Background and Purpose-Endovascular treatment has increasingly been used for aneurismal subarachnoid aneurismal hemorrhage. The aim of this analysis is to assess the current evidence regarding safety and efficiency of clipping compared with coiling. Methods-We conducted a meta-analysis of studies that compared clipping with coiling between January 1999 and July 2012. Comparison of binary outcomes between treatment groups was described using odds ratios (OR; clip versus coil). Results-Four

Background and Aims Alcohol use disorders (AUD) are often comorbid with depressive symptoms. Cohort studies on the association between AUD and subsequent depressive symptoms have produced inconsistent results. Moreover, regarding alcohol intake, the risk of developing depressive symptoms might vary with alcohol intake level. We aimed to investigate the association between AUD, alcohol intake and subsequent depressive symptoms. Design and Setting We conducted a systematic search in PubMed, Embase and PsycINFO for cohort studies on the association between AUD or alcohol intake and subsequent depressive symptoms. Participants We included 338 426 participants from 42 studies. Six and four studies analyzed only females and males, respectively. Measurements We combined risk estimates for developing depressive symptoms using a random‐effects model. We divided alcohol intake into abstinence, light (0–84 g/week), moderate (85–168 g/week) and heavy drinking (> 168 g/week or > 48 g/day at least weekly). We conducted a categorical analysis to compare the risk of depressive symptoms between abstinence and different intake categories. Further, we conducted a dose–response analysis to investigate the alcohol–depression association. Findings We analyzed 42 studies (follow‐up time: 1–40 years). AUD was associated with significantly increased risk of subsequent depressive symptoms [relative risk (RR) = 1.57, 95% confidence interval (CI) = 1.41–1.76]. Regarding alcohol intake, heavy drinking had an increased risk of depressive symptoms; however, the association was only significant when controls were limited to non‐heavy drinkers (RR = 1.13, 95% CI = 1.05–1.22). Taking into consideration the possibility of publication bias and confounding factors made the association non‐significant. We observed J‐shaped associations in both categorical and dose–response analyses where light‐moderate drinking had a significantly decreased risk of depression, while heavy drinking did not show a significant association with depressive symptoms compared with non‐drinkers. Conclusion Alcohol use disorders are associated with increased the risk of subsequent depressive symptoms. Heavy drinking does not significantly predict occurrence of depressive symptoms after adjusting for potential confounders.

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Radiation-induced brain injury (RI) commonly occurs in patients who received head and neck radiotherapy. However, the mechanism of RI remains unclear. We aimed to evaluate whether pyroptosis was involved in RI and the impact of mesenchymal stem cells (MSCs) on it. BALB/c male mice (6-8 weeks) were cranially irradiated (15 Gy), and MSCs were transplanted into the bilateral cortex 2 days later; then mice were sacrificed 1 month later. Meanwhile, irradiated BV-2 microglia cells (10 Gy) were cocultured with MSCs for 24 hours. We observed that irradiated mice brains presented NLRP3 and caspase-1 activation. RT-PCR then indicated that it mainly occurred in microglia cells but not in neurons. Further, irradiated BV-2 cells showed pyroptosis and increased production of IL-18 and IL-1 . RT-PCR also demonstrated an increased expression of several inflammasome genes in irradiated BV-2 cells, including NLRP3 and AIM2. Particularly, NLRP3 was activated. Knockdown of NLRP3 resulted in decreased LDH release. Noteworthily, in vivo, MSCs transplantation alleviated radiation-induced NLRP3 and caspase-1 activation. Moreover, in vitro, MSCs could decrease caspase-1 dependent pyroptosis, NLRP3 inflammasome activation, and ROS production induced by radiation. Thus, our findings proved that microglia pyroptosis occurred in RI. MSCs may act as a potent therapeutic tool in attenuating pyroptosis.

Background and aims Observational studies have yielded conflicting results on the association of prescription opioid use (POU) with the risk of cardiovascular diseases (CVD). Residual confounding and potential reverse causality are inevitable in such conventional observational studies. This study used Mendelian randomization (MR) design to estimate the causal effect of POU on the risk of CVD, including coronary heart disease (CHD), myocardial infarction (MI) and ischemic stroke (IS), as well as their common risk factors. Design We estimated the causal effect of genetic liability for POU on CVD in a two‐sample MR framework. Complementary sensitivity analyses were conducted to test the robustness of our results. Setting Genome‐wide association studies (GWAS) that were based on predominantly European ancestry. Participants The sample sizes of the GWAS used in this study ranged from 69 033 to 757 601 participants. Measurements Genetic variants predictive of the POU and their corresponding summary‐level information in the outcomes were retrieved and extracted from the respective GWAS. Findings Using univariable MR, we found evidence for a causal effect of genetic liability for POU on an increased risk of CHD [odds ratio (OR) = 1.09; 95% confidence interval (CI) = 1.02–1.16; P = 0.008] and MI (OR = 1.13; 95% CI = 1.04–1.22; P = 0.002). In multivariable MR, the association remained after accounting for comorbid pain conditions, but was attenuated with adjustment for potential mediators, including body mass index (BMI), waist circumference (WC) and type 2 diabetes (T2D). Conclusion Mendelian randomization estimates provide robust evidence for the causal effects of genetic liability for prescription opioid use on an increased risk of coronary heart disease and myocardial infarction, which might be mediated by obesity‐related traits.

Alcohol use disorders (AUD), including alcohol abuse and alcohol dependence, are common psychiatric disorders contribute greatly to the burden of society. 1 Alcohol-related diseases are one of the leading risk factors of disability and mortality, causing about 3.3 million deaths around the world and taking account for 5.1% of the global burden of disease according to the report of WHO. 2 Depression is a highly prevalent mental illness and is one of the important causes of premature deaths. About 350 million people around the world suffer from depression and nearly one million of

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