The current meta-analysis identified potential risk factors for PTE. The results may contribute to better prevention strategies and treatments for PTE.

Increasing evidence suggests that epilepsy is the result of synaptic reorganization and pathological excitatory loop formation in the central nervous system; however, the mechanisms that regulate this process are not well understood. We proposed that microRNA-132 (miR-132) and p250GAP might play important roles in this process by activating the downstream Rho GTPase family. We tested this hypothesis using a magnesium-free medium-induced epileptic model of cultured hippocampal neurons. We investigated whether miR-132 regulates GTPase activity through p250GAP and found that Cdc42 was significantly activated in our experimental model. Silencing miR-132 inhibited the electrical excitability level of cultured epileptic neurons, whereas silencing p250GAP had an opposite effect. In addition, we verified the effect of miR-132 in vivo and found that silencing miR-132 inhibited the aberrant formation of dendritic spines and chronic spontaneous seizure in a lithium-pilocarpine-induced epileptic mouse model. Finally, we confirmed that silencing miR-132 has a neuroprotective effect on cultured epileptic neurons; however, this effect did not occur through the p250GAP pathway. Generally, silencing miR-132 may suppress spontaneous seizure activity through the miR-132/p250GAP/Cdc42 pathway by regulating the morphology and electrophysiology of dendritic spines; therefore, miR-132 may serve as a potential target for the development of antiepileptic drugs.

BackgroundInconsistent findings have been obtained for previous studies evaluating the association between antihypertensive medication (AHM) adherence and the risk of stroke. This dose‐response meta‐analysis was designed to investigate the association between AHM adherence and stroke risk.Methods and ResultsMEDLINE and Embase databases were systematically searched to identify relevant studies. The quantification of adherence to AHM was calculated as the percentage of the sum of days with AHM actually taken divided by the total number of days in a specific period. Summary relative risks (RR) and 95% CIs were estimated using a random‐effects model. Stratified and dose‐response analyses were also performed. A total of 18 studies with 1 356 188 participants were included. The summary RR of stroke for the highest compared with the lowest AHM adherence level was 0.73 (95% CI, 0.67–0.79). Stratified by stroke subtype, a higher AHM adherence was associated with lower risks of ischemic stroke (RR, 0.74; 95% CI, 0.69–0.79) and hemorrhagic stroke (RR, 0.55; 95% CI, 0.42–0.72). Moreover, both fatal (RR, 0.51; 95% CI, 0.36–0.73) and nonfatal stroke (RR, 0.52; 95% CI, 0.28–0.94) were lower in participants with higher AHM adherence. The results of a dose‐response analysis indicated that a 20% increment in AHM adherence level was associated with a 9% lower risk of stroke (RR, 0.91; 95% CI, 0.86–0.96).ConclusionsHigher AHM adherence is dose‐dependently associated with a lower risk of stroke in patients with hypertension.

The resection of the epileptogenic area of brain is very important and useful for the treatment of uncontrolled epilepsy, especially for the patients with stereotyped partial seizures. The critical point for successful epilepsy surgery is the precise identification of epileptogenic zone. Actually, we cannot precisely localize the epileptogenic zone in about 25 % of patient with refractory seizures based on the noninvasive examination; thus for these patients, we mainly use the intracranial EEG to localize the epileptogenic zone which could be useful in 10-15 % of surgical candidates. The intracranial electrodes which are most used currently are depth electrodes, subdural strip electrodes, and subdural grid electrodes. The subject of this paper is to discuss and compare the indications, construction, insertion, interpretation, limitations, risks and accuracy of each of these methods.

Whether very early mobilization (VEM) improves outcomes in stroke patients and reduces immobilization-related complications (IRCs) is currently unknown. The objective of this systematic review and meta-analysis was to evaluate the efficacy and safety of VEM in acute stroke patients following admission. Medline, Embase, and Cochrane Central Register of Controlled Trials databases were searched for randomized controlled trials (RCTs) that examined the efficacy or safety of VEM in patients with acute stroke. VEM was defined as out of bed activity commencing within 24 or 48 hours after the onset of stroke. A total of 9 RCTs with 2,803 participants were included. Upon analysis, VEM was not associated with favorable functional outcomes (modified Ranking Scale: 0–2) at 3 months [relative risk (RR): 0.96; 95% confidence interval (CI): 0.86–1.06]; VEM did not reduce the risk of IRCs during follow up. With respect to safety outcomes, VEM was not associated with a higher risk of death (RR: 1.04; 95% CI: 0.52–2.09) and did not increase the risk of neurological deterioration or incidence of falls with injury. In conclusion, pooled data from RCTs concluded that VEM is not associated with beneficial effects when carried out in patients 24 or 48 hours after the onset of a stroke.

Epigenetics underlying refractory epilepsy is poorly understood, especially in patients without distinctive genetic alterations. DNA methylation may affect gene expression in epilepsy without affecting DNA sequences. Herein, we analyzed genome-wide DNA methylation and gene expression in brain tissues of 10 patients with refractory epilepsy using methylated DNA immunoprecipitation linked with sequencing and mRNA Sequencing. Diverse distribution of differentially methylated genes was found in X chromosome, while differentially methylated genes appeared rarely in Y chromosome. 62 differentially expressed genes, such as MMP19, AZGP1, DES, and LGR6 were correlated with refractory epilepsy for the first time. Although general trends of differentially enriched gene ontology terms and Kyoto Encyclopedia of Genes and Genome pathways in this study are consistent with previous researches, differences also exist in many specific gene ontology terms and Kyoto Encyclopedia of Genes and Genome pathways. These findings provide a new genome-wide profiling of DNA methylation and gene expression in brain tissues of patients with refractory epilepsy, which may provide a basis for further study on the etiology and mechanisms of refractory epilepsy.

The mechanisms that underlie the pathogenesis of epilepsy are still unclear. Recent studies have indicated that inflammatory processes occurring in the brain are involved in a common and crucial mechanism in epileptogenesis. C-X-C motif chemokine ligand 13 (CXCL13) and its only receptor, C-X-C motif chemokine receptor 5 (CXCR5), are highly expressed in the central nervous system (CNS) and participate in inflammatory responses. The present study aimed to assess the expression of CXCL13 and CXCR5 in the brain tissues of both patients with intractable epilepsy (IE) and a rat model (lithium-pilocarpine) of temporal lobe epilepsy (TLE) to identify possible roles of the CXCL13-CXCR5 signaling pathway in epileptogenesis. Real-time quantitative polymerase chain reaction (RT-qPCR), immunohistochemical, double-labeled immunofluorescence and Western blot analyses were performed in this study. CXCL13 and CXCR5 mRNA expression and protein levels were found to be significantly up-regulated in the TLE patients and TLE rats. Further, CXCL13 and CXCR5 protein levels were altered during the different epileptic phases after onset of status epilepticus (SE) in the pilocarpine model rats, including the acute phase (6, 24, and 72 h), latent phase (7 and 14 days) and chronic phase (30 and 60 days groups). Moreover, double-labeled immunofluorescence analysis revealed that CXCL13 was mainly expressed in the cytomembranes and cytoplasm of neurons and astrocytes, while CXCR5 was mainly expressed in the cytomembranes and cytoplasm of neurons. Thus, the CXCL13-CXCR5 signaling pathway may play a possible pathogenic role in IE. CXCL13 and CXCR5 may represent potential biomarkers of brain inflammation in epileptic patients.

Background-Inconsistent findings have been obtained for previous studies evaluating the association between antihypertensive medication (AHM) adherence and the risk of stroke. This dose-response meta-analysis was designed to investigate the association between AHM adherence and stroke risk.