Neuroscience
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High mortality and morbidity rates are observed in patients with bacterial meningitis (BM) and urge for new adjuvant treatments in addition to standard antibiotic therapies. In BM the hippocampal dentate gyrus is injured by apoptosis while in cortical areas ischemic necrosis occurs. Experimental therapies aimed at reducing the inflammatory response and brain damage have successfully been evaluated in animal models of BM. Fluoxetine (FLX) is an anti-depressant of the selective serotonin reuptake inhibitors (SSRI) and was previously shown to be neuroprotective in vitro and in vivo. We therefore assessed the neuroprotective effect of FLX in experimental pneumococcal meningitis. ⋯ A significant neuroprotective effect of FLX on the hippocampus was observed in acute pneumococcal meningitis in infant rats.
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Standards-referenced educational reform has increased the prevalence of standardized testing; however, whether these tests accurately measure students' competencies has been questioned. This may be due to domain-specific assessments placing a differing domain-general cognitive load on test-takers. ⋯ Results provide converging evidence that: (a) the spelling assessments differed in the cognitive load placed on test-takers; (b) performance decreased with increasing cognitive load of the assessment; and (c) brain regions associated with working memory were more highly activated during performance of assessments that were higher in cognitive load. These findings suggest that assessment design should optimize the cognitive load placed on test-takers, to ensure students' results are an accurate reflection of their true levels of competency.
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The aim of this study was to investigate the effects of mental fatigue on the duration of actual and imagined goal-directed arm movements involving speed-accuracy trade-off. Ten participants performed actual and imagined point-to-point arm movements as accurately and as fast as possible, before and after a 90-min sustained cognitive task inducing mental fatigue, and before and after viewing a neutral control task (documentary movie) that did not induce mental fatigue. Target width and center-to-center target distance were varied, resulting in five different indexes of difficulty. ⋯ The trial-by-trial evolution of actual and imagined movement duration remained stable with mental fatigue. The control task did not induce any change in actual and imagined movement duration. The results suggested that movement was slowed in the presence of mental fatigue, maybe due to proactive changes occurring during the preparatory state of the movement, to preserve task success.
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Hemoglobin (Hb) is a major constituent of blood and a potent mediator of oxidative or nitrative stress after intracerebral hemorrhage (ICH). Our previous study demonstrated that Hb could induce abundant peroxynitrite (ONOO(-)) formation in vivo, which may be involved in the blood-brain barrier (BBB) disruption, however, the drug intervention is absent and also the underlying mechanism. Using an experimental stroke model by injecting Hb into the caudate nucleus of male Sprague-Dawley rats, we assessed the role of ONOO(-) decomposition catalyst, 5,10,15,20-tetrakis (4-sulfonatophenyl) porphyrinato iron(III) [FeTPPS] in the activation of MMP-9 and Hb-induced neurovascular injuries. 3-Nitrotyrosine (3-NT, as an index of ONOO(-) formation) and NF-κB expression was measured by western blot (WB) and immunohistochemistry (IHC)/immunofluorescence (IF). ⋯ Hb-induced injury to tight junction protein (ZO-1), basal lamina of FN-immunopositive microvasculature and neural cells was evidently ameliorated by FeTPPS. In addition, apoptotic cell numbers as well as behavioral deficits were also improved. The present study shows that the administration of the ONOO(-) decomposition catalyst FeTPPS protects against Hb-induced neurovascular injuries and improves neurological function, which possibly in part by suppressing MMP-9 activation.
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Inner ear damage can lead to hearing disorders, including tinnitus, hyperacusis, and hearing loss. We measured the effects of severe inner ear damage, produced by cochlear ablation, on the levels and distributions of amino acids in the first brain center of the auditory system, the cochlear nucleus. Measurements were also made for its projection pathways and the superior olivary nuclei. ⋯ GABA and glycine levels showed some bilateral decreases, especially in the PVCN. These results may represent the state of amino acid metabolism in the cochlear nucleus of humans after removal of eighth nerve tumors, which may adversely result in destruction of the auditory nerve. Measurement of chemical changes following inner ear damage may increase understanding of the pathogenesis of hearing impairments and enable improvements in their diagnosis and treatment.