Neuroprotection最新文献

{"title":"Role of astrocyte in neuroinflammation-induced loss in neuroplasticity and subsequent onset of depression: A systematic review.","authors":"Gaurav Singhal, Saurabh Singhal, Bernhard T Baune","doi":"10.1002/nep3.70009","DOIUrl":"10.1002/nep3.70009","url":null,"abstract":"<p><p>Major depressive disorder (MDD) is a complex psychiatric condition increasingly linked to chronic neuroinflammation, particularly in the context of aging, stress, and systemic comorbidities. While microglia have traditionally been the focus of neuroimmune studies, growing evidence highlights astrocytes as central regulators in the pathogenesis of MDD. This review synthesizes current findings on the multifaceted roles of astrocytes in neuroplasticity, neurotransmission, metabolic support, and blood-brain barrier regulation. It explores how astrocyte reactivity and the release of pro-inflammatory cytokines are often triggered by psychosocial stress, aging, and peripheral immune activation and contribute to synaptic dysfunction and cognitive impairment. The review also examines the bidirectional crosstalk between astrocytes and microglia, astrocytic calcium signaling, epigenetic modulation via histone lactylation, and metabolic pathways involving lactate. Special attention is given to the region-specific and phenotype-dependent responses of astrocytes, as well as their influence on the onset and maintenance of depressive symptoms. Additionally, therapeutic strategies targeting astrocyte-mediated pathways, including anti-inflammatory agents, metabolic modulators, repetitive transcranial magnetic stimulation, and inflammasome inhibitors, are discussed. Finally, methodological challenges and future research directions are outlined, emphasizing the need for precision medicine approaches in developing astrocyte-targeted interventions for MDD.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 3","pages":"206-225"},"PeriodicalIF":4.1,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12699557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145758658","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":"History of pre-eclampsia negatively impacts stroke severity postpartum in rats.","authors":"Ari Kropf, Jennifer L Anderson, Milena Esposito, Sarah M Tremble, Marilyn J Cipolla","doi":"10.1002/nep3.70002","DOIUrl":"10.1002/nep3.70002","url":null,"abstract":"<p><strong>Background: </strong>Preeclampsia (PE) is a serious hypertensive disorder of pregnancy that has lifelong deleterious effects, including increased risk of stroke postpartum (PP). Here we determined if previous PE exacerbates ischemic injury in the PP period and investigated underlying mechanisms including oxidative stress and collateral perfusion.</p><p><strong>Methods: </strong>Female Sprague-Dawley rats were studied at 4-9 months PP, after either a normal pregnancy (NormP-PP <i>n</i> = 7) or experimental PE (ePE) induced via high cholesterol diet during gestation (ePE-PP <i>n</i> = 9). Animals underwent transient middle cerebral artery occlusion (tMCAO) for 2 hours with 1 hour reperfusion. Dual-site laser Doppler flowmetry measured changes in cerebral blood flow (CBF) in the MCA and collateral territories. Ischemic injury was measured by 2,3,5-triphenyl tetrazolium chloride staining. Circulating 8-isoprostane, 3-nitrotyrosine (3-NT), and oxidized low-density lipoprotein (oxLDL) were measured by enzyme-linked immunosorbent assays. In separate groups of animals, NormP-PP (<i>n</i> = 10) and ePE-PP (<i>n</i> = 9) that were 3-4 months PP, isolated pial collateral vessels, leptomeningeal anastomoses (LMAs), and mesenteric arteries were studied using pressure myography.</p><p><strong>Results: </strong>Previous ePE pregnancy worsened stroke outcome in the PP state, significantly increasing infarction in ePE-PP vs. NormP-PP animals (40.6 ± 7.6% vs. 13.7 ± 6.5%; <i>p</i> <0.01) and edema (5.1 ± 2.0% vs. 2.6 ± 0.4%; <i>p</i> < 0.01), despite comparable changes in CBF in both MCA and pial collateral territories during ischemia and reperfusion. When infarction was analyzed as a function of perfusion deficit, ePE-PP animals had greater sensitivity to ischemia. Pial collaterals had increased pressure-induced myogenic tone vs. NormP-PP rats. Percent tone at 80 mmHg for ePE-PP vs. NormP-PP was 15.5 ± 1.6% vs. 8.6 ± 1.9% (<i>p</i> <0.01). In addition, ePE-PP animals had significantly elevated circulating 8-isoprostane and 3-NT, but not oxLDL, after tMCAO (*<i>p</i><0.05 and **<i>p</i><0.01, respectively).</p><p><strong>Conclusions: </strong>We found worsened stroke outcome after ePE pregnancy that was related to increased sensitivity to ischemia, increased pial collateral tone, and elevated levels of oxidative stress markers. Thus, the pathologic effects of ePE persisted PP and negatively impacted stroke outcome.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 2","pages":"172-182"},"PeriodicalIF":4.1,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12377490/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981674","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":"Targeting gut microbiota as a therapeutic approach for neurodegenerative diseases.","authors":"Tobiloba S Olajide, Omamuyovwi M Ijomone","doi":"10.1002/nep3.70000","DOIUrl":"10.1002/nep3.70000","url":null,"abstract":"<p><p>Recent evidence suggests a more important role of the gut microbiota in neurodegenerative diseases (NDDs) given its relationship through the microbiota-gut-brain as an active communication system aiding in maintaining homeostasis between the brain and the gut. This review focuses on how modulation of gut microbiota can serves as a therapeutic strategy for NDDs, emphasizing the neuroprotective effects of probiotics. Probiotics are live microorganisms that confer health benefits, and their interaction with gut-microbiota influences neurogenesis, neurotransmitter regulation, and neuroinflammation. Recent advancements, including germ-free animal models, fecal microbiota transplantation (FMT), and diverse probiotic strains, have revealed the underlying mechanisms linking gut health to brain function. Notably, several <i>Lactobacillus</i> and <i>Bifidobacterium</i> species have been shown to exert neuroprotective effects via the upregulation of neurotrophic factors such as brain-derived neurotrophic factor and enhancing mitochondrial function through reducing the impacts of oxidative stress. Interestingly, FMT has exhibited a degree of success in overcoming cognitive impairment and motor deficits in preclinical studies and clinical trials. However, further research is warranted to explore its therapeutic potential in humans. Overall, this review highlights the significant role of gut microbiota in NDDs and advocates for gut-targeted interventions as innovative approaches to mitigate these diseases.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 2","pages":"120-130"},"PeriodicalIF":4.1,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12208687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144531466","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":"How pandemics reshape our brain: Common links and targets between long-haul COVID-19, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), oxidative stress, and neurodegeneration.","authors":"Mary E Herman","doi":"10.1002/nep3.70007","DOIUrl":"10.1002/nep3.70007","url":null,"abstract":"<p><p>Fatiguing syndromes affect millions of patients in the United States and globally, but are grossly underserved in the clinic and in the contemplative design of basic research.Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex multisystem metabolic-immune-inflammatory disorder. Although research on this condition is in its infancy, it appears to involve the immune system and central nervous system malfunction, with cellular oxidative stress as a predominant feature.Approximately half of the cases of long-haul coronavirus disease 2019 meet the diagnostic criteria for ME/CFS, burgeoning the number of affected individuals.Recent strides in neurobiology have yet to transfer the understanding of the neurodegenerative aspects, and potential for neuroprotection, of ME/CFS.ME/CFS may represent a useful paradigm and research model for the study of the impact of sustained oxidative stress on the central nervous system and the body at large.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 3","pages":"280-287"},"PeriodicalIF":4.1,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12699542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145758633","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":"Mitochondrial transfer as a novel therapeutic approach in ischemic stroke treatment: Current challenges and future perspectives.","authors":"Shuchen Meng, Min Bai, Changsheng Ma, Bo Han, Mengyuan Duan, Liying Zhang, Jinfen Guo, Changku Shi, Ke Li, Maotao He","doi":"10.1002/nep3.70004","DOIUrl":"10.1002/nep3.70004","url":null,"abstract":"<p><p>Ischemic stroke, the second leading cause of human mortality, presents a formidable challenge to healthcare. Following ischemic insult, the brain undergoes intricate pathological transformations, prominently marked by mitochondrial damage, including swelling, fission, and mitophagy, collectively termed mitochondrial quality control disorder. Mitochondria, pivotal in energy regulation and oxidative stress modulation, play a critical role in neuronal apoptosis post-stroke. To solve the problems caused by mitochondrial quality control disorders, mitochondrial transfer has become a new therapeutic strategy for central nervous system diseases. Mitochondrial transfer refers to the process by which certain cell types export their mitochondria and pass them on to other cell types, a process also known as intercellular mitochondrial transfer. Mechanistically, mitochondrial transfer occurs via tunneling nanotubes, extracellular vesicles, and free mitochondrial transfer, exerting multifaceted effects such as anti-inflammatory, anti-lipid peroxidation, ferroptosis modulation, and enhancement of mitochondrial metabolism. This review explores the therapeutic efficacy, current obstacles, and future prospects of mitochondrial transfer in ischemic stroke, offering insights to researchers and instilling hope in patients for conquering this debilitating condition.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 3","pages":"253-265"},"PeriodicalIF":4.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12699545/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145758638","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":"Vitamin E for intraventricular hemorrhage prevention in preterm neonates: A systematic review and meta-analysis.","authors":"Felipe Araujo Gouhie, Ana Clara Nogueira Cezar, Davi Alves Silva, Beatriz Rizzo Parreira, Larissa Ferreira Machado, Laura Caroline Felipe de Freitas, Paulo Roberto da Silva Lucena Patriota","doi":"10.1002/nep3.70005","DOIUrl":"10.1002/nep3.70005","url":null,"abstract":"<p><strong>Background: </strong>Some research suggests that vitamin E may help prevent intraventricular hemorrhage (IVH) in preterm neonates. However, consolidated evidence regarding its effects on brain vascular health in this population is lacking. This study systematically reviews primary research on this topic. This study examines the effectiveness of vitamin E supplementation in preventing IVH in preterm neonates than a placebo, thus addressing gaps in the literature.</p><p><strong>Methods: </strong>The Cochrane, Dimensions, Embase, and PubMed databases were searched for relevant studies based on specific inclusion criteria. Subsequently, the relevant data were extracted, and statistical analysis was conducted using R studio (version 4.3.1) by applying appropriate models to account for heterogeneity and generate a combined estimate. The results were interpreted considering potential biases and limitations.</p><p><strong>Results: </strong>Five studies involving 554 patients were included. Among them, 274 (49.45%) received vitamin E. The results (relative ratio 0.57; 95% confidence interval 0.35-0.92; <i>p</i> = 0.02; <i>I</i> ² = 56%) demonstrated a reduction in the incidence of IVH in patients who received administration of vitamin E (<i>n</i> = 274) compared with those who received a placebo (<i>n</i> = 280).</p><p><strong>Conclusion: </strong>These findings highlight the potential therapeutic benefits of vitamin E supplementation in preterm neonates, which show a significant reduction in IVH incidence than placebo. Further research and clinical trials are required to fully explore its protective effects in this population.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 2","pages":"165-171"},"PeriodicalIF":4.1,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486940/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745992","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":"The role of gut microbiota-derived metabolites in neuroinflammation.","authors":"Lingjie Mu, Yijie Wang","doi":"10.1002/nep3.70001","DOIUrl":"10.1002/nep3.70001","url":null,"abstract":"<p><p>Neuroinflammation, a key defense mechanism of the nervous system, is associated with changes in inflammatory markers and stimulation of neuroimmune cells such as microglia and astrocytes. Growing evidence indicates that the gut microbiota and its metabolites directly or indirectly regulate host health. According to recent studies, bacterial dysbiosis in the gut is closely linked to several central nervous system disorders that cause neuroinflammation, including multiple sclerosis, Alzheimer's disease, Parkinson's disease, sepsis-associated encephalopathy, and ischemic stroke. Recent findings indicate a bidirectional communication network between the gut microbiota and central nervous system that influences neuroinflammation and cognitive function. Dysregulation of this system can affect the generation of cytotoxic metabolites, promote neuroinflammation, and impair cognition. This review explores the lesser-studied microbiota-derived metabolites involved in neuroinflammation-bile acids, trimethylamine-N-oxide, and indole derivatives-as targets for creating new treatment tools for neuroinflammatory illnesses, as well as possible biomarkers for early diagnosis and prognosis.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 2","pages":"131-144"},"PeriodicalIF":4.1,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746006","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":"Protecting the brain from multifaceted damage and promoting recovery.","authors":"Piotr Walczak, Xunming Ji, Shen Li, Johannes Boltze","doi":"10.1002/nep3.70003","DOIUrl":"10.1002/nep3.70003","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 1","pages":"1-4"},"PeriodicalIF":4.1,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12020454/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144046042","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":"Unravelling the nexus of stroke and dementia: Deciphering the role of secondary neurodegeneration in orchestrating cognitive decline.","authors":"Shannon M Stuckey, Rebecca J Hood, Lin Kooi Ong, Isabella M Bilecki, Lyndsey E Collins-Praino, Renée J Turner","doi":"10.1002/nep3.74","DOIUrl":"10.1002/nep3.74","url":null,"abstract":"<p><p>Stroke is the leading cause of acquired disability. The development of acute ischemic stroke treatments, such as mechanical thrombectomy and tissue plasminogen activator, has resulted in more patients surviving the initial insult. However, long-term complications, such as post-stroke cognitive impairment (PSCI) and dementia (PSD), are at an all-time high. Notably, 80% of stroke survivors suffer from cognitive impairment, and a history of stroke doubles a patient's lifetime risk of developing dementia. A combination of greater life expectancy, an increase in the number of strokes in young individuals, and improved survival have inherently increased the number of years patients are living post-stroke, highlighting the critical need to understand the long-term effects of stroke, including how pathological changes in the brain might give rise to functional and behavioral changes in stroke survivors. Even with this increased risk of PSCI and PSD in stroke survivors, understanding of how the stroke itself develops into these conditions remains incomplete. Recently, secondary neurodegeneration (SND) following stroke has been linked with PSCI and PSD. SND is the degeneration of brain regions outside the original stroke site. Degeneration in these sites is thought to arise due to functional diaschisis with the infarct core; however, observation of SND pathology in multiple regions without direct connectivity to the stroke infarct suggests that the degeneration in these regions is likely more complex. Moreover, pathological hallmarks of dementia, such as a deposition of neurodegenerative proteins and iron, cell death, inflammation and blood-brain barrier alterations, have all been found in regions such as the thalamus, hippocampus, basal ganglia, amygdala and prefrontal cortex following stroke. Hence, in this review, we present the current understanding of PSCI and PSD in the context of SND and outline how remote anatomical and molecular changes may drive the development of these conditions.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 1","pages":"5-28"},"PeriodicalIF":4.1,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745987","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":"Advancing neuroprotection and atherosclerosis prevention through familial hypercholesterolemia management: Analyzing comorbidity burden with stroke, coronary heart disease, hypertension, and diabetes.","authors":"Jingjia Wang, Sicong Liu, Ming Zhang, Xiangbin Meng, Xuliang Wang, Wenyao Wang, Jun Gao, Jilin Zheng, Zhiyun Yang, Jun Wen, Da Liu, Lin Yang, Chen Wei, Siyan Zhan, Pei Gao, Chunli Shao","doi":"10.1002/nep3.72","DOIUrl":"10.1002/nep3.72","url":null,"abstract":"<p><strong>Background: </strong>Despite the World Health Organization's prioritization of familial hypercholesterolemia (FH), its global diagnostic rate remains critically low, leading to inadequate treatment and control, thereby increasing the risk of atherosclerotic cardiovascular disease. This study aimed to investigate the comorbidity burden of FH in China and analyze the differences between familial and general hypercholesterolemia (HC) populations.</p><p><strong>Methods: </strong>Using a national medical insurance database from 2013 to 2017 including 13,976 patients with FH and 13,976 matched control patients with HC, we utilized case-control methods to compare the composition ratio, comorbidity rates, medical expenses, and healthcare burden of patients with FH to those of control patients.</p><p><strong>Results: </strong>The FH population had a higher comorbidity rate of more than one cardiometabolic disease (83.7% [11,697/13,976]) compared to the HC group (70.3% [9279/13,976]; <i>χ</i>² = 250.45, <i>p</i> < 0.0001). The rates of coronary heart disease, hypertension, stroke, and diabetes were higher in patients with FH (39.2% [5475/13,976], 71.0% [9925/13,976], 14.2% [1982/13,976], and 31.2% [4363/13,976], respectively) compared to those in the HC group (30.4% [4255/13,976], 61.4% [8587/13,976], 11.5% [1601/13,976], and 28.1% [3923/13,976], respectively; all <i>p</i> < 0.0001). In the 40-49 age group, patients with FH had a significantly higher average number of comorbidities compared to control patients with HC (1.2 vs. 0.9; <i>t</i>  = 15.67, <i>p</i> < 0.0001). Notably, the comorbidity count in patients with FH aged 40-49 years even exceeded that in patients with HC aged 50-59 years. Furthermore, the annual per capita medical cost for patients with FH was significantly higher at 5045.5 Chinese yuan (CNY) compared to 4184.7 CNY for patients with HC (<i>t</i> = 12.54, <i>p</i> < 0.0001).</p><p><strong>Conclusion: </strong>With a large number of patients with dyslipidemia, the type and number of comorbidities significantly impact the healthcare burden. FH presents with earlier onset, more comorbidities, and heavier cardiovascular-related medical burdens than HC. Early identification, intervention, and comprehensive management of comorbidities in the FH population are crucial for neuroprotection and prevention of atherosclerotic cardiovascular disease.</p>","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"3 1","pages":"95-103"},"PeriodicalIF":4.1,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745953","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}