How does media play and ICT fit in the early childhood context?

In this chapter, Shaleen Prowse describes teaching strategies for media education and information communication technologies (ICT) and how young children’s experiences with tools of technology at home are an important starting point for building learning experiences within the classroom setting. She illustrates how digital cameras and computer editing software assist young children to share their learning.

Book Review: "Rethinking Learning in Early Childhood Education" written by Nicola Yelland, Libby Lee, Maureen O’Rourke & Cathie Harrison

There is a growing body of work that responds to the impact of the rapid uptake of information and communication technology (ICT) on education (Buckingham, 2003; Cheung, 2003; Cuban, 2003; Leung, 2003; Prensky, 2005; Green & Hannon, 2007; Brooks-Gunn & Donahue, 2008; Lyman et al, 2008). Mostly, this work has been positioned in the context of upper-primary or secondary classrooms. More recently, there has been a growing call for research about the impact of ICT on the early years or in early childhood contexts. This text initiates a response to that call. The authors concur that today’s children are a generation who create, learn, work, play and communicate very differently from their parents and teachers (Buckingham, 2003), and that classroom activity needs to reflect this difference.

Post-PC devises : a summary of early iPad technology

In just under 3 months worldwide sales of Apple's iPad tablet device stood at over 3 million units sold. The iPad device, along with rival products signify a shift in the way in which print and other media products are purchased and consumed by users. While facing initial skepticism about the uptake of the device numerous industries have been quick to adapt the device to their specific needs. Based around a newly developed six point typology of “post PC” device utility this project undertook a significant review of publicly available material to identify worldwide trends in iPad adoption and use within the tertiary sector.

Inactivation of the Huntington's disease gene (Hdh) impairs anterior streak formation and early patterning of the mouse embryo

Background Huntingtin, the HD gene encoded protein mutated by polyglutamine expansion in Huntington's disease, is required in extraembryonic tissues for proper gastrulation, implicating its activities in nutrition or patterning of the developing embryo. To test these possibilities, we have used whole mount in situ hybridization to examine embryonic patterning and morphogenesis in homozygous Hdhex4/5 huntingtin deficient embryos. Results In the absence of huntingtin, expression of nutritive genes appears normal but E7.0–7.5 embryos exhibit a unique combination of patterning defects. Notable are a shortened primitive streak, absence of a proper node and diminished production of anterior streak derivatives. Reduced Wnt3a, Tbx6 and Dll1 expression signify decreased paraxial mesoderm and reduced Otx2 expression and lack of headfolds denote a failure of head development. In addition, genes initially broadly expressed are not properly restricted to the posterior, as evidenced by the ectopic expression of Nodal, Fgf8 and Gsc in the epiblast and T (Brachyury) and Evx1 in proximal mesoderm derivatives. Despite impaired posterior restriction and anterior streak deficits, overall anterior/posterior polarity is established. A single primitive streak forms and marker expression shows that the anterior epiblast and anterior visceral endoderm (AVE) are specified. Conclusion Huntingtin is essential in the early patterning of the embryo for formation of the anterior region of the primitive streak, and for down-regulation of a subset of dynamic growth and transcription factor genes. These findings provide fundamental starting points for identifying the novel cellular and molecular activities of huntingtin in the extraembryonic tissues that govern normal anterior streak development. This knowledge may prove to be important for understanding the mechanism by which the dominant polyglutamine expansion in huntingtin determines the loss of neurons in Huntington's disease.