Source:http://linkedlifedata.com/resource/pubmed/id/16040014
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2005-8-9
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pubmed:abstractText |
Motor recovery after proximal nerve injury remains extremely poor, despite advances in surgical care. Several neurobiological hurdles are implicated, the most fundamental being extensive cell death within the motorneuron pool. N-acetyl-cysteine almost completely protects sensory neurons after peripheral axotomy, hence its efficacy in protecting motorneurons after ventral root avulsion/rhizotomy was investigated. In adult rats, the motorneurons supplying medial gastrocnemius were unilaterally pre-labelled with retrograde tracer (true-blue/fluoro-gold), prior to L5 and 6 ventral root avulsion, or rhizotomy. Groups received either intraperitoneal N-acetyl-cysteine (ip, 150 or 750 mg/kg/day), immediate or delayed intrathecal N-acetyl-cysteine treatment (it, 2.4 mg/day), or saline; untreated animals served as controls. Either 4 (avulsion model) or 8 (rhizotomy model) weeks later, the pre-labelled motorneurons' mean soma area and survival were quantified. Untreated controls possessed markedly fewer motorneurons than normal due to cell death (avulsion 53% death; rhizotomy 26% death, P<0.01 vs. normal). Motorneurons were significantly protected by N-acetyl-cysteine after avulsion (ip 150 mg/kg/day 40% death; it 30% death, P<0.01 vs. no treatment), but particularly after rhizotomy (ip 150 mg/kg/day 17% death; ip 750 mg/kg/day 7% death; it 5% death, P<0.05 vs. no treatment). Delaying intrathecal treatment for 1 week after avulsion did not impair neuroprotection, but a 2-week delay was deleterious (42% death, P<0.05 vs. 1-week delay, 32% death). Treatment prevented the decrease in soma area usually found after both types of injury. N-acetyl-cysteine has considerable clinical potential for adjuvant treatment of major proximal nerve injuries, including brachial plexus injury, in order that motorneurons may survive until surgical repair facilitates regeneration.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0007-1226
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
58
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
765-73
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16040014-Acetylcysteine,
pubmed-meshheading:16040014-Animals,
pubmed-meshheading:16040014-Cell Death,
pubmed-meshheading:16040014-Female,
pubmed-meshheading:16040014-Motor Neurons,
pubmed-meshheading:16040014-Neuroprotective Agents,
pubmed-meshheading:16040014-Rats,
pubmed-meshheading:16040014-Rats, Sprague-Dawley,
pubmed-meshheading:16040014-Rhizotomy,
pubmed-meshheading:16040014-Sciatic Nerve,
pubmed-meshheading:16040014-Spinal Nerve Roots
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pubmed:year |
2005
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pubmed:articleTitle |
Motorneuron protection by N-acetyl-cysteine after ventral root avulsion and ventral rhizotomy.
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pubmed:affiliation |
Department of Surgical and Perioperative Science, Section for Hand and Plastic Surgery, University Hospital, Umeå, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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