BACKGROUND AND PURPOSEThe renin-angiotensin system (RAS) is critical for the control of blood pressure by the CNS. Recently, direct renin inhibitors were approved as antihypertensive agents. However, the signalling mechanism of renin, which regulates blood pressure in the nucleus tractus solitarii (NTS) remains unclear. Here we have investigated the signalling pathways involved in renin-mediated blood pressure regulation, at the NTS. EXPERIMENTAL APPROACHDepressor responses to renin microinjected into the NTS of Wistar-Kyoto rats were elicited in the absence and presence of the endothelial nitric oxide synthase (eNOS)-specific inhibitor, N(5)-(-iminoethyl)-L-ornithine, Akt inhibitor IV and LY294002, a PI3K inhibitor and GP antagonist-2A [Gq inhibitor]. Lisinopril (angiotensin converting enzyme inhibitor), losartan, valsartan (angiotensin AT1 receptor antagonists), D-Ala7-Ang-(1-7) (angiotensin-(1-7) receptor antagonist) were used to study the involvement of RAS on renin-induced depressor effects. KEY RESULTSMicroinjection of renin into the NTS produced a prominent depressor effect and increased NO production. Pretreatment with Gq-PI3K-Akt-eNOS pathway-specific inhibitors significantly attenuated the depressor response evoked by renin. Immunoblotting and immunohistochemical studies further showed that inhibition of PI3K significantly blocked renin-induced eNOS-Ser 117 and Akt-Ser 473 phosphorylation in situ. In addition, pre-treatment of the NTS with RAS inhibitors attenuated the vasodepressor effects evoked by renin. Microinjection of renin also increased Ras activation in the NTS. CONCLUSIONS AND IMPLICATIONSTaken together, these results suggest renin modulated blood pressure at the NTS by AT1 and Mas receptor-mediated activation of Gq and Ras to evoke PI3K-Akt-eNOS signalling.

Blood undergoes oxidative stress during severe hypoxia or intense exercise. Excessive exposure to oxidative stress induces replicative senescence and apoptosis of lymphocytes. This study determines how various exercises with/without hypoxia affect lymphocyte subset mobilization and oxidative stress-induced lymphocyte apoptosis. Eighteen sedentary males randomly engaged in two normoxic exercise bouts [severe exercise (SE) (up to VO(2max)) and moderate-intensity exercise (ME) (50%VO(2max)) while exposed to 21%O(2)], two hypoxic exercise bouts (ME while exposed to 12%O(2) and 15%O(2)) and two hypoxic resting conditions (resting while exposed to 12%O(2) and 15%O(2)) in a normobaric hypoxia chamber. Under normoxic conditions, SE but not ME (1) increased the percentages of senescent (CD28(-) and CD57(+))/activated (CD62L(-) and CD11a(+))-form lymphocytes mobilized into the peripheral blood compartment; (2) decreased the levels of surface thiol and intracellular total (t-GSH) and reduced-form glutathione (r-GSH) of lymphocytes in blood; and (3) further enhanced the extents of H(2)O(2)-induced mitochondria trans-membrane potential diminishing, caspases 3/8/9 activation, poly(ADP-ribose) polymerase cleavage and phosphotidyl serine exposure in blood lymphocytes. However, no significant change occurred in the subset mobilization, antioxidant levels or apoptosis of lymphocytes following exposure to either 12%O(2) or 15%O(2). Although both 12%O(2) and 15%O(2) ME increased the mobilization of senescent/activated-form lymphocytes, only 12%O(2) ME enhanced H(2)O(2)-induced lymphocyte thiol, t-GSH and r-GSH consumption and apoptotic responses. Therefore, we conclude that the 12%O(2) exposure increases the mobilization of senescent/activated-form lymphocytes into the peripheral blood compartment and simultaneously enhances oxidative stress-induced lymphocyte apoptosis by diminishing cellular antioxidant levels during exercise.

The present study aimed to use event-related potentials with the stop-signal task to investigate the effects of trait anxiety on inhibitory control, error monitoring, and post-error adjustments. The stop-signal reaction time (SSRT) was used to evaluate the behavioral competence of inhibitory control. Electrophysiological signals of error-related negativity (ERN) and error positivity (Pe) were used to study error perception and error awareness, respectively. Post-error slowing (PES) was applied to examine the behavioral adjustments after making errors. The results showed that SSRT and PES did not differ significantly between individuals with high trait anxiety (HTA) and those with low trait anxiety (LTA). However, individuals with HTA demonstrated reduced ERN amplitudes and prolonged Pe latencies than those with LTA. Prolonged Pe latencies were also significantly associated with poorer post-error adjustments. In conclusion, HTA led to reduced cortical responses to error monitoring. Furthermore, inefficient conscious awareness of errors might lead to maladaptive post-error adjustments.

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BackgroundMastery motivation is the driving force behind children’s desire to explore the surrounding world and their comprehensive development. However, disease factors may lower a child’s motivation and hamper development. The aim of this review is to examine mastery motivation in preschool children with cerebral palsy (CP) and the impact of contextual factors on mastery motivation.MethodsSix electronic databases were searched (PubMed, ScienceDirect, Scopus, PsycINFO, Medline, and Airiti Library) using the keywords “Activity,” “Cerebral Palsy,” “Preschool,” “Motivation,” “Mastery motivation,” “Gross motor,” and “Toddler.” We reviewed six observational studies and one interventional study for the following features: (1) participants’ characteristics; (2) assessment, observation, and intervention methods; (3) findings.ResultsOf the seven studies, three were individual cohort studies and four were individual case–control studies. There were two types of motivation-related measures, standardized measurements and observations of structured tasks or free play. Three studies showed no significant difference in mastery motivation between children with and those without CP when given mental-age-appropriate tasks of moderate difficulty. However, environmental factors including social experience, family interaction, and caregivers’ perceptions may affect motivation in preschool children with CP.ConclusionCurrent studies on mastery motivation in preschool children with CP are very limited, and the lack of a universal, theory-based definition of mastery motivation and common assessment frameworks makes it difficult to draw clear conclusions on mastery motivation in children with CP. Future studies should investigate mastery motivation with rigorous study designs to identify ideal activities and environments for preschool children with CP.