152 resultados para neurociencia
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Resumen tomado de la publicación. El artículo forma parte del monográfico de la revista dedicado a: Pedagogía sistémica
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Resumen basado en el de la publicación
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Resumen tomado de la publicación. Resumen en inglés. Monográfico: Textos y contextos de la televisión
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Monográfico con el título: 'Evaluación psicopedagógica'
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Resumen basado en el de la publicación.
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El art??culo forma parte de la secci??n ???Opciones b??sicas de los contenidos del curr??culo??? del monogr??fico ???Los contenidos???.
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Resumen basado en el de la publicaci??n
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Resumen basado en el de la publicaci??n
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Resumen basado en el de la publicaci??n
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Hoy en día las organizaciones financieras necesitan solventar los requerimientos y necesidades de los colaboradores de un Call Center para mejorar su productividad y elevar los índices de bienestar laboral. Con base a estas necesidades el objetivo de la presente investigación es conocer los factores de estrés que existen en el área de Call Center de Pague Ya, que influencian directa o indirectamente en la productividad de esta área. Por este motivo se va a evaluar todos los factores de riesgos psicosociales que conllevan al estrés laboral. Como objetivos específicos debemos Identificar los factores transmisores de estrés laboral dentro del Call Center, establecer las características de las personas que tienen distrés y conocer los indicadores de productividad de este grupo. Se mirará el estrés desde la Neurociencia, y desde las ciencias del comportamiento, Se observará la productividad, tipos de productividad y sus características; y como estará relacionado con el estrés de un Call Center diferenciando si es Distrés o es Eustrés; también observaremos los efectos del estrés en la productividad y los casos de ausentismo más frecuentes; finalmente, obtendremos los resultados de la investigación y sus respectivas conclusiones y recomendaciones. Esta investigación empírica, intenta esclarecer las características y las diferencias entre las causas y los efectos de las personas que tienen eustrés (estrés positivo) y las que tienen distrés (estrés negativo), y cómo estas diferencias afectan la productividad en la organización.
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Rod bipolar cells in Cebus apella monkey retina were identified by an antibody against the alpha isoform of protein kinase C (PKC alpha). which has been shown to selectively identify rod bipolars in two other primates and various mammals. Vertical sections were used to confirm the identity of these cells by their characteristic morphology of dendrites and axons. Their topographic distribution was assessed in horizontal sections; counts taken along the dorsal, ventral, nasal, and temporal quadrants. The density of rod bipolar cells increased from 500 to 2900 cells/mm(2) at 1 mm from the fovea to reach a peak of 10,000-12,000 cellss/mm(2) at 4 mm, approximately 5 deg of eccentricity, and then gradually decreased toward retinal periphery to values of 5000 cells/mm(2) or less. Rod to rod bipolar density ratio remained between 10 and 20 across most of the retinal extension. The number of rod bipolar cells per retina was 6,360,000 +/- 387,433 (mean +/- S.D., n = 6). The anti-PKC alpha antibody has shown to be a good marker of rod bipolar cells of Cebus, and the cell distribution is similar to that described for other primates. In spite of the difference in the central retina, the density variation of rod bipolar cells in the Cebus and Macaca as well as the convergence from rod to rod bipolar cells are Generally similar, suggesting that both retinae stabilize similar sensitivity (as measured by rod density) and convergence.
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Methylmalonic acidemia is one of the most prevalent inherited metabolic disorders involving neurological deficits. In vitro experiments, animal model studies and tissue analyses from human patients suggest extensive impairment of mitochondrial energy metabolism in this disease. This review summarizes changes in mitochondrial energy metabolism occurring in methylmalonic acidemia, focusing mainly on the effects of accumulated methylmalonic acid, and gives an overview of the results found in different experimental models. Overall, experiments to date suggest that mitochondrial impairment in this disease occurs through a combination of the inhibition of specific enzymes and transporters, limitation in the availability of substrates for mitochondrial metabolic pathways and oxidative damage.
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2,4-Dinitrophenol (DNP) is classically known as a mitochondrial uncoupler and, at high concentrations, is toxic to a variety of cells. However, it has recently been shown that, at subtoxic concentrations, DNP protects neurons against a variety of insults and promotes neuronal differentiation and neuritogenesis. The molecular and cellular mechanisms underlying the beneficial neuroactive properties of DNP are still largely unknown. We have now used DNA microarray analysis to investigate changes in gene expression in rat hippocampal neurons in culture treated with low micromolar concentrations of DNP. Under conditions that did not affect neuronal viability, high-energy phosphate levels or mitochondrial oxygen consumption, DNP induced up-regulation of 275 genes and down-regulation of 231 genes. Significantly, several up-regulated genes were linked to intracellular cAMP signaling, known to be involved in neurite outgrowth, synaptic plasticity, and neuronal survival. Differential expression of specific genes was validated by quantitative RT-PCR using independent samples. Results shed light on molecular mechanisms underlying neuroprotection by DNP and point to possible targets for development of novel therapeutics for neurodegenerative disorders.
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NADPH oxidase (Nox) is a unique, multi-protein, electron transport system that produces large amounts of superoxide via the reduction of molecular oxygen. Nox-derived reactive oxygen species (ROS) are known to be involved in a variety of physiological processes, including host defense and signal transduction. However, over the past decade, the involvement of (Nox)-dependent oxidative stress in the pathophysiology of several neurodegenerative diseases has been increasingly recognized. ROS produced by Nox proteins contribute to neurodegenerative diseases through distinct mechanisms, such as oxidation of DNA, proteins, lipids, amino acids and metals, in addition to activation of redox-sensitive signaling pathways. In this review, we discuss the recent literature on Nox involvement in neurodegeneration, focusing on Parkinson and Alzheimer diseases.
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Overstimulation of the glutamatergic system (excitotoxicity) is involved in various acute and chronic brain diseases. Several studies support the hypothesis that guanosine-5'-monophosphate (GMP) can modulate glutamatergic neurotransmission. The aim of this study was to evaluate the effects of chronically administered GMP on brain cortical glutamatergic parameters in mice. Additionally, we investigated the neuroprotective potential of the GMP treatment submitting cortical brain slices to oxygen and glucose deprivation (OGD). Moreover, measurements of the cerebrospinal fluid (CSF) purine levels were performed after the treatment. Mice received an oral administration of saline or GMP during 3 weeks. GMP significantly decreases the cortical brain glutamate binding and uptake. Accordingly, GMP reduced the immunocontent of the glutamate receptors subunits, NR2A/B and GluR1 (NMDA and AMPA receptors, respectively) and glutamate transporters EAAC1 and GLT1. GMP treatment significantly reduced the immunocontent of PSD-95 while did not affect the content of Snap 25, GLAST and GFAP. Moreover, GMP treatment increased the resistance of neocortex to OGD insult. The chronic GMP administration increased the CSF levels of GMP and its metabolites. Altogether, these findings suggest a potential modulatory role of GMP on neocortex glutamatergic system by promoting functional and plastic changes associated to more resistance of mice neocortex against an in vitro excitotoxicity event.