Institution
Guy's and St Thomas' NHS Foundation Trust
Healthcare•London, United Kingdom•
About: Guy's and St Thomas' NHS Foundation Trust is a healthcare organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Medicine. The organization has 7686 authors who have published 9631 publications receiving 399353 citations. The organization is also known as: Guy's and St Thomas' National Health Service Foundation Trust & Guy's and St Thomas' National Health Service Trust.
Topics: Population, Medicine, Randomized controlled trial, Cancer, Breast cancer
Papers published on a yearly basis
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06 May 2010125 citations
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University of Oxford1, Foundation for Research & Technology – Hellas2, University of Crete3, Wellcome Trust Centre for Human Genetics4, Guy's and St Thomas' NHS Foundation Trust5, NHS Lothian6, Belfast City Hospital7, Great Ormond Street Hospital8, King's College London9, UCL Institute of Child Health10, Medical Research Council11
TL;DR: Reduced dosage of ERF, which encodes an inhibitory ETS transcription factor directly bound by ERK1/2, causes complex craniosynostosis in humans and mice and is identified as a novel regulator of osteogenic stimulation by RAS-ERK signaling, potentially by competing with activating ETS factors in multifactor transcriptional complexes.
Abstract: George Mavrothalassitis, Andrew Wilkie and colleagues report the identification of mutations in ERF that cause a complex craniosynostosis disorder with multiple-suture synostosis, craniofacial dysmorphism, Chiari malformation and language delay. They also show that reduced dosage of Erf in mice causes craniosynostosis.
125 citations
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University College Cork1, Food Standards Agency2, University of Southampton3, University of Nebraska–Lincoln4, Imperial College London5, Royal Children's Hospital6, University of Natural Resources and Life Sciences, Vienna7, Charité8, Hospital Clínico San Carlos9, Nestlé10, Guy's and St Thomas' NHS Foundation Trust11, Technical University of Denmark12, Manchester Academic Health Science Centre13, National and Kapodistrian University of Athens14, University of Manchester15, Hobart Corporation16, Agro ParisTech17, University Hospital Southampton NHS Foundation Trust18, St Mary's Hospital19
TL;DR: This review aims to summarize the perspectives of all the key stakeholders (including clinicians, patients, food industry and regulators), with the aim of defining common health protection and risk minimization goals.
Abstract: Precautionary allergen labelling (PAL) was introduced by the food industry to help manage and communicate the possibility of reaction from the unintended presence of allergens in foods. However, in its current form, PAL is counterproductive for consumers with food allergies. This review aims to summarize the perspectives of all the key stakeholders (including clinicians, patients, food industry and regulators), with the aim of defining common health protection and risk minimization goals. The lack of agreed reference doses has resulted in inconsistent application of PAL by the food industry and in levels of contamination that prompt withdrawal action by enforcement officers. So there is a poor relationship between the presence or absence of PAL and actual reaction risk. This has led to a loss of trust in PAL, reducing the ability of consumers with food allergies to make informed choices. The result has been reduced avoidance, reduced quality of life and increased risk-taking by consumers who often ignore PAL. All contributing stakeholders agree that PAL must reflect actual risk. PAL should be transparent and consistent with rules underpinning decision-making process being communicated clearly to all stakeholders. The use of PAL should indicate the possible, unintended presence of an allergen in a consumed portion of a food product at or above any proposed action level. This will require combined work by all stakeholders to ensure everyone understands the approach and its limitations. Consumers with food allergy then need to be educated to undertake individualized risk assessments in relation to any PAL present.
124 citations
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TL;DR: The strategy anticipates that these common adverse events are likely to occur and recommends the early use of preventive therapy to lower triglycerides and elevate thyroid hormone levels in the blood, followed by subsequent monitoring, dose adjustment during bexarotene treatment, and titration of the daily bexARotene dose, which is optimal for most patients.
Abstract: Bexarotene is an oral retinoid therapy that is effective for the treatment of early and advanced-stage cutaneous T-cell lymphoma (CTCL) in patients who have failed on other therapies. However, bexarotene treatment is associated with unavoidable side-effects, in particular hypertriglyceridaemia and hypothyroidism, which are manageable with adequate concomitant medications and are reversible on cessation of treatment. A pragmatic strategy for minimizing bexarotene-associated hypertriglyceridaemia and hypothyroidism is suggested, based on data from the studies with bexarotene in CTCL and on day-to-day experience with this agent in the clinical setting. The strategy anticipates that these common adverse events are likely to occur and recommends the early use of preventive therapy to lower triglycerides and elevate thyroid hormone levels in the blood, followed by subsequent monitoring, dose adjustment during bexarotene treatment, and titration of the daily bexarotene dose from 150 to 300 mg m(-2), which is optimal for most patients. When further information becomes available on how bexarotene interacts with lipid metabolism and thyroid function, the management approach suggested here may need to be changed.
124 citations
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University of Oxford1, King's College London2, Churchill Hospital3, Guy's and St Thomas' NHS Foundation Trust4, Imperial College London5, Royal Brisbane and Women's Hospital6, University of Edinburgh7, Hebrew University of Jerusalem8, Ohio State University9, University of Otago10, Worcestershire Acute Hospitals NHS Trust11, University of Ulsan12, Cardiff University13, Imperial College Healthcare14, Katholieke Universiteit Leuven15, Cancer Research UK16
TL;DR: Mutations in PTEN and PTCH are unlikely to cause juvenile polyposis in the absence of clinical features indicative of CS, BRRS, or GS, and a proportion of JPS patients harbour DPC4 mutations but there remains uncharacterised genetic heterogeneity in JPS.
Abstract: Background—Juvenile polyposis syndrome (JPS) is characterised by gastrointestinal (GI) hamartomatous polyposis and an increased risk of GI malignancy. Juvenile polyps also occur in the Cowden (CS), Bannayan-Ruvalcaba-Riley (BRRS) and Gorlin (GS) syndromes. Diagnosing JPS can be problematic because it relies on exclusion of CS, BRRS, and GS. Germline mutations in the PTCH, PTEN and DPC4 (SMAD4) genes can cause GS, CS/BRRS, and JPS, respectively. Aims—To examine the contribution of mutations in PTCH, PTEN, and DPC4 (SMAD4) to JPS. Methods—Forty seven individuals from 15 families and nine apparently sporadic cases with JPS were screened for germline mutations in DPC4, PTEN, and PTCH. Results—No patient had a mutation in PTEN or PTCH. Five diVerent germline mutations were detected in DPC4; three of these were deletions, one a single base substitution creating a stop codon, and one a missense change. None of these patients had distinguishing clinical features. Conclusions—Mutations in PTEN and PTCH are unlikely to cause juvenile polyposis in the absence of clinical features indicative of CS, BRRS, or GS. A proportion of JPS patients harbour DPC4 mutations (21% in this study) but there remains uncharacterised genetic heterogeneity in JPS. (Gut 2000;46:656‐660)
124 citations
Authors
Showing all 7765 results
Name | H-index | Papers | Citations |
---|---|---|---|
Christopher J L Murray | 209 | 754 | 310329 |
Bruce M. Psaty | 181 | 1205 | 138244 |
Giuseppe Remuzzi | 172 | 1226 | 160440 |
Mika Kivimäki | 166 | 1515 | 141468 |
Simon I. Hay | 165 | 557 | 153307 |
Theo Vos | 156 | 502 | 186409 |
Ali H. Mokdad | 156 | 634 | 160599 |
Steven Williams | 144 | 1375 | 86712 |
Igor Rudan | 142 | 658 | 103659 |
Mohsen Naghavi | 139 | 381 | 169048 |
Christopher D.M. Fletcher | 138 | 674 | 82484 |
Martin McKee | 138 | 1732 | 125972 |
David A. Jackson | 136 | 1095 | 68352 |
Graham G. Giles | 136 | 1249 | 80038 |
Yang Liu | 129 | 2506 | 122380 |