Journal of Neuroinflammation最新文献

{"title":"Impaired membrane lipids in ischemic stroke: a key player in inflammation and thrombosis.","authors":"Qian Wang, Dandan Wang, Yan Gao, Jie Jiang, Minghui Li, Shuhui Li, Xiaowen Hu, Jinfeng Wang, Tianqi Wang, Juan Zhang, Lei Feng, Chao Quan, Ping Zhang, Lan Zheng, Chunling Wan","doi":"10.1186/s12974-025-03464-w","DOIUrl":"https://doi.org/10.1186/s12974-025-03464-w","url":null,"abstract":"<p><strong>Background: </strong>Membrane lipids play a crucial role in brain function and cell signalling, and they serve as key biological substrates in inflammatory responses, thrombosis, and energy metabolism. Multiple clinical and molecular evidences suggest that membrane lipids are probably involved in the pathogenesis of ischemic stroke (IS). However, current knowledge about the membrane lipid landscape and its involvement in IS pathophysiology is limited.</p><p><strong>Methods: </strong>We performed untargeted lipidomic analysis on erythrocyte membranes from 56 IS patients and 55 healthy controls. Integrated with gene expression and weighted gene co-expression network analysis, we identified dysregulated lipid signalling pathways and their contributions to IS pathophysiology.</p><p><strong>Results: </strong>A total of 1392 erythrocyte membrane lipids were detected and quantified. Our results revealed significant impairment of membrane lipid homeostasis in IS patients, characterized by a marked reduction in glycerophospholipids (GPLs) and lysophospholipids (LPLs). Further analysis indicated that the impaired lipids were primarily concentrated in three disturbed signalling pathways, including the phospholipase A2-mediated GPL-LPL pathway, the phospholipase C-mediated inositol 1,4,5-trisphosphate/diglyceride pathway, and the sphingosine-1-phosphate (S1P)-S1P receptors pathway. Gene expression results indicated that these pathways were inhibited during the subacute phase of IS. Furthermore, these lipid signalling pathways form a highly interconnected network that collaboratively contributes to inflammation and thrombosis in IS, thereby influencing the progression and prognosis of the disease.</p><p><strong>Conclusion: </strong>Our findings reveal impaired erythrocyte membrane lipid homeostasis in IS, which implicates inflammatory processes and thrombosis in IS. This research offers new insights into the role of membrane lipids in IS pathogenesis, potentially informing future monitoring and therapeutic strategies.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"144"},"PeriodicalIF":9.3,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semaglultide targets Spp1⁺ microglia/macrophage to attenuate neuroinflammation following perioperative stroke.","authors":"Yan Li, Qiuyue Fan, Rui Pang, Ling Cai, Jie Qi, Weijie Chen, Yueman Zhang, Chen Chen, Weifeng Yu, Peiying Li","doi":"10.1186/s12974-025-03465-9","DOIUrl":"10.1186/s12974-025-03465-9","url":null,"abstract":"<p><p>Peripheral surgery evokes neuroimmune activation in the central nervous system and modulates immune cell polarization in the ischemic brain. However, the phenotypic change of microglia and myeloid cells within post-surgical ischemic brain tissue remain poorly defined. Using an integrated approach that combines single-cell RNA sequencing with comprehensive biological analysis in a perioperative ischemic stroke (PIS) model, we identified a distinct Spp1-positive macrophage/microglia (Spp1⁺ Mac/MG) subgroup that exhibit enriched anti-inflammatory pathways with distinct lipid metabolic reprogrammed profile. Moreover, using immunofluorescence staining, we identified the expression of Glucagon-like peptide-1 receptor (GLP1R) in Spp1⁺F4/80⁺ cells and Spp1⁺Iba-1⁺ cells. Intraperitoneal administration of semaglutide, a GLP1R agonist clinically approved for the treatment of type 2 diabetes mellitus, resulted in a significant reduction of cerebral infarct volume in PIS mice compared to that in ischemic stroke (IS) mice. Meanwhile, semaglutide treatment also increased the proportion of Spp1⁺Edu⁺Iba-1⁺ cells 3 days after PIS. Using high-parameter flow cytometry, immunofluorescence staining and RNA sequencing, we demonstrated that semaglutide treatment significantly attenuated the expression of neuroinflammatory markers in mice following PIS. We also found that semaglutide treatment significantly ameliorated sensorimotor dysfunction up to 3 days after PIS in mice. Our current finding reveal a novel protective Spp1⁺Mac/MG subset after PIS and demonstrated that it can be upregulated by semaglutide. We propose that targeting Spp1⁺Mac/MG subsets using semaglutide could serve as a promising strategy to attenuate the exacerbated neuroinflammation in PIS.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"143"},"PeriodicalIF":9.3,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144159481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial TREM-1 mediates sepsis-induced blood‒brain barrier disruption and cognitive impairment via the PI3K/Akt pathway.","authors":"Yuwen Su, Wanwan Zhu, Tong Su, Lian Huang, Mubing Qin, Qingyu Wang, Qi Xu, Yi Li, Jianbo Xiu","doi":"10.1186/s12974-025-03469-5","DOIUrl":"10.1186/s12974-025-03469-5","url":null,"abstract":"<p><p>The blood‒brain barrier (BBB) is a critical selective interface between the central nervous system (CNS) and the blood circulation. BBB dysfunction plays an important role in the neurological damage caused by sepsis. However, the mechanisms underlying the disruption of the BBB during sepsis remain unclear. We established a human induced pluripotent stem cell (iPSC)-derived BBB model and reported that treating with sepsis patient serum leads to structural and functional disruption of the BBB. In a cecal ligation and puncture (CLP)-induced mouse model of sepsis, we also observed disruption of the BBB, inflammation in the brain, and impairments in cognition. In both models, we found that the expression of TREM-1 was significantly increased in endothelial cells. TREM-1 knockout specifically in endothelial cells alleviated BBB dysfunction and cognitive impairments. Further study revealed that TREM-1 affects the expression of genes involved in the PI3K/Akt signaling pathway. The protective effects of TREM-1 inhibition on the BBB and cognition were abrogated by PI3K inhibitors. Our findings suggest that endothelial TREM-1 induces sepsis-induced BBB disruption and cognitive impairments via the PI3K/Akt signaling pathway. Targeting endothelial TREM-1 or the PI3K/Akt signaling pathway may be a promising strategy to maintain BBB integrity and improve cognitive function in sepsis patients.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"142"},"PeriodicalIF":9.3,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144158721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of M. tuberculosis and HIV-1 infection on in vitro blood-brain barrier function.","authors":"Alizé Proust, Katalin A Wilkinson, Robert J Wilkinson","doi":"10.1186/s12974-025-03467-7","DOIUrl":"10.1186/s12974-025-03467-7","url":null,"abstract":"<p><strong>Background: </strong>Tuberculous meningitis is the most severe form of tuberculosis and HIV-1 co-infection worsens the already poor prognosis. However, how Mycobacterium tuberculosis crosses the blood-brain barrier and how HIV-1 influences tuberculous meningitis pathogenesis remains unclear.</p><p><strong>Methods: </strong>Using human pericytes, astrocytes, endothelial cells, and microglia alone and combined in an in vitro blood-brain barrier model, we investigated the effect of Mycobacterium tuberculosis +/- HIV-1 co-infection on central nervous system cell entry and function. Cells and the blood-brain barrier model were infected with Mycobacterium tuberculosis and/or HIV-1 and we evaluated the effects of both infection on (i) cells susceptibility to Mycobacterium tuberculosis and its growth in cells by flow cytometry; (ii) modulation of blood-brain barrier permeability and Mycobacterium tuberculosis passage through it; (iii) viral and bacterial cytopathogenicity using the xCELLigence system; (iv) cell metabolic activity and ROS release using colorimetric assays; (v) extracellular glutamate concentration by fluorometric assay; (vi) the inflammatory response by Luminex; and (vii) endoplasmic reticulum stress by quantitative PCR.</p><p><strong>Results: </strong>We demonstrated that Mycobacterium tuberculosis infects and multiplies in all cell types with HIV-1 increasing entry to astrocytes and pericytes, and growth in HIV-1 positive pericytes and endothelial cells. Mycobacterium tuberculosis also induces an increase of the blood-brain barrier permeability resulting in translocation of bacilli across it. Cytopathic effects include (i) increased markers of cellular stress (mitochondrial metabolic activity, unfolded protein response); (ii) ROS release; (iii) the induction of neurotoxic astrocytes; (iv) and the secretion of the excitotoxic neurotransmitter glutamate. Lastly, we observed distinct cell-type specific production of inflammatory and effector mediators.</p><p><strong>Conclusion: </strong>These results indicate that Mycobacterium tuberculosis can translocate the blood-brain barrier directly to initiate meningitis.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"141"},"PeriodicalIF":9.3,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12107840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Microglial activation contributes to cognitive impairments in rotenone-induced mouse Parkinson's disease model.","authors":"Dongdong Zhang, Sheng Li, Liyan Hou, Lu Jing, Zhengzheng Ruan, Bingjie Peng, Xiaomeng Zhang, Jau-Shyong Hong, Jie Zhao, Qingshan Wang","doi":"10.1186/s12974-025-03458-8","DOIUrl":"10.1186/s12974-025-03458-8","url":null,"abstract":"","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"140"},"PeriodicalIF":9.3,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NLRP3 activation induces BBB disruption and neutrophil infiltration via CXCR2 signaling in the mouse brain.","authors":"Jaeho Lee, Wooyoung Cho, Je-Wook Yu, Young-Min Hyun","doi":"10.1186/s12974-025-03468-6","DOIUrl":"10.1186/s12974-025-03468-6","url":null,"abstract":"<p><p>NLRP3 is an intracellular sensor molecule that affects neutrophil functionality and infiltration in brain disorders such as experimental autoimmune encephalomyelitis (EAE). However, the detailed molecular mechanisms underlying the role of NLRP3 in these processes remain unknown. We found that NLRP3 is crucial for neutrophil infiltration, whereas dispensable for neutrophil priming. Notably, NLRP3 activation in neutrophils induced blood-brain barrier (BBB) disruption and neutrophil infiltration into the brain via CXCL1/2 secretion and subsequent activation of the CXCL1/2-CXCR2 signaling axis. Moreover, CXCL1 and CXCL2 in the inflamed brain directly reduced Claudin-5 expression, which regulates BBB permeability in brain endothelial cells. Furthermore, neutrophil-specific NLRP3 activation aggravated EAE pathogenesis by promoting CXCR2-mediated infiltration of both neutrophils and CD4⁺ T cells into the central nervous system at disease onset. Thus, the CXCL1/2-CXCR2 axis plays a role in EAE progression. Therefore, this chemokine axis could be a potential therapeutic target for attenuating neuroinflammatory diseases through modulating of neutrophil and CD4⁺ T cell infiltration and BBB disruption.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"139"},"PeriodicalIF":9.3,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102932/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota deficiency reduces neutrophil activation and is protective after ischemic stroke.","authors":"Ali A Tuz, Susmita Ghosh, Laura Karsch, Medina Antler, Vivian Lakovic, Sabrina Lohmann, Amber Hope Lehmann, Alexander Beer, Dennis Nagel, Marcel Jung, Nils Hörenbaum, Viola Kaygusuz, Altea Qefalia, Belal Alshaar, Niloufar Amookazemi, Silvia Bolsega, Marijana Basic, Jens T Siveke, Sven Heiles, Anika Grüneboom, Smiths Lueong, Josephine Herz, Albert Sickmann, Nina Hagemann, Anja Hasenberg, Dirk M Hermann, Matthias Gunzer, Vikramjeet Singh","doi":"10.1186/s12974-025-03448-w","DOIUrl":"10.1186/s12974-025-03448-w","url":null,"abstract":"<p><p>Neutrophils are readily activated immune cells after ischemic stroke in mice and patients. Still, the impact of gut microbiota on neutrophil activation and its influence on inflammatory brain injury remain undefined. We report that natural microbiota colonization of germ-free (GF) mice induces substantial neutrophil activation and deteriorates stroke pathology. The colonized Ex-GF stroke mice had considerably larger infarct sizes and higher sensorimotor deficits than GF littermates. Furthermore, employing an antibiotic-based mouse model of microbiota deficiency, we demonstrate that gut microbiota depletion induces a juvenile neutrophil phenotype characterized by the upregulation of resting state surface receptors, reduced inflammatory proteins, and levels of circulating NETs. This disarming of neutrophil responses was associated with decreased expression of brain inflammatory genes, vascular thrombus formation, reduced infarct size, and alleviated behavioral deficits. We conclude that gut microbes strongly influence neutrophil activation after stroke and thus directly contribute to stroke severity.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"137"},"PeriodicalIF":9.3,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12100894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diverse cell types establish a pathogenic immune environment in peripheral neuropathy.","authors":"Julie Choi, Amy Strickland, Hui Qi Loo, Wendy Dong, Lilianne Barbar, A Joseph Bloom, Yo Sasaki, Sheng Chih Jin, Aaron DiAntonio, Jeffrey Milbrandt","doi":"10.1186/s12974-025-03459-7","DOIUrl":"10.1186/s12974-025-03459-7","url":null,"abstract":"<p><p>Neuroinflammation plays a complex and context-dependent role in many neurodegenerative diseases. We identified a key pathogenic function of macrophages in a mouse model of a rare human congenital neuropathy in which SARM1, the central executioner of axon degeneration, is activated by hypomorphic mutations in the axon survival factor NMNAT2. Macrophage depletion blocked and reversed neuropathic phenotypes in this sarmopathy model, revealing SARM1-dependent neuroimmune mechanisms as key drivers of disease pathogenesis. In this study, we investigated the impact of chronic subacute SARM1 activation on the peripheral nerve milieu using single cell/nucleus RNA-sequencing (sc/snRNA-seq). Our analyses reveal an expansion of immune cells (macrophages and T lymphocytes) and repair Schwann cells, as well as significant transcriptional alterations to a wide range of nerve-resident cell types. Notably, endoneurial fibroblasts show increased expression of chemokines (Ccl9, Cxcl5) and complement components (C3, C4b, C6) in response to chronic SARM1 activation, indicating enhanced immune cell recruitment and immune response regulation by non-immune nerve-resident cells. Analysis of CD45⁺ immune cells in sciatic nerves revealed an expansion of an Il1b⁺ macrophage subpopulation with increased expression of markers associated with phagocytosis and T cell activation/proliferation. We also found a significant increase in T cells in sarmopathic nerves. Remarkably, T cell depletion rescued motor phenotypes in the sarmopathy model. These findings delineate the significant changes chronic SARM1 activation induces in peripheral nerves and highlights the potential of immunomodulatory therapies for SARM1-dependent peripheral neurodegenerative disease.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"138"},"PeriodicalIF":9.3,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12100903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elucidating the specific mechanisms of the gut-brain axis: the short-chain fatty acids-microglia pathway.","authors":"Qingyu Cao, Mengmeng Shen, Ruoqiu Li, Yan Liu, Zhen Zeng, Jidong Zhou, Dejun Niu, Quancai Zhang, Rongrong Wang, Jingchun Yao, Guimin Zhang","doi":"10.1186/s12974-025-03454-y","DOIUrl":"10.1186/s12974-025-03454-y","url":null,"abstract":"<p><p>In recent years, the gut microbiota has been increasingly recognized for its influence on various central nervous system diseases mediated by microglia, yet the underlying mechanisms remain unclear. As key metabolites of the gut microbiota, short-chain fatty acids (SCFAs) have emerged as a focal point in understanding microglia-related interactions. In this review, we further refine the connection between the gut microbiota and microglia by introducing the concept of the \"SCFAs-microglia\" pathway. We summarize current knowledge on this pathway, recent discoveries regarding its role in neurological diseases, and potential pharmacological strategies targeting it. Finally, we outlined the current challenges and limitations in this field of research. We hope this review provides new insights into the role of the gut microbiota in neuroimmune regulation.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"133"},"PeriodicalIF":9.3,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12093714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglial dynamics and neuroinflammation in prodromal and early Parkinson's disease.","authors":"Frida Lind-Holm Mogensen, Philip Seibler, Anne Grünewald, Alessandro Michelucci","doi":"10.1186/s12974-025-03462-y","DOIUrl":"10.1186/s12974-025-03462-y","url":null,"abstract":"<p><p>Parkinson's disease (PD) is characterized by a drastic loss of dopaminergic neurons already at diagnosis. As this loss of neurons starts decades before diagnosis, understanding the prodromal stages of the disease might offer novel strategies to curb its progression. While the precise pathogenic mechanisms underlying PD remain incompletely understood, growing evidence suggests that neuroinflammation and immune dysregulation play a central role in the development and progression of the disease. Here, we delve into the emerging roles of microglia, the resident immune cells of the central nervous system, in the pathogenesis of prodromal and early-stage PD. We emphasize that microglia contribute to neuroinflammation, protein aggregation and neurodegeneration, although the underlying mechanisms are not yet known. Neuroimaging studies have provided valuable insights into the patterns of microglial activation detected in individuals with prodromal PD and at the time of clinical diagnosis. Furthermore, we highlight the complex interplay between immune dysregulation and neurodegeneration along PD development, including alterations in the peripheral immune system, brain-gut interactions and brain-immune interfaces. Lastly, we outline existing models for investigating microglial involvement in prodromal PD, along with the impact of anti-inflammatory therapies and strategies to modify risk factors. In conclusion, targeting microglial activation and immune dysfunctions in individuals at risk of PD could represent a promising preventive measure and may offer novel therapeutic strategies for early intervention and disease modification.</p>","PeriodicalId":16577,"journal":{"name":"Journal of Neuroinflammation","volume":"22 1","pages":"136"},"PeriodicalIF":9.3,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}