In two experiments, false feedback given about cognitive performance influenced participants’ beliefs about whether they had been allocated to the active treatment or placebo. These beliefs also appeared to influence actual cognitive performance in that participants who believed they had taken the active treatment had higher accuracy in Experiment 1 and faster reaction times in Experiment 2 than those who believed they had been given a placebo. The addition of no treatment control groups in Experiment 2 showed that these effects could not be accounted for by

the feedback manipulation itself, thereby supporting expectancy as a causal factor.

These results indicate the importance of assessing participants’ beliefs about their treatment allocation in real double-blind RCTs and considering if and how these may have affected the trial’s outcome.”
“Genetic variants eFT-508 in vivo of the serotonergic neurotransmitter Evofosfamide system are potential contributing

factors in the pathological processes underlying Alzheimer’s disease (AD). We examined polymorphisms of the serotonin transporter (SLC6A4) and serotonin receptor 2A (HTR2A) genes for possible association with AD, and therefore genotyped 5-HTTLPR, STin2-VNTR and HTR2A T102C polymorphisms in 252 Hungarian AD patients and 234 ethnically matched control individuals. We did not detect statistically significant differences in genotype distribution comparing the AD and the control group when the polymorphisms were investigated separately. Logistic regression analyses, however, revealed an interaction effect between 5-HTTLPR and HTR2A T102C (p = 0.019), but not between 5-HTTLPR and STin2-VNTR (p = 0.494) or STin2-VNTR and HTR2A T102C (p selleck chemicals llc = 0.310) polymorphisms. Our study suggests no individual influence of the investigated polymorphisms but a

potential combined effect of the 5-HTTLPR L/L and HTR2A T102C C/C genotypes on AD risk. However, the results need to be treated with considerable caution, and further analyses in larger samples are required. (C) 2013 Elsevier Ireland Ltd. All rights reserved.”
“Infection of the chestnut blight fungus Cryphonectria parasitica with Cryphonectria hypovirus 1 (CHV1) causes disruption of virulence, pigmentation, and sporulation. Transcriptional downregulation of key developmentally regulated fungal genes occurs during infection, but vegetative growth is unaffected. Previous studies showed that CHV1 utilizes trans-Golgi network (TGN) secretory vesicles for replication. In this study, the fungal cell surface hydrophobin cryparin was chosen as a marker to follow secretion in virally infected and noninfected strains. Subcellular fractionation, cryparin-green fluorescent protein (GFP) fusion, and Western blot studies confirmed that vesicles containing cryparin copurify with the same fractions previously shown to contain elements of the viral replication complex and the TGN resident endoprotease Kex2.