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Free Radicals and Inflammation

  • Paul G. Winyard
  • David R. Blake
  • Christopher H. Evans

Part of the Progress in Inflammation Research book series (PIR)

Table of contents

  1. Front Matter
    Pages i-xi
  2. David R. Blake, Tulin Bodamyali, Cliff R. Stevens, Paul G. Winyard
    Pages 1-9
  3. Tulin Bodamyali, Cliff R. Stevens, David R. Blake, Paul G. Winyard
    Pages 11-16
  4. David R. Blake, Tulin Bodamyali, Cliff R. Stevens, Paul G. Winyard
    Pages 17-19
  5. Owen T. G. Jones, John T. Hancock
    Pages 21-46
  6. Nigel Benjamin
    Pages 47-63
  7. Roger Harrison
    Pages 65-81
  8. Vanessa Gilston, David R. Blake, Paul G. Winyard
    Pages 83-98
  9. Yvonne Y. C. Lo, Johnson M. S. Wong, Wing-Fai Cheung, Tony F. Cruz
    Pages 133-153
  10. Chris H. Evans, Maja Stefanovic-Racic
    Pages 155-168
  11. Heather MacPherson, Stuart H. Ralston
    Pages 169-181
  12. Joseph Lunec, Helen R. Griffiths
    Pages 183-194
  13. George A. C. Murrell
    Pages 195-206
  14. Christopher A. Bombeck, Jianrong Li, Timothy R. Billiar
    Pages 207-219
  15. Back Matter
    Pages 253-259

About this book

Introduction

As in so many fields of scientific endeavour following the molecular biology revo­ lution, our knowledge of the role of radicals not only in pathological states, but in basic physiology has developed exponentially. Indeed, our evolving concepts have, like so many political parties, been forced into dramatic "V-turns" and contortions. Within our working lives, we have had to debate whether radicals made any con­ tribution to any pathology, whilst now it is difficult not to entertain the view that every physiological process is pivotally controlled by exquisitely sensitive radical reactions. Inflammation is, of course, an example of pathology evolving from physiology, and in this book we have called upon both scientists and clinicians who have research interests in the complex switching mechanisms that sustain these transi­ tions. The book as a whole explores, from a physiological standpoint, how deter­ ministic radical systems sensitive to their initial conditions can interdigitate, iterate and feed back to control diverse cellular processes that create the inflammatory response. Whilst systems such as these to a mathematician would provide the basis for a chaotic response, one is forced to marvel how, for all stages of an inflammatory reaction, this system appears exquisitely controlled, making therapeutic manipula­ tion both possible and, to some extent, predictable.

Keywords

Arthritis apoptosis biology cell cell death diseases inflammation nitrogen rheumatism rheumatoid arthritis tissue

Editors and affiliations

  • Paul G. Winyard
    • 1
  • David R. Blake
    • 2
  • Christopher H. Evans
    • 3
  1. 1.St. Bartholomew’s and The Royal London School of Medicine and DentistryQueen Mary and Westfield CollegeLondonUK
  2. 2.School of Postgraduate MedicineUniversity of BathBathUK
  3. 3.Musculoskeletal InstituteUniversity of Pittsburgh School of MedicinePittsburghUSA

Bibliographic information

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