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The Cellular Mechanisms of Tumor Necrosis Factor-Induced Mortality: A Possible Role for Platelet Activating Factor and/or the Eicosanoids

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Host Defense Dysfunction in Trauma, Shock and Sepsis

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Abstract

Tumor necrosis factor (TNF) is hailed as the seminal mediator in endotoxemia and/or sepsis in animals and humans [1, 2]. Of particular interest recently has been the reported role of eicosanoids (PGS) and platelet activating factor (PAF) in mediating many of the events in the pathophysiology of endotoxemia/sepsis in animals [3, 4]. Interestingly, the putative effects of PAF and the eicosanoids alone or in endotoxemia/sepsis are very similar to those attributed to TNF. To make the situation even more complex, TNF stimulates endothelial cells or fibroblasts to synthesize PAF [5], prostacyclin [6], or PGE2 [7] as well as many other potent cellular effectors.

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Author information

Authors and Affiliations

  1. Vanderbilt University, Nashville, TN, USA

    J. M. Moore, M. Hubbard, M. Earnest, P. Williams, A. DiSimone & N. Abumrad

  2. Department of Surgery, University of South Alabama, Mobile, AL, USA

    J. R. Fletcher

Authors
  1. J. M. Moore
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  2. M. Hubbard
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  3. M. Earnest
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  4. P. Williams
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  5. A. DiSimone
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  6. N. Abumrad
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  7. J. R. Fletcher
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Editor information

Editors and Affiliations

  1. Dept. of Surgery, Ludwig-Maximilians-University Munich, Klinikum Großhadern Marchioninistr. 15, 8000, Munich 70, Germany

    Eugen Faist  & Friedrich W. Schildberg  & 

  2. Dept. of Surgery, McGill University, Room 510.34 687 Pine Avenue West, Montreal, Quebec, H3A 1A1, Canada

    Jonathan L. Meakins M.D., D.Sc.

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© 1993 Springer-Verlag, Berlin Heidelberg

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Moore, J.M. et al. (1993). The Cellular Mechanisms of Tumor Necrosis Factor-Induced Mortality: A Possible Role for Platelet Activating Factor and/or the Eicosanoids. In: Faist, E., Meakins, J.L., Schildberg, F.W. (eds) Host Defense Dysfunction in Trauma, Shock and Sepsis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77405-8_99

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  • DOI: https://doi.org/10.1007/978-3-642-77405-8_99

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-77407-2

  • Online ISBN: 978-3-642-77405-8

  • eBook Packages: Springer Book Archive

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