INT234585

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Context Info
Confidence 0.04
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.91
Pain Relevance 0.37

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

isomerase activity (Ptges) nucleus (Ptges) cytoplasm (Ptges)
Anatomy Link Frequency
microglia 2
Ptges (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 21 100.00 Very High Very High Very High
Paracetamol 1 95.20 Very High Very High Very High
COX-2 inhibitor 4 85.96 High High
Inflammatory response 6 83.52 Quite High
rheumatoid arthritis 1 55.52 Quite High
cytokine 19 22.76 Low Low
Central nervous system 8 5.00 Very Low Very Low Very Low
chemokine 8 5.00 Very Low Very Low Very Low
cINOD 4 5.00 Very Low Very Low Very Low
Intracerebroventricular 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 35 100.00 Very High Very High Very High
Hepatotoxicity 1 96.12 Very High Very High Very High
Ocular & Orbital Inflammation 1 93.20 High High
Convulsion 1 88.52 High High
Drug Induced Neurotoxicity 3 76.96 Quite High
Parkinson's Disease 1 71.40 Quite High
Familial Adenomatous Polyposis 1 56.92 Quite High
Rheumatoid Arthritis 1 55.52 Quite High
Stress 3 29.68 Quite Low
Neurodegenerative Disease 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Another study reported, in support of our observations, that selective pharmacological inhibition of COX-2 with NS-398 increases the transcription of inflammatory genes (mPGES-1, TLR2, CD14, MCP-1) in vascular associated brain cells and parenchymal microglia after systemic injection of LPS [14].
Negative_regulation (inhibition) of Positive_regulation (increases) of mPGES-1 in microglia associated with inflammation
1) Confidence 0.04 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2409311 Disease Relevance 0.91 Pain Relevance 0.37

General Comments

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