Frontiers in Cellular Neuroscience最新文献

{"title":"Investigating mouse superior colliculus function using two-photon calcium imaging.","authors":"Haesuk Lee, Greg J Stuart","doi":"10.3389/fncel.2026.1922414","DOIUrl":"10.3389/fncel.2026.1922414","url":null,"abstract":"<p><p><i>In vivo</i> two-photon calcium imaging has fuelled ongoing progress in understanding the superior colliculus (SC). This has been achieved through technical endeavors that have made this midbrain structure optically accessible. In this mini-review, we summarize these methods. New techniques, materials, and ideas will further advance these methods, making SC imaging both less invasive and more accessible in the future. In doing so, two-photon calcium imaging will undoubtedly continue to contribute to our understanding of the SC and the cellular and circuit mechanisms underlying sensory processing and sensorimotor function in the brain.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1922414"},"PeriodicalIF":4.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The cochlear macrophage in presbycusis: inflammaging, neuroinflammation, and targets for therapeutic modulation.","authors":"Reef K Al-Asad, Judith S Kempfle","doi":"10.3389/fncel.2026.1930209","DOIUrl":"10.3389/fncel.2026.1930209","url":null,"abstract":"<p><p>Age-related neurodegenerative diseases and age-related hearing loss are increasing in prevalence globally. Immune cells are novel mediators linking these diseases through shared mechanisms of chronic inflammation and maladaptive repair. In the cochlea, resident macrophages and infiltrating immune cells respond to injury, noise exposure, and aging by adopting activated phenotypes that disrupt synaptic integrity, impair myelination, and promote hair cell and neuronal loss. Similarly, in the central nervous system, microglia, the resident immune cells of the brain undergo age- and disease-associated priming, characterized by exaggerated inflammatory responses, complement activation, and impaired clearance of cellular debris. Emerging evidence suggests that cochlear macrophages and CNS microglia share transcriptional programs and signaling pathways. Importantly, these immune cells also serve as key regulators of repair and regeneration when appropriately modulated, adopting pro-regenerative phenotypes that promote tissue recovery rather than injury. As hearing loss is increasingly recognized as a contributing risk factor for neurodegenerative disease, deepening our understanding of age-related immune responses within the inner ear and the mechanisms governing immune cell modulation may help mitigate this risk while uncovering shared therapeutic targets across these related disease processes.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1930209"},"PeriodicalIF":4.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MSC-derived extracellular vesicles for spinal cord injury: inflammatory microenvironment modulation, stage-dependent repair mechanisms, and translational challenges.","authors":"Hang Yu, Yifan Liu, Shulong Yin, Haoyue Hu, Linquan Li, Taotao Zhu, Jie Liu, Sheng Liu, Chenxi Zhao, Shiqing Feng","doi":"10.3389/fncel.2026.1960271","DOIUrl":"10.3389/fncel.2026.1960271","url":null,"abstract":"<p><p>Spinal cord injury is not only an acute mechanical insult but also the beginning of a prolonged secondary pathological process dominated by inflammatory microenvironmental imbalance. Because the primary traumatic event occurs within minutes and offers a narrow therapeutic window, persistent post-traumatic inflammation, blood-spinal cord barrier disruption, edema, oxidative stress, complement activation, inflammasome signaling, astrocyte reactivity, vascular dysfunction, and extracellular matrix remodeling represent more realistic therapeutic targets. In accordance with the Minimal Information for Studies of Extracellular Vesicles recommendations, this review uses the term MSC-derived extracellular vesicles, abbreviated as MSC-EVs, to describe MSC-derived vesicle preparations reported in the cited studies, including small extracellular vesicles and exosome-like vesicles, unless endosomal biogenesis has been strictly demonstrated. Existing preclinical studies suggest that MSC-EVs may attenuate the inflammatory microenvironment after spinal cord injury by suppressing complement activation, inhibiting NLRP3 inflammasome signaling, modulating heterogeneous microglia/macrophage states, reducing neurotoxic inflammatory astrocyte responses, improving blood-spinal cord barrier integrity, and decreasing inflammatory cytokine production. These anti-inflammatory and barrier-protective effects are closely linked to downstream neuroprotection, angiogenesis, axonal plasticity, remyelination, and tissue repair. Mechanistically, MSC-EVs regulate multiple signaling pathways, including NF-κB, PI3K/Akt, ERK, RhoA/ROCK, PTEN/PI3K/Akt, and Wnt/β-catenin, and deliver regulatory microRNAs such as miR-133b, miR-21, miR-29, miR-126, and miR-486-5p. However, available evidence is uneven: some claims are supported by gain- and loss-of-function experiments, whereas others remain correlative or based on limited animal studies. Beyond microRNAs, MSC-EVs also contain mRNAs, long non-coding RNAs, circular RNAs, tRNA-derived fragments, proteins, and lipids, but their specific roles in spinal cord injury remain less well defined. Reactive astrogliosis is heterogeneous and stage-dependent; A1/A2 terminology may be useful descriptively but should not be treated as a complete classification of astrocyte states. Although MSC-EVs may reduce some risks associated with live-cell transplantation, their clinical translation remains limited by inefficient lesion delivery, biodistribution uncertainty, cargo heterogeneity, storage instability, lack of standardized potency assays, incomplete time-dose-response data, and evolving regulatory requirements. This review summarizes MSC-EVs as modulators of the spinal cord injury inflammatory microenvironment, integrates their actions into an acute-subacute-chronic stage-based model, and discusses the major preclinical and translational barriers that must be addressed before clinical application.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1960271"},"PeriodicalIF":4.4,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13669502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transient synaptic refinement and glial adaptations after whisker denervation in adult mice.","authors":"Sean Collier, Laxmi Iyer, Kimberly R Byrnes, Emily Petrus","doi":"10.3389/fncel.2026.1941129","DOIUrl":"10.3389/fncel.2026.1941129","url":null,"abstract":"<p><p>Loss of sensation after injury causes profound changes in neural circuits, impacting sensory perception and recovery. Overcoming sensory loss requires neural plasticity to support accurate processing of remaining sensory afferents, but the mechanisms by which circuit plasticity occurs in adults are not well understood. Despite decades of studies manipulating the mouse whisker sensory system, the impact of sex, glial activity, and time since injury has not yet been clarified. We performed unilateral whisker denervation in adult male and female mice and characterized synaptic and glial responses at multiple time points after injury. We determined that whisker denervation leads to a transient loss of thalamocortical and intracortical putative excitatory synapses in the deprived sensory cortex. This loss corresponds with a transient shift in microglial morphology, with increased proportions of ramified-shaped microglia and decreased proportions of amoeboid-shaped microglia. Most of these results were more robust in female mice, highlighting the importance of powering studies for sex-specific adaptations. Importantly, these results identify temporally restricted circuit plasticity that should be considered when implementing post-injury interventions to support recovery.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1941129"},"PeriodicalIF":4.4,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149192666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal dynamics between the whisker sensorimotor cortex and the olivocerebellar module in awake mice.","authors":"G Cheron, A Caballero-Tapia, D Ristori, J Márquez-Ruiz, A M Cebolla, L Ris","doi":"10.3389/fncel.2026.1781469","DOIUrl":"10.3389/fncel.2026.1781469","url":null,"abstract":"<p><strong>Introduction: </strong>The precise timing of the long-range bidirectional connections between the cerebral cortex and the cerebellum remains a critical factor in elucidating their respective and integrated functions. The key role of the cerebellum in both motor and non-motor domains is exerted through numerous cerebro-cerebellar closed loops that sustain different forms of motor coordination, in which the response timing of the various types of cerebellar neurons may constitute a significant component of neural computation.</p><p><strong>Methods: </strong>In this study, we investigated the cerebral sensorimotor cortex and the corresponding cerebellar region (Crus I) of the murine whisker system during electrical stimulation of the whisker pad. In addition, the firing of Golgi cells, Purkinje cells (PC), deep cerebellar nuclei (DCN) neurons, and inferior olive (IO) neurons was analyzed during electrical stimulation of the whisker pad (Wh), the somatosensory (wS1) and motor (wM1) cortices.</p><p><strong>Results: </strong>We demonstrated that, although peripheral Wh stimulation evoked cortical, cerebellar and IO responses at the same early latency (~3 ms), the transmission within the olivocerebellar circuit was slower when the signal was elicited by wS1 stimulation than by peripheral input, and even slower when wM1 was stimulated.</p><p><strong>Discussion: </strong>We discussed the different possibilities regarding the transmission of the efference copy and the forward dynamic model within these circuits, and we speculated that the relative slowing of wM1 input into the olivo-cerebellar circuit reflects the increased computational demand associated with the elaboration of the final motor command.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1781469"},"PeriodicalIF":4.4,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13661409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Orexins and neuregulins as exemplars of peptide physiology in the brain: experimental challenges and implications for neuropathology.","authors":"Laura Clara Grandi, Marta Cerina, Alida Amadeo, Andrea Becchetti","doi":"10.3389/fncel.2026.1933123","DOIUrl":"https://doi.org/10.3389/fncel.2026.1933123","url":null,"abstract":"<p><p>Neuropeptides and neurotrophic factors exert overlapping roles on synaptic maturation and plasticity. Although the relative intracellular signals are mostly elucidated, difficulties are met in discerning the dynamics of their extracellular action <i>in vivo</i>, which is largely determined by their peptide nature. We discuss these common mechanisms in two exemplary systems, which are otherwise biologically divergent. The hypothalamic orexin system has a low molecular complexity (two peptides, two receptors), but an intricate connection pattern covering subcortical and cortical structures. Orexins sustain motivated behavior during active waking and are implicated in narcolepsy with cataplexy, as well as psychiatric and metabolic disorders. Neuregulins control neuronal and synaptic maturation after proteolytic release in the extracellular space, or functioning as transmembrane cell-adhesion proteins. They are implicated in neurodevelopmental pathologies and display a wide molecular diversity, with multiple genes and tens of cell- and compartment-specific isoforms. Understanding how peptides regulate synaptic circuits is hampered by uncertainty about essential quantitative aspects: rate of release and diffusion; distribution and desensitization of receptor subtypes; extracellular matrix binding; kinetics of proteolytic degradation. Ongoing studies investigate the peptide-dependent interplay of different CNS populations, by applying optogenetics and ever more specific pharmacological agents to conditional animal models. These approaches need to be complemented by assessing peptide dynamics with novel amperometry or live imaging to monitor peptide release and spatiotemporal distribution, with photoactivatable drugs for spatiotemporal control of stimulus onset, with mass spectrometry to test the long-term cerebrospinal peptide concentration. Furthermore, experimental settings are needed that better mimic the situation <i>in vivo</i>.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1933123"},"PeriodicalIF":4.4,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Impacts of cytoskeletal dysregulation on spinogenesis.","authors":"Keerthana Surabhi, Erzsebet M Szatmari, Robert M Hughes","doi":"10.3389/fncel.2026.1999766","DOIUrl":"https://doi.org/10.3389/fncel.2026.1999766","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1999766"},"PeriodicalIF":4.4,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13657033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Divergent cellular responses to sciatic nerve crush versus transection: bilateral MYCN induction and distinct DRG neuronal responses.","authors":"Shilian Zhou, Ziyan Huang, Zhongyuan Lin, Jingwei Chen, Xinyu Zhang, Diya Wang, Haihua Shu, Fang Ye","doi":"10.3389/fncel.2026.1922426","DOIUrl":"10.3389/fncel.2026.1922426","url":null,"abstract":"<p><strong>Introduction: </strong>Peripheral nerve injuries can produce regenerative or persistent-disconnection outcomes depending on the injury modality, but the underlying cellular responses and their effects on the central nervous system remain incompletely defined.</p><p><strong>Methods: </strong>We compared sciatic nerve crush (SNC; axonotmesis) and sciatic nerve transection (SNT; neurotmesis) in wild-type, AdvCre;Ai14, and MYCN-eGFP reporter mice. Longitudinal assessments included functional recovery, neuronal injury responses marked by ATF3, IB4-positive sensory-neuron responses, dorsal-horn microglial activation, and spinal MYCN-eGFP signal.</p><p><strong>Results: </strong>SNC was associated with partial, measure-specific functional recovery, a transient and self-limited ATF3 response, and a limited reduction in IB4-positive neuronal profiles. In contrast, SNT produced persistent axotomy-associated neuronal stress, a reduction in IB4-positive neuronal profiles, and more protracted dorsal-horn microglial activation. MYCN-eGFP intensity was significantly increased above sham levels bilaterally in spinal ventral-horn neurons after both SNC and SNT at postoperative day 7 (POD7), with the greatest acute amplitude observed after SNC. From POD7 to POD14, MYCN-eGFP intensity declined by more than 90% after SNC but by approximately 60% after SNT, indicating distinct temporal patterns between the two injury modalities.</p><p><strong>Discussion: </strong>SNC and SNT engage overlapping but quantitatively and temporally distinct cellular programs, including modality-specific dorsal root ganglion neuronal responses associated with functional recovery. These findings refine the interpretation of two widely used peripheral nerve injury models and identify bilateral spinal MYCN-eGFP dynamics as a candidate cellular readout for future mechanistic investigation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1922426"},"PeriodicalIF":4.4,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13654848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HSV-1 infections of the prefrontal cortex: regional vulnerability, cellular mechanisms, and neurocognitive consequences.","authors":"Hannah Chau, Julia Schurr, Jonna M Leyrer-Jackson, Erin S Honsa","doi":"10.3389/fncel.2026.1887935","DOIUrl":"https://doi.org/10.3389/fncel.2026.1887935","url":null,"abstract":"<p><p>Herpes simplex encephalitis (HSE), caused by herpes simplex virus type 1 (HSV-1), is the most common cause of sporadic viral encephalitis and remains associated with substantial mortality and long-term neurological morbidity despite effective antiviral therapy. Although HSE is classically characterized by involvement of the medial temporal lobes and limbic system, recent clinical, preclinical and neuroimaging studies highlight involvement of prefrontal cortical regions, including the medial prefrontal cortex (mPFC) and orbitofrontal cortex (OFC). The functional consequences of HSV-1 associated injury may be particularly relevant to the persistent executive, cognitive, motivational, emotional, and behavioral abnormalities observed in HSE survivors. However, the mechanisms linking HSV-1 infection to prefrontal injury and subsequent neurobehavioral dysfunction remain incompletely defined. This review examines HSV-1 neuropathogenesis through a prefrontal cortical framework, with a focus on the mPFC and OFC, and evaluates potential mechanisms underlying their vulnerability. Current evidence supports a multistep hypothesis for HSV-1-associated injury involving olfactory and trigeminal neural entry, microtubule-dependent axonal transport, dissemination, and potential regional differences in cellular susceptibility. Further, we highlight cellular mechanisms of HSV-1-associated injury, including microglial and NLRP3 inflammasome activation, astrocytic dysfunction, neurovascular unit disruption, neuronal and synaptic injury, and viral immune-evasion mechanisms that facilitate viral persistence and amplify host-mediated injury. Lastly, we integrate these mechanisms with the functional organization of prefrontal-frontal-limbic networks to consider how regional injury may contribute to persistent cognitive and behavioral dysfunction following HSE. The studies discussed here provide a framework for linking HSV-1-associated prefrontal injury to long-lasting cognitive and behavioral sequelae of HSE, while highlighting critical gaps in our understanding of these HSV-driven mechanisms.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1887935"},"PeriodicalIF":4.4,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperbaric oxygen therapy in sepsis-associated encephalopathy: pathophysiological rationale, preclinical evidence, and translational challenges.","authors":"Yikun Xie, Yihao Li, Yujing Li, Shuai Chen, Guanqi Song, Hongyu Wang","doi":"10.3389/fncel.2026.1941147","DOIUrl":"10.3389/fncel.2026.1941147","url":null,"abstract":"<p><p>Sepsis-associated encephalopathy (SAE) is a serious neurological complication of sepsis that can cause acute cerebral dysfunction and long-term cognitive impairment. Its pathogenesis involves multiple pathological processes, including blood-brain barrier (BBB) disruption, neuroinflammation, microglial and astrocytic responses, oxidative stress, mitochondrial dysfunction, ferroptosis, and pyroptosis. Excessive reactive oxygen species (ROS) production and mitochondrial injury can aggravate cerebrovascular endothelial and BBB damage, promote glial inflammatory responses, and contribute to lipid peroxidation and inflammasome activation, thereby linking neuroinflammation with regulated cell death. Hyperbaric oxygen therapy (HBOT) increases tissue oxygen tension and may exert neuroprotective effects by improving microcirculation and regulating redox homeostasis and inflammatory responses. Available animal studies of SAE suggest that HBOT may attenuate certain aspects of BBB injury and hippocampal neuroinflammation and improve neurobehavioral and cognitive outcomes. Findings from systemic sepsis and other neurological injury models further suggest that antioxidant responses, mitochondrial homeostasis, and signaling pathways associated with ferroptosis and pyroptosis may contribute to these effects. This review summarizes the cellular and molecular processes potentially affected by HBOT within the major pathological mechanisms of SAE and discusses its therapeutic potential and translational challenges based on the available direct and supportive evidence. Current evidence remains predominantly preclinical, and the mechanisms and clinical value of HBOT in SAE require further investigation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1941147"},"PeriodicalIF":4.4,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13647324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}