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Institution

Nuffield Orthopaedic Centre

HealthcareOxford, United Kingdom
About: Nuffield Orthopaedic Centre is a healthcare organization based out in Oxford, United Kingdom. It is known for research contribution in the topics: Population & Arthroplasty. The organization has 2082 authors who have published 2920 publications receiving 145718 citations.


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Journal ArticleDOI
TL;DR: It is recommended that resurfacings are undertaken with caution in women, particularly those under 40 years of age but they remain a good option in young men, and further work is required to understand the aetiology of pseudotumours.
Abstract: Metal-on-metal hip resurfacing is commonly performed for osteoarthritis in young active patients. We have observed cystic or solid masses, which we have called inflammatory pseudotumours, arising around these devices. They may cause soft-tissue destruction with severe symptoms and a poor outcome after revision surgery. The aim of this study was to determine the incidence of and risk factors for pseudotumours that are serious enough to require revision surgery.Since 1999, 1419 metal-on-metal hip resurfacings have been implanted by our group in 1224 patients; 1.8% of the patients had a revision for pseudotumour. In this series the Kaplan-Meier cumulative revision rate for pseudotumour increased progressively with time. At eight years, in all patients, it was 4% (95% confidence interval (CI) 2.2 to 5.8). Factors significantly associated with an increase in revision rate were female gender (p < 0.001), age under 40 (p = 0.003), small components (p = 0.003), and dysplasia (p = 0.019), whereas implant type was ...

324 citations

Journal ArticleDOI
TL;DR: In this article, a brief discussion of the contribution of atrophy to muscle weakness is presented, focusing on inhibition of quadriceps activation and suggesting some therapeutic implications, but not dealing with reduced oxidative capacity and increased fatiguability of disused muscle since, although important, these have not been part of their programme of work.
Abstract: ‘Arthrogenous muscle weakness’ is weakness of muscles acting about an injured or inflamed joint. The weakness may be due to loss of muscle or to inability to activate the muscle (Fig. 1). Weakness of the thigh muscles, and of the quadriceps in particular, is a common and important consequence of knee trauma, surgery or arthritis. Muscle weakness contributes significantly to disability and probably also renders the joint vulnerable to further damage (Fig. 1). This review starts with a brief discussion of the contribution of atrophy to weakness. It concentrates, however, on inhibition of quadriceps activation and suggests some therapeutic implications. It does not deal with the reduced oxidative capacity and increased fatiguability of disused muscle since, although important, these have not been part of our programme of work.

321 citations

Journal ArticleDOI
TL;DR: To ascertain if IGF-1 is a regulator of local muscle growth, total RNA was extracted from rabbit muscle induced to undergo rapid hypertrophy using active stretch and from control muscles to confirm that alternative splicing of the insulin-like growth factor 1 gene occurs in muscle in response to physical activity.
Abstract: To ascertain if IGF-1 is a regulator of local muscle growth, total RNA was extracted from rabbit muscle induced to undergo rapid hypertrophy using active stretch and from control muscles. This was analysed by Northern hybridization with a 280 base pair probe containing sequences derived from exons 3 and 4 of the insulin-like growth factor 1 gene. Two types of insulin-like growth factor 1 mRNA were shown to be strong expressed in the stretched muscles. In situ hybridization using the same probe (280 base pair) showed that IGF-1 is strongly expressed in muscle that is induced to grow rapidly and is expressed in the muscle fibres themselves. Using RT-PCR a single insulin-like growth factor 1 isoform cDNA (IGF-1Ea) could be cloned from the normal resting muscles. However, an additional isoform of insulin-like growth factor 1 (insulin-like growth factor 1Eb) was found to be expressed in stretched muscle undergoing hypertrophy. The E domain sequence of the additional isoform differs from the liver insulin-like growth factor 1Ea by the presence a 52 base pair insert. This changes the reading frame of the derived carboxyl-terminal resulting in a different precursor insulin-like growth factor 1 isoform. This insulin-like growth factor 1 mRNA probably encodes the precursor insulin-like growth factor 1 isoform that is responsible for local muscle growth regulation in response to mechanical stimulation. To confirm that alternative splicing of the insulin-like growth factor 1 gene occurs in muscle in response to physical activity, oligonucleotide primers were made which specifically amplify the cDNAs of two isoforms (insulin-like growth factors 1Ea and Eb) in the human as well as the rabbit. Following altered physical activity for 2 h to 6 days, appreciable levels of insulin-like growth factor 1Eb (in human the Ec) isoform were detected in skeletal muscle by using RT-PCR. In contrast very little if any of this splice variant could be detected in control muscle not subjected to stretch or extra physical activity.

316 citations

Journal ArticleDOI
TL;DR: Guideline for the Management of Rheumatoid Arthritis (The first 2 years) R. Luqmani, S. Oliver, Z. Walsh, C. Washbrook and F. Webb on behalf of the British Society for rheumatology and British Health Professionals in R heumatology Standards, Guidelines and Audit Working Group.
Abstract: British Society for Rheumatology and British Health Professionals in Rheumatology Guideline for the Management of Rheumatoid Arthritis (The first 2 years) R. Luqmani, S. Hennell, C. Estrach, F. Birrell, A. Bosworth, G. Davenport, C. Fokke, N. Goodson, P. Jeffreson, E. Lamb, R. Mohammed, S. Oliver, Z. Stableford, D. Walsh, C. Washbrook and F. Webb on behalf of the British Society for Rheumatology and British Health Professionals in Rheumatology Standards, Guidelines and Audit Working Group

314 citations

Journal ArticleDOI
TL;DR: This review focuses on recent developments in Na+, K+-ATPase research, and in particular reportsof expression of isoforms in various tissues and experiments aimed atucidating the intrinsic structural features of iso forms important forNa+, K-atPase function.
Abstract: Na+, K+-ATPase is ubiquitously expressed in the plasma membrane of all animal cells where it serves as the principal regulator of intracellular ion homeostasis. Na+, K+-ATPase is responsible for generating and maintaining transmembrane ionic gradients that are of vital importance for cellular function and subservient activities such as volume regulation, pH maintenance, and generation of action potentials and secondary active transport. The diversity of Na+, K+-ATPase subunit isoforms and their complex spatial and temporal patterns of cellular expression suggest that Na+, K+-ATPase isozymes perform specialized physiological functions. Recent studies have shown that the alpha subunit isoforms possess considerably different kinetic properties and modes of regulation and the beta subunit isoforms modulate the activity, expression and plasma membrane targeting of Na+, K+-ATPase isozymes. This review focuses on recent developments in Na+, K+-ATPase research, and in particular reports of expression of isoforms in various tissues and experiments aimed at elucidating the intrinsic structural features of isoforms important for Na+, K+-ATPase function.

314 citations


Authors

Showing all 2120 results

NameH-indexPapersCitations
Douglas G. Altman2531001680344
George Davey Smith2242540248373
Cyrus Cooper2041869206782
James J. Collins15166989476
Richard J.H. Smith118130861779
Andrew Carr11184254974
Paul Dieppe10561853529
Matthew A. Brown10374859727
David W. Murray9769943372
Ray Fitzpatrick9547740322
Derrick W. Crook9247429885
Richard W Morris9151935165
Richard J. K. Taylor91154343893
Sharon J. Peacock9049433352
Derick T Wade9039837413
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202315
202246
2021138
2020129
2019126
2018110