Neuroprotection最新文献

{"title":"Nicolás Achúcarro: A forgotten architect of glial biology and neuroprotection.","authors":"Carlos Matute, Luis Pacheco","doi":"10.1002/nep3.70051","DOIUrl":"10.1002/nep3.70051","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" ","pages":"306-309"},"PeriodicalIF":4.1,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13394739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148581530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Graded traumatic brain injury severity differentially modulates microglial and astrocytic polarization states and response to minocycline.","authors":"Yan Yu, Chen Wang, Jinyu Zhu, Jiahui Du, Hao Li, Shuyi Ning, Rui Yang, Yiwen Ma, Mengyuan Yuan, Wei Shen, Huailin Wang, Huihui Jiang, Liping Chen, Haitao Wu","doi":"10.1002/nep3.70044","DOIUrl":"10.1002/nep3.70044","url":null,"abstract":"<p><strong>Background: </strong>Traumatic brain injury (TBI) involves complex secondary injury cascades in which neuroinflammation is a prominent driver. The lack of standardized models capturing a spectrum of injury severities has hindered a systematic understanding of the associated cellular and molecular responses. This study aims to systematically characterize the dynamic responses and phenotypic shifts of neurons, microglia, and astrocytes during the acute and subacute phases following TBI of varying severities. By integrating macroscopic histopathological assessments with microscopic cellular analyses and correlating these with early peripheral biomarker changes, we seek to provide a solid experimental foundation for understanding TBI mechanisms and developing severity-stratified diagnostic and therapeutic strategies.</p><p><strong>Methods: </strong>Male mice were randomly assigned using a computer-generated randomization sequence to the following experimental groups: Sham group, mice that underwent only craniotomy (<i>n</i> = 10 per group); Mild group, mice with a 0.5 mm depth impact on the right motor cortex (<i>n</i> = 10 per group); Moderate group, mice with a 1.0 mm depth impact on the right motor cortex (<i>n</i> = 10 per group); Severe group, mice with a 2.0 mm depth impact on the right motor cortex (<i>n</i> = 10 per group). On Days 1, 3, 7, and 14 after injury, tissue damage was assessed using Nissl staining; anxiety-like behavior was evaluated using the elevated plus maze; cognitive function was assessed using the Y-maze test; motor function was evaluated using the open field test, balance beam test, rotarod test, and gait analysis; neuronal apoptosis and glial cell polarization levels were assessed using immunofluorescence staining; and changes in peripheral serum markers were measured using enzyme-linked immunosorbent assay (Elisa). In addition, severely injured mice received minocycline treatment (45 mg/kg, <i>n</i> = 12 per group) from 30 min to Day 3 post-injury, while the control group received the same volume of saline. For comparisons between groups at a single time point, one-way analysis of variance (ANOVA) followed by Tukey's multiple comparisons test was used. For comparisons between groups across multiple time points, two-way ANOVA followed by Tukey's multiple comparisons test was applied.</p><p><strong>Results: </strong>Impact depth was directly correlated with histopathological lesion volume and dictated the trajectory of functional recovery. Motor deficits and neuronal apoptosis scaled with injury severity. The neuroimmune response was severity-dependent: mild TBI triggered a transient, reparative response dominated by M2 microglia and A2 astrocytes. In contrast, severe TBI provoked an early and sustained pro-inflammatory state, characterized by persistent M1 microglial and neurotoxic A1 astrocytic activation (<i>n </i>= 4 per group, <i>p</i> < 0.0001). Furthermore, severe injury led to significant acute elevations","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" ","pages":"275-294"},"PeriodicalIF":4.1,"publicationDate":"2026-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148586303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-Omicron cognitive decline is largely reversible: Two-year multicenter cohort study of domain-specific outcomes in hospitalized patients.","authors":"Min Qiu, Mengwen Wang, Shengcai Chen, Wenbo Zuo, Jiashuo Lin, Luojinyun Wang, Senwei Tan, Quanwei He, Yanan Li, Huijuan Jin, Xuan Niu, Wanli Li, Fengguang Li, Ming Huang, Yan Wan, Bo Hu","doi":"10.1002/nep3.70050","DOIUrl":"10.1002/nep3.70050","url":null,"abstract":"<p><strong>Background: </strong>Cognitive impairment represents a significant concern within the spectrum of post-acute sequelae of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, particularly impacting the aging population. This study aimed to assess the incidence of reversible and irreversible cognitive decline after Omicron infection, identify changes in specific cognitive domains, and determine the risk factors for progressive cognitive decline.</p><p><strong>Methods: </strong>In this multicenter longitudinal cohort, 3419 patients diagnosed with Coronavirus Disease 2019 (COVID-19) between December 2022 and March 2023 from nine hospitals in China were enrolled. Cognitive function was assessed at 6 months and 2 years post-infection using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) and Telephone Interview of Cognitive Status-40 (TICS-40). Domain-specific performance was analyzed, and logistic regression was used to identify risk factors.</p><p><strong>Results: </strong>In total, 2087 patients with COVID-19 completed both the 6-month and 2-year follow-up (1172 [56.2%] men; 915 [43.8%] women; median age 63.0 years [interquartile range]: 53.0-71.0) respectively. Two years after discharge from the hospital, 67.1% (1401/2087) of survivors maintained stable cognitive function, 22.0% (460/2087) of survivors experienced reversible cognitive decline, and 10.8% (226/2087) experienced irreversible cognitive decline (3.6% [76/2087] showed progressive cognitive decline). The profile of recovery or deterioration in cognitive domains involved attention/calculation, executive function, delayed recall, registration, and learning, all of which are multi-dimensional. Age ≥60 years (OR = 4.31, 95% CI [1.47, 12.65]), reinfection (OR = 2.12, 95% CI [1.33, 3.38]), and vaccination doses (OR = 0.69, 95% CI [0.55, 0.87]) were associated with progressive decline.</p><p><strong>Conclusion: </strong>Post-Omicron cognitive decline is largely reversible, with significant recovery observed in key domains including attention/calculation, executive function, delayed recall, registration, and learning. However, a vulnerable subset with risk factors such as older adults, reinfection, and inadequate vaccination, is at risk for progressive cognitive decline. These findings highlight the necessity of targeted long-term monitoring and early intervention for high-risk populations.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" ","pages":"248-261"},"PeriodicalIF":4.1,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148586249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian rhythms and chronotherapy in Alzheimer's disease: Mechanisms and therapeutic implications.","authors":"Bivek Singh, Filippo Pigazzani, Roberto Manfredini","doi":"10.1002/nep3.70046","DOIUrl":"10.1002/nep3.70046","url":null,"abstract":"<p><p>Alzheimer's disease (AD), the most prevalent form of dementia, has been increasingly associated with disruptions in circadian rhythms and sleep-wake regulation. This narrative review synthesizes recent literature on how circadian dysfunction may contribute to AD pathogenesis, biomarker profiles, and treatment response. Mechanistic studies suggest important interactions between core clock genes and neurodegenerative cascades involving oxidative stress, neuroinflammation, glial reactivity, and proteostasis. Disruptions in circadian-regulated molecular pathways, including brain and muscle ARNT-like 1 (<i>BMAL1</i>)-sirtuin 1 (<i>SIRT1</i>), nuclear factor kappa B (<i>NF-κB</i>)-NOD-like receptor family pyrin domain containing 3 (<i>NLRP3</i>), and period circadian regulator 2 (<i>PER2</i>)-antioxidant signaling pathways, may compromise neuronal resilience and worsen AD-related pathology. Emerging evidence also suggests distinct circadian patterns in AD-relevant biomarkers, including melatonin, cortisol, orexin, core body temperature, blood-brain barrier permeability, and glial marker oscillations. These rhythmic patterns may have diagnostic and prognostic relevance and support the need for time-aware biomarker interpretation. Chronotherapeutic strategies targeting circadian biology, including melatonin receptor agonists, light therapy, time-restricted feeding, and circadian-aligned drug delivery systems, may help improve targeted clinical endpoints in AD. This review also discusses chronoepigenetics as an emerging area in which clock-regulated epigenetic modifications may influence neurodegenerative trajectories. Future directions include next-generation chronotherapeutic targets, such as glial clocks, clock-gated inflammatory mechanisms, and systemic comorbidities with circadian modulation, including diabetes and hypertension. Overall, the available evidence supports a close association between circadian disruption and both AD pathology and therapeutic response, while also highlighting important gaps in large-scale clinical trials. This time-oriented perspective may support the development of personalized, biomarker-guided, and rhythm-informed approaches to AD care. By bridging chronobiology and neurodegeneration, this review highlights how circadian precision medicine may refine future approaches to understanding and managing AD.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" ","pages":"229-247"},"PeriodicalIF":4.1,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13398922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148586235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An open-source pipeline for longitudinal single-cell tracking and cell-cycle/migration coupling analysis for neurotherapeutic screening.","authors":"Neha Chandra, Matthew Yang, Hailey Wang, Miroslaw Janowski, Piotr Walczak, Cedric Allier, Yajie Liang","doi":"10.1002/nep3.70047","DOIUrl":"10.1002/nep3.70047","url":null,"abstract":"<p><strong>Background: </strong>Imaging-based phenotypic assays are widely used in neuroprotection, drug discovery, and neurorepair studies, but long-term, high-throughput time-lapse datasets remain difficult to analyze because of segmentation noise, photobleaching, crowded fields, cell division, and tracking errors. Fluorescent ubiquitination-based cell cycle indicator (FUCCI) reporters enable live visualization of cell-cycle phases, but their integration with migration behaviors remains limited. This study aimed to developed an open workflow for tracking cycle and motility.</p><p><strong>Methods: </strong>We combined Fiji/ImageJ preprocessing, Cellpose-based deep learning segmentation, and TrackMate-based cell tracking. FUCCI-expressing HEK293 cells were imaged using a Tecan Spark Cyto (Männedorf, Switzerland) every 15 min for 24 h. Cellpose models were retrained using manually corrected masks from brightfield and fluorescence images, and TrackMate parameters were optimized using manually curated tracks. Statistical analyses were conducted using Paleontological Statistics (PAST) software (version 4.0, Natural History Museum, University of Oslo, Oslo, Norway).</p><p><strong>Results: </strong>Iterative cellpose retraining improved segmentation accuracy in both brightfield and fluorescent datasets by reducing false-positive and false-negative errors (Brightfield Type I error improvement: <i>t</i>(10) = 33.323, <i>p</i> = 1.400 × 10^-11, Brightfield Type II error improvement: <i>t</i>(10) = 16.066, <i>p</i> = 1.805 × 10^-8, Fluorescent Type II errors: <i>U</i> = 0, <i>p</i> = 0.00077). TrackMate optimization improved trajectory continuity, especially through adjustment of frame-to-frame linking distances (Brightfield: <i>χ</i> ² (2) = 10, <i>p</i> = 0.00077, Fluorescent: <i>χ</i> ² (2) = 10, <i>p</i> = 0.00077). The workflow enabled single-cell and population-level analysis of migration distance, turning behavior, morphology, division events, and FUCCI-defined cell-cycle progression. Cells showed heterogeneous motility, with lower displacement trends during green-dominant S/G2/M phases than red-dominant G1 phases.</p><p><strong>Conclusion: </strong>This workflow links cell-cycle state with migration dynamics and can be adapted for neuroprotective screening, neural cultures, organoids, and neuron-glia co-culture studies.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" ","pages":"295-305"},"PeriodicalIF":4.1,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148586196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heparan sulfate and glycomimetics: Advances in synthesis and biological applications for post-stroke neurorepair.","authors":"Mozammel H Bhuiyan, Madeleine J Smith, Simon F R Hinkley, Andrew N Clarkson","doi":"10.1002/nep3.70043","DOIUrl":"10.1002/nep3.70043","url":null,"abstract":"<p><p>Heparan sulfate, a structurally diverse glycosaminoglycan that is abundant in the central nervous system (CNS), orchestrates essential processes fundamental to neural plasticity, neurorepair, and neuroprotection. The ability of heparan sulfate to promote regeneration, in stark contrast to the inhibitory effects of chondroitin sulfate and related glycosaminoglycans, has sparked a growing interest in harnessing heparan sulfate and synthetic glycomimetics for post-stroke neurorepair, as well as numerous other neurodegenerative diseases. However, significant gaps persist in our understanding of how sulfation patterns of heparan sulfate can govern functional outcomes, and major barriers remain for clinical translation. Here, we critically review advances in the synthesis and application of heparan sulfate-based glycomimetics, delineate the mechanistic duality of glycosaminoglycans in CNS diseases, and highlight how new preclinical and emerging clinical data are reshaping prospects for bioengineered extracellular matrix therapies. We identify unresolved challenges in delivery, specificity and efficacy, and propose future research directions to bridge these translational divides.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" ","pages":"213-228"},"PeriodicalIF":4.1,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148586301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Could limb laterality influence the efficacy of remote postischemic conditioning after stroke?","authors":"Hansen Chen, Gary K Steinberg","doi":"10.1002/nep3.70048","DOIUrl":"10.1002/nep3.70048","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" ","pages":"195-198"},"PeriodicalIF":4.1,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148586238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel approaches for neuroprotection: Focus on neurodegenerative and ischemic central nervous system diseases.","authors":"Shen Li, Xunming Ji, Piotr Walczak, Johannes Boltze","doi":"10.1002/nep3.70045","DOIUrl":"10.1002/nep3.70045","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"4 2","pages":"95-98"},"PeriodicalIF":4.1,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13306106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148347429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imaging patterns and genetic associations of brain atrophy across distinct symptom stages in Parkinson's disease.","authors":"Yi Ji, Liujia Lu, Kaidong Chen, Ruixuan Zhang, Yao Lu, Yachen Shi, Xiangming Fang","doi":"10.1002/nep3.70040","DOIUrl":"10.1002/nep3.70040","url":null,"abstract":"<p><strong>Background: </strong>Parkinson's disease (PD) involves progressive gray matter (GM) atrophy, but stage-specific imaging patterns and their genetic mechanisms remain unclear. This study aimed to characterize GM atrophy across PD stages and link these patterns to transcriptional profiles.</p><p><strong>Methods: </strong>A total of 542 patients with PD were obtained from the Parkinson's Progression Markers Initiative (PPMI) database, including early-stage (<2.5 years, <i>n</i> = 192), mid-stage (2.5-5.0 years, <i>n</i> = 235), and late-stage (>5.0 years, <i>n</i> = 115). Structural magnetic resonance imaging data underwent voxel-based morphometry analysis and group differences were assessed using voxel-wise two-sample <i>t</i>-tests with age, sex, and total intracranial volume as covariates, followed by correlation analyses between significant GM clusters and clinical features. Gene expression data from Allen Human Brain Atlas (http://www.brain-map.org) were spatially mapped to imaging patterns with gene-wise Pearson's correlations, as well as a series of enrichment, tissue-specific, and disease-association analyses.</p><p><strong>Results: </strong>Compared to early-stage PD, the mid-stage showed brain GM atrophy in brain regions such as the right angular gyrus, superior temporal gyrus, and middle frontal gyrus (<i>p</i> < 0.05, cluster-level FWE correction). As PD progressed to the late stage, GM atrophy expanded to the left angular gyrus, left temporal pole, middle occipital gyrus, and bilateral posterior cingulate gyrus (<i>p</i> < 0.05, cluster-level FWE correction). Transcriptomic analyses identified 1262 shared genes across all stages, 1222 early-mid-stage-specific genes, and 1847 mid-late-stage-specific genes (<i>p</i> < 0.05, FWE correction). Gene enrichment analysis showed that the three gene sets shared 13 cellular components and 10 biological processes that were enriched in common expression pathways, presenting both shared and specific functional changes at different stages of PD progression.</p><p><strong>Conclusion: </strong>Progressive GM atrophy in PD reflects coordinated but stage-differentiated molecular processes, revealing cellular and genetic architectures underlying disease progression.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" ","pages":"262-274"},"PeriodicalIF":4.1,"publicationDate":"2026-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148586253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prime editing in neuropsychiatric disorders: From mutation-specific target selection to clinical translation.","authors":"Tianshan Ji, Yuan Zhang, Jinyi Zhao, Yiping Lu, Chengkun Wang","doi":"10.1002/nep3.70041","DOIUrl":"10.1002/nep3.70041","url":null,"abstract":"<p><p>Prime editing, a novel clustered regularly interspaced short palindromic repeats (CRISPR)-based technology, fuses a reverse transcriptase (RT) to an engineered CRISPR-associated protein 9 (Cas9) and uses a prime editing guide RNA (pegRNA)-encoded template. It enables precise base substitutions, small insertions, and deletions without introducing double-strand breaks, thereby expanding the range of correctable mutations while reducing undesired repair outcomes. This technology offers a promising strategy for genomic correction in the nervous system. Here, we review the development of prime editing, its mechanistic rationale, and emerging preclinical evidence that supports its application in neuropsychiatric disorders. We discuss key biological and technological barriers, including limited editing efficiency in post-mitotic neurons, complex pegRNA design, reverse transcription-related errors, vector payload limitations, and blood-brain barrier (BBB) penetration. Nevertheless, in vitro and in vivo studies have demonstrated proof-of-concept correction and functional rescue in several monogenic neurodevelopmental disorders. Advances such as split-adeno-associated virus (AAV) systems, lipid nanoparticles, engineered peptides, and compact Cas variants are actively expanding their therapeutic potential. Further clinical translation will rely on improved editors with guide engineering, BBB-penetrant and neuron-targeted delivery platforms, transient or cell-type-specific expression strategies, and comprehensive genome-wide safety evaluations.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148586328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}