rdf:type |
|
lifeskim:mentions |
umls-concept:C0001554,
umls-concept:C0006684,
umls-concept:C0008976,
umls-concept:C0013682,
umls-concept:C0079809,
umls-concept:C0211011,
umls-concept:C0242485,
umls-concept:C0270611,
umls-concept:C0277785,
umls-concept:C0521451,
umls-concept:C1517004,
umls-concept:C1709630,
umls-concept:C1979963,
umls-concept:C2003903
|
pubmed:issue |
5
|
pubmed:dateCreated |
2000-11-3
|
pubmed:abstractText |
Determining the efficacy of a drug used in experimental traumatic brain injury (TBI) requires the use of one or more outcome measures such as decreased mortality or fewer neurological and neuropsychological deficits. Unfortunately, outcomes in these test batteries have a fairly large variability, requiring relatively large sample sizes, and administration of the tests themselves is also very time consuming. The authors previously demonstrated that experimental TBI and human TBI induce mitochondrial dysfunction. Because mitochondrial dysfunction is easy to assess compared with neurobehavioral endpoints, it might prove useful as an outcome measure to establish therapeutic time windows and dose-response curves in preclinical drug testing. This idea was tested in a model of TBI in rats.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
0022-3085
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
93
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
829-34
|
pubmed:dateRevised |
2004-12-31
|
pubmed:meshHeading |
pubmed-meshheading:11059665-Animals,
pubmed-meshheading:11059665-Brain,
pubmed-meshheading:11059665-Brain Injuries,
pubmed-meshheading:11059665-Calcium Channel Blockers,
pubmed-meshheading:11059665-Calcium Channels, N-Type,
pubmed-meshheading:11059665-Disease Models, Animal,
pubmed-meshheading:11059665-Dose-Response Relationship, Drug,
pubmed-meshheading:11059665-Male,
pubmed-meshheading:11059665-Mitochondria,
pubmed-meshheading:11059665-Neuroprotective Agents,
pubmed-meshheading:11059665-Oxygen,
pubmed-meshheading:11059665-Rats,
pubmed-meshheading:11059665-Rats, Sprague-Dawley,
pubmed-meshheading:11059665-Time Factors,
pubmed-meshheading:11059665-omega-Conotoxins
|
pubmed:year |
2000
|
pubmed:articleTitle |
Improvement in mitochondrial dysfunction as a new surrogate efficiency measure for preclinical trials: dose-response and time-window profiles for administration of the calcium channel blocker Ziconotide in experimental brain injury.
|
pubmed:affiliation |
Department of Neurosurgery, University of California at Davis Medical Center, Sacramento 95817, USA.
|
pubmed:publicationType |
Journal Article
|