INT131816

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Context Info
Confidence 0.19
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Abstract
Documents 1
Total Number 2
Disease Relevance 1.05
Pain Relevance 1.31

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

mitochondrion (Pars2) translation (Pars2) ligase activity (Pars2)
cytoplasm (Pars2)
Pars2 (Mus musculus)
Pain Link Frequency Relevance Heat
COX-2 inhibitor 8 99.88 Very High Very High Very High
Analgesic 2 99.42 Very High Very High Very High
Hyperalgesia 8 97.80 Very High Very High Very High
Inflammation 12 97.54 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hyperalgesia 8 97.80 Very High Very High Very High
INFLAMMATION 6 97.54 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In conclusion, NO reverses endotoxin-induced inflammatory hyperalgesia via inhibition of prostacyclin production, and also contributes to the analgesic effect of NF-kappaB, COX or PARS inhibitors.
Negative_regulation (inhibitors) of PARS associated with hyperalgesia, inflammation and analgesic
1) Confidence 0.19 Published 2006 Journal Pharmacol. Res. Section Abstract Doc Link 16310374 Disease Relevance 0.52 Pain Relevance 0.66
Injection of endotoxin (10 mg kg(-1), i.p.) to mice elicited hyperalgesia, determined by hot plate test, which is prevented by NO precursor (L-arginine), cNOS/iNOS inhibitor (N(G)-nitro-L-arginine methyl ester; L-NAME), NF-kappaB inhibitor (N-acetylserotonin), COX inhibitor (indomethacin), COX-2 inhibitor (DFU) and PARS inhibitor (3-aminobenzamide).
Negative_regulation (inhibitor) of PARS associated with hyperalgesia and cox-2 inhibitor
2) Confidence 0.14 Published 2006 Journal Pharmacol. Res. Section Abstract Doc Link 16310374 Disease Relevance 0.53 Pain Relevance 0.65

General Comments

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