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Institution

Imperial College London

EducationLondon, Westminster, United Kingdom
About: Imperial College London is a education organization based out in London, Westminster, United Kingdom. It is known for research contribution in the topics: Population & Medicine. The organization has 90019 authors who have published 209164 publications receiving 9337534 citations. The organization is also known as: Imperial College of Science, Technology and Medicine & Imperial College.


Papers
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Journal ArticleDOI
TL;DR: The current status of the technique and recommendations on the measurement of [18F]-FDG uptake for tumour response monitoring from a consensus meeting of the EORTC PET study group held in Brussels in February 1998 and confirmed at a subsequent meeting in March 1999 are summarized.

1,641 citations

Journal ArticleDOI
TL;DR: In this paper the operational and fixpoint semantics of predicate logic programs are defined, and the connections with the proof theory and model theory of logic are investigated, and it is concluded that operational semantics is a part ofProof theory and that fixpoint semantic is a special case of model-theoretic semantics.
Abstract: Sentences in first-order predicate logic can be usefully interpreted as programs. In this paper the operational and fixpoint semantics of predicate logic programs are defined, and the connections with the proof theory and model theory of logic are investigated. It is concluded that operational semantics is a part of proof theory and that fixpoint semantics is a special case of model-theoretic semantics.

1,636 citations

Journal ArticleDOI
21 Apr 1994-Nature
TL;DR: In this paper, the authors provide evidence from direct experimental manipulation of diversity by over an order of magnitude, using multi-trophic level communities and simultaneous measures of several ecosystem processes, that reduced biodiversity may indeed alter the performance of ecosystems.
Abstract: COMMUNITIES of species and their associated biological, chemical and physical processes, collectively known as ecosystems, drive the Earth's biogeochemical processes1,2. Currently most ecosystems are experiencing loss of biodiversity associated with the activities of human expansion3–5, raising the issue of whether the biogeochemical functioning of ecosystems will be impaired by this loss of species6–8. Current ecological knowledge supports a wide range of views on the subject9–13, but empirical tests are few9,14–16. Here we provide evidence from direct experimental manipulation of diversity by over an order of magnitude, using multi-trophic level communities and simultaneous measures of several ecosystem processes, that reduced biodiversity may indeed alter the performance of ecosystems.

1,632 citations

Journal ArticleDOI
Matthew Berriman1, Elodie Ghedin2, Elodie Ghedin3, Christiane Hertz-Fowler1, Gaëlle Blandin2, Hubert Renauld1, Daniella Castanheira Bartholomeu2, Nicola Lennard1, Elisabet Caler2, N. Hamlin1, Brian J. Haas2, Ulrike Böhme1, Linda Hannick2, Martin Aslett1, Joshua Shallom2, Lucio Marcello4, Lihua Hou2, Bill Wickstead5, U. Cecilia M. Alsmark6, Claire Arrowsmith1, Rebecca Atkin1, Andrew Barron1, Frédéric Bringaud7, Karen Brooks1, Mark Carrington8, Inna Cherevach1, Tracey-Jane Chillingworth1, Carol Churcher1, Louise Clark1, Craig Corton1, Ann Cronin1, Robert L. Davies1, Jonathon Doggett1, Appolinaire Djikeng2, Tamara Feldblyum2, Mark C. Field8, Audrey Fraser1, Ian Goodhead1, Zahra Hance1, David Harper1, Barbara Harris1, Heidi Hauser1, Jessica B. Hostetler2, Al Ivens1, Kay Jagels1, David W. Johnson1, Justin Johnson2, Kristine Jones2, Arnaud Kerhornou1, Hean Koo2, Natasha Larke1, Scott M. Landfear9, Christopher Larkin2, Vanessa Leech8, Alexandra Line1, Angela Lord1, Annette MacLeod4, P. Mooney1, Sharon Moule1, David M. A. Martin10, Gareth W. Morgan11, Karen Mungall1, Halina Norbertczak1, Doug Ormond1, Grace Pai2, Christopher S. Peacock1, Jeremy Peterson2, Michael A. Quail1, Ester Rabbinowitsch1, Marie-Adèle Rajandream1, Chris P Reitter8, Steven L. Salzberg2, Mandy Sanders1, Seth Schobel2, Sarah Sharp1, Mark Simmonds1, Anjana J. Simpson2, Luke J. Tallon2, C. Michael R. Turner4, Andrew Tait4, Adrian Tivey1, Susan Van Aken2, Danielle Walker1, David Wanless2, Shiliang Wang2, Brian White1, Owen White2, Sally Whitehead1, John Woodward1, Jennifer R. Wortman2, Mark Raymond Adams12, T. Martin Embley6, Keith Gull5, Elisabetta Ullu13, J. David Barry4, Alan H. Fairlamb10, Fred R. Opperdoes14, Barclay G. Barrell1, John E. Donelson15, Neil Hall16, Neil Hall2, Claire M. Fraser2, Sara E. Melville8, Najib M. El-Sayed3, Najib M. El-Sayed2 
15 Jul 2005-Science
TL;DR: Comparisons of the cytoskeleton and endocytic trafficking systems of Trypanosoma brucei with those of humans and other eukaryotic organisms reveal major differences.
Abstract: African trypanosomes cause human sleeping sickness and livestock trypanosomiasis in sub-Saharan Africa. We present the sequence and analysis of the 11 megabase-sized chromosomes of Trypanosoma brucei. The 26-megabase genome contains 9068 predicted genes, including ∼900 pseudogenes and ∼1700 T. brucei–specific genes. Large subtelomeric arrays contain an archive of 806 variant surface glycoprotein (VSG) genes used by the parasite to evade the mammalian immune system. Most VSG genes are pseudogenes, which may be used to generate expressed mosaic genes by ectopic recombination. Comparisons of the cytoskeleton and endocytic trafficking systems with those of humans and other eukaryotic organisms reveal major differences. A comparison of metabolic pathways encoded by the genomes of T. brucei, T. cruzi, and Leishmania major reveals the least overall metabolic capability in T. brucei and the greatest in L. major. Horizontal transfer of genes of bacterial origin has contributed to some of the metabolic differences in these parasites, and a number of novel potential drug targets have been identified.

1,631 citations

Journal ArticleDOI
TL;DR: A double mutation at codons 670 and 671 (APP 770 transcript) in exon 16 which co–segregates with the disease in two large (probably related) early–onset Alzheimer's disease families from Sweden is identified.
Abstract: Mutations at codon 717 in exon 17 of the beta-amyloid precursor protein (APP) gene have previously been shown to segregate with early onset Alzheimer's disease in some families. We have identified a double mutation at codons 670 and 671 (APP 770 transcript) in exon 16 which co-segregates with the disease in two large (probably related) early-onset Alzheimer's disease families from Sweden. Two base pair transversions (G to T, A to C) from the normal sequence predict Lys to Asn and Met to Leu amino acid substitutions at codons 670 and 671 of the APP transcript. This mutation occurs at the amino terminal of beta-amyloid and may be pathogenic because it occurs at or close to the endosomal/lysosomal cleavage site of the molecule. Thus, pathogenic mutations in APP frame the beta-amyloid sequence.

1,626 citations


Authors

Showing all 90798 results

NameH-indexPapersCitations
Albert Hofman2672530321405
David Miller2032573204840
Tamara B. Harris2011143163979
Mark I. McCarthy2001028187898
Peter J. Barnes1941530166618
Simon D. M. White189795231645
Patrick W. Serruys1862427173210
John Hardy1771178171694
Simon Baron-Cohen172773118071
Richard H. Friend1691182140032
Yang Gao1682047146301
Hongfang Liu1662356156290
Philippe Froguel166820118816
Salvador Moncada164495138030
Dennis R. Burton16468390959
Network Information
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023413
20221,329
202112,883
202012,473
201911,096
201810,236