pubmed-article:10411942 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C0270611 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C0333516 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C0205178 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C0205191 | lld:lifeskim |
pubmed-article:10411942 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
pubmed-article:10411942 | pubmed:issue | 15 | lld:pubmed |
pubmed-article:10411942 | pubmed:dateCreated | 1999-8-23 | lld:pubmed |
pubmed-article:10411942 | pubmed:abstractText | The present study evaluated behavioral and histopathological outcome after controlled cortical impact (CCI) brain injury in mice deficient in tumor necrosis factor [TNF(-/-)] and their wild-type (wt) littermates. Mice were subjected to CCI brain injury [TNF(-/-), n = 10; wt, n = 10] or served as uninjured controls [TNF(-/-), n = 10; wt, n = 10] and were evaluated for deficits in memory retention at 7 days postinjury. Although both brain-injured wt and TNF(-/-) mice exhibited significant memory dysfunction compared to uninjured controls (P < 0.02), the deficits in memory retention in injured TNF(-/-) mice were significantly less severe than in injured wt mice (P < 0.02). A second group of mice was subjected to CCI brain injury [TNF(-/-), n = 20; wt, n = 20] or served as uninjured controls [TNF(-/-), n = 15; wt, n = 15] and were evaluated over a 4-week period for neurological motor function. In the acute posttraumatic period (48 h postinjury), brain-injured TNF(-/-) mice were significantly less impaired than injured wt mice on composite neuroscore (P < 0.001), rotarod (P < 0.05), and beam balance (P < 0. 02) tests. However, wt mice recovered from brain injury by 2-3 weeks postinjury, whereas TNF(-/-) mice continued to demonstrate persistent motor deficits up to 4 weeks postinjury. Histopathological analysis at 2 and 4 weeks postinjury revealed that brain-injured TNF(-/-) mice had significantly more cortical tissue loss than wt mice (P < 0.02). Our results suggest that although the presence of TNF in the acute posttraumatic period may be deleterious, this cytokine may play a role in facilitating long-term behavioral recovery and histological repair after brain injury. | lld:pubmed |
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pubmed-article:10411942 | pubmed:language | eng | lld:pubmed |
pubmed-article:10411942 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10411942 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10411942 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10411942 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10411942 | pubmed:month | Jul | lld:pubmed |
pubmed-article:10411942 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:10411942 | pubmed:author | pubmed-author:NakamuraMM | lld:pubmed |
pubmed-article:10411942 | pubmed:author | pubmed-author:TrojanowskiJ... | lld:pubmed |
pubmed-article:10411942 | pubmed:author | pubmed-author:NeugebauerEE | lld:pubmed |
pubmed-article:10411942 | pubmed:author | pubmed-author:McIntoshT KTK | lld:pubmed |
pubmed-article:10411942 | pubmed:author | pubmed-author:RaghupathiRR | lld:pubmed |
pubmed-article:10411942 | pubmed:author | pubmed-author:MarinoM WMW | lld:pubmed |
pubmed-article:10411942 | pubmed:author | pubmed-author:SaatmanK EKE | lld:pubmed |