18 resultados para Wilson, Charles Edward, b. 1886.

em Deakin Research Online - Australia


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Details the operations of the Victorian Navy for the period 1883 to 1886, including information on ships, training, stores, list of officers on the active and unattached list, list of ships including their armament, and the regulations under which the navy ran.

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This paper discusses results from an international study of continuous improvement in product innovation. The empirical research is based upon a theoretical model of continuous product innovation (CPI) that identifies contingencies, behaviours, levers and performances relevant to improving product innovation processes. As successful knowledge management is widely recognised as a key capability for firms to successfully develop CPI, companies have been classified according to identified contingencies and the impact of these contingencies on key knowledge management criteria. Comparative analysis of the identified groups of companies has demonstrated important differences between the learning behaviours found present in the two groups thus identified, and in the levers used to develop and support these behaviours. The selection of performance measures by the two groups has highlighted further significant differences in the way the two groups understand and measure their CPI processes. Finally, the paper includes a discussion of appropriate mechanisms for firms with similar contingency sets to improve their approaches to organisational learning and product innovation.

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Visionnaire : A screening of postgraduate and masters films<br /><br /><b>All I Have Left b>- Merei, Daniel<br /><b>The Score b>- Holland, Thomas,<br /><b>The Beard Fairy b>- Morrison, Luke<br /><b>Retracing the End b>- Biviano, Shannon, Lee, David, Ooi, Zihui, Joo, James, Partovifar, Hadi, Karantzas, Alexandra<br /><b>Armedb> - Francisco, Mia, Weise, Timothy, Benyaminovich, Mark, Medew, Sarah, Barker, Nic, Walker, James E.<br /><b>The Library Museum b>- Song, Miru, Larmour-Reid, Ezra, Yii, Emily, Mentzoni, Kristoffer, Janssen, Hans, Yong, King<br /><b>Children Can Write Poetry b>- Carolan, Olivia, Wilson, Robert, Sebastian, Justin, Noonan, Sam, Wally, Joe, Huang, Janet<br /><b>Ill Will b>- Evans, Sheridan, Thorborg, Oscar, Tofteberg, Lise, Vawdrey, Michael, Moraes, Jamie, Meyer, Nina<br /><b>The Toothpick Man b>- Devandran, Yogashree, Arntzen, Kim, Sheah, Ju Er, Kusdina, Karina, Rahim, Amir Abdul<br /><b>Necareb> - Thomas, Rohan, Wijananda, Adi, Graham, Alice, Low, Nicholas, Wong, Aaron, Kitchen, Zachary<br /><b>Glassb> - Stringer, Blake, Anderson, Robert, Kelada, Matthew, Hafner, Katrina, Warner, Timothy, Vivian-Williams, Olivia<br /><b>Brick Road b>- Moore, Kimberley, Cleeve, Guy, Kennedy, Ryan, Terry, James, herbert, Robert, Wilson, Eleanor<br /><b>Tiesb> - Rondos, Maximo, Gordes, Liam, Ruddy, Dylan, Blakley, Jock, Pitches, Devan, Mitchell, Robert

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<b>Background/Objectivesb>:<br />Invasive procedures such as surgery cause immunosuppression, leading to increased risk of complications, infections and extended hospital stay. Emerging research around immune-enhancing nutrition supplements and their ability to reduce postoperative complications and reduce treatment costs is promising. This randomised controlled trial aims to examine the effect of preoperative immunonutrition supplementation on length of hospital stay (LOS), complications and treatment costs in both well-nourished and malnourished gastrointestinal surgery patients.<br /><br /><b>Subjects/Methodsb>:<br />Ninety-five patients undergoing elective upper and lower gastrointestinal surgery were recruited. The treatment group (n=46) received a commercial immuno-enhancing supplement 5 days preoperatively. The control group (n=49) received no supplements. The primary outcome measure was LOS, and secondary outcome measures included complications and cost.<br /><br /><b>Resultsb>:<br />A nonsignificant trend towards a shorter LOS within the treatment group was observed (7.1±4.1 compared with 8.8±6.5 days; P=0.11). For malnourished patients, this trend was greater with hospital stay reduced by 4 days (8.3±3.5 vs 12.3±9.5 days; P=0.21). Complications and unplanned intensive care admission rates were very low in both the groups. The average admission cost was reduced by AUD1576 in the treatment group compared with the control group (P=0.37).<br /><br /><b>Conclusionsb>:<br />Preoperative immunonutrition therapy in gastrointestinal surgery has the potential to reduce the LOS and cost, with greater treatment benefit seen in malnourished patients; however, there is a need for additional research with greater patient numbers.

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I am an early- to mid-career researcher, and Letters to a Young Scientist struck a chord with me from the very first page. The journey from amateur enthusiast to professional scientist is an exciting, challenging and often difficult one, and Edward Wilson - a Pulitzer prizewinner and one of the world's greatest entomologists - is well qualified to guide and advise the new generation. Written as a collection of letters filled with anecdotes and well-considered advice, this book is inspired by the author's experience of the journey from being a young boy enthused by ants to an eminent scholar. Like many in his field, Wilson's education began when he was a child fascinated by insects in the garden (my own summers spent excavating ant nests feel somewhat validated). He traces his progression through formal education to the establishment of his own scientific research programme.

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Wilson disease is an autosomal recessive copper transport disorder resulting from defective biliary excretion of copper and subsequent hepatic copper accumulation and liver failure if not treated. The disease is caused by mutations in the ATP7B (WND) gene, which is expressed predominantly in the liver and encodes a copper-transporting P-type ATPase that is structurally and functionally similar to the Menkes protein (MNK), which is defective in the X-linked copper transport disorder Menkes disease. The toxic milk (tx) mouse has a clinical phenotype similar to Wilson disease patients and, recently, the tx mutation within the murine WND homologue (Wnd) of this mouse was identified, establishing it as an animal model for Wilson disease. In this study, cDNA constructs encoding the wild-type (Wnd-wt) and mutant (Wnd-tx) Wilson proteins (Wnd) were generated and expressed in Chinese hamster ovary (CHO) cells. The tx mutation disrupted the copper-induced relocalization of Wnd in CHO cells and abrogated Wnd-mediated copper resistance of transfected CHO cells. In addition, co-localization experiments demonstrated that while Wnd and MNK are located in the trans-Golgi network in basal copper conditions, with elevated copper, these proteins are sorted to different destinations within the same cell. Ultrastructural studies showed that with elevated copper levels, Wnd accumulated in large multi-vesicular structures resembling late endosomes that may represent a novel compartment for copper transport. The data presented provide further support for a relationship between copper transport activity and the copper-induced relocalization response of mammalian copper ATPases, and an explanation at a molecular level for the observed phenotype of tx mice<br />

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The Wilson disease (WD) protein (ATP7B) is a copper-transporting P-type ATPase that is responsible for the efflux of hepatic copper into the bile, a process that is essential for copper homeostasis in mammals. Compared with other mammals, sheep have a variant copper phenotype and do not efficiently excrete copper via the bile, often resulting in excessive copper accumulation in the liver. To investigate the function of sheep ATP7B and its potential role in the copper-accumulation phenotype, cDNAs encoding the two forms of ovine ATP7B were transfected into immortalised fibroblast cell lines derived from a Menkes disease patient and a normal control. Both forms of ATP7B were able to correct the copper-retention phenotype of the Menkes cell line, demonstrating each to be functional copper-transporting molecules and suggesting that the accumulation of copper in the sheep liver is not due to a defect in the copper transport function of either form of sATP7B.<br />

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<b>Background and Aim:b> The toxic milk (tx) mouse is a non-fatal animal model for the metabolic liver disorder, Wilson's disease. The tx mouse has a mutated gene for a copper-transporting protein, causing early copper accumulation in the liver and late accumulation in other tissues. The present study investigated the efficacy of liver cell transplantation (LCT) to correct the tx mouse phenotype.<br /><br /><b>Methods:b> Congenic hepatocytes were isolated and intrasplenically transplanted into 3–4-month-old tx mice, which were then placed on various copper-loaded diets to examine its influence on repopulation by transplanted cells. The control animals were age-matched untransplanted tx mice. Liver repopulation was determined by comparisons of restriction fragment length polymorphism ratios (DNA and mRNA), and copper levels were measured by atomic absorption spectroscopy.<br /><br /><b>Results:b> Repopulation in recipient tx mice was detected in 11 of 25 animals (44%) at 4 months after LCT. Dietary copper loading (whether given before or after LCT, or both) provided no growth advantage for donor cells, with similar repopulation incidences in all copper treatment groups. Overall, liver copper levels were significantly lower in repopulated animals (538 ± 68 µg/g, n = 11) compared to non-repopulated animals (866 ± 62 µg/g, n = 14) and untreated controls (910 ± 103 µg/g, n = 6; P < 0.05). This effect was also seen in the kidney and spleen. Brain copper levels remained unchanged.<br /><br /><b>Conclusion:b> Transplanted liver cells can proliferate and correct a non-fatal metabolic liver disease, with some restoration of hepatic copper homeostasis after 4 months leading to reduced copper levels in the liver and extrahepatic tissues, but not in the brain.<br /><br /><br />

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