Institution
University of Dundee
Education•Dundee, United Kingdom•
About: University of Dundee is a education organization based out in Dundee, United Kingdom. It is known for research contribution in the topics: Population & Protein kinase A. The organization has 19258 authors who have published 39640 publications receiving 1919433 citations. The organization is also known as: Universitas Dundensis & Dundee University.
Papers published on a yearly basis
Papers
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TL;DR: The COACH system shows promise as a tool to help support older adults with moderate-levels of dementia and their caregivers, and the findings reinforce the need for flexibility and dynamic personalization in devices designed to assist elderly adults with dementia.
Abstract: Background
Many older adults with dementia require constant assistance from a caregiver when completing activities of daily living (ADL). This study examines the efficacy of a computerized device intended to assist people with dementia through ADL, while reducing caregiver burden. The device, called COACH, uses artificial intelligence to autonomously guide an older adult with dementia through the ADL using audio and/or audio-video prompts.
317 citations
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TL;DR: A mathematical model of cancer cell invasion of tissue (extracellular matrix) which focuses on the role of the plasminogen activation system and the results obtained from numerical computations carried out on the model equations produce rich, dynamic heterogeneous spatio-temporal solutions.
Abstract: The growth of solid tumours proceeds through two distinct phases: the avascular and the vascular phase. It is during the latter stage that the insidious process of cancer invasion of peritumoral tissue can and does take place. Vascular tumours grow rapidly allowing the cancer cells to establish a new colony in distant organs, a process that is known as metastasis. The progression from a single, primary tumour to multiple tumours in distant sites throughout the body is known as the metastatic cascade. This is a multistep process that first involves the over-expression by the cancer cells of proteolytic enzyme activity, such as the urokinase-type plasminogen activator (uPA) and matrix metalloproteinases (MMPs). uPA itself initiates the activation of an enzymatic cascade that primarily involves the activation of plasminogen and subsequently its matrix degrading protein plasmin. Degradation of the matrix then enables the cancer cells to migrate through the tissue and subsequently to spread to secondary sites in the body. In this paper we consider a mathematical model of cancer cell invasion of tissue (extracellular matrix) which focuses on the role of the plasminogen activation system. The model consists of a system of reaction-diffusion-taxis partial differential equations describing the interactions between cancer cells, urokinase plasminogen activator (uPA), uPA inhibitors, plasmin and the host tissue. The focus of the modelling is on the spatio-temporal dynamics of the uPA system and how this influences the migratory properties of the cancer cells through random motility, chemotaxis and haptotaxis. The results obtained from numerical computations carried out on the model equations produce rich, dynamic heterogeneous spatio-temporal solutions and demonstrate the ability of rather simple models to produce complicated dynamics, all of which are associated with tumour heterogeneity and cancer cell progression and invasion.
317 citations
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University of California, San Francisco1, King's College London2, University of California, Berkeley3, University of Dundee4, Hokkaido University5, University of Milan6, University of Kentucky7, Rockefeller University8, Gifu University9, Washington University in St. Louis10, Juntendo University11, Hacettepe University12, University of British Columbia13, Churchill Hospital14, St Thomas' Hospital15
TL;DR: Kindler syndrome is, to the authors' knowledge, the first skin fragility disorder caused by a defect in actin-ECM linkage, rather than keratin- ECM linkage.
Abstract: Kindler syndrome is an autosomal recessive disorder characterized by neonatal blistering, sun sensitivity, atrophy, abnormal pigmentation, and fragility of the skin. Linkage and homozygosity analysis in an isolated Panamanian cohort and in additional inbred families mapped the gene to 20p12.3. Loss-of-function mutations were identified in the FLJ20116 gene (renamed “KIND1” [encoding kindlin-1]). Kindlin-1 is a human homolog of the Caenorhabditis elegans protein UNC-112, a membrane-associated structural/signaling protein that has been implicated in linking the actin cytoskeleton to the extracellular matrix (ECM). Thus, Kindler syndrome is, to our knowledge, the first skin fragility disorder caused by a defect in actin-ECM linkage, rather than keratin-ECM linkage.
317 citations
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TL;DR: Best evidence medical education (BEME) is the implementation, by teachers in their practice, of methods and approaches to education based on the best evidence available, taking into account a number of factors-the QUESTS dimensions.
Abstract: There is a need to move from opinion-based education to evidence-based education. Best evidence medical education (BEME) is the implementation, by teachers in their practice, of methods and approaches to education based on the best evidence available. It involves a professional judgement by the teacher about his/her teaching taking into account a number of factors-the QUESTS dimensions. The Quality of the research evidence available-how reliable is the evidence? the Utility of the evidence-can the methods be transferred and adopted without modification, the Extent of the evidence, the Strength of the evidence, the Target or outcomes measured-how valid is the evidence? and the Setting or context-how relevant is the evidence? The evidence available can be graded on each of the six dimensions. In the ideal situation the evidence is high on all six dimensions, but this is rarely found. Usually the evidence may be good in some respects, but poor in others.The teacher has to balance the different dimensions and...
316 citations
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TL;DR: It is demonstrated that both XPD and FancJ proteins have a conserved domain near the N terminus that includes an iron-sulfur (Fe-S) cluster, which is essential for the helicase activity of XPD.
316 citations
Authors
Showing all 19404 results
Name | H-index | Papers | Citations |
---|---|---|---|
Matthias Mann | 221 | 887 | 230213 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Stefan Schreiber | 178 | 1233 | 138528 |
Kenneth C. Anderson | 178 | 1138 | 126072 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Salvador Moncada | 164 | 495 | 138030 |
Jorge E. Cortes | 163 | 2784 | 124154 |
Andrew P. McMahon | 162 | 415 | 90650 |
Philip Cohen | 154 | 555 | 110856 |
Dirk Inzé | 149 | 647 | 74468 |
Andrew T. Hattersley | 146 | 768 | 106949 |
Antonio Lanzavecchia | 145 | 408 | 100065 |
Kim Nasmyth | 142 | 294 | 59231 |
David Price | 138 | 1687 | 93535 |
Dario R. Alessi | 136 | 354 | 74753 |