Journal of Central Nervous System Disease最新文献

{"title":"The impact of interaction between verteporfin and yes-associated protein 1/transcriptional coactivator with PDZ-binding motif-TEA domain pathway on the progression of isocitrate dehydrogenase wild-type glioblastoma.","authors":"Mahmoud Osama,&nbsp;Muhammed Amir Essibayi,&nbsp;Mona Osama,&nbsp;Ismail A Ibrahim,&nbsp;Mostafa Nasr Mostafa,&nbsp;Murat Şakir Ekşi","doi":"10.1177/11795735231195760","DOIUrl":"https://doi.org/10.1177/11795735231195760","url":null,"abstract":"<p><p>Verteporfin and 5-ALA are used for visualizing malignant tissue components in different body tumors and as photodynamic therapy in treating isocitrate dehydrogenase (IDH) wild-type glioblastoma (GBM). Additionally, verteporfin interferes with Yes-associated protein 1 (YAP)/Transcriptional coactivator with PDZ-binding motif - TEA domain (TAZ-TEAD) pathway, thus inhibiting the downstream effect of these oncogenes and reducing the malignant properties of GBM. Animal studies have shown verteporfin to be successful in increasing survival rates, which have led to the conduction of phase 1 and 2 clinical trials to further investigate its efficacy in treating GBM. In this article, we aimed to review the novel mechanism of verteporfin's action, the impact of its interaction with YAP/TAZ-TEAD, its effect on glioblastoma stem cells, and its role in inducing ferroptosis.</p>","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/83/b7/10.1177_11795735231195760.PMC10439684.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10304411","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 relationships between neuroglial and neuronal changes in Alzheimer's disease, and the related controversies II: <b>gliotherapies and multimodal therapy</b>.","authors":"Adolfo Toledano-Díaz,&nbsp;M Isabel Álvarez,&nbsp;Adolfo Toledano","doi":"10.1177/11795735221123896","DOIUrl":"https://doi.org/10.1177/11795735221123896","url":null,"abstract":"<p><p>Since the original description of Alzheimer´s disease (AD), research into this condition has mainly focused on assessing the alterations to neurons associated with dementia, and those to the circuits in which they are involved. In most of the studies on human brains and in many models of AD, the glial cells accompanying these neurons undergo concomitant alterations that aggravate the course of neurodegeneration. As a result, these changes to neuroglial cells are now included in all the \"pathogenic cascades\" described in AD. Accordingly, astrogliosis and microgliosis, the main components of neuroinflammation, have been integrated into all the pathogenic theories of this disease, as discussed in this part of the two-part monograph that follows an accompanying article on gliopathogenesis and glioprotection. This initial reflection verified the implication of alterations to the neuroglia in AD, suggesting that these cells may also represent therapeutic targets to prevent neurodegeneration. In this second part of the monograph, we will analyze the possibilities of acting on glial cells to prevent or treat the neurodegeneration that is the hallmark of AD and other pathologies. Evidence of the potential of different pharmacological, non-pharmacological, cell and gene therapies (widely treated) to prevent or treat this disease is now forthcoming, in most cases as adjuncts to other therapies. A comprehensive AD multimodal therapy is proposed in which neuronal and neuroglial pharmacological treatments are jointly considered, as well as the use of new cell and gene therapies and non-pharmacological therapies that tend to slow down the progress of dementia.</p>","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2022-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/40/9d/10.1177_11795735221123896.PMC9666878.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40699653","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":"Central nervous system, spinal root ganglion and brachial plexus involvement in leprosy: A prospective study.","authors":"Sumit Verma,&nbsp;Ravindra Kumar Garg,&nbsp;Imran Rizvi,&nbsp;Hardeep Singh Malhotra,&nbsp;Neeraj Kumar,&nbsp;Amita Jain,&nbsp;Swastika Suvirya,&nbsp;Anit Parihar,&nbsp;Rajesh Verma,&nbsp;Praveen Kumar Sharma,&nbsp;Shweta Pandey,&nbsp;Ravi Uniyal,&nbsp;Shantanu Prakash","doi":"10.1177/11795735221135477","DOIUrl":"https://doi.org/10.1177/11795735221135477","url":null,"abstract":"<p><strong>Background: </strong>Leprosy is primarily a disease of peripheral nerves. Some isolated case reports and case series have communicated imaging changes in the central nervous system (CNS) and brachial plexus in patients with leprosy.</p><p><strong>Objectives: </strong>To study the neuroimaging abnormalities in patients with lepra bacilli-positive neuropathy in the context of CNS, spinal root ganglion, and brachial plexus.</p><p><strong>Design: </strong>Prospective observational study.</p><p><strong>Methods: </strong>We screened newly-diagnosed patients with multibacillary leprosy presenting with neuropathy. Patients with bacilli-positive sural nerve biopsies were included in the study and subjected to magnetic resonance imaging (MRI) of the brain and spinal cord.</p><p><strong>Results: </strong>A total of 54 patients with bacteriologically confirmed multibacillary leprosy were screened; <i>Mycobacterium leprae</i> was demonstrated in the sural nerve biopsies of 29 patients. Five patients (5/29; 17.24%) had MRI abnormalities in CNS, spinal root ganglion, and/or brachial plexus. Three patients had MRI changes suggestive of either myelitis or ganglionitis. One patient had T2/FLAIR hyperintensity in the middle cerebellar peduncle while 1 had T2/FLAIR hyperintensity in the brachial plexus.</p><p><strong>Conclusion: </strong>CNS, spinal root ganglion, and brachial plexus are involved in patients with leprous neuropathy. Immunological reaction against <i>M leprae</i> antigen might be a plausible pathogenetic mechanism for brachial plexus and CNS imaging abnormalities.</p>","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2022-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fe/eb/10.1177_11795735221135477.PMC9583215.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40655030","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":"Natalizumab extended-interval dosing in multiple sclerosis to mitigate progressive multifocal leukoencephalopathy risk: initial study evidence and real-world experience.","authors":"Julian Perncezky,&nbsp;Johann Sellner","doi":"10.1177/11795735221135485","DOIUrl":"https://doi.org/10.1177/11795735221135485","url":null,"abstract":"<p><p>The high efficacy of natalizumab in the treatment of relapsing-remitting multiple sclerosis (MS) is without controversy. Indeed, effective disease control was not only demonstrated in the pivotal trials but has been corroborated impressively in real-world observations. This monoclonal IgG4 antibody blocks the α4β1 integrin-mediated leukocyte-endothelial interaction and thereby inhibits the migration of immune cells to the brain parenchyma. However, treatment with natalizumab carries the risk of progressive multifocal leukoencephalopathy (PML). This potentially lethal side effect is a significant limitation for treatment initiation and long-term therapy. Natalizumab is given intravenously or subcutaneously in the standard dose of 300 mg every 4 weeks, allowing drug concentrations at levels that ensure continuous α4β1 integrin receptor saturation on the surface of immune cells. Extended-interval dosing (EID) is an emerging treatment approach that aims to mitigate the natalizumab-related PML risk by prolonging the standard infusion intervals to 6 weeks or even more. This treatment approach may abrogate the PML risk due to improved immune surveillance within the central nervous system while maintaining clinical efficacy. Moreover, even an individual interval dosing can be envisioned based on the availability of a biomarker that is capable of monitoring both safety and efficacy aspects. This review summarizes the early and encouraging evidence for EID from observational and randomized-controlled trials and discusses current limitations and upcoming challenges for introducing a tailored treatment approach.</p>","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2022-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ee/c2/10.1177_11795735221135485.PMC9580073.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40655029","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 relationships between neuroglial alterations and neuronal changes in Alzheimer's disease, and the related controversies I: Gliopathogenesis and glioprotection.","authors":"Adolfo Toledano-Díaz, M Isabel Álvarez, Adolfo Toledano","doi":"10.1177/11795735221128703","DOIUrl":"10.1177/11795735221128703","url":null,"abstract":"<p><p>Since Alois Alzheimer described the pathology of Alzheimer's disease in 1907, an increasing number of studies have attempted to discover its causes and possible ways to treat it. For decades, research has focused on neuronal degeneration and the disruption to the neural circuits that occurs during disease progression, undervaluing in some extent the alterations to glial cells even though these alterations were described in the very first studies of this disease. In recent years, it has been recognized that different families of neuroglia are not merely support cells for neurons but rather key and active elements in the physiology and pathology of the nervous system. Alterations to different types of neuroglia (especially astroglia and microglia but also mature oligodendroglia and oligodendroglial progenitors) have been identified in the initial neuropathological changes that lead to dementia, suggesting that they may represent therapeutic targets to prevent neurodegeneration. In this review, based on our own studies and on the relevant scientific literature, we argue that a careful and in-depth study of glial cells will be fundamental to understanding the origin and progression of Alzheimer's disease. In addition, we analyze the main issues regarding the neuroprotective and neurotoxic role of neuroglial changes, reactions and/or involutions in both humans with Alzheimer's disease and in experimental models of this condition.</p>","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2022-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ff/67/10.1177_11795735221128703.PMC9551335.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33537714","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":"Safety and efficacy of endovascular thrombectomy in patients with severe cerebral venous thrombosis: A meta-analysis.","authors":"Gaurav Nepal,&nbsp;Sanjeev Kharel,&nbsp;Riwaj Bhagat,&nbsp;Megan A Coghlan,&nbsp;Jayant K Yadav,&nbsp;Stella Goeschl,&nbsp;Rajan Lamichhane,&nbsp;Subash Phuyal,&nbsp;Rajeev Ojha,&nbsp;Gentle S Shrestha","doi":"10.1177/11795735221131736","DOIUrl":"https://doi.org/10.1177/11795735221131736","url":null,"abstract":"<p><strong>Background: </strong>Cerebral venous thrombosis (CVT) is a rare thrombotic condition which is traditionally treated with anti-coagulation therapy. Subsets of patients with severe CVT have been treated with endovascular thrombectomy (EVT). Despite the high estimated mortality associated with severe CVT, there has been only one randomized control trial done regarding safety and efficacy of EVT in severe CVT compared to standard medical management. Evidence in this area is lacking.</p><p><strong>Objective: </strong>The aim of this systematic review is to analyze all existing literature and generate robust information regarding the role of EVT in the management of patients with severe CVT.</p><p><strong>Methods: </strong>This systematic review and meta-analysis followed PRISMA guideline. PubMed, Embase, Google Scholar, and CNKI were searched for eligible studies from 2007 to 2021. Safety and efficacy of EVT were evaluated by meta-analyzing recanalization status, the good functional outcome at follow-up, recurrent CVT, new hematoma. A pooled proportion with a 95% confidence interval was derived from a meta-analysis of various outcomes (CI).</p><p><strong>Results: </strong>A total of 33 studies comprising 610 patients treated with EVT were included for analysis which comprised one randomized control trial, one prospective study and 31 retrospective studies. Based on pooled data, 85% of patients had good functional outcome, 62% had complete recanalization, 5% had all-cause mortality, and 3% had catheter related complications. The efficacy outcomes in this analysis had a significant heterogeneity and a subgroup analysis was also done to explain these findings. The minimum time of follow up was 3 months and varied EVT techniques were used across the studies.</p><p><strong>Conclusion: </strong>This meta-analysis suggests EVT may be safe and efficacious in treating patients with severe CVT.</p><p><strong>Registration: </strong>Our protocol was registered with PROSPERO: International prospective register of systematic reviews with the registration number CRD42021254760.</p>","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2022-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5f/5a/10.1177_11795735221131736.PMC9530583.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33492899","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":"Author response to comment on: Alopecia in multiple sclerosis patients treated with disease modifying therapies.","authors":"Mokshal H Porwal, Ahmed Z Obeidat","doi":"10.1177/11795735221127131","DOIUrl":"10.1177/11795735221127131","url":null,"abstract":"","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/59/7e/10.1177_11795735221127131.PMC9527983.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33490334","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":"Comment on: Neurological Manifestations Associated With SARS-CoV-2 in Children: A Case Series.","authors":"Josef Finsterer","doi":"10.1177/11795735221123915","DOIUrl":"https://doi.org/10.1177/11795735221123915","url":null,"abstract":"DECLARATION OF CONFLICTING INTERESTS: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. FUNDING: The author(s) received no financial support for the research, authorship, and/or publication of this article.","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2022-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b0/b5/10.1177_11795735221123915.PMC9478691.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40364057","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":"Rho-Kinase inhibition decreases focal cerebral ischemia-induced glial activation in rats.","authors":"Abdullah Md Sheikh,&nbsp;Shozo Yano,&nbsp;Shingo Mitaki,&nbsp;Shatera Tabassum,&nbsp;Shuhei Yamaguchi,&nbsp;Atsushi Nagai","doi":"10.1177/11795735221123910","DOIUrl":"https://doi.org/10.1177/11795735221123910","url":null,"abstract":"<p><strong>Background: </strong>Rho-kinase inhibition in a rat middle cerebral artery occlusion (MCAO) model is reported to improve neurological functions and decrease infarction size.</p><p><strong>Objective: </strong>The objective of this study is to investigate the underlying mechanisms of such improvement by evaluating the effects of Rho-kinase inhibition on astrocytes and microglial accumulation and activation in this condition.</p><p><strong>Methods: </strong>Adult male Sprague-Dawley (SD) rats were used to generate the MCAO model, which received an I.P injection of a chemical Rho-kinase inhibitor (Fasudil- 5 mg/kg/day) or vehicle (PBS) for 2 and 4 days.</p><p><strong>Results: </strong>Fasudil treatment significantly decreased the stroke volumes and water content in the lesion areas, as revealed by MRI. Immunostaining and Western blotting results demonstrated that Fasudil significantly decreased the levels of Aquaporin-4, a water channel protein. The number of GFAP⁺ astrocytes and Iba-1⁺ macrophage/microglia was decreased in the lesion areas. Proinflammatory transcription factor NF-κB protein levels were decreased in the Fasudil group 2 days after MCAO. Also, proinflammatory mediators including TNF-α, IL-1β, and iNOS levels were decreased. In vitro migration study using a human microglial cell line (HMO6) confirmed the inhibitory effects of Fasudil on the process. Fasudil also decreased combined IL-1β and IFNγ-induced NF-κB nuclear translocation in HMO6. Moreover, Fasudil transiently decreased combined IL-1β and IFNγ-induced iNOS, TNFα, and IL-1β mRNA levels in HMO6.</p><p><strong>Conclusion: </strong>Our study demonstrates the inhibitory effects of Rho-kinase on NF-κB-mediated glial activation and cerebral edema, which might be a promising therapeutic target in acute cerebral ischemia conditions.</p>","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2022-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6d/f0/10.1177_11795735221123910.PMC9465613.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40358840","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 sequential natalizumab - alemtuzumab therapy in patients with relapsing forms of multiple sclerosis (SUPPRESS) trial - Part I: Rationale and objectives.","authors":"Rehana Z Hussain,&nbsp;Peter V Sguigna,&nbsp;Annette Okai,&nbsp;Crystal Wright,&nbsp;Mariam Madinawala,&nbsp;Ann D Bass,&nbsp;Gary R Cutter,&nbsp;Navid Manouchehri,&nbsp;Olaf Stuve","doi":"10.1177/11795735221123911","DOIUrl":"https://doi.org/10.1177/11795735221123911","url":null,"abstract":"Background Natalizumab is a recombinant humanized monoclonal antibody (mAb) against α4-integrin that is approved for relapsing forms of multiple sclerosis (MS). Natalizumab is associated with an increased risk of developing progressive multifocal leukoencephalopathy (PML), and with disease reactivation after cessation of treatment that is likely mediated by an accumulation of pro-inflammatory lymphocytes in the blood during therapy. Alemtuzumab is a mAb against CD52 that reduces the number of peripheral lymphocytes. Rationale To determine if treatment with alemtuzumab after natalizumab reduces disease activity in patients with relapsing forms of MS. This review article will outline the rationale and objectives of the sequential natalizumab – alemtuzumab therapy in patients with relapsing forms of multiple sclerosis (SUPPRESS; ClinicalTrials.gov ID: NCT03135249) trial in greater detail than would be feasible in a manuscript that summarizes the study results. Methods The SUPPRESS trial is single arm, open-label, multicenter, efficacy pilot study that aims to establish a disease-free state over a 24-months period in patients who received the natalizumab- alemtuzumab sequential therapy. Participants will be recruited from four different sites. The primary endpoint is the annualized relapse rate (ARR) from the time of cessation of natalizumab treatment. Key secondary endpoint is freedom of relapse at 12-months, the number of new/enlarging T2 lesions on magnetic resonance imaging (MRI), and the number of gadolinium (Gd)-enhancing lesions on MRI. An exploratory endpoint is the Expanded Disability Status Scale (EDSS), retinal nerve fiber layer (RNFL) thickness assessment by optic coherence tomography (OCT) and assessment of quality of life (QoL) measures by a pre-defined, self-administered testing battery. To evaluate immunological effects, blood leukocytes will be collected and immunophenotyped by multi-parameter flow cytometry. Conclusion The SUPPRESS trial will provide clinical, imaging, and biological data to determine whether sequential natalizumab to alemtuzumab combination therapy establish a disease-free state in patients with relapsing forms of MS.","PeriodicalId":15218,"journal":{"name":"Journal of Central Nervous System Disease","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2022-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ef/6a/10.1177_11795735221123911.PMC9434668.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40349979","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}