Methods Eighty-four social drinkers took part in two studies that followed a counterbalanced repeated measure design. Fifteen men and 33 women were tested the morning (09:00, 11:00 or 13:00?h) following normal/usual alcohol consumption and the morning after no alcohol consumption; the order of testing was counterbalanced. In a second study, 36 participants (18 men and 18 women) were

tested after receiving alcohol to attain a blood alcohol concentration of 0.08%, and after no alcohol administration, the order of testing was counterbalanced. In both studies, participants completed LDN-193189 ic50 a task battery of memory, reaction time and attention tasks. Results Alcohol had no effect on the free recall task and the spatial attention task. Alcohol consumption, either acute or the next day, significantly affected reaction time, divided attention, selective attention and Stroop interference. The impairments during intoxication and hangover were of comparable magnitude. Performance on tasks of delayed recognition and irregular interstimulus reaction time was worse during hangover when compared with intoxication. Conclusion It is evident that awareness selleck kinase inhibitor needs to be raised

that performance the morning after alcohol consumption is at the same level if not worse than when participants are at the legal limit for driving (0.08% blood alcohol concentration). Copyright (c) 2012 John PCI-34051 inhibitor Wiley & Sons, Ltd.”
“Traditionally, medical therapy for epilepsy has aimed to suppress seizure activity, but has been unable to alter the progression of the underlying disease. Recent advances in our understanding of mechanisms of epileptogenesis open the door for the development of new therapies which prevent the pathogenic changes in the brain that predispose to spontaneous seizures. In particular, the mammalian target of rapamycin (mTOR) signaling pathway has recently

garnered interest as an important regulator of cellular changes involved in epileptogenesis, and mTOR inhibitors have generated excitement as potential antiepileptogenic agents. mTOR hyperactivation occurs in tuberous sclerosis complex (TSC), a common genetic cause of epilepsy, as a result of genetic mutations in upstream regulatory molecules. mTOR inhibition prevents epilepsy and brain pathology in animal models of TSC. mTOR dysregulation has also been demonstrated in a variety of other genetic and acquired epilepsies, including brain tumors, focal cortical dysplasias, and animal models of brain injury due to status epilepticus or trauma. Indeed, mTOR inhibitors appear to possess antiepileptogenic properties in animal models of acquired epilepsy as well. Thus, mTOR dysregulation may represent a final common pathway in epilepsies of various causes.