ICT Use in Preschool Education

Es descriu una proposta pedagògica per introduir l’ordinador en el currículum de l’educació infantil. La metodologia duta a terme segueix un procés globalitzador fonamentat en principis d’aprenentatge significatiu. S’estudiaren els coneixements previs dels alumnes i es realitzà un plantejament de la tasca atenent les necessitats individuals de cada nen i nena. Es conclou que les TIC han estat elements mediadors a l’hora de treballar aspectes com l’aprenentatge de les matemàtiques, la lectoescriptura, la comunicació, l’escriptura i el desenvolupament del llenguatge oral.Se describe una propuesta pedagógica para introducir el ordenador en el currículo de la educación infantil. La metodología llevada a cabo sigue un proceso globalizador basado en principios de aprendizaje significativo. Se estudiaron los conocimientos previos de los alumnos y se realizó un planteamiento de la tarea atendiendo a las necesidades individuales de cada niño y niña. Se concluye que las TIC han sido elementos mediadores a la hora de trabajar aspectos como el aprendizaje de las matemáticas, la lectoescritura, la comunicación, la escritura y el desarrollo del lenguaje oral.This article describes a pedagogical proposal designed to incorporate the use of computers in preschool curricula. The methodology carried out was a comprehensive process based on meaningful learning principles. The students’ previous knowledge of the ICTs was examined and a task approach was defined in keeping with the individual needs of each child. The study concludes that the Information and Communication Technologies served as intermediary tools when working on mathematics, reading and writing, communication, and written and oral language development

Utilització de les TIC a l’educació infantil

Es descriu una proposta pedagògica per introduir l’ordinador en el currículum de l’educació infantil. La metodologia duta a terme segueix un procés globalitzador fonamentat en principis d’aprenentatge significatiu. S’estudiaren els coneixements previs dels alumnes i es realitzà un plantejament de la tasca atenent les necessitats individuals de cada nen i nena. Es conclou que les TIC han estat elements mediadors a l’hora de treballar aspectes com l’aprenentatge de les matemàtiques, la lectoescriptura, la comunicació, l’escriptura i el desenvolupament del llenguatge oral

Cholecystokinin Activates a Variety of Intracellular Signal Transduction Mechanisms in Rodent Pancreatic Acinar Cells

Cholecystokinin (CCK) acting through its G protein-coupled receptor is now known to activate a variety of intracellular signaling mechanisms and thereby regulate a complex array of cellular functions in pancreatic acinar cells. The best studied mechanism is the coupling through heterotrimeric G proteins of the G q family to activate a phospholipase C leading to an increase in inositol trisphosphate and release of intracellular Ca 2+ . This pathway along with protein kinase C activation in response to the increase in diacylglycerol stimulates the secretion of digestive enzymes by the process of exocytosis. CCK also activates signaling pathways in acini more related to other processes. The three mitogen activated protein kinase cascades leading to ERKs, JNKs and p38 MAPK are all activated by CCK. CCK activates the ERK cascade by PKC activation of Raf which in turn activates MEK and ERKs. JNKs are activated by a distinct mechanism whish requires higher concentrations of CCK. Both ERKs and JNKs are presumed to regulate gene expression. CCK activation of p38 MAPK also plays a role in regulating the actin cytoskeleton through phosphorylation of the small heat shock protein HSP27. The PI3K-PKB-mTOR pathway is activated by CCK and plays a major role in regulating protein synthesis at the translational level. This includes both activation of p70 S6K leading to phosphorylation of ribosomal protein S6 and the phosphorylation of the binding protein for initiation factor 4E leading to formation of the mRNA cap binding complex. Other signaling pathways activated by CCK receptors include NF-κB and a variety of tyrosine kinases. Further work is needed to understand how CCK receptors activate most of the above pathways and to better understand the biological events regulated by these diverse signaling pathways.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72562/1/j.1600-0773.2002.910606.x.pd

InnovIB. Recursos i recerca educativa de les Illes Balears

Es descriu una proposta pedagògica per introduir l’ordinador en el currículum de l’educació infantil. La metodologia duta a terme segueix un procés globalitzador fonamentat en principis d’aprenentatge significatiu. S’estudiaren els coneixements previs dels alumnes i es realitzà un plantejament de la tasca atenent les necessitats individuals de cada nen i nena. Es conclou que les TIC han estat elements mediadors a l’hora de treballar aspectes com l’aprenentatge de les matemàtiques, la lectoescriptura, la comunicació, l’escriptura i el desenvolupament del llenguatge oral.Se describe una propuesta pedagógica para introducir el ordenador en el currículo de la educación infantil. La metodología llevada a cabo sigue un proceso globalizador basado en principios de aprendizaje significativo. Se estudiaron los conocimientos previos de los alumnos y se realizó un planteamiento de la tarea atendiendo a las necesidades individuales de cada niño y niña. Se concluye que las TIC han sido elementos mediadores a la hora de trabajar aspectos como el aprendizaje de las matemáticas, la lectoescritura, la comunicación, la escritura y el desarrollo del lenguaje oral.ES

Regulation of transforming growth factor β-induced responses by protein kinase A in pancreatic acinar cells

TGF-β is an important regulator of growth and differentiation in the pancreas and has been implicated in pancreatic tumorigenesis. We have recently demonstrated that TGF-β can activate protein kinase A (PKA) in mink lung epithelial cells (Zhang L, Duan C, Binkley C, Li G, Uhler M, Logsdon C, Simeone D. Mol Cell Biol 24: 2169–2180, 2004). In this study, we sought to determine whether TGF-β activates PKA in pancreatic acinar cells, the mechanism by which PKA is activated, and PKA's role in TGF-β-mediated growth regulatory responses. TGF-β rapidly activated PKA in pancreatic acini while having no effect on intracellular cAMP levels. Coimmunoprecipitation experiments demonstrated a physical interaction between a Smad3/Smad4 complex and the regulatory subunits of PKA. TGF-β also induced activation of the PKA-dependent transcription factor CREB. Both the specific PKA inhibitor H89 and PKI peptide significantly blocked TGF-β's ability to activate PKA and CREB. TGF-β-mediated growth inhibition and TGF-β-induced p21 and SnoN expression in pancreatic acinar cells were blocked by H89 and PKI peptide. This study demonstrates that this novel cross talk between TGF-β and PKA signaling pathways may play an important role in regulating TGF-β signaling in the pancreas

CCK-independent mTORC1 activation during dietary protein-induced exocrine pancreas growth

Dietary protein can stimulate pancreatic growth in the absence of CCK release, but there is little data on the regulation of CCK-independent growth. To identify mechanisms whereby protein stimulates pancreatic growth in the absence of CCK release, C57BL/6 control and CCK-null male mice were fed normal-protein (14% casein) or high-protein (75% casein) chow for 7 days. The weight of the pancreas increased by 32% in C57BL/6 mice and 26% in CCK-null mice fed high-protein chow. Changes in pancreatic weight in control mice were due to both cell hypertrophy and hyperplasia since there was an increase in protein-to-DNA ratio, total DNA content, and DNA synthesis. In CCK-null mice pancreatic growth was almost entirely due to hypertrophy with both protein-to-DNA ratio and cell size increasing without significant increases in DNA content or DNA synthesis. ERK, calcineurin, and mammalian target of rapamycin complex 1 (mTORC1) are activated in models of CCK-induced growth, but there were no differences in ERK or calcineurin activation between fasted and fed CCK-null mice. In contrast, mTORC1 activation was increased after feeding and the duration of activation was prolonged in mice fed high-protein chow compared with normal-protein chow. Changes in pancreatic weight and RNA content were completely inhibited, and changes in protein content were partially abated, when the mTORC1 inhibitor rapamycin was administered during high-protein chow feeding. Prolonged mTORC1 activation is thus required for dietary protein-induced pancreatic growth in the absence of CCK