics.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"251 ","pages":"Article 102796"},"PeriodicalIF":6.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuronal encoding of recognition memory for numerical quantities in macaque intraparietal and prefrontal cortices","authors":"Tobias Machts,&nbsp;Julia Grüb,&nbsp;Andreas Nieder","doi":"10.1016/j.pneurobio.2025.102794","DOIUrl":"10.1016/j.pneurobio.2025.102794","url":null,"abstract":"<div><div>The parieto-frontal number network in primates is vital for extracting and memorizing numerical information. However, how neurons in these regions retain abstract numerical categories to recognize target numbers amidst ongoing numerical input is unclear. To explore this, single neurons were recorded from the ventral intraparietal cortex (VIP) and lateral prefrontal cortex (PFC) of two male macaques trained to memorize and recognize target numerosities while viewing sequences of irrelevant numerosities. In the VIP, neuronal selectivity for both target and irrelevant numerosities declined rapidly, making it unable to distinguish relevant from irrelevant quantities. Conversely, PFC neurons maintained selective tuning for target numerosities over time but not for irrelevant ones, enabling the distinction between sought and irrelevant quantities. Match enhancement effects, where firing increased for repeated target numerosities, were observed only in the PFC. In contrast, match suppression effects, involving reduced firing for repeated target numerosities, occurred in both the VIP and PFC. These findings suggest the VIP primarily encodes displayed numerosities, while the PFC is specialized for processing, storing, and recognizing numerical quantities by enhancing familiar numerosities. This highlights the PFC’s key role in recognition memory, contrasting with the transient coding observed in the VIP.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"251 ","pages":"Article 102794"},"PeriodicalIF":6.7,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The social salience network hypothesis of autism: Disrupted network activity, oxytocin signaling, and implications for social symptoms","authors":"Aishwarya Patwardhan,&nbsp;Katrina Y. Choe","doi":"10.1016/j.pneurobio.2025.102787","DOIUrl":"10.1016/j.pneurobio.2025.102787","url":null,"abstract":"<div><div>Autism Spectrum Disorder (ASD) is a complex condition characterized by its heterogeneity, with significant variability in symptoms across subtypes and associated comorbidities. Despite the urgent need to develop mechanism-based therapies for the core social symptoms of ASD, progress has been hindered by the heterogeneous etiology of this neurodevelopmental disorder and our still limited understanding of the neural mechanisms underlying social behavior. The evaluation of sociosensory cues and the modulation of motivation to engage socially are fundamental components of social interaction, thought to be coordinated by a network of interconnected brain regions called the social salience network (SSN). This network is strongly modulated by the neurohormone oxytocin (OXT) to facilitate appropriate social responses. It is increasingly recognized that disruptions within the SSN contribute to the atypical social perception and engagement observed in autistic individuals. This review will summarize evidence from current clinical and preclinical literature that provides compelling evidence for SSN disruptions as a possible mechanism that underlies the social symptoms of ASD. Furthermore, we discuss OXT-mediated correction of SSN disruptions at the regional and circuit levels that rescues social phenotypes in preclinical models of ASD-risk factors. These molecular, cellular, and circuit mechanisms within the SSN could serve as promising treatment targets which may propel the development of novel and effective options for alleviating the social difficulties of autistic individuals.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"251 ","pages":"Article 102787"},"PeriodicalIF":6.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in astrocyte function induced by stress-induced glucocorticoid exacerbate major depressive disorder","authors":"Beomjo Park ,&nbsp;Gee Euhn Choi","doi":"10.1016/j.pneurobio.2025.102786","DOIUrl":"10.1016/j.pneurobio.2025.102786","url":null,"abstract":"<div><div>Major depressive disorder (MDD) is a prevalent psychiatric condition that affects millions of people worldwide and is a leading cause of disability. Chronic stress is a key factor in the development of MDD, leading to hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis and elevated glucocorticoid levels, which in turn affect brain function and structure. Astrocytes, crucial for maintaining central nervous system (CNS) homeostasis, play a significant role in the pathophysiology of MDD. Dysregulation of glucocorticoid signaling in astrocytes contributes to changes in astrocyte survival, reactivity, metabolism, neurotrophic support, gliotransmitter release, and neuroinflammation, exacerbating depressive symptoms. This review explains the necessity for exploring the effects of glucocorticoid on astrocytes and subsequent MDD progression. Firstly, we briefly explore the glucocorticoid signaling and the multifaceted function of astrocytes. Then, this study discusses the mechanisms by which chronic stress and glucocorticoid exposure induce astrocyte-mediated neurodegenerative changes, highlighting the importance of targeting glucocorticoid-related signaling of astrocytes in developing therapeutic interventions for MDD. Understanding these mechanisms could lead to the development of more effective treatments aimed at restoring astrocyte function and alleviating MDD.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"251 ","pages":"Article 102786"},"PeriodicalIF":6.7,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144249291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutamine transport via amino acid transporter NTT4 (SLC6A17) maintains presynaptic glutamate supply at excitatory synapses in the CNS","authors":"Angela L. Nicoli ,&nbsp;A. Shaam Al Abed ,&nbsp;Sarah R. Hulme ,&nbsp;Abhijit Das ,&nbsp;Gregory Gauthier-Coles ,&nbsp;Angelika Bröer ,&nbsp;Sarojini Balkrishna ,&nbsp;Gaetan Burgio ,&nbsp;Nathalie Dehorter ,&nbsp;Caroline D. Rae ,&nbsp;Stefan Bröer ,&nbsp;Brian Billups","doi":"10.1016/j.pneurobio.2025.102785","DOIUrl":"10.1016/j.pneurobio.2025.102785","url":null,"abstract":"<div><div>The glutamate-glutamine cycle is thought to be the principle metabolic pathway that recycles glutamate at synapses. In this cycle, synaptically released glutamate is sequestered by astrocytes and forms glutamine, before being returned to the presynaptic terminal for conversion back into glutamate to replenish the neurotransmitter pool. While many aspects of this cycle are established, a key component remains unknown: the nature of the transporter responsible for the presynaptic uptake of glutamine. We hypothesise that neurotransmitter transporter 4 (NTT4/<em>SLC6A17</em>) plays this role. Accordingly, we generated NTT4 knockout mice to assess its contribution to presynaptic glutamine transport and synaptic glutamate supply. Using biochemical tracing of ¹³C metabolites in awake mice, we observe a reduction of neuronal glutamate supply when NTT4 is absent. In addition, direct electrical recording of hippocampal mossy fibre boutons reveals a presynaptic glutamine transport current that is eliminated when NTT4 is removed or inhibited. The role of NTT4 in neurotransmission was demonstrated by electrophysiological recordings in hippocampal slices, which reveal that NTT4 is required to maintain vesicular glutamate content and to sustain adequate levels of glutamate supply during periods of high-frequency neuronal activity. Finally, behavioural studies in mice demonstrate a deficit in trace fear conditioning, and alterations in anxiety behaviour and social preference. These results demonstrate that NTT4 is a presynaptic glutamine transporter, which is a central component of the glutamate-glutamine cycle. NTT4 and hence the glutamate-glutamine cycle maintain neuronal glutamate supply for excitatory neurotransmission during high-frequency synaptic activity, and are important regulators of memory retention and normal behaviour.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"250 ","pages":"Article 102785"},"PeriodicalIF":6.7,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Switching state to engage and sustain attention: Dynamic synchronization of the frontoparietal network","authors":"Grace Ross ,&nbsp;Wei A. Huang ,&nbsp;Jared Reiling ,&nbsp;Mengsen Zhang ,&nbsp;Jimin Park ,&nbsp;Susanne Radtke-Schuller ,&nbsp;Joseph Hopfinger ,&nbsp;Agnieszka Zuberer ,&nbsp;Flavio Frohlich","doi":"10.1016/j.pneurobio.2025.102777","DOIUrl":"10.1016/j.pneurobio.2025.102777","url":null,"abstract":"<div><div>Sustained attention (SA) is essential for maintaining focus over time, with disruptions linked to various neurological and psychiatric disorders. The oscillatory dynamics and functional connectivity in the dorsal frontoparietal network (dFPN) are crucial in SA. However, the neuronal mechanisms that control the level of SA, especially in response to heightened attentional demands, remain poorly understood. To examine the role of rhythmic synchronization in the dFPN in SA, we recorded local field potential and single unit activity in ferrets that performed the 5-Choice Serial Reaction Time Task (5-CSRTT) under both low and high attentional load. Under high attentional load, dFPN exhibited a pronounced state shift that corresponded with behavioral changes in the animal. Prior to the onset of the target stimulus, animals transitioned from a stationary state, characterized by frontal theta oscillations and dFPN theta connectivity, to an active exploration state associated with sensory processing. This shift was indexed by a suppression of inhibitory alpha oscillations and an increase in excitatory theta and gamma oscillations in parietal cortex. We further show that dFPN theta connectivity predicts performance fluctuations under high attentional load. Together, these results suggest that behavioral strategies for maintaining SA are tightly linked to neuronal state dynamics in the dFPN. Importantly, these findings identify rhythmic synchronization within the FPN as a potential neural target for novel therapeutic strategies for disrupted attention.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"250 ","pages":"Article 102777"},"PeriodicalIF":6.7,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144102528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Awake reactivation of cortical memory traces predicts subsequent memory retrieval","authors":"Wei Duan ,&nbsp;Pingping Lu ,&nbsp;Zhansheng Xu ,&nbsp;Jing Wang ,&nbsp;Yue Lu ,&nbsp;Mengyang Wang ,&nbsp;Ken A. Paller ,&nbsp;Nikolai Axmacher ,&nbsp;Liang Wang","doi":"10.1016/j.pneurobio.2025.102778","DOIUrl":"10.1016/j.pneurobio.2025.102778","url":null,"abstract":"<div><div>Brief periods of rest after learning facilitate consolidation of new memories. Memory reactivation and hippocampal-cortical dialogue have been proposed as candidate mechanisms supporting consolidation. However, the study of these mechanisms has mostly concerned sleep-based consolidation. Whether and how awake reactivation can selectively consolidate cortical memory traces to guide subsequent behavior requires more human electrophysiological evidence. This study addressed these issues by utilizing intracranial electroencephalography (iEEG) recordings from 11 patients with drug-resistant epilepsy, who learned a set of object-location associations. Using representational similarity analysis, we found that, among the multiple cortical memory traces of object-location associations for the same object generated through several rounds of learning, the association corresponding to memory traces with stronger cortical activation during wakeful rest was more likely to be retrieved later. Awake reactivation of cortical memory trace was accompanied by increased hippocampal ripple rates and enhanced theta-band hippocampal-cortical communication, with hippocampal interactions with cortical regions within the default mode network preceding cortical reactivation. Together, these results suggest that awake reactivation of cortical memory trace during post-learning rest supports memory consolidation, predicting subsequent recall.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"250 ","pages":"Article 102778"},"PeriodicalIF":6.7,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}