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This could affect decision making with respect to antithrombotic strategy.Background Inflammation plays an important role in tumorigenesis. Previous studies have reported the prognostic value of several peripheral inflammatory markers in glioma patients, including the neutrophil-to-lymphocyte ratio (NLR). However, it still remains unclear whether inflammatory markers can independently predict the prognosis of glioblastoma (GBM) patients. The present study aims to explore the prognostic value of systemic inflammatory markers, including neutrophils, lymphocytes, platelets, the NLR, and the platelet-to-lymphocyte ratio (PLR), in patients with GBM. Methods A comprehensive systemic search and review was performed using the PubMed, EMBASE, and Cochrane Library databases to identify all the relevant literature (published before June 30, 2020) that evaluated the association between any of these inflammatory markers and survival in GBM. Results There were 2 (634 patients), 3 (723 patients), 2 (237 patients), 8 (1,225 patients), and 3 (505 patients) studies examining the correlation of survival with neutrophils, lymphocytes, platelets, the NLR, and the PLR, respectively. An elevated NLR and elevated neutrophil and platelet counts were associated with worse overall survival (OS) in GBM patients (NLR hazard ratio [HR] = 1.63, 95% confidence interval [CI] 1.23-2.15, p = 0.0007; neutrophil count HR = 1.46, 95% CI1.16-1.83, p = 0.001; platelet count HR = 1.58, 95% CI 1.42-1.77, p less then 0.00001). VER155008 HSP (HSP90) inhibitor However, there was no significant association between the PLR or the absolute lymphocyte count and OS in GBM patients. Conclusion The NLR and the absolute neutrophil and platelet counts may be valuable and convenient peripheral inflammatory markers to evaluate the prognosis of GBM patients. Further prospective studies are needed to verify its reliability.In the past decade, several groups have reported that microRNAs (miRNAs) can participate in the regulation of tau protein at different levels, including its expression, alternative splicing, phosphorylation, and aggregation. These observations are significant, since the abnormal regulation and deposition of tau is associated with nearly 30 neurodegenerative disorders. Interestingly, miRNA profiles go awry in tauopathies such as Alzheimer's disease, progressive supranuclear palsy, and frontotemporal dementia. Understanding the role and impact of miRNAs on tau biology could therefore provide important insights into disease risk, diagnostics, and perhaps therapeutics. In this Perspective article, we discuss recent advances in miRNA research related to tau. While proof-of-principle studies hold promise, physiological validation remains limited. To help fill this gap, we describe herein a pure tauopathy mouse model deficient for the miR-132/212 cluster. This miRNA family is strongly downregulated in human tauopathies and shown to regulate tau in vitro and in vivo. No significant differences in survival, motor deficits or body weight were observed in PS19 mice lacking miR-132/212. Age-specific effects were seen on tau expression and phosphorylation but not aggregation. Moreover, various miR-132/212 targets previously implicated in tau modulation were unaffected (GSK-3β, Foxo3a, Mapk1, p300) or, unexpectedly, reduced (Mapk3, Foxo1, p300, Calpain 2) in miR-132/212-deficient PS19 mice. These observations highlight the challenges of miRNA research in living models, and current limitations of transgenic tau mouse models lacking functional miRNA binding sites. Based on these findings, we finally recommend different strategies to better understand the role of miRNAs in tau physiology and pathology.Background Recent advanced technologies, such as high-throughput sequencing, have enabled the identification of a broad spectrum of variants. Using targeted-gene-panel resequencing for Parkinson's disease (PD)-associated genes, we have occasionally found several single-nucleotide variants (SNVs), which are thought to be disease-associated, in PD patients. To confirm the significance of these potentially disease-associated variants, we performed genome association analyses, using next-generation target resequencing, to evaluate the associations between the identified SNVs and PD. Methods We obtained genomic DNA from 766 patients, who were clinically diagnosed with PD, and 336 healthy controls, all of Japanese origin. All data were analyzed using Ion AmpliSeq panel sequences, with 29 PD- or dementia-associated genes in a single panel. We excluded any variants that did not comply with the Hardy-Weinberg equilibrium in the control group. Variant frequencies in the PD and control groups were compared using PLINK. The identified variants were confirmed to a frequency difference of P less then 0.05, after applying the Benjamini-Hochberg procedure using Fisher's exact test. The pathogenicity and prevalence of each variant were estimated based on a public gene database. Results We identified three rare variants that were significantly associated with PD rs201012663/rs150500694 in SYNJ1 and rs372754391 in DJ-1, which are intronic variants, and rs7412 in ApoE, which is an exonic variant. The variants in SYNJ1 and ApoE were frequently identified in the control group, and rs201012663/rs150500694 in SYNJ1 may play a protective role against PD. The DJ-1 variant was frequently identified in the PD group, with a high odds ratio of 2.2. Conclusion The detected variants may represent genetic modifiers or disease-related variants in PD. Targeted-gene-panel resequencing may represent a useful method for detecting disease-causing variants and genetic association studies in PD.Objective To evaluate the characteristics of F-wave in spinocerebellar ataxia type 3 (SCA3) patients and preclinical carriers of SCA3 gene mutation (PreSCA3), and explore the relationship between disease severity and F-wave parameters and evaluate F-wave parameters as potential biomarkers for monitoring of disease progression in SCA3. Methods We performed F-wave recordings in median, ulnar and tibial nerves of 39 SCA3 patients, 20 PreSCA3, and 27 healthy controls, and compared F-wave parameters between them. Results In all nerves studied, the mean F-wave amplitude, maximum F-wave amplitude, and F/M amplitude ratio were significantly increased in the SCA3 patients in comparison with the normal controls. And the minimal F-wave latency of SCA3 patients was significantly prolonged and the F-wave persistence (%) was significantly decreased in the median nerve. For the PreSCA3, the maximum F-wave amplitude was significantly higher than normal controls for both median, ulnar, and tibial nerves. The mean F-wave amplitude and F/M amplitude ratio in all nerves were comparable between PreSCA3 and normal controls.