Experimental Neurology最新文献

{"title":"Pathogenic role of CD169+ macrophages in neuronal loss and motor decline in NMO mice","authors":"Yuko Morita ,&nbsp;Oluwaseun Fatoba ,&nbsp;Takahide Itokazu ,&nbsp;Toshihide Yamashita","doi":"10.1016/j.expneurol.2025.115355","DOIUrl":"10.1016/j.expneurol.2025.115355","url":null,"abstract":"<div><div>Neuromyelitis optica (NMO) is a severe autoimmune inflammatory disease characterized by debilitating symptoms, such as blindness or paralysis, often following a single acute attack. However, effective acute treatments to prevent long-term sequelae are currently limited. This study aimed to investigate the role of CD169-expressing macrophages during the acute phase of NMO. We developed an NMO mouse model by injecting high-affinity AQP4-IgG with human complement into the striatum, inducing NMO-like lesions marked by astrocyte loss and infiltration of microglia/macrophages and neutrophils. Immunohistochemical analyses revealed that CD169-expressing macrophages were the predominant infiltrating cells within the lesion core. Based on this finding, we explored the therapeutic potential of blocking CD169 function to mitigate NMO. CD169+ macrophages were activated by astrocytopathy, partially through SYK signaling, leading to significant neuronal loss and motor deficits. Treatment with an anti-CD169 antibody significantly reduced neuronal loss, improved motor function, and inhibited the phagocytic activity of CD169+ macrophages. Our findings demonstrate that CD169-expressing macrophages play a critical role in exacerbating tissue damage and functional decline during the acute phase of NMO. Targeting CD169 signaling may represent a promising therapeutic strategy to reduce pathological phagocytosis and prevent secondary injury in NMO.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115355"},"PeriodicalIF":4.6,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495432","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":"Circadian rhythm disruption exacerbates neurodegeneration and alters proteomic profiles in a 6-OHDA induced Parkinson's disease model","authors":"Halil I. Koc ,&nbsp;Enes Dogan ,&nbsp;Hayriye E. Yelkenci ,&nbsp;Cigdem Bayraktaroglu ,&nbsp;Aysenur Ozpinar ,&nbsp;Buse Balaban ,&nbsp;Serdar Altunay ,&nbsp;Merve Beker ,&nbsp;Ertugrul Kilic ,&nbsp;Mustafa C. Beker","doi":"10.1016/j.expneurol.2025.115356","DOIUrl":"10.1016/j.expneurol.2025.115356","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra (SN) and associated motor symptoms. Recent studies suggest a strong link between circadian rhythm disruption (CRD) and PD pathogenesis. However, the underlying molecular mechanisms remain unclear. In this study, we investigated the impact of CRD on PD progression using a 6-hydroxydopamine induced experimental PD model in mice. CRD was induced using a chronic jet lag protocol and mice were divided into four main groups as Sham, CRD, PD and PD + CRD. Behavioral assessments, immunofluorescence staining, and proteomic analyses were performed to evaluate functional and molecular changes. Non-lesional CRD groups have shown that CRD can cause molecular changes that may sensitise neural tissue to degeneration. CRD significantly worsened motor asymmetry, reduced locomotor activity PD mice. Neuropathological analysis revealed a marked reduction in tyrosine hydroxylase (TH⁺) dopaminergic neurons in the SN and decreased TH fiber density in the striatum, indicating enhanced neurodegeneration. Proteomic analysis identified 427 differentially expressed proteins in the SN and 115 in the striatum, with key alterations in pathways related to mitochondrial function, oxidative phosphorylation, dopaminergic signaling, proteasome-mediated protein degradation, and ferroptosis. Notably, proteins involved in cytoskeletal stability (MARK1, Septin3), neuroinflammation (JAK2, Ifi208), and metabolic regulation (PDE4A, ACSL3) exhibited significant changes in CRD-exposed PD mice. These findings highlight the critical role of circadian dysfunction in accelerating PD progression by exacerbating neuronal loss and dysregulating key molecular pathways. Targeting circadian homeostasis may provide a novel therapeutic strategy for mitigating neurodegeneration in PD.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115356"},"PeriodicalIF":4.6,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144491266","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":"Intermittent transcutaneous auricular vagus nerve stimulation reverses acute stress-induced memory deficits via O-GlcNAc modulation","authors":"Jianhui Wang ,&nbsp;Jingying Liu ,&nbsp;Chengran Wang ,&nbsp;Feng Liu ,&nbsp;Yan Huang ,&nbsp;Hexi Yang ,&nbsp;Mengting Xia ,&nbsp;Wenxia Zhou ,&nbsp;Zhiyong Xiao","doi":"10.1016/j.expneurol.2025.115359","DOIUrl":"10.1016/j.expneurol.2025.115359","url":null,"abstract":"<div><div>In recent years, transcutaneous auricular vagus nerve stimulation (taVNS), as a non-invasive therapy, has been increasingly employed to ameliorate cognitive deficits. O-linked β-<em>N</em>-acetylglucosamine (O-GlcNAc) modification plays a crucial role in neuronal function and is closely related to stress responses and memory regulation. However, the impact of taVNS on O-GlcNAc modification and memory function under acute stress conditions remains unclear. This study aims to explore the effects of taVNS on memory impairment in acutely stressed mice and elucidate the potential mechanisms involving O-GlcNAc in this process. The results indicate that intermittent taVNS, compared to continuous taVNS, significantly improved memory function in acutely stressed mice, with the 5 Hz stimulation showing the most significant effect and effectively reducing O-GlcNAc levels in the hippocampus. Furthermore, bioinformatic analysis revealed that blocking O-GlcNAc led to abnormal activation of the STAT3 pathway. Subsequent biochemical analysis confirmed that intermittent taVNS modulated the expression of IL-6 and phosphorylated STAT3, suggesting that it protects memory function by mediating neuroinflammatory responses through the regulation of O-GlcNAc modification. Notably, the memory-protective effect of taVNS was significantly diminished after blocking hippocampal O-GlcNAc flux, supporting the hypothesis that taVNS safeguards memory function via O-GlcNAc modification. This study underscores the efficacy of intermittent 5 Hz taVNS in reversing acute stress-induced memory deficits. It highlights the pivotal role of O-GlcNAc modification in the hippocampus during this process, offering new insights for developing therapeutic strategies targeting stress-related cognitive disorders.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115359"},"PeriodicalIF":4.6,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495431","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":"Immune cell response after intracerebral hemorrhage in piglets and the treatment effects of deferoxamine and minocycline","authors":"Qing Xie,&nbsp;Yuxiang Gu,&nbsp;Guohua Xi,&nbsp;Ya Hua,&nbsp;Richard F. Keep,&nbsp;Yingfeng Wan","doi":"10.1016/j.expneurol.2025.115354","DOIUrl":"10.1016/j.expneurol.2025.115354","url":null,"abstract":"<div><h3>Background</h3><div>Intracerebral hemorrhage (ICH) induces immune cell infiltration. This study used a piglet lobar ICH model to address three questions: do immune cells use surviving or degenerating white matter within hematoma to migrate? Do certain types of immune cell preferentially migrate into the hematoma? How do two potential therapeutics, deferoxamine (DFX) and minocycline (MINO), alter the migration of different immune cells into the perihematomal zone and the hematoma itself?</div></div><div><h3>Methods</h3><div>This two-part study was conducted in piglets. In the first part, 2.5 ml of blood was injected into the right frontal lobe, and the animals were euthanized at 4 h, days 1, 3 and 7 post-ICH. In the second part, animals were treated with vehicle, DFX or MINO after ICH and euthanized on day 3. Immunohistochemistry was used to examine the distribution of B and T lymphocytes, neutrophils and microglia/macrophages in the hematoma and perihematomal areas.</div></div><div><h3>Results</h3><div>B and T lymphocytes, as well as microglia/macrophages, gradually increased in the hematoma and peri-hematomal areas from 4 h to day 7 after ICH, while neutrophils decreased from 4 h to day 1 before increasing from day 1 to day 7. The infiltration of all the types of immune cells into the hematoma core was greater in areas with surviving intra-hematoma white matter fibers. There was preferential migration of B and T lymphocytes compared to microglia/macrophages as assessed by the hematoma/perihematomal ratio. MINO treatment significantly reduced infiltration of B and T lymphocytes and microglia/macrophages into the hematoma and peri-hematomal area at day 3 post-ICH. DFX induced a non-significant reduction. However, neutrophil numbers increased in the hematoma and peri-hematomal areas with DFX, while MINO reduced neutrophil numbers.</div></div><div><h3>Conclusions</h3><div>ICH induces significant infiltration of immune cells infiltration into the hematoma core and perihematomal areas, with this infiltration associated with surviving intra-hematoma white matter fibers. DFX and MINO treatments attenuate the immune cells response, although DFX increase neutrophils number, possible due to reduced neutrophils apoptosis.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115354"},"PeriodicalIF":4.6,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144365223","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":"Modulatory effects of transcranial magneto-acoustic stimulation on behavior and corticostriatal transmission of oscillatory activity in a mouse model of Parkinson's disease induced by MPTP","authors":"Yihao Xu ,&nbsp;Shuai Zhang ,&nbsp;Jinrui Mi ,&nbsp;Xiaochao Lu ,&nbsp;Qingzhao Wang ,&nbsp;Ruiyang Fan ,&nbsp;Jiangwei Lv ,&nbsp;Lipeng Xing ,&nbsp;Haochen Zhang ,&nbsp;Guizhi Xu","doi":"10.1016/j.expneurol.2025.115352","DOIUrl":"10.1016/j.expneurol.2025.115352","url":null,"abstract":"<div><h3>Background</h3><div>Transcranial magneto-acoustic stimulation (TMAS) is a novel noninvasive neuromodulation technology that combines ultrasound within a static magnetic field to achieve high spatial resolution and deep brain penetration. However, the effects of TMAS on neural oscillations related to motor deficits in Parkinson's disease (PD) remain poorly understood.</div></div><div><h3>Objective</h3><div>The objective of this study was to investigate whether TMAS could enhance the propagation and interaction of oscillatory dynamics within the corticostriatal circuit.</div></div><div><h3>Methods</h3><div>We performed a comprehensive neurological assessment using behavioral tests, in vivo electrophysiological recordings, and immunohistochemistry in male C57BL/6 J mice treated with MPTP, followed by noninvasive brain stimulation.</div></div><div><h3>Results</h3><div>Our results demonstrate that TMAS: 1) improves locomotor performance and learning abilities in PD mice; 2) reduces phase-amplitude coupling between beta and gamma frequency bands of local field potentials, while enhancing inter-brain interactions and information transmission; 3) modulates neural activity and depresses c-Fos overexpression on the dorsal striatum of PD mice; 4) provides neuroprotection by modulating neuroinflammation and mitigating MPTP-induced neurotoxicity within neural circuits.</div></div><div><h3>Conclusion</h3><div>These findings highlight the role of TMAS in strengthening the functional organization of the corticostriatal circuit, suggesting its potential as a novel treatment for neuropsychiatric disorders characterized by activity disruptions.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115352"},"PeriodicalIF":4.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340070","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":"Electroacupuncture ameliorates sleep deprivation-induced insomnia in mice by regulating the dopaminergic projections from VTA to NAc","authors":"Weichao Pan ,&nbsp;Sijia Wang ,&nbsp;Ying Liu ,&nbsp;Shan Qin ,&nbsp;Feifei Ge ,&nbsp;Xiya Yuan ,&nbsp;Yuyang Bo ,&nbsp;Haoqing Tai ,&nbsp;Chengyong Liu ,&nbsp;Yu Fan ,&nbsp;Xiaoqiu Wang ,&nbsp;Hee Young Kim ,&nbsp;Wenzhong Wu ,&nbsp;Xiaowei Guan","doi":"10.1016/j.expneurol.2025.115351","DOIUrl":"10.1016/j.expneurol.2025.115351","url":null,"abstract":"<div><h3>Background</h3><div>The electroacupuncture (EA) has emerged as a potential therapeutic approach for the treatment of chronic insomnia, however, its underlying brain mechanism remain unclear. <em>Methods:</em> Chronic sleep deprivation (CSD) mice models was established to investigate the effect of EA at acupoints of Yintang (EX-HN3), Shenmen (HT7), and Sanyinjiao (SP6) on CSD. With the methods of EEG/EMG recordings and chemogenetic manipulations, we explore the role of the dopaminergic projections from ventral tegmental area (VTA) to nucleus accumbens (NAc) in the therapeutic effects of EA on CSD-induced insomnia.</div></div><div><h3>Results</h3><div>We found that EA significantly alleviated CSD-induced insomnia, as indicated by an increased total sleep time and non-rapid eye movement (NREM) sleep during the dark period, along with attenuating the CSD-caused hyperactivity of VTA dopamine neurons in mice. Chemogenetic inhibition of the dopaminergic projections from VTA to NAc could restore the NREM sleep in CSD mice. Most importantly, the therapeutic effects of EA on CSD-induced insomnia was counteracted by activating the dopaminergic projections from VTA to NAc of mice.</div></div><div><h3>Conclusion</h3><div>These findings suggested that the therapeutic effects of EA at EX-HN3, HT7 and SP6 are achieved by targeting the dopaminergic projections from VTA to NAc, which could be therapeutic approach for chronic insomnia.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115351"},"PeriodicalIF":4.6,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330454","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":"Response to the Editor - Exploring the Potential of routine serological markers in predicting neurological outcomes in spinal cord injury","authors":"Jan Matthias ,&nbsp;Louis P. Lukas ,&nbsp;Sarah C. Brüningk ,&nbsp;Lucie Bourguignon ,&nbsp;Catherine R. Jutzeler","doi":"10.1016/j.expneurol.2025.115346","DOIUrl":"10.1016/j.expneurol.2025.115346","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115346"},"PeriodicalIF":4.6,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324910","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":"Letter to the editor: “Exploring the potential of routine serological markers in predicting neurological outcomes in spinal cord injury” by Jan Matthias et al","authors":"Shashank Chaurasia,&nbsp;Vishal Kumar","doi":"10.1016/j.expneurol.2025.115345","DOIUrl":"10.1016/j.expneurol.2025.115345","url":null,"abstract":"","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115345"},"PeriodicalIF":4.6,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144290723","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":"Short-chain fatty acids are a key mediator of gut microbial regulation of T cell trafficking and differentiation after traumatic brain injury","authors":"Marta Celorrio ,&nbsp;Kirill Shumilov ,&nbsp;Allen Ni ,&nbsp;Leyre Ayerra ,&nbsp;Wade K. Self ,&nbsp;N.L. Vitorino de Francisca ,&nbsp;Rachel Rodgers ,&nbsp;Lawrence A. Schriefer ,&nbsp;Ben Garcia ,&nbsp;Maria S. Aymerich ,&nbsp;Brian T. Layden ,&nbsp;Gabor Egervari ,&nbsp;Megan T. Baldridge ,&nbsp;Stuart H. Friess","doi":"10.1016/j.expneurol.2025.115349","DOIUrl":"10.1016/j.expneurol.2025.115349","url":null,"abstract":"<div><div>The gut microbiota has emerged as a pivotal regulator of host inflammatory processes after traumatic brain injury (TBI). However, the mechanisms by which the gut microbiota communicates to the brain in TBI are still under investigation. We previously reported that gut microbiota depletion (GMD) using antibiotics after TBI resulted in increased microglial activation, reduced neurogenesis, and reduced T cell infiltration. In the present study, we have demonstrated that intestinal T cells contribute to the pool of cells infiltrating the brain after TBI. Depletion or genetic deletion of T cells before injury reversed GMD induced reductions in post-TBI neurogenesis. Short-chain fatty acid supplementation increased T regulatory and T helper 1 cell infiltration to the brain along with restoring neurogenesis and microglia activation after TBI with GMD. These data suggest that T cell subsets are essential cellular mediators by which the gut microbiota modulates TBI pathogenesis, a finding with important therapeutic implications.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115349"},"PeriodicalIF":4.6,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316265","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":"Role of aging in nerve and muscle changes after chronic nerve compression in mice","authors":"Allen Green ,&nbsp;Jagmeet S. Arora ,&nbsp;Jordan J. Burgess,&nbsp;Jesse Emefiele,&nbsp;Shannon D. Francis,&nbsp;Amar Singh,&nbsp;Paige M. Fox","doi":"10.1016/j.expneurol.2025.115348","DOIUrl":"10.1016/j.expneurol.2025.115348","url":null,"abstract":"<div><h3>Background and aims</h3><div>Chronic nerve compression (CNC) impacts over one million Americans annually, causing substantial functional and economic burdens. Despite its prevalence, the translational relevance of murine CNC models is limited by the use of young animals and a lack of studies investigating post-decompression recovery. This study aims to characterize CNC in aged mice compared to young mice and assess nerve and muscle recovery following surgical release in aged animals.</div></div><div><h3>Methods</h3><div>Young (20-week) and aged (67-week) male C57BL/6 J mice underwent 16 weeks of sciatic nerve compression. A subset of aged mice received surgical decompression, followed by a 4-week recovery. Electrophysiological, histological, and molecular analyses were performed on nerve and muscle tissues to evaluate changes induced by CNC and decompression.</div></div><div><h3>Results</h3><div>CNC induced demyelination in both young and aged mice, with aged mice exhibiting greater axonal atrophy. Young mice muscle demonstrated increased expression of atrophic and fibrotic markers such as <em>Atrogin1</em>, <em>MuRF1</em>, and <em>α-SMA</em>. Conversely, we observed increased expression of <em>MyoD</em> and <em>MyoG</em> myogenic markers in aged mice muscle, correlating with increased average muscle fiber cross-sectional area. In aged mice, surgical release restored electrophysiological parameters, normalized histological features, and reversed molecular gene adaptations.</div></div><div><h3>Conclusion</h3><div>The molecular and structural responses to CNC in affected muscle differ with age, with aged mice demonstrating a shift from atrophic to myogenic pathways compared to young mice. Surgical release effectively mitigates CNC-induced deficits, emphasizing its therapeutic value. This study highlights the importance of age-appropriate models for understanding CNC pathophysiology and recovery dynamics.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"392 ","pages":"Article 115348"},"PeriodicalIF":4.6,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293612","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}