Accordingly, it probably confers some advantage that other mammals either lack or attain through the

function of other structures. Yet, this advantage remains enigmatic. This is not so for other parts of the cortex. For example, certain visual areas encode, represent and store knowledge about objects. By analogy, perhaps the primate prefrontal cortex encodes, represents and stores knowledge about behaviors, including the consequences of doing (or not doing) something in complex and challenging situations. The long list of functions often attributed to the prefrontal cortex could contribute to knowing what to do and what will happen selleck chemicals when rare risks arise or outstanding opportunities knock.”
“Background. Hierarchical Cumulative scales are common and informative in psychology.

The General Health Questionnaire (GHQ) does not appear to have been subjected to an analysis that examines click here the hierarchical and cumulative nature of its items. We report an analysis of data from the 30-item GHQ (GHQ-30) as part of the Health and Lifestyle Survey (HALS).

Method. Data from 6317 participants who completed the GHQ-30 as part of the HALS were analysed using the Mokken Scaling Procedure (MSP), which is a computer program that searches polychotomous data for hierarchical and cumulative scales on the basis of a range of diagnostic criteria.

Results. A final scale consisting of nine items from the GHQ-30 was obtained that, according to the criteria for a Mokken scale, was a reliable and very strong scale. The least difficult item in the scale is ‘been (un)able to face up to your problerns?’ and the most SCH772984 mw difficult item is ‘felt that life isn’t worth living?’

Conclusions. Items from the GHQ-30 form a short hierarchical and cumulative scale. The majority of these items also appear in the GHQ-12. The nine-item GHQ shows better distribution properties than the GHQ-30 and compares

very favourably with the GHQ-12.”
“Huntington’s disease (HD) is a fatal, inherited neurodegenerative disorder that gradually robs affected individuals of memory, cognitive skills and normal movements. Although research has identified a single faulty gene, the huntingtin gene, as the cause of the disease, a cure remains elusive. Strong evidence indicates that mitochondrial impairment plays a key part in HD pathogenesis. Here, we highlight how mutant huntingtin (mtHtt) might cause mitochondrial dysfunction by either perturbing transcription of nuclear-encoded mitochondrial proteins or by direct interaction with the organelle and modulation of respiration, mitochondrial membrane potential and Ca(2+) buffering. In addition, we propose that mtHtt might convey its neurotoxicity by evoking defects in mitochondrial dynamics, organelle trafficking and fission and fusion, which, in turn, might result in bioenergetic failure and HD-linked neuronal dysfunction and cell death.