Molecular Neurobiology最新文献

{"title":"Identifying Pyroptosis-Hub Genes and Inflammation Cell Type-Related Genes in Ischemic Stroke.","authors":"Wei Ge, Liangbin Cao, Can Liu, Hao Wang, Meijing Lu, Yongquan Chen, Ye Wang","doi":"10.1007/s12035-024-04647-x","DOIUrl":"10.1007/s12035-024-04647-x","url":null,"abstract":"<p><p>Stroke is the second-leading global cause of death. The damage attributed to the immune storm triggered by ischemia-reperfusion injury (IRI) post-stroke is substantial. However, data on the transcriptomic dynamics of pyroptosis in IRI are limited. This study aimed to analyze the expression of key pyroptosis genes in stroke and their correlation with immune infiltration. Pyroptosis-related genes were identified from the obtained middle cerebral artery occlusion (MCAO) datasets. Differential expression and functional analyses of pyroptosis-related genes were performed, and differences in functional enrichment between high-risk and low-risk groups were determined. An MCAO diagnostic model was constructed and validated using selected pyroptosis-related genes with differential expression. High- and low-risk MCAO groups were constructed for expression and immune cell correlation analysis with pyroptosis-related hub genes. A regulatory network between pyroptosis-related hub genes and miRNA was also constructed, and protein domains were predicted. The expression of key pyroptosis genes was validated using an MCAO rat model. Twenty-five pyroptosis genes showed differential expression, including four hub genes, namely WISP2, MELK, SDF2L1, and AURKB. Characteristic genes were verified using real-time quantitative PCR analyses. The high- and low-risk groups showed significant expression differences for WISP2, MELK, and SDF2L1. In immune infiltration analysis, 12 immune cells showed differences in expression in MCAO samples. Further analysis demonstrated significant positive correlations between the pyroptosis-related hub gene SDF2L1 and immune cell-activated dendritic cells in the high-risk group and immune cell natural killer cells in the low-risk group. This study identified four pyroptosis-related hub genes, with elevated WISP2, MELK, and SDF2L1 expression closely associated with the high-risk group. The analysis of inflammatory cell types in immune infiltration can predict ischemic stroke risk levels and help to facilitate treatment.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"6228-6255"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11953102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142965958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into the Role of the Glymphatic System in the Pathogenesis of Post-hemorrhagic Hydrocephalus.","authors":"Ahmed T Massoud, Dillon A Noltensmeyer, Jenifer Juranek, Charles S Cox, Fred Christian Velasquez, Banghe Zhu, Eva M Sevick-Muraca, Manish N Shah","doi":"10.1007/s12035-025-04692-0","DOIUrl":"10.1007/s12035-025-04692-0","url":null,"abstract":"<p><p>Recently, it has been well-established that the glymphatic or glial-lymphatic system plays a vital role in the pathophysiology of various neurological compromise, especially hydrocephalus (HCP). Till now, the complete pathway is not yet fully understood, and little evidence is available from the literature that links hydrocephalus to disorders of the glymphatic system. Most published molecular studies and animal research have shown that, in models with hydrocephalus, the drainage of cerebrospinal fluid (CSF) via the glymphatic system is disrupted. This is strongly observed in normal pressure and post-hemorrhagic hydrocephalus cases. A thorough search of the literature to date yields scarce evidence on studies conducted on humans. Despite major similarities between non-human and human glymphatic pathways, the need for studies conducted on humans is becoming more urgent as the glymphatic pathway has been shown to be a good candidate for therapeutic intervention. In this review, we collect and report the most updated evidence addressing the glymphatic drainage pathways and their associations with the development of various types of hydrocephalus. In addition, we reveal the current scientific gap in human studies and our recommendations for the conduction of future clinical studies.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"6537-6543"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11952971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterizing Genetic-Predisposed Proteins Involving Insomnia by Integrating Genome-Wide Association Study Summary Statistics.","authors":"Jiang Long, Meng Dou, Xiangdong Tang, Xiaojing Gu","doi":"10.1007/s12035-025-04695-x","DOIUrl":"10.1007/s12035-025-04695-x","url":null,"abstract":"<p><p>Large case-control genome-wide association studies (GWASs) have detected loci associated with insomnia, but how these risk loci confer disease risk remains largely unknown. By integrating brain protein quantitative trait loci (pQTL) (N_pQTL1 = 376, N_pQTL2 = 152) and expression QTL (eQTL) (N = 452) datasets, with the latest insomnia GWAS summary statistics (N_case = 109,548, N_Controls = 277440), we conducted proteome/transcriptome-wide association study (PWAS/TWAS) and Mendelian randomization (MR) analysis, aiming to identify causal proteins involving in the pathogenesis of insomnia. We also explored the bi-directional causality between insomnia and several common diseases. As a result, the altered protein level of 28 genes in the brain was associated with the risk of insomnia in the discovery stage of PWAS, of which 18 genes' associations were replicated in the confirmatory stage of PWAS. Among them, four proteins (2-aminoethanethiol dioxygenase (ADO), calcium-modulating cyclophilin ligand (CAMLG), islet cell autoantigen 1 like (ICA1L) and latexin (LXN)) were found to be the most likely causal genes for insomnia with validations from TWAS, MR, and colocalization results. Specifically, the higher protein level of ADO, CALMG, and ICA1L was causally associated with a lower risk of insomnia. In comparison, the higher protein level of LXN was causally associated with an increased risk for insomnia. Moreover, genetically predicted insomnia was causally associated with an increased risk of developing cardiovascular diseases and depression. In conclusion, our study identified ADO, CAMLG, ICA1L, and LXN as potentially causal proteins in the pathogenesis of insomnia. This could provide insights into further mechanistic studies and therapeutic development for insomnia.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"6576-6586"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11953091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk Between Mitochondrial DNA and Immune Response: Focus on Autism Spectrum Disorder.","authors":"Wenxuan Qu, Ge Yan, Yajuan Du, Xinyang Zhou, Chutian Huang, Bei Li, Junmei Zhou, Qian Li","doi":"10.1007/s12035-024-04637-z","DOIUrl":"10.1007/s12035-024-04637-z","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by multiple dysfunctions in behavior, the nervous system, and the immune system. Increasing evidence suggests that mitochondrial DNA (mtDNA) plays a crucial role in the pathology of ASD. In clinical practice, altered mtDNA levels have been observed in various tissues of individuals with ASD. Mutation or oxidation of mtDNA is also closely related to the immune response associated with the pathology of autism. With mtDNA identified as a causal factor, much interest has focused on how its production affects neurodevelopment and neurophysiology. Here, we review how mtDNA leads to dysfunction of cellular mitochondria and immune response. We also illustrate the relationship between mtDNA alterations and the pathology of autism. Finally, we discuss the existing evidence on cell-free mtDNA associated with ASD and look forward to its application in clinical diagnosis and treatment.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"5629-5639"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716567","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":"Exogenous α-Synuclein Induces Oxidative Damage to Dopaminergic Neurons Through p-NMDAR2B/Nur77.","authors":"Xiaoyi Lai, Jiannan Wu, Xuanfen Kou, Yongjiang Zhang, Mengmeng Shen, Miao Yu, Yibo Zhai, Junqiang Yan","doi":"10.1007/s12035-024-04625-3","DOIUrl":"10.1007/s12035-024-04625-3","url":null,"abstract":"<p><p>Alpha-synuclein (α-syn) is a major pathological marker of Parkinson's disease (PD), and its abnormal expression and aggregation lead to dopaminergic neuron degeneration, in which oxidative stress plays an important role. However, the exact molecular mechanism by which α-syn causes PD remains unclear. In this study, exogenous α-syn, also known as α-syn preformed fibrils (α-syn PFFs), was used to construct in vivo and in vitro models of PD. Behavioral, Western blotting, biochemical, immunofluorescence, flow cytometry, electron microscopy, etc. were used to investigate the pathological mechanism of PD induced by α-syn. We found that 6 months after striatum injection of α-syn PFFs, mice exhibited motor deficits. Meanwhile, the protein expression of pS129-α-syn (p-α-syn) and α-syn oligomer significantly increased, while the expression of TH significantly decreased, and the oxidative stress in the substantia nigra was aggravated. In addition, we found an increase in the protein expression of NMDAR2B and p-Tyr1472-NMDAR2B (p-NMDAR2B) and a decrease in the protein expression of Nur77. However, in α-syn PFFs-induced SH-SY5Y cells, we found that inhibiting p-NMDAR2B increased the protein expression of Nur77, while overexpression of Nur77 did not affect the expression of p-NMDAR2B. Inhibition of p-NMDAR2B and overexpression of Nur77 reversed α-syn PFF-induced oxidative stress, thus reducing mitochondrial damage and cytotoxicity. Therefore, we speculate that α-syn PFF-induced oxidative stress in dopaminergic neurons may be mediated by p-NMDAR2B/Nur77. Our study provides novel insights into the pathology mechanism underlying α-syn-induced PD.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"5664-5678"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142730672","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":"Light Treatment Ameliorates Sub-chronic MK-801-Induced Cognitive Deficits in Mice Through Up-regulating BDNF/p-CREB/p-ERK Signaling Pathway.","authors":"Keke Cui, Yiying Zhou, Lizhi Zhang, Yudong Ying, Yan Xue, Xiaoqin Zhang, Qinwen Wang, Haowei Shen, Wenhua Zhou, Feng Gao, Zhengchun Wang","doi":"10.1007/s12035-024-04653-z","DOIUrl":"10.1007/s12035-024-04653-z","url":null,"abstract":"<p><p>Cognitive impairment associated with schizophrenia (CIAS) is considered a core symptom of the illness, yet effective treatments remain limited. Light plays an important role in regulating cognitive functions. However, the potential of light treatment (LT) to improve CIAS remains unknown. The current study aimed to investigate the efficacy of LT on CIAS and explore the underlying molecular mechanisms in a CIAS animal model. The CIAS group and the control group were sub-chronically administered MK-801 and saline, respectively. Concurrently, the LT/CIAS group, consisting of CIAS mice, received LT exposure (3000 Lux, 2 h/day, for 3 weeks). Results showed a significant enhancement in cognitive performance among LT/CIAS mice, as evidenced by improvements in the novel object recognition (NOR) test, novel location recognition (NLR) test, and Morris water maze (MWM) compared to the CIAS group. Remarkably, these beneficial effects of LT persisted for over 4 weeks after the termination of LT. Furthermore, Golgi-cox staining unveiled an increased dendritic spine density and enhanced morphological complexity in hippocampal CA1 pyramidal neurons following 3 weeks of LT. Subsequent investigations revealed elevated levels of brain-derived neurotrophic factor (BDNF) and heightened phosphorylation of cAMP response element-binding phosphorylation protein (p-CREB) in the hippocampus of the LT/CIAS group compared to the CIAS group. Moreover, LT elevated the phosphorylated extracellular signal-regulated kinase (p-ERK) in the hippocampus of the LT/CIAS group relative to the CIAS group. In conclusion, the current study demonstrates that long-term LT effectively ameliorated sub-chronic MK-801-induced cognitive deficits in mice, and the altered dendritic spine density and morphology of CA1 pyramidal neurons were rescued in the LT/CIAS group, potentially through the up-regulation of the BDNF/p-CREB/p-ERK signaling pathway in LT/CIAS mice.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"5947-5960"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824381","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":"Acute Treatment with Fucoidan Ameliorates Traumatic Brain Injury-Induced Neurological Damages and Memory Deficits in Rats: Role of BBB Integrity, Microglial Activity, Neuroinflammation, and Oxidative Stress.","authors":"Shahla Eyvari-Brooshghalan, Rasool Haddadi, Siamak Shahidi, Shahab Ghaderi, Masome Rashno, Ali Kalantari, Iraj Salehi, Alireza Komaki, Abdolrahman Sarihi","doi":"10.1007/s12035-024-04668-6","DOIUrl":"10.1007/s12035-024-04668-6","url":null,"abstract":"<p><p>There is no acquiesced remedy for the treatment of traumatic brain injury (TBI)-associated impairment, especially cognitive decline. The first 24 h after TBI is a golden time for preventing the progress of the impairments. The present study aimed to examine the acute effects of fucoidan on neurological outcomes and memory performance and investigate its potential mechanisms in rats with TBI. Fucoidan (25, 50, and 100 mg/kg, i.p.) was injected immediately after TBI induction. Veterinary coma scale (VCS), brain edema, blood-brain barrier (BBB) integrity, passive avoidance memory and spatial memory, neuroplasticity, myeloperoxidase (MPO) activity, oxidative stress, and histological alteration were evaluated after TBI induction and fucoidan treatment. The findings revealed that TBI resulted in an enhancement in brain water content and BBB permeability and diminished the performance of passive avoidance memory and spatial memory. These were accompanied by long-term potentiation (LTP) suppression in the hippocampus and the prevention of activities of SOD, catalase, and GPx and enhancement of MPO activity, TNF-α, IL-6, and lipid peroxidation levels in the hippocampus as well as hippocampal neuronal loss. Fascinatingly, acute treatment of TBI rats with fucoidan especially in the higher doses (50 and 100 mg/kg) significantly ameliorated (p < 0.05) neurological outcomes of VCS, cerebral edema, BBB integrity, passive avoidance memory, spatial memory, LTP impairment, and oxidative-antioxidative balance. Also, fucoidan significantly ameliorated hippocampal neuronal loss, TNF-α and IL-6 levels, and MPO activity as an indicator of microglial activation. These outcomes imply that fucoidan can be a hopeful remedy for TBI-associated neuronal impairments. However, further research is necessary to endorse this issue.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"5990-6013"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846852","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":"Genome-Wide Network Analysis of DRG-Sciatic Nerve Network-Inferred Cellular Senescence and Senescence Phenotype in Peripheral Sensory Neurons.","authors":"Sora Kawabata, Hirotaka Iijima, Naohiko Kanemura, Kenji Murata","doi":"10.1007/s12035-024-04666-8","DOIUrl":"10.1007/s12035-024-04666-8","url":null,"abstract":"<p><p>Accumulation of senescent neurons in the dorsal root ganglion (DRG) is an important tissue phenotype that causes age-related degeneration of peripheral sensory nerves. Senescent neurons are neurons with arrested cell cycle that have undergone cellular senescence but remain in the tissue and play various biological roles. To understand the accumulation of senescent neurons in the DRG during aging, we aimed to elucidate the mechanism that induces cellular senescence in DRG neurons and the role of senescent DRG neurons. We integrated multiple public transcriptome datasets for DRGs, which include cell bodies in neurons, and the sciatic nerve, which includes axons in neurons, using network medicine-based bioinformatics analysis. We thus inferred the molecular mechanisms involved in cellular senescence of DRG neurons, from molecular responses to senescence, in the DRG-sciatic nerve network. Network medicine-based bioinformatics analysis revealed that age-related Mapk3 decline leads to impaired cholesterol metabolism and biosynthetic function in axons, resulting in compensatory upregulation of Srebf1, a transcription factor involved in lipid and cholesterol metabolism. This in turn leads to CDKN2A-mediated cellular senescence. Furthermore, our analysis revealed that senescent DRG neurons develop a senescence phenotype characterized by activation of antigen-presenting cells via upregulation of Ctss as a hub gene. B cells were inferred as antigen-presenting cells activated by Ctss, and CD8-positive T cells were inferred as cells that receive antigen presentation from B cells.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"6112-6127"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142877081","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 Roles of DMT1 in Inflammatory and Degenerative Diseases.","authors":"Haigang Liu, Mi Li, Yi Deng, Yanjun Hou, Liangcai Hou, Xiong Zhang, Zehang Zheng, Fengjing Guo, Kai Sun","doi":"10.1007/s12035-025-04687-x","DOIUrl":"10.1007/s12035-025-04687-x","url":null,"abstract":"<p><p>Iron homeostasis is critical for multiple physiological and pathological processes. DMT1, a core iron transporter, is expressed in almost all cells and organs and altered in response to various conditions, whereas, there is few reviews focusing on DMT1 in diseases associated with aberrant iron metabolism. Based on available knowledge, this review described a full view of DMT1 and summarized the roles of DMT1 and DMT1-mediated iron metabolism in the onset and development of inflammatory and degenerative diseases. This review also provided an overview of DMT1-related treatment in these disorders, highlighting its therapeutic potential in chronic inflammatory and degenerative diseases.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"6317-6332"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951889","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":"Clusterin Deficiency Promotes Cellular Senescence in Human Astrocytes.","authors":"Pinky Sultana, Ondrej Honc, Zdenek Hodny, Jiri Novotny","doi":"10.1007/s12035-024-04650-2","DOIUrl":"10.1007/s12035-024-04650-2","url":null,"abstract":"<p><p>The glycoprotein clusterin (CLU) is involved in cell proliferation and DNA damage repair and is highly expressed in tumor cells. Here, we aimed to investigate the effects of CLU dysregulation on two human astrocytic cell lines: CCF-STTG1 astrocytoma cells and SV-40 immortalized normal human astrocytes. We observed that suppression of CLU expression by RNA interference inhibited cell proliferation, triggered the DNA damage response, and resulted in cellular senescence in both cell types tested. To further investigate the underlying mechanism behind these changes, we measured reactive oxygen species, assessed mitochondrial function, and determined selected markers of the senescence-associated secretory phenotype. Our results suggest that CLU deficiency triggers oxidative stress-mediated cellular senescence associated with pronounced alterations in mitochondrial membrane potential, mitochondrial mass, and expression levels of OXPHOS complex I, II, III and IV, indicating mitochondrial dysfunction. This report shows the important role of CLU in cell cycle maintenance in astrocytes. Based on these data, targeting CLU may serve as a potential therapeutic approach valuable for treating gliomas.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"5774-5786"},"PeriodicalIF":4.6,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11953114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}