ASN NEURO最新文献

{"title":"Polyglutamine-Expanded Ataxin-3 Accelerates CFTR Degradation Through K63-Linked Ubiquitination to Exacerbate Microglial Inflammation.","authors":"Zixin Wang, Xue Fan, Bingbing Bai, Mengxue Song, Ye Shi, Yinghao Zhao, Pengyu Xie, Tao Shi, Chunjiu He, Yuhong Hu, Qingtian Wu, Xia Hou","doi":"10.1080/17590914.2026.2662867","DOIUrl":"10.1080/17590914.2026.2662867","url":null,"abstract":"<p><p>The deubiquitinase Ataxin-3 causes spinocerebellar ataxia type 3 (SCA3) upon polyglutamine (polyQ) expansion. While expressed in the nervous system, the function of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel therein remains unclear, as does its potential regulation by Ataxin-3. This study reveals that Ataxin-3 interacts with and promotes CFTR degradation in human microglia by its K63-linked polyubiquitination, thereby shortening CFTR's half-life. Paradoxically, K63-linked polyubiquitin chains also promote the degradation of Ataxin-3 itself, suggesting a complex feedback mechanism. The pathogenic Ataxin-3Q80 mutant exerts a stronger effect than the wild-type protein. Consequently, this Ataxin-3-CFTR axis drives microglial polarization toward a pro-inflammatory phenotype and amplifies neuroinflammation. We thus identify a novel \"Ataxin-3-K63 ubiquitin chain-CFTR\" pathway that controls microglial activation, offering new mechanistic insight and therapeutic targets for SCA3. <b>Abbreviations:</b> MJDM: achado-Joseph disease; SCA3: spinocerebellar ataxia type 3; PolyQ: polyglutamine; CNS: central nervous system; CFTR: cystic fibrosis transmembrane conductance regulator; CF: cystic fibrosis; UIMs: ubiquitin-interacting motifs; MEM: Minimum Essential Medium; FBS: fetal bovine serum; P/S: penicillin/streptomycin; siRNA: small interfering RNA; BSA: bovine serum albumin; Co-IP: Co-immunoprecipitation; LPS: lipopolysaccharide; WT-CFTR: wild-type CFTR; CHX: Cycloheximide; 3-MA: 3-Methyladenine; IF: Immunofluorescence; IB: immunoblot; Ub: ubiquitin.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2662867"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13215304/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148026375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transferrin Promotes Oligodendroglial Differentiation Independently of Iron Binding and Release.","authors":"Estefania Chamorro-Aguirre, Martina Garmendia, María Julia Pérez, Paula G Franco, Agustín Byrne, Hugo Adamo, Jorge Correale, Juana María Pasquini","doi":"10.1080/17590914.2026.2720203","DOIUrl":"10.1080/17590914.2026.2720203","url":null,"abstract":"<p><p>Transferrin (Tf), classically known as the major iron-transport protein in mammals, also engages in potent promyelinating activity within the central nervous system by accelerating oligodendrocyte maturation. Since 1994, our group has shown that intrathecal or intranasal administration of apoTransferrin (aTf) promotes oligodendroglial differentiation and myelin protein expression <i>in vivo</i> and <i>in vitro</i>. A long-standing question, however, has been whether these effects depend on iron delivery or instead reflect an intrinsic trophic property of the protein. To directly address this point, we used the oligodendroglial precursor cell line Oli-Neu and two previously characterized non-glycosylated human Tf mutants with selective defects in iron handling: TfY (Y95F/Y188F/Y426F/Y517F), an iron-binding-deficient mutant unable to bind iron, in either lobe, and TfK (K206E/E534A), an iron-release-deficient mutant that binds iron but cannot release it. We first confirmed that Oli-Neu cells express endogenous Tf and Tf receptor 1 (TfR1), internalize exogenous human Tf, and display low, non-colocalizing TfR2 expression. Transient expression of wild-type Tf, TfY, or TfK increased myelin basic protein (MBP) immunoreactivity and induced complex oligodendrocyte-like morphologies compared with non-transfected cells. Both mutants promoted maturation despite their opposite iron-binding defects, with TfK generating highly branched arbors and TfY inducing a more compact process architecture. AlphaFold-based structural modelling demonstrated the preservation of the canonical bilobalTf scaffold in both mutants. These findings provide direct evidence that the promyelinating and promaturational actions of Tf do not require iron binding or release, but rather reside in the protein itself. By decoupling Tf's biological activity from iron metabolism, this work expands the current understanding of Tf biology and identifies Tf as an iron-independent signaling cue for oligodendrocyte differentiation.This insight opens new avenues for developing Tf-based or Tf-mimetic therapeutic strategies to enhance remyelination in demyelinating disorders such as multiple sclerosis.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2720203"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13505439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutamate-Dependent Dynamic DNA Methylation Regulates Excitatory Amino Acid Transporters in Bergmann Glia Cells: Role of AMPA Receptors.","authors":"Bolaji O Oyetayo, Temitayo Subair, Natalia Morales-Ramírez, Luisa C Hernández-Kelly, Ada G Rodríguez-Campuzano, Leticia Ramírez-Martínez, Luz Nolasco-Hiniesta, Emma S Calderón, Francisco Castelán, Esther López-Bayghen, Marie-Paule Felder-Schmittbuhl, Arturo Ortega","doi":"10.1080/17590914.2025.2604823","DOIUrl":"10.1080/17590914.2025.2604823","url":null,"abstract":"<p><p>Glial glutamate uptake through sodium-dependent excitatory amino acid transporters (EAATs) is essential for synaptic homeostasis. Epigenetic modifications and neurotransmitter receptor signaling influence glial function although their interactive effects on glutamate transporter regulation remain poorly understood. To investigate how DNA methylation affects glutamate receptor-mediated regulation of its own removal, primary cultures from chick cerebellar Bergmann glial cells were used. Confluent monolayers were treated with a DNA methylation inhibitor. Glutamate transporter activity was assessed through radioactive uptake assays, while methylation levels within distinct regions of the <i>chGLAST</i> promoter were analyzed by methylated DNA immunoprecipitation (MeDIP)-PCR. The role of cytoskeletal dynamics and calcium signaling was evaluated using pharmacological modulators. DNA hypomethylation sensitizes glial cells to glutamate receptors stimulation. Kinetic analyses show a statistically significant increase in the Michaelis-Menten constant V<i>_Max</i> and a non-significant change in K<i>_M</i>, changes in <i>V_Max</i> reflect alterations in plasma membrane transporter numberinity. Pharmacological analysis revealed the involvement of the phosphatidyl inositol 3 kinase (PI3K), the Ca²⁺/calmodulin-dependent kinase II (CaMKII) and the mammalian target of rapamycin (mTOR) pathways, suggesting coordinated regulation of glutamate transport. Importantly, short-term activation of AMPA receptors induced hypomethylation of the <i>chglast</i> promoter, suggesting the engagement of active demethylation pathways that sustain transporter expression during heightened excitatory activity. Together, these findings reveal a novel mechanism in which epigenetic flexibility and synaptic receptor activity converge to enhance glutamate uptake in glial cells. This synergy between DNA methylation and AMPA receptor signaling provide new insights into the mechanisms by which glial cells dynamically adapt to excitatory stress.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2604823"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12721094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145792881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-Synaptic Mechanism of Ocular Dominance Plasticity.","authors":"Maxwell K Foote, William C Huffman, Erin N Santos, Philip R Lee, Michal Jarnik, Wei Li, Juan S Bonifacino, R Douglas Fields","doi":"10.1080/17590914.2026.2616376","DOIUrl":"10.1080/17590914.2026.2616376","url":null,"abstract":"<p><p>Classic experiments showing that monocular visual disruption alters synaptic connections to binocular neurons established the fundamental concept of synaptic plasticity. Synaptic inputs that are activated coincidently with postsynaptic action potential firing are strengthened, and inputs from cells firing before or after the postsynaptic action potential are weakened. An implicit assumption, however, is that the speed of impulse transmission is not altered by visual deprivation. If so, spike time arrival at binocular neurons would be affected, thereby inducing synaptic plasticity. This possibility is tested here in adult mice by monocular eyelid suture and monocular action potential inhibition in retinal axons. The results show that spike time arrival in visual cortex is altered by monocular visual disruption in association with morphological changes in myelin (nodes of Ranvier) on axons in optic nerve and optic tract. This non-synaptic mechanism of ocular dominance plasticity, mediated by myelin-forming cells, supplements and may drive synaptic plasticity.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2616376"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Fatty Acid Oxidation by Neural Stem and Progenitor Cells Increases Proliferation but Does Not Improve Long-Term Neurogenesis After Mild Traumatic Brain Injury.","authors":"Javier Allende Labastida, Regina F Fernandez, Tiffany Chu, Noelle Puleo, Maria Shishikura, Michael J Wolfgang, Joseph Scafidi, Susanna Scafidi","doi":"10.1080/17590914.2025.2610198","DOIUrl":"10.1080/17590914.2025.2610198","url":null,"abstract":"<p><p>Neurogenesis in the dentate gyrus of the hippocampus is a conserved and highly regulated process throughout the lifespan. Hippocampal neural stem and progenitor cells (NSPCs) can either transition into an activated proliferative state or remain quiescent. Accumulating data suggests that mitochondrial fatty acid β-oxidation is important in maintaining NSPCs quiescence under normal physiological conditions; however, the contribution of this pathway in NSPCs following brain injury remains unknown. While severe traumatic brain injury (TBI) is characterized by increased NSPCs proliferation in the hippocampus, the extent of this proliferative response after mild TBI, the most prevalent form of TBI, has not been fully delineated. Using closed head injury as a model of mild TBI and a brain-specific knockout mouse of carnitine palmitoyltransferase 2 (CPT2; an obligate gene in mitochondrial fatty acid β-oxidation), we investigated the role of fatty acid oxidation in hippocampal NSPCs proliferation in naïve and injured male and female mice. Our results show that loss of CPT2 in the brain does not affect hippocampal proliferation in naïve mice. Furthermore, mild TBI upregulates proliferation at day 3 post-injury, and is further increased only in male CPT2-deficient mice. Despite the post-injury increase in hippocampal NSPCs proliferation in CPT2^B-/- mice, long-term neurogenesis remained unchanged. Together, these data provides a new insight into the metabolic regulation of NSPCs neurogenesis in the hippocampus following mild traumatic brain injury.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2610198"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12818800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galectin-3 in the Lateral Ventricle Regulates Immune Functions.","authors":"Luana Campos Soares, Hana Bernhardova, Francis G Szele","doi":"10.1080/17590914.2026.2622750","DOIUrl":"10.1080/17590914.2026.2622750","url":null,"abstract":"<p><p>Galectin-3 (Gal-3) is a protein expressed by glia that belongs to an ancient family. Gal-3 recognises molecular patterns on pathogens due to the high degree of its binding specificity with carbohydrate recognition domains. Thus, in sponges as well as other invertebrates, galectins are an important component of the primitive innate immune system. Whereas Gal-3's function in driving mammalian inflammation is well known, its function in warding off bacterial and viral infections is not well appreciated. One route of brain infection is via the cerebrospinal fluid brain interface (CSFBI) which is primarily composed of ependymal cells (EC). ECs express high levels of Gal-3, and their motile cilia are compromised in Gal-3 KOs. In this mini-review, we discuss fundamentally important potential roles of Gal-3 in pathogen recognition at the CSFBI and suggest avenues of further study.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2622750"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12885407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal Dynamics and Cellular States of Neuroinflammation in Amyotrophic Lateral Sclerosis: Implications for Stage‑Specific Therapeutics.","authors":"Congwen Lv, Wenjia Zhu, Xinmei Wen, Yuwei Da","doi":"10.1080/17590914.2026.2715625","DOIUrl":"https://doi.org/10.1080/17590914.2026.2715625","url":null,"abstract":"<p><p>Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with a complex and heterogeneous pathogenesis. Accumulating preclinical and clinical evidence indicates that neuroinflammation is an important modulator of ALS pathophysiology, involving activation of resident central nervous system immune cells, dysfunction of glial support systems, disruption of neurovascular barriers, and altered recruitment of peripheral immune cells. ALS-associated neuroinflammation is temporally dynamic and varies across anatomical compartments and cellular contexts. Multiple animal models, human neuroimaging, and post-mortem tissue suggest that relatively regulated or compensatory immune responses during early stage may progressively shift to persistent, maladaptive, and potentially neurotoxic inflammatory circuits in later stage. Although previous studies have described stage-dependent changes in individual immune cell populations, an integrated stage-dependent systematic framework that unifies dynamic alterations in both central and peripheral immune compartments remains insufficiently established. In this review, we propose a four-phase conceptual framework for ALS neuroinflammation across the progressive ALS pathogenesis, aiming to provide theoretical guidance for staging inflammatory therapeutic interventions.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2715625"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13488473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148787653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of E3 Ubiquitin Ligases in Oligodendrocyte Health and Disease.","authors":"Angela M Mabb, Dhanya N Pyaram, Jayshree Samanta","doi":"10.1080/17590914.2026.2682220","DOIUrl":"10.1080/17590914.2026.2682220","url":null,"abstract":"<p><p>Protein ubiquitination is a type of posttranslational modification that occurs in all cells to regulate numerous biological processes. Ubiquitination of proteins is carried out by an enzymatic cascade where E3 ubiquitin ligases facilitate the final step in the transfer of ubiquitin to substrates. This review focuses on the role of E3 ubiquitin ligases in the regulation of oligodendrocytes, a glial cell type in the central nervous system that is critical for axon myelination and overall neuronal health. Here we focus on how protein ubiquitination dominantly driven by E3 ubiquitin ligase enzymes alters the development, maintenance, and disease pathogenesis in oligodendrocytes.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2682220"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13336288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148366794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting NLRP3 Inflammasome and Metabolic Dysregulation by Electroacupuncture: A Novel Therapeutic Strategy for Methamphetamine Withdrawal-Induced Depression.","authors":"Xiong Zhang, Xiao-Rui Zhao, Chun-Li You, Fang Zhang, Hong-Yi Zhu, Tian Gu, Jia Li","doi":"10.1080/17590914.2026.2624589","DOIUrl":"10.1080/17590914.2026.2624589","url":null,"abstract":"<p><p>This study demonstrates that electroacupuncture (EA) produces robust antidepressant effects in a rat model of methamphetamine (METH) withdrawal. Behavioral tests showed that EA applied at GV20, PC6, and HT7 significantly reduced immobility in the forced swim test and enhanced exploratory activity in the open field test. Mechanistically, EA repaired blood-brain barrier (BBB) disruption, as shown by reduced hippocampal water content, decreased Evans Blue leakage, and restored expression of tight-junction proteins (Occludin, Claudin-5, ZO-1). EA also inhibited neuronal apoptosis, suppressed microglial activation, and lowered pro-inflammatory cytokines IL-6 and TNF-α. Multi-omics analyses revealed that EA reversed METH-induced alterations in 32 differentially expressed genes related to the NLRP3 inflammasome pathway (Nlrp3, Pycard, Il1b) and BBB function, while metabolomic profiling identified 13 key metabolites involved in glutamate metabolism, TCA cycle, and tryptophan pathways. Crucially, the therapeutic benefits of EA were abolished by intracerebroventricular administration of the NLRP3 activator nigericin, confirming the essential role of NLRP3 inflammasome inhibition in EA's mechanism of action. In summary, EA represents a promising non-pharmacological approach for treating METH withdrawal-induced depression by coordinating BBB protection, suppression of neuroinflammation, and metabolic network regulation.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2624589"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146194010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myelin <i>g</i> Ratios: The Model Is in the Details.","authors":"Alexander Gow","doi":"10.1080/17590914.2025.2612034","DOIUrl":"10.1080/17590914.2025.2612034","url":null,"abstract":"<p><p>In contemporary myelin biology, there is a growing trend to prioritize faster, more convenient methodologies for evaluating white matter structure over quality of the analysis. This shift is often accompanied by less attention to the mechanistic foundations of the methods in preclinical and clinical research. To address such worrisome trends, the current article assesses three approaches for estimating the myelin <i>g</i> ratio from electron microscopy data, which is the gold standard approach to measure the impacts of neuropathology and treatment strategies on white matter integrity. Of the mathematical models examined, two are consistent with and equivalent to the linear relation defined by the axon versus fiber diameter plot (the principal data). The final model is the canonical almost universally accepted approach to measuring <i>g</i> ratios. This model is demonstrated to be internally inconsistent and discordant with the axon versus fiber diameter relation and can lead to inaccurate conclusions about myelin integrity. Furthermore, the increasing interest in non-invasive neuroimaging approaches to measure <i>g</i> ratios clinically in both physiologic and pathophysiologic studies necessitates calibration with electron microscopy-derived <i>g</i> ratios. In this vein, mathematical models applicable to these methodologies are concordant; thus, magnetic resonance imaging holds significant promise for accurate determination of myelin integrity in patients. On the other hand, the metrics measurable by this voxel-based technology may preclude application to gray matter myelin and perhaps limit its use to linearly-organized white matter tracts.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"18 1","pages":"2612034"},"PeriodicalIF":4.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12802999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145958267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}