616 research outputs found

    Learning from the early adopters: developing the digital practitioner

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    This paper explores how Sharpe and Beetham’s Digital Literacies Framework which was derived to model students’ digital literacies, can be applied to lecturers’ digital literacy practices. Data from a small-scale phenomenological study of higher education lecturers who used Web 2.0 in their teaching and learning practices are used to examine if this pyramid model represents their motivations for adopting technology-enhanced learning in their pedagogic practices. The paper argues that whilst Sharpe and Beetham’s model has utility in many regards, these lecturers were mainly motivated by the desire to achieve their pedagogic goals rather than by a desire to become a digital practitioner

    Solidification behavior of intensively sheared hypoeutectic Al-Si alloy liquid

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    The official published version of this article can be found at the link below.The effect of the processing temperature on the microstructural and mechanical properties of Al-Si (hypoeutectic) alloy solidified from intensively sheared liquid metal has been investigated systematically. Intensive shearing gives a significant refinement in grain size and intermetallic particle size. It also is observed that the morphology of intermetallics, defect bands, and microscopic defects in high-pressure die cast components are affected by intensive shearing the liquid metal. We attempt to discuss the possible mechanism for these effects.Funded by the EPSRC

    Intentional rounding in hospital wards to improve regular interaction and engagement between nurses and patients: a realist evaluation

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    BACKGROUND: The government response to the care failures at the Mid Staffordshire NHS Foundation Trust led to the policy imperative of ‘regular interaction and engagement between nurses and patients’ (Francis R. Report of the Mid Staffordshire NHS Foundation Trust Public Inquiry. London: The Stationery Office; 2013. © Crown copyright 2013. Contains public sector information licensed under the Open Government Licence v3.0) in the NHS. The pressure on nursing to act resulted in the introduction of the US model, known as ‘intentional rounding’, into nursing practice. This is a timed, planned intervention that sets out to address fundamental elements of nursing care by means of a regular bedside ward round. OBJECTIVES: The study aims were to examine what it is about intentional rounding in hospital wards that works, for whom and in what circumstances. DESIGN: A multimethod study design was undertaken using realist evaluation methodology. The study was conducted in four phases: (1) theory development; (2) a national survey of all NHS acute trusts in England; (3) in-depth case studies of six wards, involving individual interviews, observations, retrieval of routinely collected ward outcome data and analysis of costs; and (4) synthesis of the study findings. SETTING: The study was conducted in acute NHS trusts in England. PARTICIPANTS: A total of 108 acute NHS trusts participated in the survey. Seventeen senior managers, 33 front-line nurses, 28 non-nursing professionals, 34 patients and 28 carers participated in individual interviews. Thirty-nine members of nursing staff were shadowed during their delivery of intentional rounding and the direct care received by 28 patients was observed. REVIEW METHODS: A realist synthesis was undertaken to identify eight context–mechanism–outcome configurations, which were tested and refined using evidence collected in subsequent research phases. RESULTS: The national survey showed that 97% of NHS trusts had implemented intentional rounding in some way. Data synthesis from survey, observation and interview findings showed that only two of the original eight mechanisms were partially activated (consistency and comprehensiveness, and accountability). The evidence for two mechanisms was inconclusive (visibility of nurses and anticipation); there was minimal evidence for one mechanism (multidisciplinary teamwork and communication) and no evidence for the remaining three (allocated time to care, nurse–patient relationships and communication, and patient empowerment). A total of 240 intentional rounds were observed within 188 hours of care delivery observation. Although 86% of all intentional rounding interactions were observed to be documented, fidelity to the original intervention [i.e. the Studer Group protocol (Studer Group. Best Practices: Sacred Heart Hospital, Pensacola, Florida. Hourly Rounding Supplement. Gulf Breeze, FL: Studer Group; 2007)] was generally low. LIMITATIONS: Intentional rounding was often difficult for researchers to observe, as it was rarely delivered as a discrete activity but instead undertaken alongside other nursing activities. Furthermore, a lack of findings about the influence of intentional rounding on patient outcomes in the safety thermometer data limits inferences on how mechanisms link to clinical outcomes for patients. CONCLUSIONS: The evidence from this study demonstrates that the effectiveness of intentional rounding, as currently implemented and adapted in England, is very weak and falls short of the theoretically informed mechanisms. There was ambivalence and concern expressed that intentional rounding oversimplifies nursing, privileges a transactional and prescriptive approach over relational nursing care, and prioritises accountability and risk management above individual responsive care. FUTURE WORK: It is suggested that the insights and messages from this study inform a national conversation about whether or not intentional rounding is the optimum intervention to support the delivery of fundamental nursing care to patients, or if the time is right to shape alternative solutions. FUNDING: The National Institute for Health Research Health Services and Delivery Research programme

    cAMP/PKA signaling balances respiratory activity with mitochondria dependent apoptosis via transcriptional regulation

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    Background Appropriate control of mitochondrial function, morphology and biogenesis are crucial determinants of the general health of eukaryotic cells. It is therefore imperative that we understand the mechanisms that co-ordinate mitochondrial function with environmental signaling systems. The regulation of yeast mitochondrial function in response to nutritional change can be modulated by PKA activity. Unregulated PKA activity can lead to the production of mitochondria that are prone to the production of ROS, and an apoptotic form of cell death. Results We present evidence that mitochondria are sensitive to the level of cAMP/PKA signaling and can respond by modulating levels of respiratory activity or committing to self execution. The inappropriate activation of one of the yeast PKA catalytic subunits, Tpk3p, is sufficient to commit cells to an apoptotic death through transcriptional changes that promote the production of dysfunctional, ROS producing mitochondria. Our data implies that cAMP/PKA regulation of mitochondrial function that promotes apoptosis engages the function of multiple transcription factors, including HAP4, SOK2 and SCO1. Conclusions We propose that in yeast, as is the case in mammalian cells, mitochondrial function and biogenesis are controlled in response to environmental change by the concerted regulation of multiple transcription factors. The visualization of cAMP/TPK3 induced cell death within yeast colonies supports a model that PKA regulation plays a physiological role in coordinating respiratory function and cell death with nutritional status in budding yeast

    Application of pharmacogenomics and bioinformatics to exemplify the utility of human <i>ex vivo</i> organoculture models in the field of precision medicine

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    Here we describe a collaboration between industry, the National Health Service (NHS) and academia that sought to demonstrate how early understanding of both pharmacology and genomics can improve strategies for the development of precision medicines. Diseased tissue ethically acquired from patients suffering from chronic obstructive pulmonary disease (COPD), was used to investigate inter-patient variability in drug efficacy using ex vivo organocultures of fresh lung tissue as the test system. The reduction in inflammatory cytokines in the presence of various test drugs was used as the measure of drug efficacy and the individual patient responses were then matched against genotype and microRNA profiles in an attempt to identify unique predictors of drug responsiveness. Our findings suggest that genetic variation in CYP2E1 and SMAD3 genes may partly explain the observed variation in drug response

    Thymosin β10 Expression Driven by the Human TERT Promoter Induces Ovarian Cancer-Specific Apoptosis through ROS Production

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    Thymosin β10 (Tβ10) regulates actin dynamics as a cytoplasm G-actin sequestering protein. Previously, we have shown that Tβ10 diminishes tumor growth, angiogenesis, and proliferation by disrupting actin and by inhibiting Ras. However, little is known about its mechanism of action and biological function. In the present study, we establish a new gene therapy model using a genetically modified adenovirus, referred to as Ad.TERT.Tβ10, that can overexpress the Tβ10 gene in cancer cells. This was accomplished by replacing the native Tβ10 gene promoter with the human TERT promoter in Ad.TERT.Tβ10. We investigated the cancer suppression activity of Tβ10 and found that Ad.TERT.Tβ10 strikingly induced cancer-specific expression of Tβ10 as well as apoptosis in a co-culture model of human primary ovarian cancer cells and normal fibroblasts. Additionally, Ad.TERT.Tβ10 decreased mitochondrial membrane potential and increased reactive oxygen species (ROS) production. These effects were amplified by co-treatment with anticancer drugs, such as paclitaxel and cisplatin. These findings indicate that the rise in ROS production due to actin disruption by Tβ10 overexpression increases apoptosis of human ovarian cancer cells. Indeed, the cancer-specific overexpression of Tβ10 by Ad.TERT.Tβ10 could be a valuable anti-cancer therapeutic for the treatment of ovarian cancer without toxicity to normal cells
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