Clinical and Experimental Neuroimmunology最新文献

{"title":"Absolute Counts of Circulating T Follicular Helper Cell Subsets in Acute-Phase AQP4-IgG–Positive Neuromyelitis Optica Spectrum Disorder","authors":"Takafumi Hosokawa,&nbsp;Hideto Nakajima,&nbsp;Manami Matsushita,&nbsp;Takahiro Akamatsu,&nbsp;Shoji Ogawa,&nbsp;Shin Ota,&nbsp;Hiroko Tanada,&nbsp;Shigeki Arawaka","doi":"10.1111/cen3.70084","DOIUrl":"https://doi.org/10.1111/cen3.70084","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease characterized by pathogenic anti-aquaporin-4 (AQP4) antibodies. Previous studies have shown increased circulating T follicular helper (cTfh) cells and altered Tfh subset frequencies in NMOSD, but the absolute counts of Tfh subsets remain unclear. We evaluated relative frequencies and absolute counts of cTfh subsets in acute-phase AQP4-IgG–positive NMOSD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This retrospective single-center study included 12 patients with AQP4-IgG–positive NMOSD and seven disease controls. Flow cytometry assessed the frequency of cTfh cells among CD4⁺ T cells, the relative frequencies of Tfh1, Tfh2, and Tfh17 subsets, and their absolute counts. Acute-phase NMOSD was compared with chronic-phase NMOSD and disease controls.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The frequency of cTfh cells among CD4⁺ T cells was significantly higher in acute-phase NMOSD than in chronic-phase NMOSD (15.7% vs. 12.7%, <i>p</i> = 0.026) and disease controls (15.7% vs. 12.2%, <i>p</i> = 0.012). Neither the relative frequencies of Tfh1, Tfh2, and Tfh17 subsets nor the (Tfh2 + Tfh17)/Tfh1 ratio differed significantly between groups. However, the absolute Tfh1 count was significantly higher in acute-phase NMOSD than in chronic-phase NMOSD (72.5 vs. 30.7 cells/μL, <i>p</i> = 0.034), whereas the absolute Tfh2 count was significantly higher than that in disease controls (50.5 vs. 32.4 cells/μL, <i>p</i> = 0.038).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Acute-phase AQP4-IgG–positive NMOSD is characterized by a higher absolute Tfh1 count than chronic-phase NMOSD and a higher absolute Tfh2 count than disease controls, together with an increased cTfh frequency, despite unchanged relative Tfh-subset frequencies and an unchanged (Tfh2 + Tfh17)/Tfh1 ratio. Analysis of absolute cTfh-subset counts may complement conventional assessments based on relative Tfh-subset frequencies and the (Tfh2 + Tfh17)/Tfh1 ratio, providing additional insight into the immunopathogenesis of NMOSD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.70084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149205896","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":"Are Adolescent Dimethyl Fumarate Outcomes Obscured by Broad Age Categories?","authors":"Ercan Yılmaz","doi":"10.1111/cen3.70086","DOIUrl":"https://doi.org/10.1111/cen3.70086","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149146305","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":"Progressive Multifocal Leukoencephalopathy Mimicking Relapse of Anti-GABAB Receptor Encephalitis After Rituximab-Containing Immunotherapy: A Case Report","authors":"Tomohide Ando,&nbsp;Nobuaki Yoshikura,&nbsp;Akio Kimura,&nbsp;Keiko Tanaka,&nbsp;Kazuo Nakamichi,&nbsp;Takayoshi Shimohata","doi":"10.1111/cen3.70083","DOIUrl":"https://doi.org/10.1111/cen3.70083","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Rituximab is widely used as second-line therapy for autoimmune encephalitis; however, progressive multifocal leukoencephalopathy (PML) after rituximab-containing immunotherapy for autoimmune encephalitis has not been reported.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>An 82-year-old woman with anti-GABA_B receptor encephalitis was treated with immunotherapy including rituximab. Six months later, she developed progressive neurological deterioration. MRI showed new white matter lesions suggestive of PML, and CSF JC virus (JCV) PCR was positive. Retrospective review revealed that a small right frontal lesion had already appeared 1 month after rituximab, when ultrasensitive CSF JCV PCR remained below the detection limit.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>To our knowledge, this is the first reported case of PML after immunotherapy for autoimmune encephalitis. PML should be considered when neurologic deterioration or new white matter lesions emerge after rituximab-containing immunotherapy, even when initial CSF JCV PCR is negative.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149146203","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":"Post-Immune Checkpoint Inhibitor Paraneoplastic Syndrome Presenting With a Longitudinally Extensive Lesion Confined to the Dorsal Columns of the Spinal Cord","authors":"Hiroaki Yokote,&nbsp;Kageaki Watanabe,&nbsp;Yoshiharu Miura","doi":"10.1111/cen3.70082","DOIUrl":"https://doi.org/10.1111/cen3.70082","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048522","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":"Sequential and Concurrent C5 and Neonatal Fc Receptor Inhibition in Prolonged Myasthenic Crisis due to Advanced Invasive Thymoma-Associated Myasthenia Gravis: A Case Report and Literature Review","authors":"Yuta Kizuka,&nbsp;Yuriko Nakamura,&nbsp;Kensuke Okada,&nbsp;Yu Okubo,&nbsp;Kaoru Kaseda,&nbsp;Hirofumi Toyama,&nbsp;Keisuke Asakura,&nbsp;Atsuya Takeda,&nbsp;Jin Nakahara,&nbsp;Kei Ishizuchi","doi":"10.1111/cen3.70080","DOIUrl":"https://doi.org/10.1111/cen3.70080","url":null,"abstract":"<p>Thymoma-associated myasthenia gravis (TAMG) is frequently refractory, particularly when complicated by myasthenic crisis in advanced invasive disease. Complement C5 inhibitors and neonatal Fc receptor (FcRn) inhibitors have expanded the treatment of acetylcholine receptor (AChR) antibody-positive generalized myasthenia gravis; however, their optimal selection, sequencing, and combined use in refractory TAMG remain undefined. We report a case of a 46-year-old man with Masaoka–Koga stage IVa invasive thymoma and pleural dissemination who developed a prolonged ventilator-dependent myasthenic crisis after debulking surgery. Immunoadsorption plasmapheresis, intravenous immunoglobulin, and ravulizumab produced only transient benefit. Serum complement activity became undetectable after ravulizumab was switched to zilucoplan (a peptide C5 inhibitor chosen because it is not affected by FcRn blockade), yet sustained respiratory stability was not achieved. Only after subcutaneous efgartigimod was added to ongoing zilucoplan did the patient attain sustained daytime ventilator independence, with a parallel decline in anti-AChR antibody titer and total immunoglobulin G. He was discharged and remained clinically stable, with no worsening during a subsequent mild infection. Reviewing this case together with previously reported patients who received concurrent or sequentially overlapping C5 and FcRn inhibition, we discuss the biological rationale for dual-pathway targeting, pharmacological considerations relevant to agent selection and sequencing, and infectious-safety implications. This temporal association does not establish efficacy; however, combined C5 and FcRn inhibition may be considered, on an individualized basis, in selected refractory TAMG cases when single-pathway therapy is insufficient.</p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.70080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048273","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":"Chimeric Antigen Receptor T-Cell Therapy in Multiple Sclerosis: Rationale, Mechanisms, and Clinical Perspectives","authors":"Raghavi Nagabhushan Malepati,&nbsp;Vansh Patel,&nbsp;Aken Kayastha,&nbsp;Praveen Nandha Kumar,&nbsp;Rucha Bahekar,&nbsp;Aashray Raj,&nbsp;Yusuf Kagzi,&nbsp;Muthu Kuzhali Ganapathy,&nbsp;Shitiz Sriwastava","doi":"10.1111/cen3.70081","DOIUrl":"https://doi.org/10.1111/cen3.70081","url":null,"abstract":"<div>\u0000 \u0000 <p>To systematically review the emerging clinical evidence on CAR-T cell therapy in adults with multiple sclerosis, including relapsing–remitting and progressive phenotypes, with particular emphasis on safety, clinical outcomes, biological effects, and evidence of CNS activity. Multiple Sclerosis is a progressive neuroinflammatory disease caused due to autoimmune assault on the central nervous system. Despite the earliest description being found in the 14th century, the autoimmune nature of MS was only confirmed in the 1960s. The discovery of Interferon Beta-1b, a DMT, was revolutionary in reducing the frequency of exacerbations in MS. However, there remains a lacuna in the treatment of MS that focuses on neuroprotection and remyelination. CAR-T cell therapy is a rapidly evolving treatment to combat the neurodegeneration in this autoimmune disease. Systematic search up to March 2026 was conducted across PubMed and Google Scholar. A total of 1046 records were identified, of which 36 were assessed for eligibility and 10 studies were inducted. Quantitative synthesis was not suitable considering the early-stage nature of the data. Data was extracted methodically into a standardized table format. Results were interpreted descriptively with consideration of study design limitations and consistency of reported outcomes. A total of 32 patients were treated with CAR-T cell therapy. CRS was the most frequently reported adverse event, occurring in 15 of 24 patients with reported multiple sclerosis-specific CRS status (62.5%). ICANS was suspected in one patient (1/26, 3.8%). EDSS improvement was reported in 8 of 12 evaluable patients (66.7%). Peripheral B-cell depletion was consistently reported across evaluated cohorts, including complete depletion in all four patients in the BreakFree-2 cohort. Evidence of CNS penetration was reported in 13 patients across four cohorts. Current targets for CAR-T cell therapy include CD-19 and BCMA. All studies showed an admissible safety profile, encouraging further exploration of this therapy. Favorable clinical outcomes suggest possibility of combating neurodegeneration. Peripheral B-cell depletion implies possible chances of immune reconstitution. However, longer follow up periods are required to note long term effects and efficacy. All the studies were case reports or Phase 1 trials, further investigation is needed to fully understand and implement the usage of CAR-T therapy in MS.</p>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048188","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":"Beyond Thymectomy: Optimizing Perioperative Immunotherapy to Prevent Postoperative Myasthenic Crisis (POMC)","authors":"Abeer Khalid","doi":"10.1111/cen3.70079","DOIUrl":"https://doi.org/10.1111/cen3.70079","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148942814","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":"Bidirectional Neuro-Immune Interactions of the Orexin/Hypocretin System: A Systematic Review With Conceptual Synthesis","authors":"Jean Claude Hakizimana,&nbsp;Zephyrin Izukwizabigenza,&nbsp;Marie Gorette Kampire,&nbsp;Joseph Mucumbitsi,&nbsp;Abdullateef Isiaka Alagbonsi","doi":"10.1111/cen3.70078","DOIUrl":"https://doi.org/10.1111/cen3.70078","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Beyond regulating sleep, the orexin/hypocretin system participates in bidirectional neuro-immune interactions that may influence neurodegenerative diseases (NDs) and chronic inflammatory conditions. This systematic review aimed to conceptually synthesize evidence on these interactions and their clinical implications.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Following PRISMA 2020 guidelines, a comprehensive search was performed in PubMed, Embase, Web of Science, Scopus, and PsycINFO. Studies were included if they reported original empirical data (human, animal, or in vitro) examining orexin signaling in relation to cytokines, microglial activation, or neuroinflammation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of 1248 records screened, 18 studies (three human, 13 animal, two in vitro/ex vivo) were included. Human studies, albeit limited, showed consistent suppression of the immune-to-orexin signaling: an 11-fold increase in CD4⁺ T cells was observed specifically in the hypocretin region in NT1 brains; peripheral LPS reduced orexin neuron activity, and lower orexin-A levels correlated with elevated pro-inflammatory cytokines and worse cognitive/fatigue outcomes in epilepsy, depression, and Sjögren's syndrome. Conversely, preclinical studies showed that orexin-to-immune signaling demonstrated consistent anti-inflammatory effects. Orexin-A shifted microglia toward an anti-inflammatory phenotype, inhibited key pathways (NF-κB, ERK, NEK7/NLRP3), reduced cytokines (IL-1β, IL-6, TNF-α), and attenuated astrogliosis across models of intracerebral hemorrhage, chronic hypoperfusion, sepsis-associated encephalopathy, experimental autoimmune encephalomyelitis, and gut-brain inflammation. Sex- and region-specific effects were noted.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Inflammation generally suppresses orexin signaling, while orexin-A signaling exerts predominantly anti-inflammatory effects by modulating microglial phenotype and key inflammatory pathways. These bidirectional interactions highlight the orexin system as a potential bridge between sleep dysregulation and neuroinflammation. However, most evidence on orexin-to-immune signaling derives from preclinical models, and significant gaps remain in human mechanistic studies and clinical translation on immune-to-orexin signaling. Orexin receptor agonists warrant further investigation as candidate adjunctive therapies in neurodegenerative and chronic inflammatory conditions.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148942291","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":"Myelin Oligodendrocyte Glycoprotein Antibody-Associated Optic Neuritis With Perineuritis Treated With Immunoadsorption Plasmapheresis in a 91-Year-Old Woman: A Case Report","authors":"Isamu Takai,&nbsp;Yuji Tomizawa,&nbsp;Yasunobu Hoshino,&nbsp;Chikage Kijima,&nbsp;Natsumi Takemura,&nbsp;Naoto Arawaka,&nbsp;Rei Iwamoto,&nbsp;Eitaro Yoshida,&nbsp;Takashi Kyomoto,&nbsp;Kazumasa Yokoyama,&nbsp;Shintaro Nakao,&nbsp;Taku Hatano","doi":"10.1111/cen3.70077","DOIUrl":"https://doi.org/10.1111/cen3.70077","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Myelin oligodendrocyte glycoprotein antibody-associated disease can occur in older adults, but onset in nonagenarians is uncommon. In this age group, acute or subacute visual loss often requires differentiation from ischemic, diabetic retinal, and glaucomatous disorders.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>A 91-year-old woman presented with subacute bilateral visual loss over 9 days. Ophthalmological examination showed severe bilateral visual impairment, optic disc edema, and visual field constriction. Serum myelin oligodendrocyte glycoprotein antibodies were positive. Contrast-enhanced orbital magnetic resonance imaging showed bilateral optic nerve enlargement, optic nerve sheath enhancement, and perineural inflammatory changes. Temporal artery ultrasonography showed no halo sign. High-dose intravenous methylprednisolone followed by oral prednisolone led to limited visual recovery. Further corticosteroid exposure was undesirable because of poorly controlled diabetes. Immunoadsorption plasmapheresis was performed under close monitoring, and visual function improved without bleeding or hemodynamic complications. Delayed corticosteroid effects cannot be excluded, but immunoadsorption plasmapheresis may be an option when further corticosteroid exposure is undesirable in very elderly patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This case describes the diagnostic and therapeutic management of myelin oligodendrocyte glycoprotein antibody-associated optic neuritis with perineuritis in a nonagenarian. Immunoadsorption plasmapheresis may be considered in selected elderly patients when corticosteroid response is insufficient or further corticosteroid exposure is clinically difficult.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148807735","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":"Concurrent Hashimoto Encephalopathy and Papillary Thyroid Carcinoma: Separate Diagnostic Pathways, Shared Clinical Vigilance","authors":"Yun-Han Yang,&nbsp;Lien-Chung Wei","doi":"10.1111/cen3.70076","DOIUrl":"https://doi.org/10.1111/cen3.70076","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148752763","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}