Trait Aggressiveness Predicting Aggressive Behavior: The Moderating Role of Meta-Cognitive Certainty.

Research on aggression has benefitted from using individual-difference measures to predict aggressive behavior. Research on meta-cognition has recently identified that the predictive utility of individual-difference inventories can be improved by considering the certainty with which people hold their self-views. Merging these two frameworks, the present research examines whether assessing certainty in trait aggressiveness improves its ability to predict aggressive outcomes. Across two studies, participants reported their level of trait physical aggressiveness and the certainty with which they held their responses to the scale (predictor variables). Aggressive behavioral intentions (Study 1 and 2) and actual aggressive behavior (Study 2) were used as dependent measures. As hypothesized, results indicated that certainty moderated the effects of individual-differences in aggressiveness on both aggressive outcomes. Therefore, considering the certainty with which people hold their relevant traits can be useful for understanding aggression, and also for predicting the consistency between personality and behavior.pre-print741 K

Spin physics with antiprotons

New possibilities arising from the availability at GSI of antiproton beams, possibly polarised, are discussed. The investigation of the nucleon structure can be boosted by accessing in Drell-Yan processes experimental asymmetries related to cross-sections in which the parton distribution functions (PDF) only appear, without any contribution from fragmentation functions; such processes are not affected by the chiral suppression of the transversity function $h_1(x)$. Spin asymmetries in hyperon production and Single Spin Asymmetries are discussed as well, together with further items like electric and magnetic nucleonic form factors and open charm production. Counting rates estimations are provided for each physical case. The sketch of a possible experimental apparatus is proposed.Comment: Presented for the proceedings of ASI "Spin and Symmetry", Prague, July 5-10, 2004, to be published in Czech. J. Phys. 55 (2005

Bun splitting: a practical cutting stock problem

We describe a new hierarchical 2D-guillotine Cutting Stock Problem. In contrast to the classic cutting stock problem, waste is not an issue. The problem relates to the removal of a defective part and assembly of the remaining parts into homogeneous size blocks. The context is the packing stages of cake manufacturing. The company's primary objective is to minimise total processing time at the subsequent, packing stage. This objective reduces to one of minimising the number of parts produced when cutting the tray load of buns. We offer a closed form optimization approach to this class of problems for certain cases, without recourse to mathematical programming or heuristics. The methodology is demonstrated through a case study in which the number of parts is reduced by almost a fifth, and the manufacturer's subsidiary requirement to reduce isolated single bun parts and hence customer complaints is also satisfied

Exendin-4 Improves Glycemic Control, Ameliorates Brain and Pancreatic Pathologies, and Extends Survival in a Mouse Model of Huntington's Disease

OBJECTIVE—The aim of this study was to find an effective treatment for the genetic form of diabetes that is present in some Huntington's disease patients and in Huntington's disease mouse models. Huntington's disease is a neurodegenerative disorder caused by a polyglutamine expansion within the huntingtin protein. Huntington's disease patients exhibit neuronal dysfunction/degeneration, chorea, and progressive weight loss. Additionally, they suffer from abnormalities in energy metabolism affecting both the brain and periphery. Similarly to Huntington's disease patients, mice expressing the mutated human huntingtin protein also exhibit neurodegenerative changes, motor dysfunction, perturbed energy metabolism, and elevated blood glucose levels

Extra-Visual Functional and Structural Connection Abnormalities in Leber's Hereditary Optic Neuropathy

We assessed abnormalities within the principal brain resting state networks (RSNs) in patients with Leber's hereditary optic neuropathy (LHON) to define whether functional abnormalities in this disease are limited to the visual system or, conversely, tend to be more diffuse. We also defined the structural substrates of fMRI changes using a connectivity-based analysis of diffusion tensor (DT) MRI data. Neuro-ophthalmologic assessment, DT MRI and RS fMRI data were acquired from 13 LHON patients and 13 healthy controls. RS fMRI data were analyzed using independent component analysis and SPM5. A DT MRI connectivity-based parcellation analysis was performed using the primary visual and auditory cortices, bilaterally, as seed regions. Compared to controls, LHON patients had a significant increase of RS fluctuations in the primary visual and auditory cortices, bilaterally. They also showed decreased RS fluctuations in the right lateral occipital cortex and right temporal occipital fusiform cortex. Abnormalities of RS fluctuations were correlated significantly with retinal damage and disease duration. The DT MRI connectivity-based parcellation identified a higher number of clusters in the right auditory cortex in LHON vs. controls. Differences of cluster-centroid profiles were found between the two groups for all the four seeds analyzed. For three of these areas, a correspondence was found between abnormalities of functional and structural connectivities. These results suggest that functional and structural abnormalities extend beyond the visual network in LHON patients. Such abnormalities also involve the auditory network, thus corroborating the notion of a cross-modal plasticity between these sensory modalities in patients with severe visual deficits

Neuroimaging in cluster headache and other trigeminal autonomic cephalalgias

The central nervous system mechanisms involved in trigeminal autonomic cephalalgias, a group of primary headaches characterized by strictly unilateral head pain that occurs in association with ipsilateral craniofacial autonomic features, are still not comprehensively understood. However, functional imaging methods have revolutionized our understanding of mechanisms involved in these primary headache syndromes. The present review provides a brief overview of the major modern functional neuroimaging techniques used to examine brain structure, biochemistry, metabolic state, and functional capacity. The available functional neuroimaging data in cluster headache and other TACs will thus be summarized. Although the precise brain structures responsible for these primary headache syndromes still remain to be determined, neuroimaging data suggest a major role for posterior hypothalamus activation in initiating and maintaining attacks. Furthermore, pathophysiological involvement of the pain neuromatrix and of the central descending opiatergic pain control system was observed. Given the rapid advances in functional and structural neuroimaging methodologies, it can be expected that these non-invasive techniques will continue to improve our understanding into the nature of the brain dysfunction in cluster headache and other trigeminal autonomic cephalalgias

The C. elegans Opa1 Homologue EAT-3 Is Essential for Resistance to Free Radicals

The C. elegans eat-3 gene encodes a mitochondrial dynamin family member homologous to Opa1 in humans and Mgm1 in yeast. We find that mutations in the C. elegans eat-3 locus cause mitochondria to fragment in agreement with the mutant phenotypes observed in yeast and mammalian cells. Electron microscopy shows that the matrices of fragmented mitochondria in eat-3 mutants are divided by inner membrane septae, suggestive of a specific defect in fusion of the mitochondrial inner membrane. In addition, we find that C. elegans eat-3 mutant animals are smaller, grow slower, and have smaller broodsizes than C. elegans mutants with defects in other mitochondrial fission and fusion proteins. Although mammalian Opa1 is antiapoptotic, mutations in the canonical C. elegans cell death genes ced-3 and ced-4 do not suppress the slow growth and small broodsize phenotypes of eat-3 mutants. Instead, the phenotypes of eat-3 mutants are consistent with defects in oxidative phosphorylation. Moreover, eat-3 mutants are hypersensitive to paraquat, which promotes damage by free radicals, and they are sensitive to loss of the mitochondrial superoxide dismutase sod-2. We conclude that free radicals contribute to the pathology of C. elegans eat-3 mutants