998 resultados para cameron ulcer


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Mr C, a 68-year-old Chinese male with diabetes mellitus, previous stroke and ischaemic cardiomyopathy on clopidogrel, presented with haematochezia. Colonoscopy showed a sigmoid ulcer, which was treated endoscopically. Histology of the biopsy from the ulcer revealed non-specific changes. However, he presented with recurrent bleeding from this non-healing sigmoid ulcer. A review of the histologic specimen revealed CMV intranuclear inclusion bodies. He was treated with intravenous ganciclovir, with no further hematochezia.

Keywords Hematochezia, cytomegalovirus, ulcer

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Management of dyspepsia remains a controversial area. Although the European Helicobacter pylori study group has advised empirical eradication therapy without oesophagogastroduodenoscopy (OGD) in young H pylori positive dyspeptic patients who do not exhibit alarm symptoms, this strategy has not been subjected to clinical trial.

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1. Decreasing the prevalence of pressure ulcers in a chronic care hospital presents a challenge to care providers. 2. The promotion of staff nurses as educational resources has a positive effect on their participation in a wound and skin care team. 3. When basic prevention practices are not in place, risk factors are less useful indicators to predict the development of pressure ulcers. 4. Educating nurses about pressure ulcer etiology, prevention strategies, and treatments has a positive impact on reducing the number of patients who develop pressure ulcers and the number of pressure ulcers that develop on patients in a chronic care hospital.

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Cameron’s flagship policy of the ‘Big Society’ rests on a society/government dichotomy, diagnosing a ‘broken society’ caused by ‘big government’ having assumed the role communities once played. The remedy is greater social responsibility and the ‘Big Society’. This article argues that the dichotomy is
deceptive. We aim to show that the Big Society is big government, as it employs techniques for managing the conduct of individuals and communities such that the mentality of government, far from being removed or reduced, is bettered and made more efficient. To illustrate this, we explore two major initiatives: the National Citizen Service and the Community Resilience programme. These
projects demonstrate how practices of informing and guiding the conduct of individuals both produce agents and normalise certain values, resulting in the population being better known and controlled. Thus, far from lessening government and empowering people, the Big Society extends governmentality
throughout the social body.

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While there is an acknowledgement in apology research that political apologies are highly mediated, the process of mediation itself has lacked scrutiny. This article suggests that the idea of reconstruction helps to understand how apologies are mediated and evaluated. David Cameron's apology for Bloody Sunday is examined to see how he constructs four aspects of apology: social actors, consequences, categorization, and reasons. The reconstruction of those aspects by British, Unionist, and Nationalist press along with reconstructions made by soldiers in an online forum are considered. Data analysis was informed by thematic analysis and discourse analysis which helped to explore key aspects of reconstruction and how elements of Cameron's apology are altered in subsequent mediated forms of the apology. These mediated reconstructions of the apology allowed their authors to evaluate the apology in different ways. Thus, in this article, it is suggested that the evaluation of the apology by different groups is preceded by a reconstruction of it in accordance with rhetorical goals. This illuminates the process of mediation and helps to understand divergent responses to political apologies.

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This is one of a series of short case studies describing how academic tutors at the University of Southampton have made use of learning technologies to support their students.

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As the date approaches for Prime Minister Cameron’s long-awaited speech setting out his policy intentions towards the EU, a new CEPS Commentary by Michael Emerson chronicles a plethora of problems his propositions are going to encounter for their successful implementation in the both the British and European interests.

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A well-known histopathological feature of diseased skin in Buruli ulcer (BU) is coagulative necrosis caused by the Mycobacterium ulcerans macrolide exotoxin mycolactone. Since the underlying mechanism is not known, we have investigated the effect of mycolactone on endothelial cells, focussing on the expression of surface anticoagulant molecules involved in the protein C anticoagulant pathway. Congenital deficiencies in this natural anticoagulant pathway are known to induce thrombotic complications such as purpura fulimans and spontaneous necrosis. Mycolactone profoundly decreased thrombomodulin (TM) expression on the surface of human dermal microvascular endothelial cells (HDMVEC) at doses as low as 2ng/ml and as early as 8hrs after exposure. TM activates protein C by altering thrombin’s substrate specificity, and exposure of HDMVEC to mycolactone for 24 hours resulted in an almost complete loss of the cells’ ability to produce activated protein C. Loss of TM was shown to be due to a previously described mechanism involving mycolactone-dependent blockade of Sec61 translocation that results in proteasome-dependent degradation of newly synthesised ER-transiting proteins. Indeed, depletion from cells determined by live-cell imaging of cells stably expressing a recombinant TM-GFP fusion protein occurred at the known turnover rate. In order to determine the relevance of these findings to BU disease, immunohistochemistry of punch biopsies from 40 BU lesions (31 ulcers, nine plaques) was performed. TM abundance was profoundly reduced in the subcutis of 78% of biopsies. Furthermore, it was confirmed that fibrin deposition is a common feature of BU lesions, particularly in the necrotic areas. These findings indicate that there is decreased ability to control thrombin generation in BU skin. Mycolactone’s effects on normal endothelial cell function, including its ability to activate the protein C anticoagulant pathway are strongly associated with this. Fibrin-driven tissue ischemia could contribute to the development of the tissue necrosis seen in BU lesions.