22 research outputs found

    Why Does Exercise “Triggerâ€? Adaptive Protective Responses in the Heart?

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    Numerous epidemiological studies suggest that individuals who exercise have decreased cardiac morbidity and mortality. Pre-clinical studies in animal models also find clear cardioprotective phenotypes in animals that exercise, specifically characterized by lower myocardial infarction and arrhythmia. Despite the clear benefits, the underlying cellular and molecular mechanisms that are responsible for exercise preconditioning are not fully understood. In particular, the adaptive signaling events that occur during exercise to “trigger� cardioprotection represent emerging paradigms. In this review, we discuss recent studies that have identified several different factors that appear to initiate exercise preconditioning. We summarize the evidence for and against specific cellular factors in triggering exercise adaptations and identify areas for future study

    On the Functional Significance of the P1 and N1 Effects to Illusory Figures in the Notch Mode of Presentation

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    The processing of Kanizsa figures have classically been studied by flashing the full “pacmen” inducers at stimulus onset. A recent study, however, has shown that it is advantageous to present illusory figures in the “notch” mode of presentation, that is by leaving the round inducers on screen at all times and by removing the inward-oriented notches delineating the illusory figure at stimulus onset. Indeed, using the notch mode of presentation, novel P1and N1 effects have been found when comparing visual potentials (VEPs) evoked by an illusory figure and the VEPs to a control figure whose onset corresponds to the removal of outward-oriented notches, which prevents their integration into one delineated form. In Experiment 1, we replicated these findings, the illusory figure was found to evoke a larger P1 and a smaller N1 than its control. In Experiment 2, real grey squares were placed over the notches so that one condition, that with inward-oriented notches, shows a large central grey square and the other condition, that with outward-oriented notches, shows four unconnected smaller grey squares. In response to these “real” figures, no P1 effect was found but a N1 effect comparable to the one obtained with illusory figures was observed. Taken together, these results suggest that the P1 effect observed with illusory figures is likely specific to the processing of the illusory features of the figures. Conversely, the fact that the N1 effect was also obtained with real figures indicates that this effect may be due to more global processes related to depth segmentation or surface/object perception

    Early Category-Specific Cortical Activation Revealed by Visual Stimulus Inversion

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    Visual categorization may already start within the first 100-ms after stimulus onset, in contrast with the long-held view that during this early stage all complex stimuli are processed equally and that category-specific cortical activation occurs only at later stages. The neural basis of this proposed early stage of high-level analysis is however poorly understood. To address this question we used magnetoencephalography and anatomically-constrained distributed source modeling to monitor brain activity with millisecond-resolution while subjects performed an orientation task on the upright and upside-down presented images of three different stimulus categories: faces, houses and bodies. Significant inversion effects were found for all three stimulus categories between 70–100-ms after picture onset with a highly category-specific cortical distribution. Differential responses between upright and inverted faces were found in well-established face-selective areas of the inferior occipital cortex and right fusiform gyrus. In addition, early category-specific inversion effects were found well beyond visual areas. Our results provide the first direct evidence that category-specific processing in high-level category-sensitive cortical areas already takes place within the first 100-ms of visual processing, significantly earlier than previously thought, and suggests the existence of fast category-specific neocortical routes in the human brain

    Développement cognitif à l’âge de 5 ans de très grands prématurés sans anomalies cérébrales néonatales sévères. Relations avec l’EEG à 6 semaines de vie

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    International audienceAims of the studyThis prospective study aimed to analyze the relationship between EEG at 6 weeks after birth and cognitive outcome at the age of 5 in children born very preterm who did not present with severe neonatal cerebral abnormalities.Patients and methodsEEGs were recorded at 6 weeks of age in infants born < 29 weeks of gestation or weighing < 1000 g at birth. At 5 years, study participants underwent a neurological assessment and cognitive evaluation with the Kaufman Assessment Battery for Children (K-ABC).ResultsFifty-eight children had an EEG at 6 weeks after birth. Fifty-one were evaluated at 5 years. Twenty-six children (51.0%) had one or more disabilities: neuromotor, sensory, behavioral, and/or cognitive. Children with EEG abnormalities had significantly more disabilities (20 of 25, 80%) than children with normal EEG (6 of 26, 23%) (P = 0.0002). Thirty-five children underwent complete K-ABC assessment. Multiple linear regression analysis indicated a significant relationship between the overall EEG abnormalities (normal, dysmature, and/or disorganized) and two scales: mental processing composite (MPC) scales (P = 0.0121), and sequential processing scales (P = 0.0012). Dysmature EEGs were more predictive of lower MPC and sequential processing scales than disorganized EEGs. Immature occipital slow waves (i.e., too high for conceptional age) were consistently recorded in children with dysmature EEGs and associated with the lowest K-ABC scores.ConclusionEEG abnormalities recorded at 6 weeks after birth, such as immature occipital slow waves, were associated with later cognitive impairments. EEG at 6 weeks can be an early and reliable tool for assessing the risk of future cognitive impairment.ObjectifsAnalyser prospectivement les relations entre l’EEG à 6 semaines de vie et l’évolution cognitive à l’âge de 5 ans d’anciens très grands prématurés sans anomalies cérébrales néonatales précoces sévères.MéthodesLes EEG ont été enregistrés à 6 semaines de vie chez des prématurés très immatures ou hypotrophes (< 29 semaines d’âge gestationnel ou moins de 1000 g de poids de naissance). Les enfants ont bénéficié à l’âge de 5 ans d’un bilan neurologique et d’une évaluation cognitive par le test psychométrique de Kaufman (K-ABC).RésultatsUne évaluation neurologique a été réalisée chez 51 enfants. Vingt-six d’entre eux (51 %) présentaient une ou plusieurs déficiences : neuromotrices, sensorielles, comportementales et/ou cognitives. Les enfants chez lesquels des anomalies EEG avaient été observées présentaient significativement plus de déficiences (20/25, 80 %) que les enfants avec EEG normal (6/26, 23 %) (p = 0,0002). Trente-cinq enfants ont effectué complètement le K-ABC. L’analyse statistique par régression linéaire multiple a montré une relation significative entre l’aspect global de l’EEG (normal, dysmature et désorganisé) et les échelles des processus mentaux composites (PMC) (p = 0,0121) et des processus séquentiels (p = 0,0012). Les scores aux processus mentaux composites (PMC) et aux processus séquentiels étaient significativement plus bas après des EEG dysmatures qu’après des EEG désorganisés. Des ondes lentes occipitales immatures (c.-à-d. trop amples pour l’âge conceptionnel) étaient constamment enregistrées chez les enfants avec tracés dysmatures et étaient associées aux scores les plus faibles au K-ABC.ConclusionDes anomalies EEG telles que des ondes lentes occipitales immatures étaient associées à des déficiences cognitives ultérieures. L’EEG à 6 semaines de vie est un outil utile pour déterminer un risque de déficience cognitive
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