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
Papers
More filters
••
University of Cambridge1, University of Lyon2, QIMR Berghofer Medical Research Institute3, University of Helsinki4, Laval University5, University of California, Irvine6, Mayo Clinic7, Charles University in Prague8, Ghent University9, National Institutes of Health10, Technion – Israel Institute of Technology11, Cancer Care Ontario12, University of Toronto13, University of Southern Denmark14, Aarhus University15, University of Pisa16, Tel Aviv University17, Rambam Health Care Campus18, Lund University19, Karolinska Institutet20, Uppsala University21, University of Gothenburg22, University of Pennsylvania23, Carlos III Health Institute24, Autonomous University of Barcelona25, German Cancer Research Center26, Netherlands Cancer Institute27, Erasmus University Rotterdam28, Leiden University29, Radboud University Nijmegen30, Utrecht University31, University of Amsterdam32, VU University Amsterdam33, Maastricht University34, The Royal Marsden NHS Foundation Trust35, Guy's and St Thomas' NHS Foundation Trust36, Princess Anne Hospital37, University of London38, Fox Chase Cancer Center39, University of Paris40, Curie Institute41, Institut Gustave Roussy42, University of Bordeaux43, University of Utah44, Harvard University45, Stanford University46, Cancer Prevention Institute of California47, University of Melbourne48, Columbia University49, Medical University of Vienna50, University of Copenhagen51, Memorial Sloan Kettering Cancer Center52, Roswell Park Cancer Institute53, University of Chicago54, Tufts University55, University of North Carolina at Chapel Hill56, Yale University57, New York University58, Ohio State University59, University of Turin60, University of Cologne61, Leipzig University62, Technische Universität München63, Ludwig Maximilian University of Munich64, University of Düsseldorf65, University of Ulm66, University of Regensburg67, Heidelberg University68, University of Würzburg69, Hannover Medical School70, Complutense University of Madrid71
TL;DR: The LSP1 and 2q35 SNPs appear to interact multiplicatively on breast cancer risk for BRCA2 mutation carriers and there was no evidence that the associations vary by mutation type depending on whether the mutated protein is predicted to be stable or not.
Abstract: Genome-wide association studies of breast cancer have identified multiple single nucleotide polymorphisms (SNPs) that are associated with increased breast cancer risks in the general population. In a previous study, we demonstrated that the minor alleles at three of these SNPs, in FGFR2, TNRC9 and MAP3K1, also confer increased risks of breast cancer for BRCA1 or BRCA2 mutation carriers. Three additional SNPs rs3817198 at LSP1, rs13387042 at 2q35 and rs13281615 at 8q24 have since been reported to be associated with breast cancer in the general population, and in this study we evaluated their association with breast cancer risk in 9442 BRCA1 and 5665 BRCA2 mutation carriers from 33 study centres. The minor allele of rs3817198 was associated with increased breast cancer risk only for BRCA2 mutation carriers [hazard ratio (HR) = 1.16, 95% CI: 1.07-1.25, P-trend = 2.8 x 10(-4)]. The best fit for the association of SNP rs13387042 at 2q35 with breast cancer risk was a dominant model for both BRCA1 and BRCA2 mutation carriers (BRCA1: HR = 1.14, 95% CI: 1.04-1.25, P = 0.0047; BRCA2: HR = 1.18 95% CI: 1.04-1.33, P = 0.0079). SNP rs13281615 at 8q24 was not associated with breast cancer for either BRCA1 or BRCA2 mutation carriers, but the estimated association for BRCA2 mutation carriers (per-allele HR = 1.06, 95% CI: 0.98-1.14) was consistent with odds ratio estimates derived from population-based case-control studies. The LSP1 and 2q35 SNPs appear to interact multiplicatively on breast cancer risk for BRCA2 mutation carriers. There was no evidence that the associations vary by mutation type depending on whether the mutated protein is predicted to be stable or not.
117 citations
••
TL;DR: A review of the different classes of possible biomarkers explored in psoriasis and PsA so far is summarised and novel strategies for biomarker discovery are discussed.
Abstract: Psoriasis is a common immune-mediated disease of the skin, which associates in 20–30% of patients with psoriatic arthritis (PsA). The immunopathogenesis of both conditions is not fully understood as it is the result of a complex interaction between genetic, environmental and immunological factors. At present there is no cure for psoriasis and there are no specific markers that can accurately predict disease progression and therapeutic response. Therefore, biomarkers for disease prognosis and response to treatment are urgently needed to help clinicians with objective indications to improve patient management and outcomes. Although many efforts have been made to identify psoriasis/PsA biomarkers none of them has yet been translated into routine clinical practice. In this review we summarise the different classes of possible biomarkers explored in psoriasis and PsA so far and discuss novel strategies for biomarker discovery.
116 citations
••
TL;DR: Further research is required to establish the complexities of the haemostatic changes with these devices, and to elucidate the mechanistic changes that are mainly responsible so that plans can be made to reduce their complications and improve management.
Abstract: Extracorporeal membrane oxygenators are used in critical care for the management of severe respiratory and cardiac failure. Activation of the coagulation system is initiated by the exposure of blood to synthetic surfaces and the shear stresses of the circuit, especially from device pumps. Initial fibrinogen deposition and subsequent activation of coagulation factors and complement allow platelets and leucocytes to adhere to oxygenator surfaces and enhance thrombin generation. These changes and others contribute to higher rates of thrombosis seen in these patients. In addition, bleeding rates are also high. Primary haemostasis is impaired by platelet dysfunction and loss of their key adhesive molecules and shear stress causes an acquired von Willebrand defect. In addition, there is also altered fibrinolysis and lastly, administration of systemic anticoagulation is required to maintain circuit patency. Further research is required to fulyl establish the complexities of the haemostatic changes with these devices, and to elucidate the mechanistic changes that are mainly responsible so that plans can be made to reduce their complications and improve management.
116 citations
••
TL;DR: British Association of Dermatologists’ guidelines for the management of tinea capitis 2014 L.C. Fuller, R.P. Proudfoot, S.E. Punjabi and E.F. Mustapa.
Abstract: British Association of Dermatologists’ guidelines for the management of tinea capitis 2014 L.C. Fuller, R.C. Barton, M.F. Mohd Mustapa, L.E. Proudfoot, S.P. Punjabi and E.M. Higgins Department of Dermatology, Chelsea & Westminster Hospital, Fulham Road, London SW10 9NH, U.K. Department of Microbiology, Leeds General Infirmary, Leeds LS1 3EX, U.K. British Association of Dermatologists, Willan House, 4 Fitzroy Square, London W1T 5HQ, U.K. St John’s Institute of Dermatology, Guy’s and St Thomas’ NHS Foundation Trust, St Thomas’ Hospital, Westminster Bridge Road, London SE1 7EH, U.K. Department of Dermatology, Hammersmith Hospital, 150 Du Cane Road, London W12 0HS, U.K. Department of Dermatology, King’s College Hospital, Denmark Hill, London SE5 9RS, U.K.
116 citations
••
TL;DR: Mice lacking complex gangliosides are improved hosts for raising high‐affinity, high‐titer anti‐ganglioside IgG antibodies for probing for the distribution and physiology of ganglioides and the pathophysiology of anti-ganglioide antibodies.
Abstract: Gangliosides, sialic acid-bearing glycosphingolipids, are highly enriched in the vertebrate nervous system. Anti-ganglioside antibodies are associated with various human neuropathies, although the pathogenicity of these antibodies remains unproven. Testing the pathogenic role of anti-ganglioside antibodies will be facilitated by developing high-affinity IgG-class complement-fixing monoclonal anti-bodies against major brain gangliosides, a goal that has been difficult to achieve. In this study, mice lacking complex gangliosides were used as immune-naive hosts to raise anti-ganglioside antibodies. Wild-type mice and knockout mice with a disrupted gene for GM2/GD2 synthase (UDP-N-acetyl-D-galactosamine : GM3/GD3 N-acetyl-D-glactosaminyltransferase) were immunized with GD1a conjugated to keyhole limpet hemocyanin. The knockout mice produced a vigorous anti-GD1a IgG response, whereas wildtype littermates failed to do so. Fusion of spleen cells from an immunized knockout mouse with myeloma cells yielded numerous IgG anti-GD1a antibody-producing colonies. Ganglioside binding studies revealed two specificity classes; one colony representing each class was cloned and characterized. High-affinity monoclonal antibody was produced by each hybridoma : an IgG1 that bound nearly exclusively to GD1a and an IgG2b that bound GD1a, GT1b, and GT1aalpha. Both antibodies readily readily detected gangliosides via ELISA, TLC immune overlay, immunohistochemistry, and immunocytochemistry. In contrast to prior reports using anti-GD1a and anti-GT1b IgM class monoclonal antibodies, the new antibodies bound avidly to granule neurons in brain tissue sections and cell cultures. Mice lacking complex gangliosides are improved hosts for raising high-affinity, high-titer anti-ganglioside IgG antibodies for probing for the distribution and physiology of gangliosides and the pathophysiology of anti-ganglioside antibodies.
116 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 |