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.