Clinical and Experimental Neuroimmunology最新文献

{"title":"Efficacy and Safety of Glatiramer Acetate in Japanese Multiple Sclerosis Patients","authors":"Akihito Hao,&nbsp;Yoko Warabi,&nbsp;Kazushi Takahashi","doi":"10.1111/cen3.70014","DOIUrl":"https://doi.org/10.1111/cen3.70014","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Since its approval in Japan in 2015, glatiramer acetate (GA) has been used as a disease-modifying drug (DMD) for relapsing–remitting multiple sclerosis (RRMS). However, there are still few real-world data on its safety and efficacy in Japanese patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The present study aimed to evaluate the clinical safety and efficacy of GA in Japanese patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The present, single-center, retrospective study enrolled patients with RRMS who were admitted to the study center between November 2015 and April 2024 and received GA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Twenty-two patients with RRMS were included. During GA therapy, the median annualized relapse rate and the number of new T2 lesions per year decreased from 0.6 to 0.1 and 1.8 to 0.9, respectively. As a result, nine patients (40.9%) were able to continue the treatment, and 13 patients (59.1%) switched to a different DMD, mostly because GA was ineffective. During the observation period, two of three pregnant subjects continued to receive GA therapy and experienced a safe delivery, while one subject discontinued the treatment. Furthermore, the rate of GA discontinuation due to inefficacy tended to be higher in patients who were positive for oligoclonal IgG bands.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>GA was well tolerated, had few, severe, adverse effects, and was safe for pregnant women. The present study demonstrated the clinical and radiological efficacy of GA in Japanese patients, and approximately 40% of the patients were considered suitable candidates for the treatment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145750512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathogenic Roles of Age-Associated B Cells in Neuromyelitis Optica Spectrum Disorder","authors":"Eiichiro Amano,&nbsp;Wakiro Sato,&nbsp;Takashi Yamamura","doi":"10.1111/cen3.70012","DOIUrl":"https://doi.org/10.1111/cen3.70012","url":null,"abstract":"<div>\u0000 \u0000 <p>Age-associated B cells (ABCs), initially identified in aged mice, are a distinct B cell subset that plays crucial roles in autoimmune diseases through the production of autoantibodies, proinflammatory cytokines, and antigen presentation. Although a definitive set of markers for identifying ABCs has not yet been established, they are commonly characterized by the expression of CD11c, CD11b, and the transcription factor T-bet, along with reduced levels of CD21, either alone or in combination. ABC differentiation is driven by Toll-like receptor 7 (TLR7) signaling in conjunction with cytokines such as interleukin-21 (IL-21) and interferon-gamma (IFNγ). Importantly, ABCs expand in the blood or inflamed tissues and exhibit pathogenic functions in various autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome, Crohn's disease, axial spondyloarthritis, Grave's disease, and multiple sclerosis. Recently, ABCs have been implicated in neuromyelitis optica spectrum disorder (NMOSD), a chronic inflammatory astrocytopathy mediated by anti-AQP4 antibody-producing B cells characterized by relapses and remissions. In the acute phase, CD21^lo B cells can differentiate into anti-AQP4 antibody-producing cells and expand in both cerebrospinal fluid and blood. In the chronic phase, an increased frequency of CD11c^hi B cells in the blood correlates with chronic neurological damage or brain injury. T peripheral helper type 1 cells, which produce IFNγ and IL-21, may support ABC differentiation in both phases. This review explores the role of ABCs in NMOSD, highlighting key studies that link ABC subsets to disease pathology. Understanding ABC-mediated mechanisms in NMOSD may open avenues for novel therapeutic strategies.</p>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 3","pages":"198-207"},"PeriodicalIF":0.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulmonary Nodular Lymphoid Hyperplasia in a Case of Overlapping Neuromyelitis Optica Spectrum Disorder and Myasthenia Gravis","authors":"Masashi Higashino,&nbsp;Juichi Fujimori,&nbsp;Takanobu Sasaki,&nbsp;Takafumi Sugawara,&nbsp;Fumiyoshi Fujishima,&nbsp;Kimihiko Kaneko,&nbsp;Ichiro Nakashima","doi":"10.1111/cen3.70013","DOIUrl":"https://doi.org/10.1111/cen3.70013","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Anti-aquaporin 4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (NMOSD) is a neuroinflammatory autoimmune astrocytopathy. While the precise mechanism of autoantibody production has not been completely elucidated, most AQP4-IgG is believed to originate in the peripheral lymphoid tissue.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>Herein, we present a rare case of overlapping anti-AQP4 antibody-positive NMOSD and anti-acetylcholine receptor (anti-AChR) antibody-positive myasthenia gravis (MG), incidentally accompanied by pulmonary nodular lymphoid hyperplasia (NLH), a condition also observed in several cases with Sjögren's syndrome.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The present case suggests that NLH, which may have been overlooked, can be found in NMOSD and MG. Although NLH was not considered a source of pathological autoantibodies, further analysis is required to clarify whether NLH is involved in the pathogenesis of chronic inflammatory conditions.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathogenic Role of Age-Associated B Cells in Autoimmune Disorders and Myasthenia Gravis","authors":"Hiroyuki Akamine,&nbsp;Akiyuki Uzawa","doi":"10.1111/cen3.70011","DOIUrl":"https://doi.org/10.1111/cen3.70011","url":null,"abstract":"<p>Age-associated B cell (ABC) is a distinctive B cell subset characterized by CD11c and T-bet expression that accumulates with aging and in autoimmune conditions. This review summarizes current understanding of ABCs in the immunological function and autoimmune pathogenesis of autoimmune diseases, including myasthenia gravis (MG). ABCs arise when B cells are stimulated via B cell receptors and innate immune receptors (notably TLR7/9), in the presence of cytokines secreted by Th1 cells. ABCs behave as antigen-presenting cells, secrete inflammatory cytokines, and can differentiate into antibody-secreting cells. In autoimmune disorders, ABCs are thought to undergo expansion, efficiently present self-antigens to T cells, generate inflammatory mediators, and contribute to autoantibody production. Contemporary single-cell transcriptomic investigations of MG patients experiencing myasthenic crisis have identified clonally expanded ABC-like populations. These cells potentially contribute to MG pathogenesis through multiple mechanisms: enhancing T cell activation, sustaining autoreactive plasma cell development, and producing inflammatory cytokines. The increased number of ABCs in late-onset MG suggests a link between aging and autoimmunity. Targeting ABC development may be a useful treatment approach for antibody-mediated autoimmune diseases such as MG. Understanding ABCs helps explain how aging affects autoimmunity.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 3","pages":"194-197"},"PeriodicalIF":0.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.70011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782559","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":"Correction to “Human Monocyte-Derived Microglia-Like (iMG) Cells: A Tool to Explore Microglial Dynamics”","authors":"","doi":"10.1111/cen3.70010","DOIUrl":"https://doi.org/10.1111/cen3.70010","url":null,"abstract":"<p>S. Kyuragi, S. Inamine, M. Ohgidani, and T. A. Kato, “Human Monocyte-Derived Microglia-Like (iMG) Cells: A Tool to Explore Microglial Dynamics,” <i>Clinical and Experimental Neuroimmunology</i> 15, no. 4 (2024): 222–227. https://doi.org/10.1111/cen3.12815.</p><p>The above article was published under the article category “Review Article.” This has been updated with the correct article category “Invited Review.”</p><p>We apologize for this error.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.70010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144782803","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":"Clinical and Radiological Advances in Autoimmune GFAP Astrocytopathy: Analysis of 387 Patients in Japan","authors":"Akio Kimura","doi":"10.1111/cen3.70007","DOIUrl":"https://doi.org/10.1111/cen3.70007","url":null,"abstract":"<div>\u0000 \u0000 <p>Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy (GFAP-A) is an autoimmune inflammatory central nervous system disease. Recent neuropathological findings indicate that GFAP-specific cluster of differentiation (CD)8⁺ T cells are likely the effectors of GFAP-A. Of 387 individuals in Japan identified as having GFAP-A, most presented with headache and/or fever followed by neurological symptoms including consciousness disturbance, urinary dysfunction, hyperreflexia, movement disorders, and papilledema. Sixteen (5.9%) of the 270 GFAP-A patients tested had coexisting antibodies. Cerebrospinal fluid (CSF) examination revealed lymphocytic pleocytosis and increased protein levels. Moreover, transiently increased CSF adenosine deaminase, decreased glucose, and positive oligoclonal band results were sometimes observed. Brain magnetic resonance imaging (MRI) occasionally showed T2-hyperintensity lesions. Linear perivascular radial gadolinium-enhancement patterns were observed and may be an imaging hallmark of GFAP-A. Spinal cord MRI sometimes exhibited T2-hyperintensity spinal cord lesions, most of which were longitudinally extensive. Most patients were treated with immunotherapies, including intravenous methylprednisolone pulse therapy with or without intravenous immunoglobulin therapy and/or plasma exchange; this was followed by oral corticosteroid therapy, which was gradually tapered. Some refractory patients received second-line immunotherapies including rituximab or cyclophosphamide. In 203 patients with follow-up ≥ 6 months, the median modified Rankin scale score at last follow-up was 1 (range: 0–6); however, 44 patients (21.7%) had scores of 3 or greater, and six patients died. The most common neurological finding at last follow-up was cognitive dysfunction, followed by urinary dysfunction; the recurrence rate was 10.5%. CSF GFAP-immunoglobulin G should be examined in patients who present with these characteristic clinical and radiological features.</p>\u0000 <p>\u0000 <b>Trial Registration:</b> Autoimmune GFAP astrocytopathy registry (UMIN: 000054387).</p>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 2","pages":"174-187"},"PeriodicalIF":0.0,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the Mysteries of Rare Neuroimmunological Disorders","authors":"Yoshihisa Yamano","doi":"10.1111/cen3.70009","DOIUrl":"https://doi.org/10.1111/cen3.70009","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 2","pages":"148"},"PeriodicalIF":0.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Disease-Modifying Treatments in Japanese Patients With Multiple Sclerosis During the Coronavirus Disease 2019 Pandemic","authors":"Taisuke Ogawa,&nbsp;Juichi Fujimori,&nbsp;Daisuke Kikuchi,&nbsp;Ichiro Nakashima","doi":"10.1111/cen3.70008","DOIUrl":"https://doi.org/10.1111/cen3.70008","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Most disease-modifying treatments (DMTs) for patients with multiple sclerosis (PwMS) do not influence the risk and outcome of coronavirus disease (COVID-19), except for anti-CD20 monoclonal antibodies (ocrelizumab and rituximab). However, data on Japanese PwMS are lacking. Thus, we evaluated the risk of COVID-19 in Japanese PwMS undergoing DMTs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this retrospective cross-sectional study, we used the Japanese administrative database. The incidence of COVID-19 between January 1, 2022, and December 31, 2024 was compared between PwMS who were administered different DMTs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In total, 61 of 1044 (5.8%) PwMS who were administered baseline treatments and 102 of 1253 (8.1%) PwMS who were administered high-efficacy treatments had COVID-19. The prevalence of COVID-19 was significantly higher in PwMS receiving high-efficacy treatments than in those receiving baseline treatments. However, this prevalence did not differ significantly among PwMS on different individual DMTs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Although high-efficacy therapy may increase the overall prevalence of COVID-19, no specific DMT approved in Japan was associated with an increased prevalence of COVID-19 among Japanese PwMS.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Concentration-Dependent Increase in the Expression of Junctional Adhesion Molecule-A in Brain Microvascular Endothelial Cells in Response to Proinflammatory Cytokines and Hyperthermic Decrease in the Expression of Vascular Endothelial Cadherin in These Cells","authors":"Tomohiro Matsui,&nbsp;Yuji Mochiduki","doi":"10.1111/cen3.70006","DOIUrl":"https://doi.org/10.1111/cen3.70006","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The mechanisms underlying therapeutic hypothermia, which protects neurons after severe brain damage, are not completely understood. Based on a previous study, hypothermia reduced the release of tumor necrosis factor (TNF)-α and interleukin (IL)-17. Meanwhile, hyperthermia promoted the release of TNF-α and IL-17. Leukocyte transmigration via the endothelium is mediated by endothelial cell junctional molecules, such as junctional adhesion molecule (JAM)-A and vascular endothelial cadherin (VE-cadherin), positively and negatively, respectively. In the ischemic brain, the diapedesis of leukocytes into the tissues results in enhanced postischemic brain inflammation and intensified brain injury. The current study aimed to evaluate the mechanisms underlying this treatment by assessing the effects of TNF-α and IL-17 on brain microvascular endothelial cell (BMVEC) junctional molecule and the effects of hypothermia and hyperthermia on its expression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The expression of JAM-A and VE-cadherin, which are BMVEC junctional molecules, was measured at the protein level via immunocytochemistry.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>TNF-α and IL-17 increased the expression of JAM-A in BMVECs in a concentration-dependent manner. Compared with normothermia, hypothermia did not affect the expression of JAM-A and VE-cadherin in BMVECs stimulated with TNF-α or IL-17. Meanwhile, hyperthermia reduced the basal expression of VE-cadherin in BMVECs, with this expression being further reduced by stimulation with IL-17.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The hypothermic suppression of TNF-α and IL-17 release may decrease JAM-A expression in BMVECs. Meanwhile, hyperthermia itself may decrease VE-cadherin expression in BMVECs. The former may contribute to suppressing, while the latter may promote, leukocyte extravasation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoimmune cerebellar ataxia: An overlooked, but treatable, neuroimmune condition","authors":"Hiroaki Yaguchi,&nbsp;Akihiko Kudo,&nbsp;Ichiro Yabe","doi":"10.1111/cen3.70004","DOIUrl":"https://doi.org/10.1111/cen3.70004","url":null,"abstract":"<p>Autoimmune cerebellar ataxia (ACA) is a condition in which the cerebellum is the primary location of inflammation due to autoimmune encephalitis caused by neuroimmune conditions. Although ACA is rare, it remains an important differential diagnosis, distinct from other neurodegenerative conditions, such as multiple system atrophy. An accurate diagnosis requires the integration of clinical history, blood tests, cerebrospinal fluid analysis, magnetic resonance imaging and malignancy screening. Over 30 neural antibodies associated with ACA have been reported as diagnostic biomarkers. The clinical profile of frequently reported antibodies, such as anti-Yo and anti-GAD, are well-defined, although that of rarer antibodies remain unclear. Cell-based assays are the standard method for detecting most neural antibodies, but testing for a wide range of antibodies is costly. Immunoblots assays and tissue-based assays are useful for screening. Further investigations into clinical profiles and advancements in screening methods are required to identify neural antibodies. ACA should not be overlooked, due to its treatable nature. Acute phase treatments, such as intravenous methylprednisolone and immunoglobulin, plasma exchange, and rituximab, are effective. Maintenance therapy using steroids and/or immunosuppressants is used to prevent relapse and progression. However, maintenance therapy requires individualized decisions due to limited clinical evidence. Additionally, treatment responses might vary depending on the type of neural antibody. In the future, the development of biomarkers and improved autoantibody testing methods is important to develop novel therapies and optimal immunotherapy for patients with ACA.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"16 2","pages":"161-173"},"PeriodicalIF":0.0,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}