London, United Kingdom
London, United Kingdom

University College London , formerly styled University College, London, is a public research university in London, England and a constituent college of the federal University of London. Founded in 1826 as London University, UCL was the first university institution established in London and the first in England to be entirely secular, to admit students regardless of their religion, and to admit women on equal terms with men. The philosopher Jeremy Bentham is commonly regarded as the spiritual father of UCL, as his radical ideas on education and society were the inspiration to its founders, although his direct involvement in its foundation was limited. UCL became one of the two founding colleges of the University of London in 1836. It has grown through mergers, including with the Institute of Neurology , the Eastman Dental Institute , the School of Slavonic and East European Studies , the School of Pharmacy and the Institute of Education .UCL's main campus is located in the Bloomsbury area of central London, with a number of institutes and teaching hospitals elsewhere in central London, and satellite campuses in Adelaide, Australia and Doha, Qatar. UCL is organised into 11 constituent faculties, within which there are over 100 departments, institutes and research centres. UCL has around 36,000 students and 11,000 staff and had a total income of £1.02 billion in 201315 Times Higher Education World University Rankings. For the period 1999 to 2009 it was the 13th most-cited university in the world . There are 32 Nobel Prize winners and three Fields Medalists amongst UCL's alumni and current and former staff. UCL alumni include the "Father of the Nation" of each of India, Kenya and Mauritius, the inventor of the telephone, and one of the co-discoverers of the structure of DNA. All five of the naturally-occurring noble gases were discovered at UCL by William Ramsay.UCL is part of three of the 11 biomedical research centres established by the NHS in England and is a founding member of the Francis Crick Institute and UCL Partners, the world's largest academic health science centre. UCL has hundreds of research and teaching partnerships, including a major collaboration with Yale University, the Yale UCL Collaborative. UCL is a member of numerous academic organisations including the G5, the League of European Research Universities and the Russell Group and forms part of the 'golden triangle' of British universities. Wikipedia.

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Price S.L.,University College London
Chemical Society Reviews | Year: 2014

Currently, organic crystal structure prediction (CSP) methods are based on searching for the most thermodynamically stable crystal structure, making various approximations in evaluating the crystal energy. The most stable (global minimum) structure provides a prediction of an experimental crystal structure. However, depending on the specific molecule, there may be other structures which are very close in energy. In this case, the other structures on the crystal energy landscape may be polymorphs, components of static or dynamic disorder in observed structures, or there may be no route to nucleating and growing these structures. A major reason for performing CSP studies is as a complement to solid form screening to see which alternative packings to the known polymorphs are thermodynamically feasible. This journal is © the Partner Organisations 2014.

Buchan D.W.,University College London
Nucleic acids research | Year: 2013

Here, we present the new UCL Bioinformatics Group's PSIPRED Protein Analysis Workbench. The Workbench unites all of our previously available analysis methods into a single web-based framework. The new web portal provides a greatly streamlined user interface with a number of new features to allow users to better explore their results. We offer a number of additional services to enable computationally scalable execution of our prediction methods; these include SOAP and XML-RPC web server access and new HADOOP packages. All software and services are available via the UCL Bioinformatics Group website at

A number of autobiographical memory theories and clinical theories of posttraumatic stress disorder (PTSD) make claims that are different from standard views of memory and have been the subject of controversy. These claims include the existence of a long-term perceptual memory system supporting conscious experience separate to episodic memory; greater involvement of perceptual memory in the response to emotion-laden and personally meaningful events; increased perceptual memory intrusions accompanied by impaired episodic memory for the traumatic event among PTSD patients; and a lack of association, or inverse association, between indices of voluntary recall and involuntary images relating to the same traumatic materials. In this article I review current research on perceptual memory, which supports the presence of long-term representations that are selective or incomplete reflections of sensory input. The functional independence of perceptual and episodic memory is illustrated by research on verbal overshadowing but is most clearly exemplified by the strong evidence in favor of enhanced perceptual memory and impaired episodic memory in PTSD. Theoretical predictions concerning the relation between perceptual priming and the development of intrusive images, the effect of verbal versus visuospatial secondary tasks on intrusive trauma images, and the independence of voluntary and involuntary memory for the same materials have garnered widespread support. Reasons for the continuing controversy over traumatic memory are discussed, and some implications of the review for general theories of recall and recognition, clinical theories of PTSD, and "special mechanism" views of memory are set out. © 2014 American Psychological Association.

Mauri C.,University College London | Bosma A.,University College London
Annual Review of Immunology | Year: 2012

B cells are regarded for their capacity to produce antibody. However, recent advances in B cell biology have capitalized on old findings and demonstrated that B cells also release a broad variety of cytokines. As with T helper cells, B cells can be classified into subsets according to the cytokine milieu that they produce. One functional B cell subset, regulatory B cells (Bregs), has recently been shown to contribute to the maintenance of the fine equilibrium required for tolerance. Bregs restrain the excessive inflammatory responses that occur during autoimmune diseases or that can be caused by unresolved infections. Pivotal to Breg function is interleukin-10 (IL-10), which inhibits proinflammatory cytokines and supports regulatory T cell differentiation. This review reports and discusses the factors that are important for Breg differentiation and for their effector function in both mouse and human. © 2012 by Annual Reviews. All rights reserved.

Background Individual participant data meta-analyses of postoperative chemotherapy have shown improved survival for patients with non-small-cell lung cancer (NSCLC). We aimed to do a systematic review and individual participant data meta-analysis to establish the effect of preoperative chemotherapy for patients with resectable NSCLC. Methods We systematically searched for trials that started after January, 1965. Updated individual participant data were centrally collected, checked, and analysed. Results from individual randomised controlled trials (both published and unpublished) were combined using a two-stage fi xed-effect model. Our primary outcome, overall survival, was defi ned as the time from randomisation until death (any cause), with living patients censored on the date of last follow-up. Secondary outcomes were recurrence-free survival, time to locoregional and distant recurrence, cause-specifi c survival, complete and overall resection rates, and postoperative mortality. Prespecifi ed analyses explored any variation in effect by trial and patient characteristics. All analyses were by intention to treat. Findings Analyses of 15 randomised controlled trials (2385 patients) showed a signifi cant benefi t of preoperative chemotherapy on survival (hazard ratio [HR] 087, 95% CI 078-096, p=0007), a 13% reduction in the relative risk of death (no evidence of a difference between trials; p=018, I=25%). This fi nding represents an absolute survival improvement of 5% at 5 years, from 40% to 45%. There was no clear evidence of a difference in the effect on survival by chemotherapy regimen or scheduling, number of drugs, platinum agent used, or whether postoperative radiotherapy was given. There was no clear evidence that particular types of patient defi ned by age, sex, performance status, histology, or clinical stage benefi ted more or less from preoperative chemotherapy. Recurrence-free survival (HR 085, 95% CI 076-094, p=0002) and time to distant recurrence (069, 058-082, p<00001) results were both signifi cantly in favour of preoperative chemotherapy although most patients included were stage IB-IIIA. Results for time to locoregional recurrence (088, 073-107, p=020), although in favour of preoperative chemotherapy, were not statistically signifi cant. Interpretation Findings, which are based on 92% of all patients who were randomised, and mainly stage IB-IIIA, show preoperative chemotherapy signifi cantly improves overall survival, time to distant recurrence, and recurrencefree survival in resectable NSCLC. The fi ndings suggest this is a valid treatment option for most of these patients. Toxic effects could not be assessed.

Schapira A.H.V.,University College London
The Lancet | Year: 2012

Mitochondria have a crucial role in cellular bioenergetics and apoptosis, and thus are important to support cell function and in determination of cell death pathways. Inherited mitochondrial diseases can be caused by mutations of mitochondrial DNA or of nuclear genes that encode mitochondrial proteins. Although many mitochondrial disorders are multisystemic, some are tissue specific-eg, optic neuropathy, sensorineural deafness, and type 2 diabetes mellitus. In the past few years, several disorders have been associated with mutations of nuclear genes responsible for mitochondrial DNA maintenance and function, and the potential contribution of mitochondrial abnormalities to progressive neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease has been recognised. The process of mitochondrial fission-fusion has become a focus of attention in human disease. Importantly, the mitochondrion is now a target for therapeutic interventions that encompass small molecules, transcriptional regulation, and genetic manipulation, offering opportunities to treat a diverse range of diseases.

Lloyd A.C.,University College London
Cell | Year: 2013

An adult animal consists of cells of vastly different size and activity, but the regulation of cell size remains poorly understood. Recent studies uncovering some of the signaling pathways important for size/growth control, together with the identification of diseases resulting from aberrations in these pathways, have renewed interest in this field. This Review will discuss our current understanding of how a cell sets its size, how it can adapt its size to a changing environment, and how these processes are relevant to human disease. © 2013 Elsevier Inc.

McAlpine D.,University College London
Physiological Reviews | Year: 2010

The ability to determine the location of a sound source is fundamental to hearing. However, auditory space is not represented in any systematic manner on the basilar membrane of the cochlea, the sensory surface of the receptor organ for hearing. Understanding the means by which sensitivity to spatial cues is computed in central neurons can therefore contribute to our understanding of the basic nature of complex neural representations. We review recent evidence concerning the nature of the neural representation of auditory space in the mammalian brain and elaborate on recent advances in the understanding of mammalian subcortical processing of auditory spatial cues that challenge the "textbook" version of sound localization, in particular brain mechanisms contributing to binaural hearing. Copyright © 2010 the American Physiological Society.

Marson C.M.,University College London
Chemical Society Reviews | Year: 2012

Reactions in which several components are combined in sequence, and without isolation of intermediates, are greatly sought because of the inherent molecular diversity, efficiency, and atom-economy. However, organocatalytic reactions, employing an organic catalyst to assemble products of high enantiomeric excess (a single optical isomer), are also cutting-edge methodology. This tutorial review covers the overlap of these two areas, outling the structural diversity and stereocontrol arising from one-pot combinations of at least three components, powerful approaches with great potential that minimise formation of by-products and operating costs. This journal is © The Royal Society of Chemistry 2012.

Flores-Borja F.,University College London
Science translational medicine | Year: 2013

The relevance of regulatory B cells in the maintenance of tolerance in healthy individuals or in patients with immune disorders remains understudied. In healthy individuals, CD19(+)CD24(hi)CD38(hi) B cells suppress CD4(+)CD25(-) T cell proliferation as well as the release of interferon-γ and tumor necrosis factor-α by these cells; this suppression is partially mediated through the production of interleukin-10 (IL-10). We further elucidate the mechanisms of suppression by CD19(+)CD24(hi)CD38(hi) B cells. Healthy CD19(+)CD24(hi)CD38(hi) B cells inhibited naïve T cell differentiation into T helper 1 (T(H)1) and T(H)17 cells and converted CD4(+)CD25(-) T cells into regulatory T cells (T(regs)), in part through the production of IL-10. In contrast, CD19(+)CD24(hi)CD38(hi) B cells from patients with rheumatoid arthritis (RA) failed to convert CD4(+)CD25(-) T cells into functionally suppressive T(regs) or to curb T(H)17 development; however, they maintained the capacity to inhibit T(H)1 cell differentiation. Moreover, RA patients with active disease have reduced numbers of CD19(+)CD24(hi)CD38(hi) B cells in peripheral blood compared with either patients with inactive disease or healthy individuals. These results suggest that in patients with active RA, CD19(+)CD24(hi)CD38(hi) B cells with regulatory function may fail to prevent the development of autoreactive responses and inflammation, leading to autoimmunity.

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