Source:http://linkedlifedata.com/resource/pubmed/id/10383613
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rdf:type | |
lifeskim:mentions |
umls-concept:C0009813,
umls-concept:C0020517,
umls-concept:C0021760,
umls-concept:C0026809,
umls-concept:C0027740,
umls-concept:C0027895,
umls-concept:C0205191,
umls-concept:C0205227,
umls-concept:C0221912,
umls-concept:C0234402,
umls-concept:C0332281,
umls-concept:C0392747,
umls-concept:C0443172,
umls-concept:C1261287,
umls-concept:C1760025,
umls-concept:C1880177,
umls-concept:C2684089
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pubmed:issue |
7
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pubmed:dateCreated |
1999-7-30
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pubmed:abstractText |
Partial nerve injury is a potential cause of distressing chronic pain for which conventional analgesic treatment with opiates or anti-inflammatory agents is not very effective. Constriction nerve injury, widely used to study neuropathic pain, was shown here to induce interleukin-6 (IL-6) mRNA in a subset of rat primary sensory neurons. When we inflicted chronic nerve constriction on mice with null mutation of the IL-6 gene, the hypersensitivity to cutaneous heat and pressure that is induced in wild-type mice was not evident, the loss of substance P in sensory neurons was excessive and the induction of galanin in central sensory projections was reduced. In additional experiments, intrathecal infusion of IL-6 in rats was shown to stimulate synthesis of galanin in approximately one-third of lumbar dorsal root ganglion neurons. The results of these experiments indicate that endogenous IL-6 mediates some of the hypersensitive responses that characterize peripheral neuropathic pain, and influences two neuropeptides that have been implicated in pain transmission.
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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 |
Jul
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pubmed:issn |
0953-816X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
11
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2243-53
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10383613-Animals,
pubmed-meshheading:10383613-Behavior, Animal,
pubmed-meshheading:10383613-Chronic Disease,
pubmed-meshheading:10383613-Female,
pubmed-meshheading:10383613-Ganglia, Spinal,
pubmed-meshheading:10383613-Hyperesthesia,
pubmed-meshheading:10383613-Interleukin-6,
pubmed-meshheading:10383613-Mice,
pubmed-meshheading:10383613-Mice, Knockout,
pubmed-meshheading:10383613-Nerve Compression Syndromes,
pubmed-meshheading:10383613-Neuropeptides,
pubmed-meshheading:10383613-Physical Stimulation,
pubmed-meshheading:10383613-RNA, Messenger,
pubmed-meshheading:10383613-Rats,
pubmed-meshheading:10383613-Rats, Sprague-Dawley,
pubmed-meshheading:10383613-Skin,
pubmed-meshheading:10383613-Wounds and Injuries
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pubmed:year |
1999
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pubmed:articleTitle |
Endogenous interleukin-6 contributes to hypersensitivity to cutaneous stimuli and changes in neuropeptides associated with chronic nerve constriction in mice.
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pubmed:affiliation |
Department of Physiology, Queen's University, Kingston, Canda K7L 3N63.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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