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

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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.

Background and PurposePersons who perceive their risk for stroke can promote the intervention of stroke risk factors and reduce the risk of stroke occurrence. Our purpose was to assess the knowledge of stroke risk factors and the level of perceived risk for stroke.MethodsIn 2011, a population-based face-to-face interview survey was conducted in Yuzhong district, Chongqing. A total of 1500 potential participants aged ≥18 years old were selected using a multi-stage sampling method. The knowledge of stroke risk factors and perceived risk for stroke was surveyed.ResultsA total of 941 participants completed the questionnaire survey. The respondents’ awareness rate of stroke risk factors ranged between 53.3% and 87.2%. The community residents’ perceived risk for stroke was only 17.7%. Multiple logistic regression analysis showed that 45–64 years age group, a history of hypertension, hyperlipidemia, heart disease, and stroke were independent predictors of perceived risk for stroke. Perceived risk for stroke increased as the number of risk factors increased (P<0.001). However, even for respondents with three or more risk factors, only 41% perceived themselves to be at risk for stroke.ConclusionsIn this population-based survey, few community residents perceived risk for stroke, even among those with multiple stroke risk factors, most did not perceive themselves to be at risk for stroke. Persons with 45–64 years old, a history of hypertension, hyperlipidemia, heart disease or stroke were more likely to perceive risk for stroke. The awareness of the risk for stroke has yet to be enhanced among community residents.

We consider the hydration structure and thermodynamic energetics of solutes in aqueous solution. On the basis of the dominant local correlation between the solvent and the chemical nature of the solute atoms, proximal distribution functions (pDF) can be used to quantitatively estimate the hydration pattern of the macromolecules. We extended this technique to study the solute–solvent energetics including the van der Waals terms representing excluded volume and tested the method with butane and propanol. Our results indicate that the pDF-reconstruction algorithm can reproduce van der Waals solute–solvent interaction energies to useful kilocalorie per mole accuracy. We subsequently computed polyalanine–water interaction energies for a variety of conformers, which also showed agreement with the simulated values.

Objective To evaluate the effectiveness and safety of episodic migraine prevention with the percutaneous mastoid electrical stimulator (PMES). Methods This was a randomized, double-blind, and sham-controlled trial that involved four medical centers. Episodic patients with at least two migraine attacks every month were randomly 1:1 to PMES or sham stimulation treatment. The treatments were performed daily for 45 minutes over 3 months. The primary outcomes were change in migraine days per month and the 50% response rate. Results The PMES group had a significantly greater reduction of migraine days in the third month than the sham group (-71.3% vs. -14.4%, p < 0.001). The 50% response rate of migraine days in the PMES group (≥50% reduction of migraine days compared with the baseline) was significantly higher than that in the sham group (82.5% vs. 17.5%, p < 0.001). In the PMES group, 60% of the patients had a ≥75% reduction of migraine days in the third month, and 35% of the patients had no migraine attack in the third month. No patients in the sham group had a ≥75% reduction of migraine days. There were no adverse events in either group. Conclusion Treatment of migraine using non-invasive PMES was safe and effective.

Background: Lung epithelial cells play critical roles in idiopathic pulmonary fibrosis. Methods: In the present study, we investigated whether transforming growth factor-β (TGF-β)-induced expression of connective tissue growth factor (CTGF) was regulated by the extracellular signal-regulated kinase (ERK)/a disintegrin and metalloproteinase 17 (ADAM17)/ribosomal S6 kinases 1 (RSK1)/CCAAT/enhancer-binding protein β (C/EBPβ) signaling pathway in human lung epithelial cells (A549). Results: Our results revealed that TGF-β-induced CTGF expression was weakened by ADAM17 small interfering RNA (ADAM17 siRNA), TNF-α processing inhibitor-0 (TAPI-0, an ADAM17 inhibitor), U0126 (an ERK inhibitor), RSK1 siRNA, and C/EBPβ siRNA. TGF-β-induced ERK phosphorylation as well as ADAM17 phosphorylation was attenuated by U0126. The TGF-β-induced increase in RSK1 phosphorylation was inhibited by TAPI-0 and U0126. TGF-β-induced C/EBPβ phosphorylation was weakened by U0126, ADAM17 siRNA, and RSK1 siRNA. In addition, TGF-β increased the recruitment of C/EBPβ to the CTGF promoter. Furthermore, TGF-β enhanced fibronectin (FN), an epithelial–mesenchymal transition (EMT) marker, and CTGF mRNA levels and reduced E-cadherin mRNA levels. Moreover, TGF-β-stimulated FN protein expression was reduced by ADAM17 siRNA and CTGF siRNA. Conclusion: The results suggested that TGF-β induces CTGF expression through the ERK/ADAM17/RSK1/C/EBPβ signaling pathway. Moreover, ADAM17 and CTGF participate in TGF-β-induced FN expression in human lung epithelial cells.