INT88651

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Context Info
Confidence 0.41
First Reported 2000
Last Reported 2008
Negated 0
Speculated 0
Reported most in Abstract
Documents 5
Total Number 5
Disease Relevance 2.92
Pain Relevance 4.04

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

mitochondrion (Cpox) oxidoreductase activity (Cpox) cytoplasm (Cpox)
Anatomy Link Frequency
arms 1
microglial cells 1
Cpox (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 4 100.00 Very High Very High Very High
cINOD 22 98.30 Very High Very High Very High
analgesia 2 95.12 Very High Very High Very High
COX-2 inhibitor 3 94.64 High High
Antinociceptive 4 94.36 High High
substance P 7 92.16 High High
Inflammation 23 91.48 High High
Spinal cord 3 89.84 High High
Lasting pain 1 88.72 High High
agonist 3 83.04 Quite High
Disease Link Frequency Relevance Heat
Enteropathy 1 98.52 Very High Very High Very High
INFLAMMATION 33 98.02 Very High Very High Very High
Disease 23 96.08 Very High Very High Very High
Apoptosis 5 95.68 Very High Very High Very High
Cancer 3 90.64 High High
Arthritis 1 81.88 Quite High
Death 11 77.68 Quite High
Nociception 1 77.00 Quite High
Toxicity 1 76.48 Quite High
Ganglion Cysts 4 75.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The pathogenesis of nonsteroidal anti-inflammatory drug (NSAID) enteropathy is a complex process involving the uncoupling of mitochondrial oxidative phosphorylation and inhibition of cyclooxygenase (COX).
Phosphorylation (phosphorylation) of COX associated with inflammation, enteropathy and cinod
1) Confidence 0.41 Published 2004 Journal Braz. J. Med. Biol. Res. Section Abstract Doc Link 15060699 Disease Relevance 0.27 Pain Relevance 0.31
Resveratrol also prevented the bilateralisation of COX-2 expression.
Phosphorylation (bilateralisation) of COX
2) Confidence 0.35 Published 2008 Journal Pain Section Abstract Doc Link 18814970 Disease Relevance 0.90 Pain Relevance 0.87
In addition to inhibiting cyclooxygenase (COX) activity, this includes interfering with glucose metabolism through both arms of the pentose phosphate pathways and energy production via glycolysis and oxidative phosphorylation.
Phosphorylation (phosphorylation) of COX in arms
3) Confidence 0.27 Published 2000 Journal Eur. J. Pharmacol. Section Abstract Doc Link 10844092 Disease Relevance 0.75 Pain Relevance 0.76
The increase in the TRPV1 phosphorylated forms induced by a 60-min exposure to GR73632 was completely abolished by the inhibition of either PKC, COX or PLC, p38 or p42/44 MAP kinases.
Phosphorylation (phosphorylated) of COX associated with kinase c
4) Confidence 0.18 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18809416 Disease Relevance 0.07 Pain Relevance 1.04
NSAIDs target p38 mitogen-activated protein kinase (MAPK) in addition to their main target COX [23] and inhibition of p38MAPK phosphorylation blocks NO release from activated microglial cells [24].
Phosphorylation (phosphorylation) of COX in microglial cells associated with cinod
5) Confidence 0.11 Published 2004 Journal J Neuroinflammation Section Body Doc Link PMC483059 Disease Relevance 0.91 Pain Relevance 1.06

General Comments

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