These findings contribute to our understanding of the processes through which implicit associations are learned in the context of addiction. Understanding cognitive as well as other potential biological and environmental factors that may predict drinking behaviors in youth will aid in the development of more effective evidence-based strategies for the prevention of alcoholism.Cognitive decline (CD), which related to vascular dementia, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis and diabetes mellitus, is a growing health concern that has a great impact on the patients' quality of life. Although extensive efforts, the mechanisms of CD are still far from being clarified, not to mention the effective treatment and prevention strategies. Caveolin-1 (Cav-1), a trans-membrane protein, is a major component of the caveolae structure and scaffolding proteins. Recently, ample evidence depicts a strong correlation between Cav-1 and CD, however, the specific role of Cav-1 in CD has not been clearly examined and how they might be connected have yet to be identified. This review seeks to provide a comprehensive overview about how Cav-1 modulates pathogeneses of CD-associated diseases. In summary, Cav-1 can promote structural and functional plasticity of neurons, improve neurogenesis, relieve mitochondrial dysfunction, inhibit inflammation and suppress oxidative stress, which have shed light on the idea that Cav-1 may be an efficacious therapeutic target to treat CD.Affinin is mainly recognized by its antinociceptive effect. Recently, our research group demonstrated that this compound produces vasodilation via activation of the gasotransmitters signaling pathways. However, the molecular targets of affinin were not identified. Considering the structural similarity of this alkamide with anandamide, we hypothesized that affinin-induced vasodilation could involve participation of TRP channels and cannabinoid receptors. In this work, by using the isolated rat aorta assay, we assessed involvement of TRP channels, the cannabinoid system, and the HNO-CGRP-TRPA1 pathway on the mechanism of action of affinin. Additionally, we measured NO and H2S levels elicited by affinin on rat aorta homogenates and carried out computer simulations of molecular interactions between affinin and the TRPA1 and TRPV1 channels and the CB1 receptor. Our results indicated that affinin induces an increase in aortic NO and H2S levels. We found evidence that the vasodilator effect induced by affinin involves activation of TRPA1 and TRPV1 channels and the CB1 and eCB receptors. In silico analyses showed that affinin is able to bind with high affinity to these molecular targets. Moreover, we also proved that affinin-induced vasodilation is partly mediated via activation of the HNO-TRPA1-CGRP pathway. Based on these results we propose a novel mechanism of action to explain the vasodilatory effect of affinin, which could be developed as an alternative drug to treat cardiovascular diseases.Burst suppression (BS) is an electroencephalogram (EEG) pattern in which signals alternates between high-amplitude slow waves (burst waves) and nearly flat low-amplitude waves (suppression waves). In this study, we used wide-field (8.32 mm × 8.32 mm) fluorescent calcium imaging to record the activity of glutamatergic neurons in the parietal and occipital cortex, in conjunction with EEG recordings under BS induced by different anesthetics (sevoflurane, isoflurane, and propofol), to investigate the spatiotemporal pattern of neural activity under BS. The calcium signal of all observed cortices was decreased during the phase of EEG suppression. However, during the phase of EEG burst, the calcium signal in areas of the medial cortex, such as the secondary motor and retrosplenial area, was excited, whereas the signal in areas of the lateral cortex, such as the hindlimb cortex, forelimb cortex, barrel field, and primary visual area, was still suppressed or only weakly excited. Correlation analysis showed a strong correlation between the EEG signal and the calcium signal in the medial cortex under BS (except for propofol induced signals). As the burst-suppression ratio (BSR) increased, the regions with strong correlation coefficients became smaller, but strong correlation coefficients were still noted in the medial cortex. JNK inhibitor purchase Taken together, our results reveal the landscape of cortical activity underlying BS. Several studies reported beneficial effects of chromium supplementation for management of type 2 diabetes mellitus (T2DM). The present study aimed to provide a systematic review and meta-analysis of randomized controlled trials (RCTs) examining the effects of chromium supplementation on blood pressure, body mass index (BMI), liver function enzymes and malondialdehyde (MDA) in patients with T2DM. PubMed, Scopus, and Embase were searched up to 15 November 2020 with no language and time restriction. RCTs that reported the effects of chromium supplementation on blood pressure, BMI, liver function enzymes and MDA in patients with T2DM were included. A random-effects model was used to compute weighted mean differences (WMDs) with 95 % confidence intervals (CIs). Between-study heterogeneity was assessed by Cochran's Q test and quantified by I statistic. Of 3586 publications, 15 RCTs were included for the meta-analysis. Pooled effect sizes indicated that chromium significantly reduced diastolic blood pressure (DBP) (WMD) -2.36 mmHg, 95 % CI -4.14, -0.60; P = 0.008), and MDA (WMD -0.55 umol/l, 95 % CI -0.96, -0.14; P = 0.008). However, chromium supplementation did not significantly affect BMI, systolic blood pressure (SBP), alanine aminotransferase (ALT), aspartate aminotransferase (AST). Meta-regression analysis did not show significant linear relationship between dose of chromium and change in BMI (p = 0.412), SBP (p = 0. 319), DBP (p = 0.102), ALT (p = 0.923), AST (p = 0.986) and MDA (p = 0.055). The present systematic review and meta-analysis shows that supplementation with chromium at dose of 200-1000 μg/day may reduce DBP and MDA in T2DM patients.The present systematic review and meta-analysis shows that supplementation with chromium at dose of 200-1000 μg/day may reduce DBP and MDA in T2DM patients.