Molecular Neurobiology最新文献

{"title":"Neural Expression of IL-16 Mediates Neuropathic Pain after Sciatic Injury in Mice.","authors":"Alba Coro-Martín, Alejandro Álvarez-Artime, Sara González-Rodríguez, María González-Amor, David Corral-Fontecha, Ana Baamonde, Luis Menéndez","doi":"10.1007/s12035-026-06280-2","DOIUrl":"https://doi.org/10.1007/s12035-026-06280-2","url":null,"abstract":"<p><p>The neutralization of interleukin-16 (IL-16) or of its main target, CD4 receptors, as well as the reduction of its synthesis by inhibiting caspase-3 have been recently considered as possible strategies to inhibit pain. Here we study the involvement of peripheral mechanisms related to the IL-16/CD4 axis in the nociceptive responses evoked after ligation of sciatic nerve in mice. Systemic administration of anti-IL-16 or anti-CD4 antibodies inhibited hyperalgesia and allodynia measured 2 days after ligation in male and female mice. In addition, both antibodies were also analgesic 9 days after nerve ligation, supporting the participation of IL-16 and CD4 in the establishment and maintenance of neuropathic pain. Following nerve injury, Il16 expression remained unaltered in dorsal root ganglia (DRGs) and damaged nerves, whereas Casp3 expression increased in DRGs and the enzymatic activity of caspase-3 was enhanced in damaged nerves. Immunofluorescence assays demonstrated a limited presence of IL-16 in DRG neurons, that remained unmodified after injury, and a clear up-regulation of this cytokine in injured nerves. Double immunofluorescence assays with βIII-tubulin and S100β antibodies demonstrated that IL-16 is expressed both in axons and Schwann cells after nerve ligation. The ability of IL-16 to evoke nociception by directly acting on nerves was confirmed by intra-sciatic administration. Immunofluorescence labelling of CD4 receptors was also present in injured nerves, being also up-regulated both in axons and Schwann cells. Finally, hyperalgesia and allodynia were prevented by the intra-sciatic administration of anti-IL-16 or anti-CD4 antibodies, thus supporting the relevance of the IL-16/CD4 axis in neuropathic hypernociception.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149245461","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":"HDAC3 Inhibitor RGFP966 Enhances Memory Persistence in a Biphasic Manner and Modulates NF-kB Nuclear Localization.","authors":"Agustina Robles, Santiago D'hers, Mariana Feld, Arturo Romano","doi":"10.1007/s12035-026-06268-y","DOIUrl":"https://doi.org/10.1007/s12035-026-06268-y","url":null,"abstract":"<p><p>Nearly five decades ago, it was first observed that long-term memory consolidation requires waves of transcriptional activity and protein synthesis, with the first two waves occurring within hours after learning. While numerous studies have examined the effects of protein synthesis inhibitors, how specific epigenetic regulators contribute to these waves remains poorly understood. Here, we aimed to determine whether HDAC3, a key modulator of memory, is involved in memory consolidation at these two time points through its potential relationship with the transcription factor NF-kB, one of its deacetylation targets and a critical player in memory formation. Pharmacological inhibition of HDAC3 with RGFP966, either immediately or 6 h after training, enhanced memory persistence in the NOR task in mice. Conversely, inhibition of NF-kB with BAY 11-7082 impaired memory at the same time points. Moreover, RGFP966 injection increased the nuclear proportion of NF-kB in the CA1 region of the hippocampus, suggesting that HDAC3 inhibition is associated with changes in NF-kB nuclear localization. To our knowledge, this study provides the first in vivo evidence that HDAC3 inhibition is associated with altered NF-kB localization during memory consolidation, extending previous observations from cell culture and electrophysiological studies in brain slices. Although these findings support a functional association between HDAC3 inhibition and NF-kB signaling during consolidation, further experiments will be required to determine whether this relationship is mechanistically causal.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149238842","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":"Multi-omics Genetic Prioritization and Cross-species Analysis of Mitochondrial Genes in Trigeminal Neuralgia.","authors":"Yi Wei, Zhixuan Lan, Yongguo Xie, Zihao Yi, Xueke Du, Zongbin Jiang","doi":"10.1007/s12035-026-06279-9","DOIUrl":"https://doi.org/10.1007/s12035-026-06279-9","url":null,"abstract":"<p><p>To identify mitochondrial genes associated with trigeminal neuralgia (TN) and characterize their expression in patient blood and experimental trigeminal nerve injury. We integrated methylation, expression, and protein quantitative trait loci with FinnGen TN genome-wide association data, focusing on MitoCarta3.0 genes. Summary-data-based Mendelian randomization, heterogeneity testing, colocalization, and tissue-specific analyses prioritized candidates. An exploratory case-control expression analysis measured candidate-gene expression by reverse-transcription quantitative polymerase chain reaction in pretreatment blood from 12 patients with TN and 12 controls; experimental analyses examined blood and selected tissues from six rats with infraorbital nerve chronic constriction injury (ION-CCI) and six sham-operated rats. Longitudinal behavioral testing characterized the injury model. NIT2, HDHD3, and GRHPR overlapped across the three molecular screens. Colocalization supported NIT2 in the anterior cingulate cortex (PP.H4 = 0.949) and GRHPR in tibial nerve (PP.H4 = 0.818). All three genes showed increased expression in patient blood (all false-discovery-rate q < 0.001). HDHD3 and GRHPR also increased in rat blood (both q = 0.0188), and GRHPR increased in the injured infraorbital nerve (q = 0.0076). Genetically predicted higher GRHPR expression was associated with lower TN risk. Human genetics and cross-species expression analyses identify mitochondrial candidates associated with TN and trigeminal nerve injury. The protective genetic direction and injury-associated expression of GRHPR support a hypothesis of compensatory metabolic adaptation in trigeminal pain.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228195","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":"Failure of Neuroinflammatory Resolution in Brain Aging: Molecular Mechanisms and an Integrative Framework of Microglial Inflammometabolic Locking.","authors":"Xi Zhao, Jiawei He, Wenjing Yu, Han Lin, Qijun He, Zhenyan Song, Shaowu Cheng","doi":"10.1007/s12035-026-06281-1","DOIUrl":"https://doi.org/10.1007/s12035-026-06281-1","url":null,"abstract":"<p><p>Persistent neuroinflammation is a central feature of brain aging and a common pathological context across neurodegenerative diseases. Although microglial activation has been extensively studied, why inflammatory responses in aging brains become increasingly difficult to resolve remains insufficiently understood. In this review, we propose inflammometabolic locking as an evidence-informed working framework describing impaired recovery and declining reversibility of microglial states. Rather than viewing persistent neuroinflammation simply as prolonged activation, the framework emphasizes failure of inflammatory exit and homeostatic re-entry. We integrate current evidence across four interrelated domains: metabolic remodeling, defective lipid handling and post-phagocytic processing, disrupted organelle homeostasis, and persistent transcriptional and epigenetic remodeling. Abnormalities across these domains may become functionally coupled and mutually reinforcing, progressively limiting microglial plasticity and recovery. Their pathological significance therefore depends not only on their presence, but also on whether they resolve as pathological burden declines and whether clearance, repair, and homeostatic functions recover. By distinguishing transient adaptation from locking-like states, this recovery-oriented framework suggests that therapeutic strategies should aim not only to suppress inflammatory output but also to restore microglial recovery capacity. Inflammometabolic locking remains a working hypothesis requiring longitudinal and intervention-based validation.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149238829","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":"Carbon-12 and Gamma-Rays Combined Irradiation Ameliorates Behavioral and Biochemical Alterations in Tau P301S Homozygous Transgenic Mice.","authors":"Viktor S Kokhan, Kseniia V Belokopytova, Vladimir A Pikalov, Denis A Abaimov, Ruslan A Ageldinov, Kirill Chaprov","doi":"10.1007/s12035-026-06283-z","DOIUrl":"https://doi.org/10.1007/s12035-026-06283-z","url":null,"abstract":"<p><p>No effective treatments currently exist for tauopathies. Given emerging evidence that moderate-dose ionizing radiation (IR) may exert neuroreparative effects in neurodegeneration, we investigated the impact of combined IR exposure on disease progression in the Tau P301S mouse model. Tau P301S mice received combined gamma-ray (0.24 Gy) and carbon-12 nuclei (0.18 Gy, 400 MeV/n) irradiation at the presymptomatic stage. Following longitudinal behavioral testing until the terminal stage, post-mortem brains were analyzed via RT-qPCR, ELISA, and HPLC to assess gene expression, protein levels, and monoamine quantification. At the symptomatic stage, Tau+R mice showed normalized endurance, fear-dependent memory, and disinhibition-like behavior, reaching wild-type levels. At the terminal stage, Tau+R mice demonstrated significantly superior balance, coordination, and grip strength compared to untreated Tau P301S mice. These benefits correlated with restored striatal serotonin and a 76% reduction in cerebellar tau protein (transcription-independent). Furthermore, IR normalized Gsk3b expression in the hippocampus and cerebellum, and Trem2 in the cerebellum, to WT levels. Notably, IR up-regulated cerebellar Iba1 by 31% and 86% compared to WT and Tau mice, respectively. Combined radiotherapy not only alleviates behavioral symptoms but also modulates key neurochemical parameters. These findings demonstrate robust symptomatic improvements and suggest a potential neuroprotective capacity of combined radiotherapy in a mouse model of severe tauopathy.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224332","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":"Unraveling Tyrosine Hydroxylase in the Brain of a Crustacean: An Integrative Investigation Using Different Approaches.","authors":"Carlos Augusto Borges de Andrade Gomes, Thyago R Cardim-Pires, Rafaela Rocha Dos Santos, Maria Clara da Costa Simas, Andressa de Abreu Mello, Louise Caroline Vitorino, Paula Grazielle Chaves da Silva, Debora Foguel, Clynton Lourenço Correa, Rosane Silva, Silvana Allodi","doi":"10.1007/s12035-026-06269-x","DOIUrl":"10.1007/s12035-026-06269-x","url":null,"abstract":"<p><p>Tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine (DA) synthesis, is conserved across most animal phyla. DA regulates motor activity, sensory processing motivation, neural homeostasis, and protection against oxidative stress. TH and DA have been described in vertebrates and in some invertebrates, including arthropods. This study investigated the anatomical location of TH and DA and characterized the biochemical and molecular structure of TH in the brain of the mangrove crab Ucides cordatus. This species is a useful environmental model for neurodegeneration studies, due to its occurrence in metal-contaminated mangrove ecosystems, and as prey of other species, including humans. Using immunohistochemistry, immunoblotting, and structural modeling, we mapped TH presence and distribution in the crustacean brain and analyzed its molecular and evolutionary characteristics. Our results revealed a TH fragment structurally similar to fragments found in 21 other species and in a complex dopaminergic network in U. cordatus, characterized by diverse neuronal morphologies, widespread projections, and sensitivity to dopaminergic neurotoxins. These findings may support further studies on catecholaminergic neurobiology.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13683526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228214","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":"Identification of Succinylation-Related Transcriptional Signatures in Alzheimer's Disease: Integrated Bioinformatics Analysis and Clinical Validation.","authors":"Yuanyuan Cheng, Yue Pu, Hong Chen, Ying Ma, Chuanbing Huang, Juan Zhang","doi":"10.1007/s12035-026-06275-z","DOIUrl":"https://doi.org/10.1007/s12035-026-06275-z","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder involving mitochondrial dysfunction, oxidative stress, proteostasis imbalance, and immune-inflammatory alterations. Protein succinylation is closely linked to mitochondrial metabolic status, but peripheral blood transcriptomic signatures related to succinylation in AD remain insufficiently characterized. This study aimed to identify peripheral blood transcriptional candidate biomarkers associated with a predefined succinylation-related gene set in AD. The GSE63061 dataset was used as the discovery cohort, and GSE63060 served as an external validation cohort. Differential expression analysis, ssGSEA-derived succinylation scoring, and WGCNA were integrated with a predefined succinylation-related gene set. Candidate biomarkers were then refined through four feature selection approaches: LASSO, random forest, SVM-RFE, and Boruta, and their discriminatory performance was evaluated by ROC analysis, nomogram construction, calibration analysis, decision curve analysis, and SHAP analysis. Functional enrichment, GSVA/GSEA, GeneMANIA, immune-cell signature analysis, and single-cell analyses were used to explore biological relevance and cellular distribution. qRT-PCR was performed using peripheral blood-derived PBMC samples for experimental validation. Five genes, NDUFA1, NDUFS5, RPS27A, AIF1, and PRDX1, were identified as candidate biomarkers associated with a succinylation-related transcriptional signature in AD. These genes were mainly involved in mitochondrial complex I activity, oxidative phosphorylation, ribosomal function, protein homeostasis, redox balance, and immune inflammation. Immune-cell signatures and single-cell analyses further suggested that the signature was associated with T cells, B cells, NK cells, and monocytes/macrophages. qRT-PCR confirmed significant downregulation of all five genes in AD PBMC samples (P < 0.05). These findings suggest that peripheral blood transcriptional signatures associated with succinylation-related genes may provide candidate biomarkers and hypothesis-generating clues for AD.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224248","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 molecular footprint of valproic acid in human hippocampal organoid.","authors":"Bishwa R Pokharel, Paul P Cook, Shaw M Akula","doi":"10.1007/s12035-026-06260-6","DOIUrl":"10.1007/s12035-026-06260-6","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental condition characterized by neuroinflammation, and disruption in neuronal development. Valproic acid (VPA) is a known environmental risk factor for ASD. Induced pluripotent stem cells (IPSCs IMR90-4)-derived human hippocampal organoids (hHOs) at 60 days of development were used to investigate VPA-induced changes in mRNA and microRNA (miRNA) profiles. The molecular effects of VPA on hHOs were deciphered by meaningfully integrating the ability of miRNA to regulate expression of their predicted mRNA targets crucial to altering neuroinflammatory pathways. Molecular footprint can be defined as the VPA-induced changes to the miRNA profile resulting in coordinated post-transcriptional (mRNA) regulation of neuronal and inflammatory pathways associated with ASD. Based on the results, the molecular footprint of VPA in hHOs was generated for the first time. These findings highlight the contribution of miRNA-mediated regulatory mRNA networks to VPA-induced neuroinflammation-associated with ASD in hHOs.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13680533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224438","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":"Neuroprotective Role of Withaferin A in Huntington's Disease: Current Evidence and Future Perspectives.","authors":"Risha Kumari, Vrinda Gupta, Komal Devi, Diwan Chand, Muralikrishnan Dhanasekaran, Shweta Agarwal","doi":"10.1007/s12035-026-06274-0","DOIUrl":"https://doi.org/10.1007/s12035-026-06274-0","url":null,"abstract":"<p><p>Huntington's disease (HD) is an inherited neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin (HTT) gene. Its pathogenesis involves mutant huntingtin aggregation, impaired proteostasis and autophagy, transcriptional dysregulation, mitochondrial dysfunction, oxidative stress, neuroinflammation and progressive neuronal loss. Withaferin A (WA), a steroidal lactone derived from Withania somnifera, has demonstrated antioxidant, anti-inflammatory, proteostasis-modulating and stress-response effects in experimental studies. In a transgenic HD mouse model, WA-induced heat-shock-response activation was associated with reduced mutant huntingtin aggregation and attenuation of selected disease-related abnormalities. In contrast, evidence for nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) activation, autophagy regulation, mitochondrial protection and suppression of inflammatory signaling is derived predominantly from cellular experiments and non-HD neurological or inflammatory models rather than from validated HD models. The direct relevance of these proposed mechanisms to HD therefore remains to be established. No clinical studies have demonstrated the safety or therapeutic efficacy of WA in individuals with HD. Moreover, its bioavailability, pharmacokinetic behavior, optimal dose, long-term toxicity, central nervous system exposure and possible drug interactions remain insufficiently characterized. This review critically evaluates HD-specific and indirect evidence concerning the neuroprotective actions of WA, identifies important methodological and translational limitations and discusses priorities for future investigation. Current evidence supports WA as an experimental compound for further preclinical study rather than as an established or clinically applicable treatment for HD.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216499","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":"A Review of the Molecular Evidence for Near-Infrared Light in Astrocyte-Mediated Neurorehabilitation.","authors":"Xi Li, Ai Liu, Xing Qi, Dong Li, Duo Liu, Shuwei Liu, Qiji Liu","doi":"10.1007/s12035-026-06273-1","DOIUrl":"https://doi.org/10.1007/s12035-026-06273-1","url":null,"abstract":"<p><p>Near-infrared (NIR) light represents a promising, noninvasive therapeutic for neurological disorders, predicated on its capacity to modulate astrocyte function. As the primary glial population in the central nervous system, astrocytes are indispensable for maintaining neuronal homeostasis, regulating glutamate metabolism, and supporting metabolic energetics. This review synthesizes recent advancements in NIR-driven neurorehabilitation, elucidating the molecular signaling cascades and transduction pathways activated within the astrocytic network. We specifically examine translational applications across preclinical and clinical models of stroke, Alzheimer's disease, epilepsy, and psychiatric disorders. Furthermore, we evaluate how the integration of optogenetic tools and nanomaterials has refined NIR therapies, establishing a foundation for high-precision neurology. Given the rising demand for nonsurgical interventions, this review provides a timely framework for the next generation of photobiomodulation and neural modulation strategies.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":"63 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216490","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}