Leer para aprender: Cómo interactúan los profesores con sus alumnos en la educación primaria.

This work studies the oral exchanges between teacher (as an expert reader) and student (as trainee) to determine the type of coaching provided during group reading activities as a joint construction of meaning 3rd, 5th and 7th grade of primary education. The system of analysis of the practice proposed by Sánchez et al. (2008) was used to describe the internal organization of those readings as episodes and to typify the aids or mediations by their function (regulation, production or feedback) and the level of autonomy provided. The results show essentially the presence of variable nuclear episodes in group reading (reading aloud and interpreting for evaluation). The mediations show a scarce presence of regulatory aids and a moderate number of non-invasive internal and feedback aids in the interpretation episode. There are differences among levels only, and not among subjects. The implications for teachers training and innovation are discussed.A partir del estudio de los intercambios orales del profesor como experto lector y el alumno como aprendiz se caracterizó el tipo de acompañamiento en la actividades de lectura colectiva  como construcción conjunta de significado en las asignaturas de Lenguaje, Historia y Ciencias Naturales en 3º, 5º y 7º de primaria. Se utilizó un sistema analítico de la práctica de Sánchez et al. (2008) para describir la organización general de episodios y las ayudas en los episodios de interpretación según su función: regulatoria, de elaboración o de retroalimentación  y según el nivel de autonomía propiciado. Los resultados muestran organización de episodios sencilla, escasa presencia de ayudas regulatorias y moderado número de ayudas internas y de feedback, con carácter no invasivo en el episodio de interpretación. Se observan diferencias solo por nivel y no por asignatura. Se discuten las implicaciones para la innovación y formación  de profesores

Regionally Impaired Redox Homeostasis in the Brain of Rats Subjected to Global Perinatal Asphyxia: Sustained Effect up to 14 Postnatal Days

© 2018, Springer Science+Business Media, LLC, part of Springer Nature. The present report evaluates the effect of global perinatal asphyxia on several parameters of oxidative stress and cell viability in rat brain tissue sampled at an extended neonatal period up to 14 days, a period characterised by intensive neuritogenesis, synaptogenesis, synaptic consolidation, pruning and delayed cell death. Perinatal asphyxia was induced by immersing foetus-containing uterine horns removed by a caesarean section from on term rat dams into a water bath at 37 °C for 21 min. Asphyxia-exposed and sibling caesarean-delivered foetuses were manually resucitated and nurtured by surrogate dams for 1 to 14 postnatal (P) days. Brain samples (mesencephalon, telencephalon and hippocampus) were assayed for glutathione (reduced and oxidated levels; spectrophotometry), tissue reducing capacity (potassium ferricyanide reducing assay, FRAP), catalase (the key enzyme protecting against oxidative stress and reactiv

Sustained Energy Deficit Following Perinatal Asphyxia: A Shift towards the Fructose-2,6-bisphosphatase (TIGAR)-Dependent Pentose Phosphate Pathway and Postnatal Development

Labor and delivery entail a complex and sequential metabolic and physiologic cascade, culminating in most circumstances in successful childbirth, although delivery can be a risky episode if oxygen supply is interrupted, resulting in perinatal asphyxia (PA). PA causes an energy failure, leading to cell dysfunction and death if re-oxygenation is not promptly restored. PA is associated with long-term effects, challenging the ability of the brain to cope with stressors occurring along with life. We review here relevant targets responsible for metabolic cascades linked to neurodevelopmental impairments, that we have identified with a model of global PA in rats. Severe PA induces a sustained effect on redox homeostasis, increasing oxidative stress, decreasing metabolic and tissue antioxidant capacity in vulnerable brain regions, which remains weeks after the insult. Catalase activity is decreased in mesencephalon and hippocampus from PA-exposed (AS), compared to control neonates (CS), in parallel with increased cleaved caspase-3 levels, associated with decreased glutathione reductase and glutathione peroxidase activity, a shift towards the TIGAR-dependent pentose phosphate pathway, and delayed calpain-dependent cell death. The brain damage continues long after the re-oxygenation period, extending for weeks after PA, affecting neurons and glial cells, including myelination in grey and white matter. The resulting vulnerability was investigated with organotypic cultures built from AS and CS rat newborns, showing that substantia nigra TH-dopamine-positive cells from AS were more vulnerable to 1 mM of H2O2 than those from CS animals. Several therapeutic strategies are discussed, including hypothermia; N-acetylcysteine; memantine; nicotinamide, and intranasally administered mesenchymal stem cell secretomes, promising clinical translation