Evaluación formativa del aprendizaje: autoevaluación y coevaluación de problemas en una asignatura del Grado en Bioquímica de la UAM

La autoevaluación y la coevaluación, o evaluación por pares, constituyen estrategias de aprendizaje activo que, entre otros aspectos positivos, promueven la implicación cognitiva, estimulan la reflexión crítica y proporcionan al estudiante la retroalimentación necesaria para conocer el grado de aprendizaje, conocimientos y competencias, que ha alcanzado. Además, a través del ejercicio de aplicar criterios de evaluación y calificación, los estudiantes van adquiriendo la capacidad de juzgar la calidad de su propio trabajo y del de otros. Con el objetivo de incorporar la evaluación formativa al proceso de aprendizaje en la asignatura Función de Macromoléculas de 2º curso del Grado en Bioquímica de la UAM, hemos diseñado y desarrollado una actividad de auto- y co-evaluación basada en la resolución de problemas durante los cursos académicos 2011/12 y 2012/13. En el contexto del estudio de la cinética y mecanismos de las reacciones enzimáticas, los estudiantes resolvieron un caso práctico que integraba datos experimentales e información proporcionada por libros de texto, y lo entregaron en las fechas asignadas a través del Moodle de la asignatura. Cada estudiante recibió el ejercicio de otro compañero, codificado númericamente y seleccionado de forma aleatoria, y una plantilla con el ejercicio resuelto que incluía criterios de evaluación y/o de calificación de cada apartado. Aunque el principal objetivo de las evaluaciones era formativo, para estimular la motivación y la responsabilidad de los estudiantes hacia esta actividad, la media de las calificaciones individuales de auto- y co-evaluación representó un 5% de la nota final de la asignatura. Los resultados obtenidos en el análisis por regresión de las calificaciones de auto- y co-evaluación y las calificaciones de la profesora indicaron que existía una mejor correlación de la evaluación de la profesora con la autoevaluación que con la coevaluación. Sin embargo, y en coincidencia con otros estudios, la mayoría de los estudiantes sobrevaloraron su propio trabajo. La mejor correlación entre las calificaciones medias individuales y la calificación de la profesora, nos anima a mantener el valor calificativo de esta actividad formativa. Con el propósito de conocer qué percepción tiene los estudiantes sobre el valor formativo de la auto- y co-evaluación y de otras actividades desarrolladas, realizamos una encuesta al final del semestre de impartición de la asignatura. Además de los aspectos esencialmente cognitivos, la encuesta incluyó también aspectos afectivos (sentimientos, actitudes). La mayoría de los estudiantes valoraron la auto- y co-evaluación como una experiencia significativa de aprendizaje, tanto a nivel de procedimiento como por los resultados derivados del mismo.</p

Impairment of skeletal muscle insulin action with aging in Wistar rats: Role of leptin and caloric restriction

Insulin resistance develops with aging in rats in parallel to fat mass accretion, central leptin resistance and hyperleptinemia. Previous studies demonstrated that insulin resistance appears earlier in adipose tissue than in muscle during aging and pointed to a role of hyperleptinemia in the impairment of insulin action. Here we explored the evolution along aging of insulin sensitivity in soleus and EDL muscles by analyzing insulin signaling in vivo and insulin-dependent glucose transport ex vivo. A decrease in insulin action was observed in both muscles. Caloric restriction improves insulin sensitivity at early aging but not in older animals. We also tested the role of leptin on insulin action in skeletal muscle. Short-term pretreatment with leptin inhibits in vivo muscle insulin signaling and insulin-dependent glucose transport in isolated muscle strips. This effect is mediated by its action on early insulin signaling as well as by the inhibition of p38. In contrast, chronic central administration of leptin elicits an insulin sensitizing effect on soleus. These data suggest that leptin can act as muscle insulin sensitizer, when acting at central level, and as insulin antagonistic when interacting directly with soleus muscle. This effect may be relevant in situations of hyperleptinemia such as aging. © 2012 Elsevier Ireland Ltd.Peer Reviewe

Regulation of tau phosphorylation and protection against β-amyloid-induced neurodegeneration by lithium. Possible implications for Alzheimer's disease

Alzheimer's disease is a neurodegenerative disorder characterized by the accumulation of the β-amyloid peptide and the hyperphosphorylation of the tau protein, among other features. The most widely accepted hypothesis on the etiopathogenesis of this disease proposes that the aggregates of the β-amyloid peptide are the main triggers of tau hyperphosphorylation and the subsequent degeneration of affected neurons. In support of this view, fibrillar aggregates of synthetic β-amyloid peptide induce tau hyperphosphorylation and cell death in cultured neurons. We have previously reported that lithium inhibits tau hyperphosphorylation and also significantly protects cultured neurons from cell death triggered by β-amyloid peptide. As lithium is a relatively specific inhibitor of glycogen synthase kinase-3 (in comparison with other protein kinases), and other studies also point to a relevant role of this enzyme, we favor the view that glycogen synthase kinase-3 is a crucial element in the pathogenesis of Alzheimer's disease. In our opinion, the possibility of using lithium, or other inhibitors of glycogen synthase kinase-3, in experimental trials aimed to ameliorate neurodegeneration in Alzheimer's disease should be considered.Peer reviewe

Lithium protects cultured neurons against β-amyloid-induced neurodegeneration

The deposition of β-amyloid peptide (Aβ), the hyperphosphorylation of tau protein and the death of neurons in certain brain regions are characteristic features of Alzheimer's disease. It has been proposed that the accumulation of aggregates of Aβ is the trigger of neurodegeneration in this disease. In support of this view, several studies have demonstrated that the treatment of cultured neurons with Aβ leads to the hyperphosphorylation of tau protein and neuronal cell death. Here we report that lithium prevents the enhanced phosphorylation of tau protein at the sites recognized by antibodies Tau-1 and PHF-1 which occurs when cultured rat cortical neurons are incubated with Aβ. Interestingly, lithium also significantly protects cultured neurons from Aβ-induced cell death. These results raise the possibility of using chronic lithium treatment for the therapy of Alzheimer's disease.This research was supported by grants from the Spanish Direccion General de Investigacion Cientifica y Tecnica (PB 94-0040 and PM 95-0039) and an institutional grant to the Centro de Biologia Molecular `Severo Ochoa' from the Fundacion Ramon Areces. G.A. is the recipient of a fellowship from the Ministerio de Educacion y Cultura.Peer reviewe

Age-associated decrease of SIRT1 expression in rat hippocampus. Prevention by late onset caloric restriction

We have studied the effect of aging and late onset caloric restriction (CR) on the expression of SIRT1 in hippocampus and cerebral cortex of the rat. Quantitative analysis showed that there is a significant reduction of SIRT1 protein levels in hippocampus with aging. Late onset, moderate CR prevented the deleterious effect of aging on SIRT1 content. Examination of SIRT1 immunoreactivity in coronal sections from hippocampus supported these results, and confirmed that old animals are able to respond to the beneficial effects of CR by regulating SIRT1 protein expression. Differences in the amounts of SIRT1 transcripts among animal groups were not found, which suggest that post-transcriptional mechanisms could be involved in the effects of aging and CR on SIRT1 expression. © 2011 Elsevier Inc.BFU2005-07647-C03-01-03; BFU2010-18297 DGI-BFU2008-C03-02/BFI; Ramón Areces FoundationPeer Reviewe

Intracellular compartmentation of pyruvate in primary cultures of cortical neurons as detected by (13)C NMR spectroscopy with multiple (13)C labels

The intracellular compartmentation of pyruvate in primary cultures of cortical neurons was investigated by high resolution (13)C NMR using mixtures of different pyruvate precursors conveniently labeled with (13)C or unlabeled. Cells were incubated with 1-5 mM (1-(13)C, 1,2-(13)C(2) or U-(13)C(6)) glucose only or with mixtures containing 1.5 mM (1-(13)C or U-(13)C(6)) glucose, 0.25-2.5 mM (2-(13)C or 3-(13)C) pyruvate and 1 mM malate. Extracts from cells and incubation media were analyzed by (13)C NMR to determine the relative contributions of the different precursors to the intracellular pyruvate pool. When ((13)C) glucose was used as the sole substrate fractional (13)C enrichments and (13)C isotopomer populations in lactate and glutamate carbons were compatible with a unique intracellular pool of pyruvate. When mixtures of ((13)C) glucose, ((13)C) pyruvate and malate were used, however, the fractional (13)C enrichments of the C2 and C3 carbons of lactate were higher than those of the C2 and C3 carbons of alanine and depicted a different (13)C isotopomer distribution. Moreover, neurons incubated with 1 mM (1,2-(13)C(2)) glucose and 0.25-5 mM (3-(13)C) pyruvate produced exclusively (3-(13)C) lactate, revealing that extracellular pyruvate is the unique precursor of lactate under these conditions. These results reveal the presence of two different pools of intracellular pyruvate; one derived from extracellular pyruvate, used mainly for lactate and alanine production and one derived from glucose used primarily for oxidation. A red-ox switch using the cytosolic NAD(+)/NADH ratio is proposed to modulate glycolytic flux, controlling which one of the two pyruvate pools is metabolized in the tricarboxylic acid cycle when substrates more oxidized or reduced than glucose are used.Contract grant sponsor: Spanish Ministry of Science and Technology; Contract grant number: MCT PB96-0864-C02; Contract grant sponsor: Community of Madrid; Contract grant number: CAM 97/105, 08.1/0023/ 97, 08.1/0046/98, strategic group grant 2000-3; Contract grant sponsor: Fundación Ramón Areces. F.C. and M.V. received fellowships from Spanish Ministry of Science and Technology.Peer Reviewe

Developmental changes in the Ca2+-regulated mitochondrial aspartate–glutamate carrier aralar1 in brain and prominent expression in the spinal cord

14 páginas, 7 figuras.Aralar1 and citrin are two isoforms of the mitochondrial carrier of aspartate–glutamate (AGC), a calcium regulated carrier, which is important in the malate–aspartate NADH shuttle. The expression and cell distribution of aralar1 and citrin in brain cells has been studied during development in vitro and in vivo. Aralar1 is the only isoform expressed in neurons and its levels undergo a marked increase during in vitro maturation, which is higher than the increase in mitochondrial DNA in the same time window. The enrichment in aralar1 per mitochondria during neuronal maturation is associated with a prominent rise in the function of the malate–aspartate NADH shuttle. Paradoxically, during in vivo development of rat or mouse brain there is very little postnatal increase in total aralar1 levels per mitochondria. This is explained by the fact that astrocytes develop postnatally, have aralar1 levels much lower than neurons, and their increase masks that of aralar1. Aralar1 mRNA and protein are widely expressed throughout neuron-rich areas in adult mouse CNS with clear enrichments in sets of neuronal nuclei in the brainstem and, particularly, in the ventral horn of the spinal cord. These aralar1-rich neurons represent a subset of the cytochrome oxidase-rich neurons in the same areas. The presence of aralar1 could reflect a tonic activity of these neurons, which is met by the combination of high malate–aspartate NADH shuttle and respiratory chain activities.This work was supported by grants from the Spanish Dirección General de Investigación del Ministerio de Ciencia y Tecnologı́a, Comunidad Autónoma de Madrid, Fondo de Investigaciones Sanitarias del Ministerio de Sanidad y Consumo, by Health Sciences Research Grants (H11-Genome-002) from the Ministry of Health and Welfare in Japan, by Grants-in-Aid for Scientific Research (B-12470518) from the Japan Society for the Promotion of Science and by an institutional grant from the Fundación Ramón Areces to the Centro de Biologı́a Molecular ‘Severo Ochoa’.Peer reviewe