19 research outputs found

    What technology for autism needs to be invented? Idea generation from the autism community via the ASCmeI.T. App

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    In autism and technology research, technologies are often developed by researchers targeting specific social and communication difficulties experienced by individuals with autism. In some technology-based projects, children and adults with autism as well as parents, carers, teachers, and other professionals, are involved as users, informers, and (more rarely) as co-designers. However, much less is known about the views of the autism community about the needs they identify as areas that could be addressed through innovative technological solutions. This paper describes the ASCmeI.T. project which encourages members of the autism community to download a free app to answer the question: If there was one new technology to help people with autism, what would it be? This project provides a model of e-participation in which people from the autism community are involved from the start so that new developments in digital technologies can be better matched to support the needs of users

    The p53 Inhibitor MDM2 Facilitates Sonic Hedgehog-Mediated Tumorigenesis and Influences Cerebellar Foliation

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    Disruption of cerebellar granular neuronal precursor (GNP) maturation can result in defects in motor coordination and learning, or in medulloblastoma, the most common childhood brain tumor. The Sonic Hedgehog (Shh) pathway is important for GNP proliferation; however, the factors regulating the extent and timing of GNP proliferation, as well as GNP differentiation and migration are poorly understood. The p53 tumor suppressor has been shown to negatively regulate the activity of the Shh effector, Gli1, in neural stem cells; however, the contribution of p53 to the regulation of Shh signaling in GNPs during cerebellar development has not been determined. Here, we exploited a hypomorphic allele of Mdm2 (Mdm2puro), which encodes a critical negative regulator of p53, to alter the level of wild-type MDM2 and p53 in vivo. We report that mice with reduced levels of MDM2 and increased levels of p53 have small cerebella with shortened folia, reminiscent of deficient Shh signaling. Indeed, Shh signaling in Mdm2-deficient GNPs is attenuated, concomitant with decreased expression of the Shh transducers, Gli1 and Gli2. We also find that Shh stimulation of GNPs promotes MDM2 accumulation and enhances phosphorylation at serine 166, a modification known to increase MDM2-p53 binding. Significantly, loss of MDM2 in Ptch1+/− mice, a model for Shh-mediated human medulloblastoma, impedes cerebellar tumorigenesis. Together, these results place MDM2 at a major nexus between the p53 and Shh signaling pathways in GNPs, with key roles in cerebellar development, GNP survival, cerebellar foliation, and MB tumorigenesis

    PadrÔes alimentares estimados por técnicas multivariadas: uma revisão da literatura sobre os procedimentos adotados nas etapas analíticas

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    Chloroplast genomes: diversity, evolution, and applications in genetic engineering

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    THE NUDIBRANCH GENERA ONCHIDORIS AND DIAPHORODORIS (MOLLUSCA, OPISTHOBRANCHIA) IN THE NORTHEASTERN PACIFIC

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    Volume: 28Start Page: 80End Page: 9

    OPISTHOBRANCH RANGE EXTENSIONS IN ALASKA WITH THE 1ST RECORDS OF CUTHONA-VIRIDIS (FORBES, 1840) FROM THE PACIFIC

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    Volume: 32Start Page: 64End Page: 6

    RECORDS OF CUTHONA-PUSTULATA (ALDER AND HANCOCK, 1854) FROM THE CANADIAN PACIFIC

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    Volume: 26Start Page: 183End Page: 18
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