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POSSIBLE PATHOGENIC ROLE OF ENDOTOXIN IN REYE'S SYNDROME

dc.contributor.authorCooperstock, Michael S.en_US
dc.contributor.authorTucker, Richard Paulen_US
dc.contributor.authorBaublis, Joseph V.en_US
dc.date.accessioned2006-04-07T16:36:58Z
dc.date.available2006-04-07T16:36:58Z
dc.date.issued1975-06-07en_US
dc.identifier.citationCooperstock, MichaelS., Tucker, RichardPaul, Baublis, JosephV. (1975/06/07)."POSSIBLE PATHOGENIC ROLE OF ENDOTOXIN IN REYE'S SYNDROME." The Lancet 305(7919): 1272-1274. <http://hdl.handle.net/2027.42/22039>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6T1B-49BYX0C-R1/2/f5da6e134a4f5518c47865d458691d06en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/22039
dc.description.abstractEvidence of circulating endotoxin was sought in children with Reye's syndrome, on the thesis that severe hepatic failure is likely to result in loss of capacity to detoxify intestinal endotoxins entering the circulation. A modification of the Limulus assay was used to demonstrate high levels of endotoxin-like activity (E.L.A.) in nine comatose patients with Reye's syndrome and in one of the two non-comatose patients. The symptom-free sibling of one patient had raised liver enzymes and a negative Limulus test. Plasma E.L.A. correlated significantly with degree of electroencephalographic disturbance early in the course of the illness. E.L.A. was also found in both of two cerebrospinal fluids evaluated. Preliminary in-vitro characterisation of this substance indicated that it resembled endotoxin derived from anaerobic intestinal bacteria. Intestinally derived endotoxin could be one factor in the pathogenesis of encephalopathy and other features of Reye's syndrome.en_US
dc.format.extent437069 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titlePOSSIBLE PATHOGENIC ROLE OF ENDOTOXIN IN REYE'S SYNDROMEen_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.affiliationumDepartments of Pediatrics and Communicable Diseases, and Neurology, University of Michigan Medical Center, Ann Arbor, Michigan, U.S.A.en_US
dc.contributor.affiliationumDepartments of Pediatrics and Communicable Diseases, and Neurology, University of Michigan Medical Center, Ann Arbor, Michigan, U.S.A.en_US
dc.contributor.affiliationumDepartments of Pediatrics and Communicable Diseases, and Neurology, University of Michigan Medical Center, Ann Arbor, Michigan, U.S.A.en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/22039/1/0000457.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/S0140-6736(75)92553-2en_US
dc.identifier.sourceThe Lanceten_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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