Differential effects of task-specific practice on performance in a simulated penalty kick under high-pressure

Objectives The current study investigated to what extent task-specific practice can help reduce the adverse effects of high-pressure on performance in a simulated penalty kick task. Based on the assumption that practice attenuates the required attentional resources, it was hypothesized that task-specific practice would enhance resilience against high-pressure. Method Participants practiced a simulated penalty kick in which they had to move a lever to the side opposite to the goalkeeper's dive. The goalkeeper moved at different times before ball-contact. Design Before and after task-specific practice, participants were tested on the same task both under low- and high-pressure conditions. Results Before practice, performance of all participants worsened under high-pressure; however, whereas one group of participants merely required more time to correctly respond to the goalkeeper movement and showed a typical logistic relation between the percentage of correct responses and the time available to respond, a second group of participants showed a linear relationship between the percentage of correct responses and the time available to respond. This implies that they tended to make systematic errors for the shortest times available. Practice eliminated the debilitating effects of high-pressure in the former group, whereas in the latter group high-pressure continued to negatively affect performance. Conclusions Task-specific practice increased resilience to high-pressure. However, the effect was a function of how participants responded initially to high-pressure, that is, prior to practice. The results are discussed within the framework of attentional control theory (ACT).

Differential effects of undernourishment on the differentiation and maturation of rat enteric neurons

The colocalization, number, and size of various classes of enteric neurons immunoreactive (IR) for the purinergic P2X2 and P2X7 receptors (P2X2R, P2X7R) were analyzed in the myenteric and submucosal plexuses of control, undernourished, and re-fed rats. Pregnant rats were exposed to undernourishment (protein-deprivation) or fed a control diet, and their offspring comprised the following experimental groups: rats exposed to a normal diet throughout gestation until postnatal day (P)42, rats protein-deprived throughout gestation and until P42, and rats protein-deprived throughout gestation until P21 and then given a normal diet until P42. Immunohistochemistry was performed on the myenteric and submucosal plexuses to evaluate immunoreactivity for P2X2R, P2X7R, nitric oxide synthase (NOS), choline acetyltransferase (ChAT), calbindin, and calretinin. Double-immunohistochemistry of the myenteric and submucosal plexuses demonstrated that 100% of NOS-IR, calbindin-IR, calretinin-IR, and ChAT-IR neurons in all groups also expressed P2X2R and P2X7R. Neuronal density increased in the myenteric and submucosal plexuses of undernourished rats compared with controls. The average size (profile area) of some types of neurons in the myenteric and submucosal plexuses was smaller in the undernourished than in the control animals. These changes appeared to be reversible, as animals initially undernourished but then fed a normal diet at P21 (re-feeding) were similar to controls. Thus, P2X2R and P2X7R are present in NOS-positive inhibitory neurons, calbindin- and calretinin-positive intrinsic primary afferent neurons, cholinergic secretomotor neurons, and vasomotor neurons in rats. Alterations in these neurons during undernourishment are reversible following re-feeding

Differential inflammasome expression and IL-1β secretion in monocyte-derived dendritic cells differentiated with IL-4 or IFN-α

NLRP3-inflammasome activation was evaluated in monocyte-derived dendritic cells (DC) obtained through IL-4 (IL4-DC) or IFN-α (IFN-DC) protocols and pulsed with chemically inactivated HIV-1. Inflammasome' genes expression and IL-1β secretion were compared in DC isolated from 15 healthy subjects (HC) and 10 HIV-1 infected individuals (HIV+). FINDINGS: Whether HIV was able to increased NLRP3-inflammasome genes expression and IL-1β secretion in IL4-DC from HC, the induction of inflammasome appeared significantly reduced in IFN-DC from HC, suggesting a different responsive state of IFN-DC compared to IL4-DC. No inflammasome activation was observed in IL4-DC as well as in IFN-DC derived from HIV + subjects, confirming previous findings on "unresponsive" state of DC derived from HIV + possibly due to chronic inflammatory state of these individuals. CONCLUSIONS: Our results showed that IFN-α differently modulates inflammasome expression during monocytes-DC in vitro differentiation. These findings could be of interest considering the on-going research about DC manipulation and therapeutic strategies for HIV + involving DC-based immune-vaccines.