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Magalhaes-Sant'ana M.,Abel Salazar Biomedical Sciences Institute | Lassen J.,Copenhagen University | Millar K.M.,University of Nottingham | Sandoe P.,Copenhagen University | Olsson I.A.S.,Institute for Molecular and Cell Biology IBMC
Journal of Veterinary Medical Education | Year: 2014

Although it is widely agreed that veterinary students need to be introduced to ethics, there is limited empirical research investigating the reasons why veterinary ethics is being taught. This study presents the first extensive investigation into the reasons for teaching veterinary ethics and reports data collected in semi-structured interviews with educators involved in teaching undergraduate veterinary ethics at three European schools: the University of Copenhagen, the University of Nottingham, and the Technical University of Lisbon (curricular year 2010-2011). The content of the interview transcripts were analyzed using Toulmin's argumentative model. Ten objectives in teaching veterinary ethics were identified, which can be grouped into four overarching themes: ethical awareness, ethical knowledge, ethical skills, and individual and professional qualities. These objectives include recognizing values and ethical viewpoints, identifying norms and regulations, developing skills of communication and decision making, and contributing to a professional identity. Whereas many of the objectives complement each other, there is tension between the view that ethics teaching should promote knowledge of professional rules and the view that ethics teaching should emphasize critical reasoning skills. The wide range of objectives and the possible tensions between them highlight the challenges faced by educators as they attempt to prioritize among these goals of ethics teaching within a crowded veterinary curriculum. © 2014 AAVMC.

Sousa J.L.R.,Institute for Molecular and Cell Biology IBMC
ICETA 2011 - 9th IEEE International Conference on Emerging eLearning Technologies and Applications, Proceedings | Year: 2011

Traditional approaches to information system architecture development have a little concerns with information technology interdependency. They are sustained in a positivist vision of the world, where the information systems, can be constructed from a set of requirements, done by a detached observer, who captures or elicits it. Organizations are each more concerned about information flow and knowledge availability as the central element for innovation and empowerment. This flow and knowledge have always a relation of interdependency. There is clear construction of a technosocial system whose relevance and differentiation come from user interrelation with information technology. It's the structure of this technosocial system that is the key element for the information system architecture dynamic development. This paper presents information technology as a commodity, resulting from a positivist development, and blueprints a definition of three loosely IT coupled structures namely, software as service, computation as a service and infrastructure as a service, structured under an information system modeling architecture. This modeling approach addresses an interpretive vision, and aims to give directions to achieve and promote differentiation, for enterprise development. An exploratory use case, regarding a two-year e-learning project, is presented as a result of the adoption of the presented modulation vision. © 2011 IEEE.

Dias A.M.,University of Porto | Dourado J.,University of Porto | Lago P.,Centro Hospitalar do Porto | Cabral J.,Centro Hospitalar do Porto | And 17 more authors.
Human Molecular Genetics | Year: 2014

The incidence of inflammatory bowel disease is increasing worldwide and the underlying molecular mechanisms are far from being fully elucidated. Herein, we evaluated the role of N-glycosylation dysregulation in T cells as a key mechanism in the ulcerative colitis (UC) pathogenesis. The evaluation of the branched N-glycosylation levelsandprofile of intestinalTcell receptor (TCR)wereassessedin colonic biopsies fromUCpatientsand healthy controls. Expression alterations of the glycosyltransferase gene MGAT5 were also evaluated. We demonstrated thatUCpatients exhibit a dysregulation ofTCRbranchedN-glycosylationonlamina propriaTlymphocytes. Patients with severe UC showed the most pronounced defect on N-glycan branching in T cells. Moreover, UC patients showed a significant reduction of MGAT5 gene transcription in T lymphocytes. In this study, we disclose for the first time that a deficiency in branched N-glycosylation on TCR due to a reduced MGAT5 gene expression is a new molecular mechanism underlying UC pathogenesis, being a potential novel biomarker with promising clinical and therapeutic applications. © The Author 2013. Published by Oxford University Press. All rights reserved.

Rodrigues A.-J.,University of Minho | do Carmo Costa M.,University of Minho | do Carmo Costa M.,University of Michigan | Silva T.-L.,University of Minho | And 6 more authors.
Biochimica et Biophysica Acta - Molecular Cell Research | Year: 2010

Ataxin-3 (ATXN3) is a widely expressed protein that binds to ubiquitylated proteins, has deubiquitylating activity in vitro and is thought to modulate substrate degradation through the ubiquitin-proteasome pathway. Expansion of a polyglutamine tract in ATXN3 causes Machado-Joseph disease, a late-onset neurodegenerative disorder characterized by ubiquitin-positive aggregate formation and specific neuronal death. Although ATXN3 has been involved in transcriptional repression and in the ubiquitin-proteasome pathway, its biological function is still unknown. In this work, we show that depletion of ATXN3 using small-interference RNA (siRNA) causes a prominent phenotype in both human and mouse cell lines. A mild increase in ubiquitylation occurs and cells exhibit ubiquitin-positive foci, which is consistent with ATXN3 putative function as a deubiquitylating enzyme. In addition, siATXN3-silenced cells exhibit marked morphological changes such as rounder shape and loss of adhesion protrusions. At a structural level, the microtubule, microfilament and intermediate filament networks are severely compromised and disorganized. This cytoskeletal phenotype is reversible and dependent on ATXN3 levels. Cell-extracellular matrix connection is also affected in ATXN3-depleted cells as talin expression is reduced in the focal adhesions and lower levels of α-1 integrin subunit are expressed at their surface. Although the cytoskeletal and adhesion problems do not originate any major change in the cell cycle of siATXN3-depleted cells, cell death is increased in siATXN3 cultures compared to controls. In summary, in this work we show that the absence of ATXN3 leads to an overt cytoskeletal/adhesion defect raising the possibility that this protein may play a role in the cytoskeleton. © 2010 Elsevier B.V.

Santos S.D.,Institute for Molecular and Cell Biology IBMC | Lambertsen K.L.,University of Southern Denmark | Clausen B.H.,University of Southern Denmark | Akinc A.,Abel Salazar Biomedical Sciences Institute | And 4 more authors.
Journal of Neurochemistry | Year: 2010

Brain injury caused by ischemia is a major cause of human mortality and physical/cognitive disability worldwide. Experimentally, brain ischemia can be induced surgically by permanent middle cerebral artery occlusion. Using this model, we studied the influence of transthyretin in ischemic stroke. Transthyretin (TTR) is normally responsible for the transport of thyroid hormones and retinol in the blood and CSF. We found that TTR null mice (TTR -/-) did not show significant differences in cortical infarction 24 h after permanent middle cerebral artery occlusion compared with TTR +/+ control littermates. However, TTR null mice, heterozygous for the heat-shock transcription factor 1 (TTR-/-HSF1+/- mice), which compromised the stress response, showed a significant increase in cortical infarction, cerebral edema and the microglial-leukocyte response compared with TTR+/+HSF1+/- mice. Unexpectedly, we observed novel TTR distribution throughout the infarct, localized to disintegrated β-tubulin III+ neurons and cell debris. Specific elimination of TTR synthesis in the liver by RNAi had no effect on TTR distribution in the infarct, indicating that the observed TTR infiltration derived from CSF and not from the serum. This finding is corroborated by results from 'in situ' hybridization and real time PCR that excluded the presence of transthyretin mRNA in the infarct and peri-infarct areas. Our data suggest that in conditions of a compromised heat-shock response, CSF TTR contributes to control neuronal cell death, edema and inflammation, thereby influencing the survival of endangered neurons in cerebral ischemia. © 2010 The Authors. Journal of Neurochemistry © 2010 International Society for Neurochemistry.

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