Co-operative learning and adaptive instruction in a mathematics curriculum

The AGO 12 to 16 Project (the acronym AGO stands for the Dutch equivalent of 'Adaptive Instruction and Co-operative Learning') seeks to develop and evaluate a mathematics curriculum which is suitable for mixed-ability groups in secondary education. The research questions we will address here are, first, whether this curriculum is feasible and effective, and, second, what effects, if any, the context variables time and mean cognitive level of the class have on learning. Many mathematics programmes make insufficient allowance for the differences in intellectual ability that exist in mixed-ability classes. In order to change this situation we developed a mathematics curriculum with adaptive qualities. The evaluation of the experimental curriculum was carried out in two stages. During the first stage the curriculum was used at two schools with the aim of investigating the feasibility of the programme. Experience with the implementation of the programme led to some improvements in the experimental materials. By and large the AGO model appeared to be feasible in secondary classrooms. In the second stage, which was on a large scale, the focus was on the effectiveness of the programme. Six hundred students, 13 teachers and six schools were involved in the research. Teachers in the experimental group were trained in AGO methods and in implementing the new AGO curriculum. Teachers in the control groups worked with the existing programme following their usual methods of teaching. The main conclusion of the study is positive. The AGO model as a whole proved to be practical and effective in learning mathematics. The AGO model has a positive effect on the intercept, which means that the mean scores of AGO classes are higher than the mean scores of non-AGO classes. It may be concluded that, on the average, students benefit from learning in AGO classes as compared with non-AGO classes. AGO does not increase or decrease the differences between students in the same class. As expected, positive effects of two context variables were found: (1) the total amount of time spent in class covering the mathematical content and (2) class composition as indicated by the mean pretest score (aptitude) of the class

Vitamin K supplementation increases vitamin K tissue levels but fails to counteract ectopic calcification in a mouse model for pseudoxanthoma elasticum

Pseudoxanthoma elasticum (PXE) is an autosomal recessive disorder in which calcification of connective tissue leads to pathology in skin, eye and blood vessels. PXE is caused by mutations in ABCC6. High expression of this transporter in the basolateral hepatocyte membrane suggests that it secretes an as-yet elusive factor into the circulation which prevents ectopic calcification. Utilizing our Abcc6−/− mouse model for PXE, we tested the hypothesis that this factor is vitamin K (precursor) (Borst et al. 2008, Cell Cycle). For 3 months, Abcc6−/− and wild-type mice were put on diets containing either the minimum dose of vitamin K required for normal blood coagulation or a dose that was 100 times higher. Vitamin K was supplied as menaquinone-7 (MK-7). Ectopic calcification was monitored in vivo by monthly micro-CT scans of the snout, as the PXE mouse model develops a characteristic connective tissue mineralization at the base of the whiskers. In addition, calcification of kidney arteries was measured by histology. Results show that supplemental MK-7 had no effect on ectopic calcification in Abcc6−/− mice. MK-7 supplementation increased vitamin K levels (in skin, heart and brain) in wild-type and in Abcc6−/− mice. Vitamin K tissue levels did not depend on Abcc6 genotype. In conclusion, dietary MK-7 supplementation increased vitamin K tissue levels in the PXE mouse model but failed to counteract ectopic calcification. Hence, we obtained no support for the hypothesis that Abcc6 transports vitamin K and that PXE can be cured by increasing tissue levels of vitamin K

Restoration of Podocyte Structure and Improvement of Chronic Renal Disease in Transgenic Mice Overexpressing Renin

Proteinuria is a major marker of the decline of renal function and an important risk factor of coronary heart disease. Elevated proteinuria is associated to the disruption of slit-diaphragm and loss of podocyte foot processes, structural alterations that are considered irreversible. The objective of the present study was to investigate whether proteinuria can be reversed and to identify the structural modifications and the gene/protein regulation associated to this reversal.We used a novel transgenic strain of mouse (RenTg) that overexpresses renin at a constant high level. At the age of 12-month, RenTg mice showed established lesions typical of chronic renal disease such as peri-vascular and periglomerular inflammation, glomerular ischemia, glomerulosclerosis, mesangial expansion and tubular dilation. Ultrastructural analysis indicated abnormal heterogeneity of basement membrane thickness and disappearance of podocyte foot processes. These structural alterations were accompanied by decreased expressions of proteins specific of podocyte (nephrin, podocin), or tubular epithelial cell (E-cadherin and megalin) integrity. In addition, since TGFbeta is considered the major pro-fibrotic agent in renal disease and since exogenous administration of BMP7 is reported to antagonize the TGFbeta-induced phenotype changes in kidney, we have screened the expressions of several genes belonging in the TGFbeta/BMP superfamily. We found that the endogenous inhibitors of BMPs such as noggin and Usag-1 were several-fold activated inhibiting the action of BMPs and thus reinforcing the deleterious action of TGFbeta.Treatment with an AT1 receptor antagonist, at dose that did not decrease arterial pressure, gradually reduced albuminuria. This decrease was accompanied by re-expression of podocin, nephrin, E-cadherin and megalin, and reappearance of podocyte foot processes. In addition, expressions of noggin and Usag-1 were markedly decreased, permitting thus activation of the beneficial action of BMPs.These findings show that proteinuria and alterations in the expression of proteins involved in the integrity and function of glomerular and renal epithelial phenotype are reversible events when the local action of angiotensin II is blocked, and provide hope that chronic renal disease can be efficiently treated

ER stress protein AGR2 precedes and is involved in the regulation of pancreatic cancer initiation

The work was supported by a grant A12008 from CR-UK (L. Dumartin, N.R. Lemoine and T. Crnogorac-Jurcevic)

REC : revista de estudios del currículum

Resumen basado en el de la publicaciónEn este artículo se informa de un estudio sobre los efectos que un currículum de matemáticas y dos variables de contexto, el tiempo y el nivel cognitivo medio de la clase, tienen sobre los resultados del aprendizaje. Primero se indica el objetivo del proyecto y se plantean las preguntas de la investigación, para dar a continuación una descripción del modelo de enseñanza. Tras ofrecer una descripción del diseño, las hipótesis, los métodos y el modelo de análisis, se presentan los resultados del estudio. El artículo termina con algunas conclusiones y un análisis de los resultados. El modelo aplicado, modelo AGO (equivalente holandés de 'Enseñanza adaptativa y aprendizaje cooperativo) demostró ser en conjunto práctico y efectivo para el aprendizaje de las matemáticas. Tiene un efecto positivo sobre la interceptación y no aumenta ni disminuye las diferencias entre los alumnos de la misma clase. También se encontraron efectos positivos de las dos variables de contexto. Como conclusión: primero, el porcentaje de tiempo dedicado a trabajar en pequeños grupos tiene un efecto positivo sobre la inclinación de una clase: los alumnos se benefician de la cooperación en pequeños grupos pero el trabajo de grupo aumenta las diferencias en el rendimiento entre los estudiantes de clase; segundo, hay una parte del modelo en lo referente a vías alternativas de aprendizaje y la adaptación de la enseñanza a las diferencias individuales, que no produjeron los efectos positivos esperados.CataluñaBiblioteca de Educación del Ministerio de Educación, Cultura y Deporte; Calle San Agustín, 5; 28014 Madrid; Tel. +34917748000; [email protected]