Institution
University of Cambridge
Education•Cambridge, United Kingdom•
About: University of Cambridge is a education organization based out in Cambridge, United Kingdom. It is known for research contribution in the topics: Population & Galaxy. The organization has 118293 authors who have published 282289 publications receiving 14497093 citations. The organization is also known as: Cambridge University & Cambridge.
Topics: Population, Galaxy, Context (language use), Gene, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: This review focuses on mammalian autophagy, and an overview of the understanding of its machinery and the signaling cascades that regulate it is given, and the possibility of autophagic upregulation as a therapeutic approach for various conditions is considered.
Abstract: (Macro)autophagy is a bulk degradation process that mediates the clearance of long-lived proteins and organelles. Autophagy is initiated by double-membraned structures, which engulf portions of cytoplasm. The resulting autophagosomes ultimately fuse with lysosomes, where their contents are degraded. Although the term autophagy was first used in 1963, the field has witnessed dramatic growth in the last 5 years, partly as a consequence of the discovery of key components of its cellular machinery. In this review we focus on mammalian autophagy, and we give an overview of the understanding of its machinery and the signaling cascades that regulate it. As recent studies have also shown that autophagy is critical in a range of normal human physiological processes, and defective autophagy is associated with diverse diseases, including neurodegeneration, lysosomal storage diseases, cancers, and Crohn's disease, we discuss the roles of autophagy in health and disease, while trying to critically evaluate if the coincidence between autophagy and these conditions is causal or an epiphenomenon. Finally, we consider the possibility of autophagy upregulation as a therapeutic approach for various conditions.
1,616 citations
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TL;DR: In this paper, it was shown that pl-flips exist in dimension n − 1, assuming finite generation in dimension N − 1 and assuming that pl flips exist in all dimensions.
Abstract: Assuming finite generation in dimension n − 1, we prove that pl-flips exist in dimension n.
1,612 citations
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University of California, Riverside1, University of Leeds2, University of Cambridge3, Max Planck Society4, National Institute of Standards and Technology5, Commonwealth Scientific and Industrial Research Organisation6, Imperial College London7, École Polytechnique Fédérale de Lausanne8, University of Göttingen9
TL;DR: In this article, the IUPAC Subcommittee on GasKinetic Data Evaluation for Atmospheric Chemistry presented the first in the series, presenting kinetic and photochemical data evaluated by the committee.
Abstract: . This article, the first in the series, presents kinetic and photochemical data evaluated by the IUPAC Subcommittee on GasKinetic Data Evaluation for Atmospheric Chemistry. It covers the gas phase and photochemical reactions of Ox, HOx, NOx and SOx species, which were last published in 1997, and were updated on the IUPAC website in late 2001. The article consists of a summary sheet, containing the recommended kinetic parameters for the evaluated reactions, and five appendices containing the data sheets, which provide information upon which the recommendations are made.
1,612 citations
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TL;DR: According to this analysis, vulnerability to anxiety stems mainly from a lower threshold for appraising threat, rather than a bias in the direction of attention deployment, and relatively innocuous stimuli are evaluated as having higher subjective threat value by high than low trait anxious individuals.
1,609 citations
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TL;DR: The 'new view' of these diseases suggests that other degenerative conditions could have similar underlying origins to those of the amyloidoses, and suggests some intriguing new factors that could be of great significance in the evolution of biological molecules and the mechanisms that regulate their behaviour.
Abstract: The deposition of proteins in the form of amyloid fibrils and plaques is the characteristic feature of more than 20 degenerative conditions affecting either the central nervous system or a variety of peripheral tissues. As these conditions include Alzheimer's, Parkinson's and the prion diseases, several forms of fatal systemic amyloidosis, and at least one condition associated with medical intervention (haemodialysis), they are of enormous importance in the context of present-day human health and welfare. Much remains to be learned about the mechanism by which the proteins associated with these diseases aggregate and form amyloid structures, and how the latter affect the functions of the organs with which they are associated. A great deal of information concerning these diseases has emerged, however, during the past 5 years, much of it causing a number of fundamental assumptions about the amyloid diseases to be re-examined. For example, it is now apparent that the ability to form amyloid structures is not an unusual feature of the small number of proteins associated with these diseases but is instead a general property of polypeptide chains. It has also been found recently that aggregates of proteins not associated with amyloid diseases can impair the ability of cells to function to a similar extent as aggregates of proteins linked with specific neurodegenerative conditions. Moreover, the mature amyloid fibrils or plaques appear to be substantially less toxic than the pre-fibrillar aggregates that are their precursors. The toxicity of these early aggregates appears to result from an intrinsic ability to impair fundamental cellular processes by interacting with cellular membranes, causing oxidative stress and increases in free Ca2+ that eventually lead to apoptotic or necrotic cell death. The 'new view' of these diseases also suggests that other degenerative conditions could have similar underlying origins to those of the amyloidoses. In addition, cellular protection mechanisms, such as molecular chaperones and the protein degradation machinery, appear to be crucial in the prevention of disease in normally functioning living organisms. It also suggests some intriguing new factors that could be of great significance in the evolution of biological molecules and the mechanisms that regulate their behaviour.
1,607 citations
Authors
Showing all 119522 results
Name | H-index | Papers | Citations |
---|---|---|---|
Albert Hofman | 267 | 2530 | 321405 |
Zhong Lin Wang | 245 | 2529 | 259003 |
Solomon H. Snyder | 232 | 1222 | 200444 |
Trevor W. Robbins | 231 | 1137 | 164437 |
George Davey Smith | 224 | 2540 | 248373 |
Nicholas J. Wareham | 212 | 1657 | 204896 |
Cyrus Cooper | 204 | 1869 | 206782 |
Eric B. Rimm | 196 | 988 | 147119 |
Martin White | 196 | 2038 | 232387 |
Simon D. M. White | 189 | 795 | 231645 |
Michael Rutter | 188 | 676 | 151592 |
George Efstathiou | 187 | 637 | 156228 |
Mark Hallett | 186 | 1170 | 123741 |
David H. Weinberg | 183 | 700 | 171424 |
Paul G. Richardson | 183 | 1533 | 155912 |