72 research outputs found

    The self which enacts learning, a research with/through the Bay Area Artists for Women's Art (BAAWA)

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    This thesis reveals and clarifies through creative research practices and forms a movement towards, and a recognition of, embodied arts learning through and as a result of an association with the Bay Area Artists for Women's Art (BAAWA), a particular feminist art educational community. Interpretive inquiry on a present learning process both locates and frames this research. The components which inform this interpretation include: a study of the associated literature on feminist art communities, a participant research study with the BAAWA community presented as a notated theatrical performance script, and an exhibition. They relate to and through each other in a complementary relationship and record the various values, perspectives and orientations I have taken on at different occasions in my learning. It is the relationship and specificity of these occasions or events which point to naming my learning process as curriculum as I have understood it from, and applied it beyond, BAAWA. This research is multi-layered, multi-textured, dialogic, open and aesthetic and points to the particular complexities, needs, and practices of contemporary North American women artists in reaching to name, affirm and expand their practices as artists

    This is Research; Patterson: Land Liminality Loss

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    Canada’s historical and contemporary crisis and the impact of related trauma on bodies result from an inherited colonial legacy. The construction is about power. Many who fled and/or were lured to Canada bear the trappings of the rewards they reaped from this place to which they migrated. But didn’t the acquisition of privilege and power have something to do with why they left in the first place

    Coming of age [Exhibition catalogue]

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    Publication to accompany the exhibition Coming of Age at the Visual Arts Centre of Clarington September 3 to October 1, 201

    What You Need to Know about Bar-Code Medication Administration

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    Medication errors are the most common type of preventable error. Bar-code medication administration (BCMA) technology was designed to reduce medication administration errors. Poor system design, implementation and workarounds remain a cause of errors. This paper reviews the literature on BCMA, identifies a gap in the findings and identifies three evidence based practices that could be used to improve system implementation and reduce error. The literature review identified that Bar-code medication administration and system workarounds are well documented and affect patient safety. Based on the critical analysis of 10 studies, we identified gaps in the standardization of BCMA planning, implementation, and sustainability. The themes that emerged from the literature were poor BCMA design and implementation that resulted in workarounds.The three evidence based strategies proposed to address this gap are, evidence based standardization in planning and implementation, the identification and elimination of workarounds and hard wiring. An evidence based checklist evaluates compliance with standard procedures. The LEAN model of Jodoka is used to assure adaptation of the machine to human workflow. Direct observation provides valuable workflow assessment. An effective BCMA implementation involves careful system design, identification of workflow issues which cause workarounds, and adapting the machine to nursing needs

    A Novel Mouse Fgfr2 Mutant, Hobbyhorse (hob), Exhibits Complete XY Gonadal Sex Reversal

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    The secreted molecule fibroblast growth factor 9 (FGF9) plays a critical role in testis determination in the mouse. In embryonic gonadal somatic cells it is required for maintenance of SOX9 expression, a key determinant of Sertoli cell fate. Conditional gene targeting studies have identified FGFR2 as the main gonadal receptor for FGF9 during sex determination. However, such studies can be complicated by inefficient and variable deletion of floxed alleles, depending on the choice of Cre deleter strain. Here, we report a novel, constitutive allele of Fgfr2, hobbyhorse (hob), which was identified in an ENU-based forward genetic screen for novel testis-determining loci. Fgr2hob is caused by a C to T mutation in the invariant exon 7, resulting in a polypeptide with a mis-sense mutation at position 263 (Pro263Ser) in the third extracellular immunoglobulin-like domain of FGFR2. Mutant homozygous embryos show severe limb and lung defects and, when on the sensitised C57BL/6J (B6) genetic background, undergo complete XY gonadal sex reversal associated with failure to maintain expression of Sox9. Genetic crosses employing a null mutant of Fgfr2 suggest that Fgr2hob is a hypomorphic allele, affecting both the FGFR2b and FGFR2c splice isoforms of the receptor. We exploited the consistent phenotype of this constitutive mutant by analysing MAPK signalling at the sex-determining stage of gonad development, but no significant abnormalities in mutant embryos were detected

    Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

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    Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

    Mouse hitchhiker mutants have spina bifida, dorso-ventral patterning defects and polydactyly: identification of Tulp3 as a novel negative regulator of the Sonic hedgehog pathway

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    The mammalian Sonic hedgehog (Shh) signalling pathway is essential for embryonic development and the patterning of multiple organs. Disruption or activation of Shh signalling leads to multiple birth defects, including holoprosencephaly, neural tube defects and polydactyly, and in adults results in tumours of the skin or central nervous system. Genetic approaches with model organisms continue to identify novel components of the pathway, including key molecules that function as positive or negative regulators of Shh signalling. Data presented here define Tulp3 as a novel negative regulator of the Shh pathway. We have identified a new mouse mutant that is a strongly hypomorphic allele of Tulp3 and which exhibits expansion of ventral markers in the caudal spinal cord, as well as neural tube defects and preaxial polydactyly, consistent with increased Shh signalling. We demonstrate that Tulp3 acts genetically downstream of Shh and Smoothened (Smo) in neural tube patterning and exhibits a genetic interaction with Gli3 in limb development. We show that Tulp3 does not appear to alter expression or processing of Gli3, and we demonstrate that transcriptional regulation of other negative regulators (Rab23, Fkbp8, Thm1, Sufu and PKA) is not affected. We discuss the possible mechanism of action of Tulp3 in Shh-mediated signalling in light of these new data
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