Frontiers in Molecular Neuroscience最新文献

{"title":"SH3BP2 deficiency in skeletal muscle leads to neuromuscular junction abnormalities and decreased muscle strength.","authors":"Bhola Shankar Pradhan, Krzysztof M Bernadzki, Yauhen Bandaruk, Anna Siudzińska, Teresa De Cicco, Małgorzata Sotomska, Marta Gawor, Margareta Jabłońska, Joanna Krzemień, Grzegorz Chodaczek, Said Hashemolhosseini, Tomasz J Prószyński","doi":"10.3389/fnmol.2026.1985823","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1985823","url":null,"abstract":"<p><p>Assembly and stabilization of a high density of acetylcholine receptors (AChRs) at the neuromuscular junction postsynaptic domain is fundamental for proper synaptic transmission. Here, we report the identification of a scaffold protein, SH3BP2, that exhibits polyvalent and direct interactions with the dystrophin-glycoprotein complex (DGC) and AChR pentamers. Loss-of-function experiments in cultured myotubes revealed that SH3BP2 promotes formation of AChR assemblies in muscle cells. Similarly, muscle-specific deletion of SH3BP2 in mice impairs AChR clustering during embryonic development and causes multiple neuromuscular junction morphological and ultrastructural abnormalities in adult animals. Mutant mice also exhibit defects in synaptic transmission, muscle strength, and general fitness. Our study identifies a novel role for SH3BP2 in modulating the neuromuscular junction in skeletal muscles.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1985823"},"PeriodicalIF":4.4,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13677847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tissue-specific peripheral sensory remodeling in chronic low back pain: established and emerging nociceptive niches.","authors":"Yizhuan Huang, Han Wang","doi":"10.3389/fnmol.2026.1972635","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1972635","url":null,"abstract":"<p><p>Chronic low back pain arises from heterogeneous peripheral and central mechanisms, yet the sensory biology of individual lumbar tissues is rarely considered within a unified framework. This Mini Review compares peripheral sensory remodeling and sensitization across four candidate nociceptive niches: the intervertebral disc, vertebral endplate, thoracolumbar fascia, and paraspinal muscle. Disc pathology is characterized by nociceptive ingrowth, endplate pathology by osteochondral sensory remodeling and afferent sensitization, and thoracolumbar fascia by inflammation-associated remodeling of a pre-existing sensory network. Paraspinal muscle remains an emerging sensory-inflammatory niche in which muscle-spindle remodeling is distinct from unproven nociceptor remodeling. Across tissues, recurrent neurotrophic, inflammatory, neuropeptide, and mechanosensory mediators indicate molecular overlap but do not establish functional convergence within common sensory circuits. Dorsal root ganglia and the spinal dorsal horn are therefore considered candidate sites of downstream integration. We propose a dynamic multi-niche model with testable predictions for identifying active niches, tracking shifts in tissue contribution, and distinguishing causal nociceptive mechanisms from incidental degeneration. Future spatial, longitudinal, and epigenomic studies may enable molecular definition of active pain-generating states and mechanism-guided treatment.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1972635"},"PeriodicalIF":4.4,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multimodal assessment of NIBS-induced adaptive plasticity in aging prefrontal networks: ERP and cognitive evidence.","authors":"Davide Crivelli, Michela Balconi","doi":"10.3389/fnmol.2026.1954473","DOIUrl":"10.3389/fnmol.2026.1954473","url":null,"abstract":"<p><p>Non-invasive brain stimulation may enhance age-sensitive executive functions by modulating task-engaged prefrontal networks, but behavioral effects remain heterogeneous and their physiological specificity is poorly understood. This pre-post study examined neuropsychological and electrophysiological responses to cognitive training paired with active or sham transcranial direct current stimulation (tDCS) over the dorsolateral prefrontal cortex. Thirty-three older adults were randomly assigned to active tDCS plus cognitive training, sham tDCS plus cognitive training, or wait-list control. Training groups completed 24 sessions across 8 weeks. Before and after intervention, participants underwent neuropsychological assessment and EEG recording during a Stroop-like task; N2 amplitude and latency were extracted at F3, Fz, and F4. Linear mixed-effects models tested Group × Time effects. Significant interactions emerged for non-verbal executive functions and associative fluency, with improvements confined to the active-tDCS group. Other cognitive measures improved over time without group-specific effects. Active tDCS selectively increased N2 amplitude in correspondence to the stimulated site, whereas no comparable change occurred after sham stimulation or in controls. These findings suggest that repeated right-prefrontal tDCS may specifically support higher-order executive functions and induce selective modulation near the stimulation site. Physiological measures may help clarify the anatomical and functional specificity of NIBS-related modulation.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1954473"},"PeriodicalIF":4.4,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13668833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Olfactory dysfunction and submicroscopic abnormalities: unveiling hidden pathologies.","authors":"Katarzyna Bilińska, Magdalena Pasińska, Fernando de Castro","doi":"10.3389/fnmol.2026.1861373","DOIUrl":"10.3389/fnmol.2026.1861373","url":null,"abstract":"<p><p>Recent advances in high-resolution genomic technologies have revealed that several syndromes are associated with submicroscopic chromosomal deletions and, less frequently, duplications, thereby substantially contributing to the functional annotation of the human genome. Among these structural variants, recurrent microdeletions or microduplications often disrupt dosage-sensitive genes, leading to shared phenotypic outcomes in affected individuals. While features such as congenital heart defects, neurodevelopmental delays, and intellectual disability (ID) have been extensively studied, phenotypes resulting in olfactory dysfunction remain largely underexplored. Here, we review reported cases of copy number variants (CNVs) in patients with isolated or syndromic olfactory impairment and stratify the strength of associations between CNVs and olfactory dysfunction using predefined evidence levels. The available evidence ranges from well-supported <i>loci</i> with documented human olfactory phenotypes and mechanistic evidence to hypothesis-generating observations based primarily on isolated cases or biological plausibility. By distinguishing these levels of evidence, we highlight both established dosage-sensitive pathways involved in olfactory development and major limitations of the current literature, including incomplete olfactory phenotyping and the difficulty of interpreting large multigenic CNVs. This framework may facilitate more rigorous genotype-phenotype interpretation in congenital and syndromic olfactory disorders.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1861373"},"PeriodicalIF":4.4,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149181131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial dysfunction and PANoptosis-related signaling in acute central nervous system injuries: mechanistic convergence and therapeutic opportunities.","authors":"Hongbo Zhang, Ruoxin Tu, Dawei Zhang, Hao Tian, Hongna Yin","doi":"10.3389/fnmol.2026.1982074","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1982074","url":null,"abstract":"<p><p>Acute central nervous system (CNS) injuries comprise a heterogeneous group of disorders caused by vascular or traumatic factors, including ischemic stroke, intracerebral hemorrhage (ICH), traumatic brain injury (TBI), and spinal cord injury (SCI). These injuries initiate secondary cascades that combine metabolic failure, oxidative stress, neuroinflammation, and regulated cell death. Mitochondrial dysfunction is positioned near the center of these processes because impaired bioenergetics, excessive mitochondrial reactive oxygen species (mtROS), abnormal fission and fusion, defective mitophagy, and mitochondrial DNA (mtDNA) release can simultaneously disturb cellular homeostasis and activate inflammatory signaling. PANoptosis is an inflammatory form of regulated cell death that integrates pyroptotic, apoptotic, and necroptotic machinery through PANoptosome complexes. Emerging evidence suggests that mitochondrial stress can create conditions that favor PANoptotic convergence by increasing mtROS and damage-associated molecular patterns (DAMPs), activating DNA-sensing and inflammasome pathways, and sustaining receptor-interacting protein kinase and caspase signaling. This review examines the potential mechanistic links between mitochondrial dysfunction and PANoptosis-related signaling across ischemic stroke, ICH, SCI, and TBI. We summarize changes in mitochondrial bioenergetics, oxidative stress, dynamics, mitophagy, mitochondria-derived vesicles (MDVs), and mitochondrial transfer, and evaluate how these changes intersect with PANoptosis-related signaling. Importantly, we distinguish direct evidence of PANoptosis from studies that only demonstrate coordinated changes in individual death pathways. We also assess therapeutic strategies that target mitochondrial oxidative stress, dynamics, mitophagy, biogenesis, mitochondrial DAMP signaling, and mitochondrial transplantation and transfer. Current findings support mitochondria as a promising upstream intervention point, but complete causal evidence linking mitochondrial damage to defined PANoptosome assembly remains limited in acute CNS injury. Clarifying cell-specific and time-dependent mechanisms will be essential for translating this framework into effective neuroprotective strategies.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1982074"},"PeriodicalIF":4.4,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149192668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Prenatal and neonatal housing conditions affect anxiety-like behavior in adulthood in rats and interact with brain-derived neurotrophic factor (BDNF) Val66Met to alter expression of BDNF and stress markers in the ventral hippocampus.","authors":"Maarten van den Buuse, Michelle Corrone, Emily J Jaehne, Veronica Begni, Alessia Marchesin, Marco A Riva","doi":"10.3389/fnmol.2026.1992919","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1992919","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fnmol.2026.1844602.].</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1992919"},"PeriodicalIF":4.4,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13656404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149181155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From dynamic condensates to pathological assemblies: the phase behavior of tau and <i>α</i>-synuclein.","authors":"Suelen Camargo, Kevin Novelo, Scott D Ryan","doi":"10.3389/fnmol.2026.1965177","DOIUrl":"https://doi.org/10.3389/fnmol.2026.1965177","url":null,"abstract":"<p><p>Neurons rely on precise protein folding, trafficking, and turnover to maintain synaptic function. Disruption of proteostasis promotes misfolded proteins that impair axonal transport, mitochondrial function, and signalling, contributing to neuronal loss. Although neurodegeneration has traditionally focused on stable amyloid deposits, many disease-associated proteins contain intrinsically disordered regions (IDRs) that can organize through liquid-liquid phase separation (LLPS). LLPS concentrates proteins and nucleic acids into dynamic condensates that regulate cellular processes, but these adaptive interactions can also promote condensate aging and less reversible, aggregation-prone states. Here, we review how sequence-encoded properties of tau and α-synuclein (α-syn) link physiological condensation to pathological protein assembly, while emphasizing that LLPS and amyloid formation are related but not obligatorily linked.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1965177"},"PeriodicalIF":4.4,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond development: LINX/Islr2 expression and TrkA interaction in the adult nervous system under neuroinflammatory challenge.","authors":"Pamela Rosso, Elena Fico, Viviana Triaca, Annamaria Di Criscio, Ari-Pekka Koivisto, Katja Kuokkanen, Mikko Ares, Kaisa Auvinen, Andrii Domanskyii, Johanna Kela, Carina Stenfors, Paola Tirassa","doi":"10.3389/fnmol.2026.1863350","DOIUrl":"10.3389/fnmol.2026.1863350","url":null,"abstract":"<p><strong>Introduction: </strong>LINX, also known as immunoglobulin superfamily containing leucine-rich repeat 2 (Islr2), was identified as a TrkA pathway component and demonstrated to modulate the NGF/TrkA-mediated axonal growth, guidance, and branching during development. However, there is limited information on LINX expression in the adult nervous system, and the possible functions of LINX in mature neurons remain unexplored. These two questions are addressed by the present study, which first investigates LINX expression in the adult spinal cord (SC), dorsal root ganglia (DRG), and cerebral cortex (Cx), and subsequently explores LINX/TrkA functions using the DRG organ culture model.</p><p><strong>Methods: </strong>Different commercially available anti-LINX antibodies were tested, and the most selective antibody was used to investigate LINX expression in the SC, Cx, and DRG of healthy rats, and to explore the LINX/TrkA action in DRG organ cultures using a model of neuroinflammation/injury induced by lipopolysaccharides (LPS). The LINX/TrkA interaction was demonstrated by immunoprecipitation in the Cx of healthy and LPS-treated rats. The DRG from healthy and LPS-treated rats were dissected and cultured in the presence of anti-LINX, with or without stimulation using NGF, and a TrkA selective inhibitor. TrkA phosphorylation levels and the expression of the axonal growth marker GAP43 were analyzed by bio-molecular assays and confocal immunofluorescence microscopy.</p><p><strong>Results: </strong>The WB analysis shows that LINX is expressed in the adult central and peripheral nervous systems, and the immunoprecipitation analysis demonstrates LINX and TrkA interaction in the Cx of both adult healthy and LPS-treated rats. <i>In vitro</i> experiments using an LPS-DRG model confirm the association between LINX and TrkA. However, it was found that while anti-LINX administration abolishes the effects of NGF and TrkA activation in LPS-DRG, it results in GAP43 increase in the presence of a TrkA inhibitor.</p><p><strong>Discussion: </strong>Our study confirms that LINX is expressed in the adult central nervous system and demonstrates that the LINX/TrkA interaction is maintained following LPS-induced systemic inflammation. Moreover, our findings that antibody-mediated perturbation of endogenous LINX is associated with the modulation of axonal growth markers in adult LP-DRG cultures, in serum-free conditions and/or in the presence of a TrkA inhibitor, suggest a potential role for LINX in regulating neurotrophin-dependent responses in injured adult neurons.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1863350"},"PeriodicalIF":4.4,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Garlic-derived bioactive components in neuropathic pain: molecular mechanisms and therapeutic promise.","authors":"Asif Ali, Sorimuthu Revathi, Koilmani Emmanuvel Rajan, Chin Kun Wang, Subramanian Thangaleela","doi":"10.3389/fnmol.2026.1886063","DOIUrl":"10.3389/fnmol.2026.1886063","url":null,"abstract":"<p><p>Neuropathic pain is a chronic condition associated with maladaptive changes in nociceptive pathways, driven by oxidative stress, mitochondrial impairment, neuroinflammation, ion channel dysfunction, and apoptotic dysregulation. Current pharmacological therapies often provide limited relief but with adverse effects highlighting the need for more safer therapeutic approaches. Garlic (<i>Allium sativum</i>) and its bioactive organosulfur compounds including allicin, S-allyl cysteine, diallyl disulfide, diallyl trisulfide have gained increasing attention for their neuroprotective potential. This review summarizes the mechanistic role of garlic-derived compounds in neuropathic pain modulation, focusing on their antioxidant, anti-inflammatory, anti-apoptotic, and mitochondrial-stabilizing properties. These bioactives regulate key signaling pathways such as NF-κB, Nrf2/HO-1, PI3K/Akt, and JNK, while also modulating TRPV1 and TRPA1 ion channels involved in nociception and central sensitization furthermore, garlic compounds enhance endogenous antioxidant defense, preserve mitochondrial bioenergetics, and inhibit caspase-mediated neuronal apoptosis, thereby contributing to neuroprotection. Despite promising preclinical evidence, challenges such as variability in garlic preparations, limited clinical studies, and insufficient pharmacokinetic data remain. Overall, garlic-derived compounds represent a promising complementary strategy for neuropathic pain management, warranting further standardized clinical investigations to validate their therapeutic efficacy and safety.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1886063"},"PeriodicalIF":4.4,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13643696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tanshinone IIA and sodium tanshinone IIA sulfonate in ischemic stroke: evidence, exposure, and translational readiness.","authors":"Aiyue Fan, Weiting Chen, Min Tang, Yangtian Ye, Yaling Jin","doi":"10.3389/fnmol.2026.1959038","DOIUrl":"10.3389/fnmol.2026.1959038","url":null,"abstract":"<p><p>Ischemic stroke remains a major cause of death and long-term disability despite reperfusion therapy. Tanshinone IIA (Tan IIA), a lipophilic diterpene quinone, and sodium tanshinone IIA sulfonate (STS), its water-soluble sulfonated derivative, show broad activity in experimental cerebral ischemia. They are often treated as interchangeable despite differences in formulation and exposure. We critically reviewed representative pharmacological, preclinical, formulation, and clinical evidence through 28 July 2026. We distinguished active entity, formulation, causal support, replication, exposure linkage, treatment window, and patient-centered relevance. Reported effects span oxidative and mitochondrial injury, endothelial barrier failure, neuroinflammation, regulated cell death, metabolism, and repair. Most pathway claims, however, rely on single laboratories, early dosing, young healthy rodents, short follow-up, or surrogate outcomes. Human evidence comprises one 42-patient STS-plus-rt-PA trial and a 2025 meta-analysis of 22 trials involving 2,289 participants. These findings suggest short-term signals but do not establish benefits for ordinal disability, survival, recurrent stroke, or uncommon bleeding. An injectable product and human plasma pharmacokinetic methods make STS more operationally tractable; superior efficacy remains unproven. Progression should require a fixed product, exposure-linked target engagement, durable benefit in aged and comorbid reperfusion models, and independent multicenter validation. Biological plausibility remains substantially stronger than translational readiness.</p>","PeriodicalId":12630,"journal":{"name":"Frontiers in Molecular Neuroscience","volume":"19 ","pages":"1959038"},"PeriodicalIF":4.4,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13643747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}