INT110956

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Context Info
Confidence 0.41
First Reported 2003
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 5
Total Number 5
Disease Relevance 3.68
Pain Relevance 3.11

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

cytosol (Pparg) signal transduction (Pparg) nucleus (Pparg)
enzyme binding (Pparg) DNA binding (Pparg) cytoplasm (Pparg)
Anatomy Link Frequency
spinal 2
Pparg (Mus musculus)
Pain Link Frequency Relevance Heat
COX-2 inhibitor 24 99.18 Very High Very High Very High
Inflammation 5 99.16 Very High Very High Very High
cINOD 16 98.56 Very High Very High Very High
Neuropathic pain 2 98.48 Very High Very High Very High
allodynia 1 96.60 Very High Very High Very High
antagonist 2 94.60 High High
intrathecal 1 84.56 Quite High
Dorsal horn 1 82.56 Quite High
agonist 2 75.68 Quite High
Pain 6 75.00 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 7 99.16 Very High Very High Very High
Disease 10 98.94 Very High Very High Very High
Neuropathic Pain 3 98.48 Very High Very High Very High
Nervous System Injury 2 97.76 Very High Very High Very High
Hypersensitivity 1 88.92 High High
Targeted Disruption 5 85.68 High High
Apoptosis 3 85.20 High High
Alzheimer's Dementia 1 84.00 Quite High
Cancer 30 75.52 Quite High
Pain 4 75.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It has been postulated that some NSAIDs target pathological hallmarks of AD by interacting with several pathways, including the inhibition of cyclooxygenases (COX) and activation of the peroxisome proliferator-activated receptor gamma.
Negative_regulation (inhibition) of Positive_regulation (activation) of peroxisome proliferator-activated receptor gamma associated with cinod and disease
1) Confidence 0.41 Published 2004 Journal J. Neurochem. Section Abstract Doc Link 15485484 Disease Relevance 1.16 Pain Relevance 0.57
Some of the COX-independent mechanisms for NSAIDs and selective COX-2 inhibitors include activation of protein kinase G, inhibition of NF-kappa B activation, downregulation of the antiapoptotic protein Bcl-XL, inhibition of PPAR delta, and activation of PPAR gamma.
Negative_regulation (inhibition) of Positive_regulation (activation) of PPAR gamma associated with cinod and cox-2 inhibitor
2) Confidence 0.19 Published 2003 Journal Prog Exp Tumor Res Section Abstract Doc Link 12795055 Disease Relevance 0.49 Pain Relevance 0.54
Some of the COX-independent mechanisms for NSAIDs and selective COX-2 inhibitors include activation of protein kinase G, inhibition of NF-kappa B activation, downregulation of the antiapoptotic protein Bcl-XL, inhibition of PPAR delta, and activation of PPAR gamma.
Negative_regulation (downregulation) of Positive_regulation (activation) of PPAR gamma associated with cinod and cox-2 inhibitor
3) Confidence 0.19 Published 2003 Journal Prog Exp Tumor Res Section Abstract Doc Link 12795055 Disease Relevance 0.49 Pain Relevance 0.54
Some of the COX-independent mechanisms for NSAIDs and selective COX-2 inhibitors include activation of protein kinase G, inhibition of NF-kappa B activation, downregulation of the antiapoptotic protein Bcl-XL, inhibition of PPAR delta, and activation of PPAR gamma.
Negative_regulation (inhibition) of Positive_regulation (activation) of PPAR gamma associated with cinod and cox-2 inhibitor
4) Confidence 0.19 Published 2003 Journal Prog Exp Tumor Res Section Abstract Doc Link 12795055 Disease Relevance 0.48 Pain Relevance 0.54
These data suggest that ligand-dependent, non-genomic activation of spinal PPARgamma decreases behavioral signs of inflammatory and neuropathic pain.
Negative_regulation (decreases) of Positive_regulation (activation) of PPARgamma in spinal associated with inflammation and neuropathic pain
5) Confidence 0.10 Published 2009 Journal Brain research reviews Section Abstract Doc Link 19162071 Disease Relevance 1.06 Pain Relevance 0.92

General Comments

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