INT169363

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Context Info
Confidence 0.20
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 4
Disease Relevance 3.35
Pain Relevance 1.22

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 (PTGIS) small molecule metabolic process (PTGIS) endoplasmic reticulum (PTGIS)
lipid metabolic process (PTGIS)
PTGIS (Homo sapiens)
Pain Link Frequency Relevance Heat
Pain 6 97.20 Very High Very High Very High
Inflammation 21 96.84 Very High Very High Very High
withdrawal 1 95.92 Very High Very High Very High
cINOD 16 95.28 Very High Very High Very High
COX-2 inhibitor 7 95.04 Very High Very High Very High
Potency 1 52.48 Quite High
ischemia 2 41.96 Quite Low
cOX1 1 25.00 Low Low
COX2 1 25.00 Low Low
fibrosis 3 22.16 Low Low
Disease Link Frequency Relevance Heat
Toxicity 5 98.74 Very High Very High Very High
Pain 4 97.20 Very High Very High Very High
INFLAMMATION 19 96.84 Very High Very High Very High
Cardiovascular Disease 2 95.56 Very High Very High Very High
Myocardial Infarction 1 91.76 High High
Missed Abortion 1 88.24 High High
Infection 7 87.08 High High
Reperfusion Injury 1 86.64 High High
Reprotox - General 1 3 86.08 High High
Systemic Sclerosis 62 84.64 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Since these five synthases, are involved in various important biological processes, they are potential drug targets and drugs are already in the market for the inhibition of PGDS, PGFS, PGIS and TXAS. mPGES-1 is being sought after as a novel target to relieve pain and inflammation after the withdrawal of popular COX-2 inhibitors from the market [8].
Negative_regulation (inhibition) of PGIS associated with pain, inflammation, cox-2 inhibitor and withdrawal
1) Confidence 0.20 Published 2010 Journal BMC Bioinformatics Section Body Doc Link PMC3009524 Disease Relevance 0.70 Pain Relevance 0.41
Subsequent endothelial dysfunction results in the imbalance of vasoactive factors: decreased levels of vasodilators such as endothelial nitric oxide synthase and prostacyclin synthase, as well as increased levels of the vasoconstrictor endothelin-1 and vascular endothelial growth factor [5, 6].
Negative_regulation (decreased) of prostacyclin synthase
2) Confidence 0.07 Published 2010 Journal International Journal of Rheumatology Section Body Doc Link PMC2952802 Disease Relevance 1.41 Pain Relevance 0.08
Moreover, the cardiovascular toxicity of rofecoxib could be increased by its capability to directly inhibit prostacyclin synthase activity, as demonstrated by our group [25].


Negative_regulation (inhibit) of prostacyclin synthase associated with toxicity
3) Confidence 0.07 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2896898 Disease Relevance 0.66 Pain Relevance 0.12
Convincing evidence suggests that cardiovascular toxicity associated with the administration of these compounds occurs through a common mechanism involving inhibition of COX-2-dependent prostacyclin.
Negative_regulation (inhibition) of prostacyclin associated with toxicity
4) Confidence 0.05 Published 2010 Journal Pharmacol Rep Section Abstract Doc Link 20631418 Disease Relevance 0.59 Pain Relevance 0.60

General Comments

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