164 research outputs found

    Interdisciplinary Student Teams Projects: A Case Study

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    In today’s organizations team work has become an integral part of the day-to-day routine. For this reason, University professors are including group projects in many courses. In such group assessments, we advocate the use of interdisciplinary teams, where possible. As a case study, we report an interdisciplinary group technical project with members from a Master of Business Administration course and a Master of Science in Accounting course. We also describe the refinements made to the course in order to enhance the collaboration between students from two classes

    Covert action failure and fiasco construction: William Hague’s 2011 Libyan venture

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    In 2011 William Hague, then British Foreign Secretary, authorized a Special Forces team to enter Libya and attempt to contact rebels opposed to Muammar Gaddafi in the unfolding civil war. However, its members were detained by the rebels, questioned and ejected from the country. This article puts the literature on public policy failures into dialogue with that on covert action as a tool of foreign policy. It asks: why did this not develop into a fully-fledged policy fiasco when journalists and politicians alike judged it to have been a major error of judgement on Hague’s part? Using narrative analysis of the contemporary reporting of this incident, we argue that the government – possessing the advantage of information asymmetry accruing from operational secrecy – was ultimately able to win the battle of narratives in a frame contestation process. The study of information asymmetry can enhance the recently revivified research into foreign policy failures

    Use of anticoagulants and antiplatelet agents in stable outpatients with coronary artery disease and atrial fibrillation. International CLARIFY registry

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    Molecular signatures for CCN1, p21 and p27 in progressive mantle cell lymphoma

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    Mantle cell lymphoma (MCL) is a comparatively rare non-Hodgkin’s lymphoma characterised by overexpression of cyclin D1.Many patients present with or progress to advanced stage disease within 3 years. MCL is considered an incurable disease withmedian survival between 3 and 4 years. We have investigated the role(s) of CCN1 (CYR61) and cell cycle regulators inprogressive MCL. We have used the human MCL cell lines REC1 G519 > JVM2 cells by RQ-PCR, depicting a decrease in CCN1expression with disease progression. Investigation of CCN1 isoform expression by western blotting showed that whilst expres-sion of full-length CCN1 was barely altered in the cell lines, expression of truncated forms (18–20 and 28–30 kDa) decreasedwith disease progression. We have then demonstrated that cyclin D1 and cyclin dependent kinase inhibitors (p21CIP1and p27KIP1)are also involved in disease progression. Cyclin D1 was highly expressed in REC1 cells (OD: 1.0), reduced to one fifth in G519cells (OD: 0.2) and not detected by western blotting in JVM2 cells. p27KIP1followed a similar profile of expression as cyclin D1.Conversely, p21CIP1was absent in the REC1 cells and showed increasing expression in G519 and JVM2 cells. Subcellularlocalization detected p21CIP1/p27KIP1primarily within the cytoplasm and absent from the nucleus, consistent with altered roles in treatment resistance. Dysregulation of the CCN1 truncated forms are associated with MCL progression. In conjunction withreduced expression of cyclin D1 and increased expression of p21, this molecular signature may depict aggressive disease andtreatment resistance

    The epigenetic landscape of renal cancer

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    This is an accepted manuscript of an article published by Nature in Nature Reviews: Nephrology on 28/11/2016, available online: https://doi.org/10.1038/nrneph.2016.168 The accepted version of the publication may differ from the final published version.The majority of kidney cancers are associated with mutations in the von Hippel-Lindau gene and a small proportion are associated with infrequent mutations in other well characterized tumour-suppressor genes. In the past 15 years, efforts to uncover other key genes involved in renal cancer have identified many genes that are dysregulated or silenced via epigenetic mechanisms, mainly through methylation of promoter CpG islands or dysregulation of specific microRNAs. In addition, the advent of next-generation sequencing has led to the identification of several novel genes that are mutated in renal cancer, such as PBRM1, BAP1 and SETD2, which are all involved in histone modification and nucleosome and chromatin remodelling. In this Review, we discuss how altered DNA methylation, microRNA dysregulation and mutations in histone-modifying enzymes disrupt cellular pathways in renal cancers
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