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A relatively common polymorphism in the human brain-derived neurotrophic factor (BDNF) gene (Val66Met, which corresponds to Val68Met in mice) has been shown to modulate cognitive function and vulnerability to mental health disorders. This substitution impairs trafficking and activity-dependent release of BDNF. A number of studies with both humans and transgenic mice suggest that carriers of the Met allele have deficits in the structure and/or function of the hippocampal formation. Using a relatively new transgenic mouse model of this polymorphism, we recently demonstrated that it modulates the effects of developmental ethanol exposure in the hippocampus. Here, we further characterized the effect of this polymorphism on hippocampal morphology and its interaction with ethanol vapor exposure during the 2nd and 3rd trimester equivalents of human pregnancy. We found that BDNFmet/met mice have slightly larger hippocampal volumes than BDNFval/val mice. Ethanol vapor exposure during the 2nd and 3rd trimester equivalents of human pregnancy increased hippocampal volume in a single hippocampal subregion, the CA1 stratum radiatum. Ethanol exposure did not interact with BDNF genotype to affect volume in any hippocampal subregion. These results suggest that the Val66Met polymorphism does not reduce hippocampal size (i.e., it rather increases it slightly) or increase susceptibility to prenatal ethanol exposure-induced structural hippocampal damage during adulthood. Engagement of programmed death-1 (PD-1) receptor by its ligands (PD-L1/PD-L2) in activated immune cells is known to be involved in inflammatory neurological disease via a co-inhibitory signal pathway. Interaction of PD-1/PD-L1 is believed to occur only in activated neuroimmune cells because there are undetectable levels of PD-1/PD-L1 in normal physiological conditions. Here, we evaluated whether activation of neuroimmune cells such as human macrophage, brain endothelial cells (hBECs), astrocytes, microglia, and neurons by non-toxic concentrations of ethanol (EtOH) exposure can alter PD-1/PD-L1 expression. Thus, the present study is limited to the screening of PD-1/PD-L1 alterations in neuroimmune cells following ethanol exposure. We found that exposure of human macrophage or microglia to EtOH in primary culture immediately increased the levels of PD-L1 and gradually up-regulated PD-1 levels (beginning at 1-2 hours). Similarly, ethanol exposure was able to induce PD-1/PD-L1 levels in hBECs and neuronal culture in a delayed process (occurring at 24 hours). Astrocyte culture was the only cell type that showed endogenous levels of PD-1/PD-L1 that was decreased by EtOH exposure time-dependently. We concluded that ethanol (alcohol) mediated the induction of PD-1/PD-L1 differentially in neuroimmune cells. Taken together, our findings suggest that up-regulation of PD-1/PD-L1 by chronic alcohol use may dampen the innate immune response of neuroimmune cells, thereby contributing to neuroinflammation and neurodegeneration. BACKGROUND Alcohol-induced blackouts are a common high-risk outcome of heavy episodic drinking and considered a marker of problematic alcohol consumption. One’s estimates of the prevalence and peer approval of heavy episodic drinking (i.e., social norm perception; descriptive and injunctive norms respectively) strongly relates to high-risk alcohol consumption. However, it is unknown if the intention to blackout and the occurrence of alcohol-induced blackouts also associates with these estimates. Therefore, the purpose of this paper is to explore the relation between participants’ social norm perception and alcohol-induced blackout intentions and recent blackout history. METHOD A total of 4430 participants completed an online survey with an average age of 19.97 (SD = 1.70) years. A series of ANOVAs and a structural equation model examined the relation between social norm perception, intention to blackout, and recent blackout history. RESULTS In the structural equation model, the social norm variables (descriptive and injunctive norms) were associated with higher levels of blackout intentions and recent blackout history. The global fit indices suggest that the data fit the model, χ2(n = 4248, 442) = 7755.90, p less then . 001, CFI = .96, TLI = .96, RMSEA = .06 (CI90 .061-.064). CONCLUSIONS Participants with a higher likelihood of having a past 30-day history of alcohol-induced blackouts and higher blackout intentions believed that many of their peer groups approved of certain alcohol-related behaviors and that their peer groups drink frequently and higher quantities. Future interventions may assess the impact of adjusting social norms on both the intention to blackout and experiencing blackouts. Alcoholism and high fat diet (HFD)-induced obesity individually promote insulin resistance and glucose intolerance in clinical populations, increasing risk for metabolic diseases. HFD can also stimulate alcohol intake in short term clinical studies. Unfortunately, there is currently a disconnect between animal models and the clinical findings as animal studies typically show that HFD decreases ethanol intake while ethanol intake mitigates HFD-induced effects on insulin and glucose dysfunction. However, most previous animal studies utilized forced or continuous HFD and/or ethanol. In three experiments we sought to determine if HFD (HFD=60% calories from fat) vs control diet (Chow=16% fat) alters voluntary two-bottle choice ethanol intake in male C57Bl/6J mice given differing access schedules for 6-7 weeks and assessed resultant impact on metabolic function via insulin and glucose tolerance tests. SGI1776 Experiment 1 Unlimited Access Ethanol+HFD (UAE+HFD; n=15; 10% ethanol v/v, ad libitum diet and ethanol) or UAE+Chownge eating-like behaviors can transfer to binge drinking behaviors. This study aims to estimate dietary exposure to deoxynivalenol and fumonisins (FBs) of infants and toddlers in Turkey. A total of 75 processed cereal-based foods intended for infants and toddlers collected between July and October 2018, were analysed by high performance liquid chromatography (HPLC). DON was determined in 21.3% of samples with mean middle bound (MB) level of 28.4 μg/kg. Of the 16 quantifiable samples, only one showed values above 200 μg/kg. Fumonisin B1 (FB1) was detected at quantifiable levels only in three samples, while FB2 was not found in any sample. Estimated mean MB chronic dietary exposures to DON in infants and toddlers were 0.161 and 0.118 μg/kg b.w. per day, while 95th percentile (P95) MB exposures to DON were estimated at 0.564 and 0.414 μg/kg b.w. per day, respectively. Mean MB dietary exposures to FBs for infants and toddlers, respectively, were 0.093 and 0.068 μg/kg b.w. per day; P95 exposure estimates were 0.079 and 0.058 μg/kg b.w. per day. Both for DON and FBs, mean and P95 exposures of infants and toddlers did not exceeded the threshold level of 1 μg/kg b.