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 & Randomized controlled trial. 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.
Papers published on a yearly basis
Papers
More filters
••
TL;DR: This review highlights the landmark studies which revealed nitrite's function in biological systems, and inspect its evolving role in cardiovascular protection, and discusses newly-identified mechanisms, including nitrite anhydration, the involvement of s-nitrosothiols, nitro-fatty acids, and direct nitrite normoxic signalling.
93 citations
••
Ludwig Maximilian University of Munich1, Guy's and St Thomas' NHS Foundation Trust2, University of Bern3, University of Sheffield4, Gentofte Hospital5, University Hospital Bonn6, Utrecht University7, Aarhus University Hospital8, University of Bordeaux9, University of Toulouse10, Gdańsk Medical University11, Hannover Medical School12, Technische Universität München13, Erasmus University Rotterdam14, University of Milan15, Children's Institute Inc.16, Free University of Brussels17, University of Amsterdam18, Lund University19, University Hospital of Lausanne20
TL;DR: The ETFAD decided to address some of questions regarding the continuation of systemic immune-modulating treatment of AD patients in these days of uncertainty, reallocation of medical resources, curfew, hoarding, and shutdown of normal social life.
Abstract: Atopic dermatitis (AD) is a complex disease with elevated risk of respiratory comorbidities.1,2 Severely affected patients are often treated with immune-modulating systemic drugs.3,4 On March 11th 2020, the World Health Organization declared the 2019 novel coronavirus severe acute respiratory syndrome (SARS-Cov-2) epidemic to be a pandemic. The number of cases worldwide is increasing exponentially and poses a major health threat, especially for those who are elderly, immuno-compromised, or have comorbidities. This also applies to AD patients on systemic immune-modulating treatment. In these days of uncertainty, reallocation of medical resources, curfew, hoarding, and shutdown of normal social life, patients, caregivers and doctors ask questions regarding the continuation of systemic immune-modulating treatment of AD patients. The ETFAD decided to address some of these questions here.
93 citations
••
TL;DR: Mutations of the SMARCB1 gene have been implicated in several human tumour predisposing syndromes and are found in a significant proportion of schwannomatosis patients, but there remains the possibility that further causative genes remain to be found.
Abstract: Mutations of the SMARCB1 gene have been implicated in several human tumour predisposing syndromes. They have recently been identified as an underlying cause of the tumour suppressor syndrome schwannomatosis. There is a much higher rate of mutation detection in familial disease than in sporadic disease. We have carried out extensive genetic testing on a cohort of familial and sporadic patients who fulfilled clinical diagnostic criteria for schwannomatosis. In our current cohort, we identified novel mutations within the SMARCB1 gene and detected several mutations that have been previously identified in other schwannomatosis cohorts. Of the schwannomatosis screens reported to date, including our current dataset, SMARCB1 mutations have been found in 45 % of familial probands and 7 % of sporadic patients. The exon 1 mutation, c.41C >A, and the 3′ untranslated region mutation, c.*82C >T, are the most common changes reported in schwannomatosis disease so far, indicating mutation hotspots at both 5′ and 3′ portions of the gene. SMARCB1 mutations are found in a significant proportion of schwannomatosis patients, but there remains the possibility that further causative genes remain to be found.
93 citations
••
TL;DR: Data show that although most of the screen-detected survival advantage is due to a shift in NPI, the mode of detection does impact on survival in patients with equivalent NPI scores, and is likely to be due to differences in tumour biology.
Abstract: This paper examines whether screen-detected breast cancer confers additional prognostic benefit to the patient, over and above that expected by any shift in stage at presentation. In all, 5604 women (aged 50–70 years) diagnosed with invasive breast cancer between 1998 and 2003 were identified by the Eastern Cancer Registration and Information Centre (ECRIC) and mammographic screening status was determined. Using proportional hazards regression, we estimated the effect of screen detection compared with symptomatic diagnosis on 5-year survival unadjusted, then adjusted for age and Nottingham Prognostic Index (NPI). A total of 72% of the survival benefit associated with screen-detected breast cancer can be accounted for by age and shift in NPI. Survival analysis by continuous NPI showed a small but systematic survival benefit for screen-detected cancers at each NPI value. These data show that although most of the screen-detected survival advantage is due to a shift in NPI, the mode of detection does impact on survival in patients with equivalent NPI scores. This residual survival benefit is small but significant, and is likely to be due to differences in tumour biology. Current prognostication tools may, therefore, overestimate the benefit of systemic treatments in screen-detected cancers and lead to overtreatment of these patients.
93 citations
••
TL;DR: Increased understanding of the pathogenic role of the IL-23–IL-17 axis, the cellular sources of these cytokines and their molecular regulation in SpA is essential to develop novel therapeutic strategies that target this pathway.
Abstract: Spondyloarthritis (SpA) is a term that refers to a group of inflammatory diseases that includes psoriatic arthritis, axial SpA and nonradiographic axial SpA, reactive arthritis, enteropathic arthritis and undifferentiated SpA. The disease subtypes share clinical and immunological features, including joint inflammation (peripheral and axial skeleton); skin, gut and eye manifestations; and the absence of diagnostic autoantibodies (seronegative). The diseases also share genetic factors. The aetiology of SpA is still the subject of research by many groups worldwide. Evidence from genetic, experimental and clinical studies has accumulated to indicate a clear role for the IL-17 pathway in the pathogenesis of SpA. The IL-17 family consists of IL-17A, IL-17B, IL-17C, IL-17D, IL-17E and IL-17F, of which IL-17A is the best studied. IL-17A is a pro-inflammatory cytokine that also has the capacity to promote angiogenesis and osteoclastogenesis. Of the six family members, IL-17A has the strongest homology with IL-17F. In this Review, we discuss how IL-17A and IL-17F and their cellular sources might contribute to the immunopathology of SpA.
93 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 |