POSSIBLE PATHOGENIC ROLE OF ENDOTOXIN IN REYE'S SYNDROME
dc.contributor.author | Cooperstock, Michael S. | en_US |
dc.contributor.author | Tucker, Richard Paul | en_US |
dc.contributor.author | Baublis, Joseph V. | en_US |
dc.date.accessioned | 2006-04-07T16:36:58Z | |
dc.date.available | 2006-04-07T16:36:58Z | |
dc.date.issued | 1975-06-07 | en_US |
dc.identifier.citation | Cooperstock, 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.uri | http://www.sciencedirect.com/science/article/B6T1B-49BYX0C-R1/2/f5da6e134a4f5518c47865d458691d06 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/22039 | |
dc.description.abstract | Evidence 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.extent | 437069 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | POSSIBLE PATHOGENIC ROLE OF ENDOTOXIN IN REYE'S SYNDROME | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Medicine (General) | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Departments of Pediatrics and Communicable Diseases, and Neurology, University of Michigan Medical Center, Ann Arbor, Michigan, U.S.A. | en_US |
dc.contributor.affiliationum | Departments of Pediatrics and Communicable Diseases, and Neurology, University of Michigan Medical Center, Ann Arbor, Michigan, U.S.A. | en_US |
dc.contributor.affiliationum | Departments of Pediatrics and Communicable Diseases, and Neurology, University of Michigan Medical Center, Ann Arbor, Michigan, U.S.A. | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/22039/1/0000457.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/S0140-6736(75)92553-2 | en_US |
dc.identifier.source | The Lancet | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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