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IS REYE'S SYNDROME CAUSED BY AUGMENTED RELEASE OF TUMOUR NECROSIS FACTOR?

dc.contributor.authorLarrick, James W.en_US
dc.contributor.authorKunkel, Steven L.en_US
dc.date.accessioned2006-04-07T19:28:23Z
dc.date.available2006-04-07T19:28:23Z
dc.date.issued1986-07-19en_US
dc.identifier.citationLarrick, JamesW., Kunkel, StevenL. (1986/07/19)."IS REYE'S SYNDROME CAUSED BY AUGMENTED RELEASE OF TUMOUR NECROSIS FACTOR?." The Lancet 328(8499): 132-133. <http://hdl.handle.net/2027.42/26096>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6T1B-49M0F53-75/2/4d04570c41b734d6fdd64b0b8ef3542een_US
dc.identifier.urihttps://hdl.handle.net/2027.42/26096
dc.description.abstractReye's syndrome affects children with a history of viral infection treated with aspirin. Its pathogenesis is unclear. Tumour necrosis factor (TNF) is released by macrophages activated by viral infection, endotoxin, and phagocytosis, and it has been shown to be a mediator of the toxic and metabolic effects of endotoxaemia. The metabolic effects of endotoxin and TNF are similar to those found in Reye's syndrome. Raised levels of TNF are released from macrophages treated with non-steroidal anti-inflammatory drugs, and young animals are known to be more sensitive than mature animals to both TNF and endotoxin. These observations lead to the hypothesis that an increased release of TNF in selected young patients treated with aspirin contributes to the development of Reye's syndrome.en_US
dc.format.extent331480 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titleIS REYE'S SYNDROME CAUSED BY AUGMENTED RELEASE OF TUMOUR NECROSIS FACTOR?en_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMedicine (General)en_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Pathology, University of Michigan, Ann Arbor, Michigan, USA; Cetus Immune Research Laboratories,, Palo Alto, California, USA.en_US
dc.contributor.affiliationumDepartment of Pathology, University of Michigan, Ann Arbor, Michigan, USA; Cetus Immune Research Laboratories,, Palo Alto, California, USA.en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/26096/1/0000172.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/S0140-6736(86)91947-1en_US
dc.identifier.sourceThe Lanceten_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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