2 resultados para Development of Competence

em Aston University Research Archive


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UK engineering standards are regulated by the Engineering Council (EC) using a set of generic threshold competence standards which all professionally registered Chartered Engineers in the UK must demonstrate, underpinned by a separate academic qualification at Masters Level. As part of an EC-led national project for the development of work-based learning (WBL) courses leading to Chartered Engineer registration, Aston University has started an MSc Professional Engineering programme, a development of a model originally designed by Kingston University, and build around a set of generic modules which map onto the competence standards. The learning pedagogy of these modules conforms to a widely recognised experiential learning model, with refinements incorporated from a number of other learning models. In particular, the use of workplace mentoring to support the development of critical reflection and to overcome barriers to learning is being incorporated into the learning space. This discussion paper explains the work that was done in collaboration with the EC and a number of Professional Engineering Institutions, to design a course structure and curricular framework that optimises the engineering learning process for engineers already working across a wide range of industries, and to address issues of engineering sustainability. It also explains the thinking behind the work that has been started to provide an international version of the course, built around a set of globalised engineering competences. © 2010 W J Glew, E F Elsworth.

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Neurons in the developing brain die via apoptosis after DNA damage, while neurons in the adult brain are generally resistant to these insults. The basis for this resistance is a matter of conjecture. We report here that cerebellar granule neurons (CGNs) in culture lose their competence to die in response to DNA damage as a function of time in culture. CGNs at either 1 day in vitro (DIV) or 7 DIV were treated with the DNA damaging agents camptothecin, UV or gamma-irradiation and neuronal survival measured. The younger neurons were effectively killed by these agents, while the older neurons displayed a significant resistance to killing. Neuronal survival did not change with time in culture when cells were treated with C2-ceramide or staurosporine, agents which do not target DNA. The resistance to UV irradiation developed over time in culture and was not due to changes in mitotic rate. Increases in DNA strand breakage, up-regulation of the levels of both p53 and its phosphorylated form and nuclear translocation of p53 were equivalent in both older and younger neurons, indicating a comparable p53 stress response. In addition, we show that treatment of older neurons with pharmacological inhibitors of distinct components of the DNA repair machinery promotes the accumulation of DNA damage and sensitizes these cells to the toxic effects of UV exposure. These data demonstrate that older neurons appear to be more proficient in DNA repair in comparison to their younger counterparts, and that this leads to increased survival after DNA damage.