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: Qualitative proteomics data show that sumoylation is strongly associated with transcription because nearly one-third of the identified target proteins are putative transcriptional regulators.
316 citations
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TL;DR: A mechanism for proving global convergence in SQP--filter methods for nonlinear programming (NLP) is described, and the main point of interest is to demonstrate how convergence for NLP can be induced without forcing sufficient descent in a penalty-type merit function.
Abstract: A mechanism for proving global convergence in SQP--filter methods for nonlinear programming (NLP) is described. Such methods are characterized by their use of the dominance concept of multiobjective optimization, instead of a penalty parameter whose adjustment can be problematic. The main point of interest is to demonstrate how convergence for NLP can be induced without forcing sufficient descent in a penalty-type merit function.
The proof relates to a prototypical algorithm, within which is allowed a range of specific algorithm choices associated with the Hessian matrix representation, updating the trust region radius, and feasibility restoration.
316 citations
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TL;DR: Electronic record linkage was more sensitive than general practice registers in identifying diabetic subjects and identified an additional 0.18% of the population with a history of hyperglycaemia who might warrant screening for undiagnosed diabetes.
Abstract: Objectives: To identify all patients with diabetes in a community using electronic record linkage of multiple data sources and to compare this method of case ascertainment with registers of diabetic patients derived from primary care. Design: Electronic capture-recapture linkage of records included data on all patients attending hospital diabetes clinics, all encashed prescriptions for diabetes related drugs and monitoring equipment, all patients discharged from hospital, patients attending a mobile unit for eye screening, and results for glycated haemoglobin and plasma glucose concentrations from the regional biochemistry database. Diabetes registers from primary care were from a random sample of eight Tayside general practices. A detailed manual study of relevant records for the 35 144 patients registered with these eight general practices allowed for validation of the case ascertainment. Setting: Tayside region of Scotland, population 391 274 on 1 January 1996. Main outcome measures: Prevalence of diabetes; population of patients identified by different data sources; sensitivity and positive predictive value of ascertainment methods. Results: Electronic record linkage identified 7596 diabetic patients, giving a prevalence of known diabetes of 1.94% (0.21% insulin dependent diabetes, 1.73% non-insulin dependent): 63% of patients had attended hospital diabetes clinics, 68% had encashed diabetes related prescriptions, 72% had attended the mobile eye screening unit, and 48% had biochemical results diagnostic of diabetes. A further 701 patients had isolated hyperglycaemia (plasma glucose >11.1 mmol/l) but were not considered diabetic by general practitioners. Validation against the eight general practices (636 diabetic patients) showed electronic linkage to have a sensitivity of 0.96 and a positive predictive value of 0.95 for ascertainment of known diabetes. General practice lists had a sensitivity of 0.91 and a positive predictive value of 0.98. Conclusions: Electronic record linkage was more sensitive than general practice registers in identifying diabetic subjects and identified an additional 0.18% of the population with a history of hyperglycaemia who might warrant screening for undiagnosed diabetes. Key messages It has been recommended that regional registers of patients with diabetes are established in order to facilitate effective monitoring and treatment of diabetes In Tayside we created a diabetes register by record linkage of multiple data sources: all patients attending hospital diabetes clinics, all encashed prescriptions for diabetes related drugs and monitoring equipment, all patients discharged from hospital, patients attending a mobile unit for eye screening, and results for glycated haemoglobin and plasma glucose concentrations from the regional biochemistry database This register identified 7596 patients with diabetes in Tayside, giving a prevalence of diabetes of 1.94% Record linkage was more sensitive than general practice registers in ascertaining cases of known diabetes A unique patient identifier, the community health number, was fundamental for successful record linkage
316 citations
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TL;DR: The results of this study suggest that muscle contraction, phenformin, or AICAR activates AMPK by a mechanism that does not involve direct activation of LKB1, and suggest that the effects of excercise, phen formin, and AICar on metabolic processes in muscle may be mediated through activation of AMPK rather than activation ofLKB1 or the AMPK-related kinases.
Abstract: Activation of AMP-activated protein kinase (AMPK) by exercise and metformin is beneficial for the treatment of type 2 diabetes. We recently found that, in cultured cells, the LKB1 tumor suppressor ...
316 citations
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TL;DR: It is demonstrated that sustained Erk1/2 activation controls the transition from an Fgf5-positive, primitive ectoderm-like cell state to a neural progenitor cell state without attenuating bone morphogenetic protein (BMP) signalling and the minimum period of Erk 1/2 activity required to mediate this key developmental step is defined.
Abstract: Neural tissue formation is induced by growth factors that activate networks of signal transduction cascades that ultimately lead to the expression of early neural genes, including transcription factors of the SoxB family. Here, we report that fibroblast growth factor (FGF)-induced Erk1/2 (Mapk3 and Mapk1, respectively) mitogen-activated protein kinase (MAPK), but not phosphatidylinositol 3'-OH kinase (PI3K, Pik3r1), signalling is required for neural specification in mouse embryonic stem (ES) cells and in the chick embryo. Further, blocking Erk1/2 inhibits the onset of key SoxB genes in both mouse ES cells (Sox1) and chick embryos (Sox2 and Sox3) and, in both contexts, Erk1/2 signalling is required during only a narrow time window, as neural specification takes place. In the absence of Erk1/2 signalling, differentiation of ES cells stalls following Fgf5 upregulation. Using differentiating ES cells as a model for neural specification, we demonstrate that sustained Erk1/2 activation controls the transition from an Fgf5-positive, primitive ectoderm-like cell state to a neural progenitor cell state without attenuating bone morphogenetic protein (BMP) signalling and we also define the minimum period of Erk1/2 activity required to mediate this key developmental step. Together, these findings identify a conserved, specific and stage-dependent requirement for Erk1/2 signalling downstream of FGF-induced neural specification in higher vertebrates and provide insight into the signalling dynamics governing this process.
315 citations
Authors
Showing all 19404 results
Name | H-index | Papers | Citations |
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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 |