13 research outputs found

    Syntactic learning by mere exposure - An ERP study in adult learners

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    <p>Abstract</p> <p>Background</p> <p>Artificial language studies have revealed the remarkable ability of humans to extract syntactic structures from a continuous sound stream by mere exposure. However, it remains unclear whether the processes acquired in such tasks are comparable to those applied during normal language processing. The present study compares the ERPs to auditory processing of simple Italian sentences in native and non-native speakers after brief exposure to Italian sentences of a similar structure. The sentences contained a non-adjacent dependency between an auxiliary and the morphologically marked suffix of the verb. Participants were presented four alternating learning and testing phases. During learning phases only correct sentences were presented while during testing phases 50 percent of the sentences contained a grammatical violation.</p> <p>Results</p> <p>The non-native speakers successfully learned the dependency and displayed an N400-like negativity and a subsequent anteriorily distributed positivity in response to rule violations. The native Italian group showed an N400 followed by a P600 effect.</p> <p>Conclusion</p> <p>The presence of the P600 suggests that native speakers applied a grammatical rule. In contrast, non-native speakers appeared to use a lexical form-based processing strategy. Thus, the processing mechanisms acquired in the language learning task were only partly comparable to those applied by competent native speakers.</p

    Conséquence de l'utilisation des nouvelles technologies de l'information et de la communication pendant la conduite automobile : rapport final COUNTIC

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    Convention DSCR/INRETS, Contrat COUBTICRapport de rechercheL'objectif principal de cette recherche est de mettre au point des méthodes d'évaluation des effets distracteurs de diverses activités de communication vocale sur l'activité de conduite. Ces effets peuvent être évalués à plusieurs niveaux : - dégradation du traitement de l'information routière - analyse des performances résultantes - modifications de la charge mentale liée à l'adjonction d'une tâche supplémentaire Au final, ceci va permettre de disposer d'échelles d'évaluation de ces effets dont la variation dépend de l'exigence en attention de la tâche ajoutée de communication

    MyD88 is a critical regulator of hematopoietic cell-mediated neuroprotection seen after stroke

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    Neuroinflammation is critical in the neural cell death seen in stroke. It has been shown that CNS and peripheral responses drive this neuroinflammatory response in the brain. The Toll-like receptors (TLRs) are important regulators of inflammation in response to both exogenous and endogenous stressors. Taking advantage of a downstream adapter molecule that controls the majority of TLR signalling, this study investigated the role of the TLR adaptor protein myeloid differentiation factor 88 (MyD88) in the control of CNS and peripheral inflammation. Reversible middle-cerebral artery occlusion was used as the model of stroke in vivo; in vitro primary cultured neurons and glia were subject to four hours of oxygen and glucose deprivation (OGD). Both in vitro and in vivo Myd88(-/-) animals or cells were compared with wild type (WT). We found that after stroke Myd88(-/-) animals have a larger infarct volume compared to WT animals. Interestingly, in vitro there was no difference between the survival of Myd88(-/-) and WT cells following OGD, suggesting that peripheral responses were influencing stroke outcome. We therefore generated bone marrow chimeras and found that Myd88(-/-) animals have a smaller stroke infarct than their radiation naive counterparts if their hematopoietic cells are WT. Furthermore, WT animals have a larger stroke than their radiation naive counterparts if the hematopoietic cells are Myd88(-/-) . We have demonstrated that MyD88-dependent signalling in the hematopoietic cell lineage reduces infarct size following stroke and that infiltrating cells to the site of neuroinflammation are neuroprotective following stroke.Catherine E. Downes, Connie H. Y. Wong, Katya J. Henley, Pedro L. Guio-Aguilar, Moses Zhang, Robert Ates, Ashley Mansell, Benjamin T. Kile, Peter J. Crac
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