La connaissance du gain d'autrui. Une incitation au risque ?

International audienceThis research aims at suggesting a causal model of risk taking, following the announcement of another player's gains in a gamble with elementary characteristics. Risk taking was measured by investment ratio, the amount the participant decided to bet divided by his current total assets. According with Langer's definition (1975), the illusion of control was measured by the level of personal success. The results show that the knowledge of another's gain increased risk taking and the expectancy of personal success. These results validated the causal model wherein the effect of the knowledge of another's gain on risk taking was mediated by the expectancy of personal success. The discussion relates mainly to the need for taking into account the fact that gamblers are not isolated decision makers, but takes account of some social parameters which guide their choices and actions.L'objectif de cette recherche était de proposer un modèle causal de la prise de risque après l'annonce d'un gain d'autrui, dans un jeu de pur hasard d'apparence élémentaire. La prise de risque était mesurée par le ratio d'investissement, soit le nombre de points misés sur le nombre de points possédés au moment de la mise. En accord avec la définition princeps de Langer (1975), l'illusion de contrôle était mesurée par le niveau d'attente de réussite personnelle. Les résultats montrent que l'annonce d'un gain notable d'autrui produit une augmentation de la perception de réussite personnelle et une hausse de la prise de risque. Ces résultats valident le modèle causal selon lequel l'effet de l'annonce d'un gain notable d'autrui sur la prise de risque est médiatisé par le niveau d'attente de réussite personnelle. La discussion porte principalement sur la nécessité de prendre en compte le fait que les joueurs ne sont pas des décideurs isolés, mais tiennent compte d'un certain nombre de paramètres sociaux qui guident leurs choix et leurs actions

Active Involvement, not Illusory Control, increases Risk Taking in a Gambling Game

International audienceThe research considers the influence of Choice (the possibility for the player to choose a gamble or another) and Involvement (the physical interaction with the gambling device) on risk taking in gambling games, and whether this influence is mediated by illusory control over the outcome of the gamble. Results of a laboratory experiment (n=100) show that (a) although Choice does increase illusory control, this influence does not translate in increased risk taking, and (b) whilst Involvement does increase risk taking, this effect is not mediated by illusory control. These results are discussed in relation to problem gambling, beliefs in the deployability of personal luck, and arousal approaches to risk taking

EMBARAZADAS [Material gráfico]

** APROXIMACIÓN HECHA DE PLACA ORIGINAL. ADQUIRIDA POR EL COLECCIONISTA EN LAS PALMAS DE GRAN CANARIAFOTO POSTAL DE TRES CHICAS CON MANTILLAS CANARIASCopia digital. Madrid : Ministerio de Educación, Cultura y Deporte. Subdirección General de Coordinación Bibliotecaria, 201

A coiled-coil affinity-based system for the controlled release of biofunctionalized gold nanoparticles from alginate hydrogels

Affinity-based systems represent a promising solution to control the delivery of therapeutics using hydrogels. Here, we report a hybrid system that is based on the peptidic E/K coiled coil affinity pair to mediate the release of gold nanoparticles (NPs) from alginate scaffolds. On one hand, the gold NPs were functionalized with the Ecoil-tagged epidermal growth factor (EGF). The bioactivity of the grafted EGF and the bioavailability of the Ecoil moiety were confirmed by EGF receptor phosphorylation assays and by capturing the functionalized NPs on a Kcoil-derivatized surface. On the other hand, alginate chains were modified with azido-homoalanine Kcoil (Aha-Kcoil) by azide–alkyne click chemistry. The hybrid system was formed by dispersing NPs functionalized with the Ecoil-tagged EGF in alginate hydrogels containing either 0, 10, or 20% of Kcoil-modified alginate (Alg-Kcoil). With 20% of Alg-Kcoil, the release of Ecoil-functionalized NPs was reduced by half when compared to the release of NPs without Ecoil, whereas little to no differences were noticed with either 0 or 10% of Alg-Kcoil. Differential dynamic microscopy was used to determine the diffusion coefficient of the NPs, and the results showed a decrease in the diffusion coefficient of Ecoil-functionalized NPs, when compared to bare PEGylated NPs. Altogether, our data demonstrated that the E/K coiled coil system can control the release of NPs in a high Kcoil content alginate gel, opening diverse applications in drug delivery

Defective involuntary attention to novelty in type 1 diabetes and impaired awareness of hypoglycaemia

Altres ajuts: Sociedad Española de DiabetesAim: To determine if there are differences in terms of neurophysiology and neurocognitive functioning in a group of type 1 diabetes (T1D) patients regarding hypoglycaemia awareness. Methods: 27 patients with T1D were classified according to Clarke score as having impaired awareness of hypoglycaemia (IAH; n = 11) or normal awareness to hypoglycaemia (NAH; n = 16). We measured several clinical and sociodemographic variables and cognitive performance using neuropsychological tests. Electroencephalography was assessed during an auditory oddball task. We compared the groups in terms of clinical/sociodemographic variables as well as two event-related brain potentials (ERPs): The P3a which is associated with automatic orientation of attention to novelty, and the P3b which is associated with target detection and processing. Results: The IAH group performed significantly worse on the Trail Making Test part A (TMT-A) (p = 0.05). Compared to the NAH group, P3a and P3b amplitudes in the frontal-central sites were significantly lower in the IAH group (p < 0.05). The P3a was strongly associated with worse performance on the TMT-A in the IAH group (r = 0.540; p < 0.005) Conclusion: IAH is accompanied by decreased neurophysiological activity in ERPs associated with information processing and with the automatic orientation of attention to novelty and environmental changes. These findings suggest a possible framework to better understand the cognitive origin of IAH in this patient population

El papel de la movilidad geográfica en la expansión de Aedes albopictus y en la transmisión de enfermedades infecciosas

Ponencia sobre el papel de la movilidad geográfica en la expansión de Aedes albopictus y en la transmisión de enfermedades infecciosas. Se estudia la dispersión de Aedes albopictus basados en el análisis de datos de la invasión en la provincia de Girona durante 2009-2011; y la dispersión epidémica en redes desarrollando un marco teórico para la modelización de la propagación de enfermedades infecciosas.N

An epilepsy-associated SV2A mutation disrupts synaptotagmin-1 expression and activity-dependent trafficking

The epilepsy-linked gene , has a number of potential roles in the synaptic vesicle (SV) life cycle. However, how loss of SV2A function translates into presynaptic dysfunction and ultimately seizure activity is still undetermined. In this study, we examined whether the first SV2A mutation identified in human disease (R383Q) could provide information regarding which SV2A-dependent events are critical in the translation to epilepsy. We utilized a molecular replacement strategy in which exogenous SV2A was expressed in mouse neuronal cultures of either sex, which had been depleted of endogenous SV2A to mimic the homozygous human condition. We found that the R383Q mutation resulted in a mislocalization of SV2A from SVs to the plasma membrane, but had no effect on its activity-dependent trafficking. This SV2A mutant displayed reduced mobility when stranded on the plasma membrane and reduced binding to its interaction partner synaptotagmin-1 (Syt1). Furthermore, the R383Q mutant failed to rescue reduced expression and dysfunctional activity-dependent trafficking of Syt1 in the absence of endogenous SV2A. This suggests that the inability to control Syt1 expression and trafficking at the presynapse may be key in the transition from loss of SV2A function to seizure activity. SV2A is a synaptic vesicle (SV) protein, the absence or dysfunction of which is linked to epilepsy. However, the series of molecular events that result in this neurological disorder is still undetermined. We demonstrate here that the first human mutation in SV2A identified in an individual with epilepsy displays reduced binding to synaptotagmin-1 (Syt1), an SV protein essential for synchronous neurotransmitter release. Furthermore, this mutant cannot correct alterations in both Syt1 expression and trafficking when expressed in the absence of endogenous SV2A (to mimic the homozygous human condition). This suggests that the inability to control Syt1 expression and trafficking may be key in the transition from loss of SV2A function to seizure activity

IVOA Recommendation: Vocabularies in the Virtual Observatory Version 1.19

This document specifies a standard format for vocabularies based on the W3C's Resource Description Framework (RDF) and Simple Knowledge Organization System (SKOS). By adopting a standard and simple format, the IVOA will permit different groups to create and maintain their own specialised vocabularies while letting the rest of the astronomical community access, use, and combine them. The use of current, open standards ensures that VO applications will be able to tap into resources of the growing semantic web. The document provides several examples of useful astronomical vocabularies

Measuring the functional impact of cognitive impairment in Huntington's disease

Acord transformatiu CRUE-CSICBackground: Patients with Huntington's disease (HD) exhibit a variable predominance of cognitive, behavioral and motor symptoms. A specific instrument focusing on the impact of cognitive impairment in HD over functional capacity is lacking. Objective: To address the need for a brief and specifically developed HD questionnaire able to capture functional aspects suspected to be sensitive to cognitive impairment. Methods: We developed and validated the "Huntington's Disease-Cognitive Functional Rating Scale" (HD-CFRS) in 78 symptomatic carriers of the Huntington's disease mutation. We also administered the HD-CFRS to a knowledgeable informant to measure the level of agreement. To explore the association between HD-CFRS scores and participants' cognitive status, we administered objective measures of cognition. Participants were classified as cognitively preserved (HD-NC), as having mild cognitive impairment (HD-MCI), or as having dementia (HD-Dem). Results: The HD-CFRS showed concurrent validity and internal consistency in the three groups. HD carriers and informants in the HD-NC group obtained similar HD-CFRS scores. However, in patients with mild cognitive impairment and dementia, informers reported greater functional impairment than HD participants. The HD-CFRS total score showed strong correlations with measures assessing cognition. Conclusions: These findings support the utility of the HD-CFRS as a brief and reliable instrument to measure functional defects associated with cognitive impairment in HD. We believe this questionnaire could be a useful tool both for clinical practice and research