INT306913

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Context Info
Confidence 0.45
First Reported 2010
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 2
Total Number 4
Disease Relevance 2.36
Pain Relevance 0.31

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

cytosol (Ephx2) Golgi apparatus (Ephx2) nucleolus (Ephx2)
peroxisome (Ephx2) cytoplasm (Ephx2)
Anatomy Link Frequency
plasma 1
blood 1
Ephx2 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 84 97.16 Very High Very High Very High
aspirin 4 80.84 Quite High
cINOD 4 79.80 Quite High
fibrosis 12 64.80 Quite High
cytokine 8 47.88 Quite Low
antagonist 4 33.44 Quite Low
Potency 10 5.00 Very Low Very Low Very Low
cva 6 5.00 Very Low Very Low Very Low
Bioavailability 4 5.00 Very Low Very Low Very Low
Pain 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Chronic Renal Failure 20 99.60 Very High Very High Very High
Renal Failure 18 99.40 Very High Very High Very High
Sprains And Strains 14 98.44 Very High Very High Very High
INFLAMMATION 86 97.16 Very High Very High Very High
Atherosclerosis 106 96.60 Very High Very High Very High
Asthma 2 87.04 High High
Hypertension 66 82.88 Quite High
Atherosclerotic Plaque 6 77.64 Quite High
Coronary Artery Disease 12 71.72 Quite High
Fibrosis 20 64.80 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A major function of the sEH is to metabolize the epoxides of AA and linoleic acid that are the regioisomers of epoxyeicosatrienoic acids (EETs) and epoxyoctadecenoic acids (EpOMEs) to their corresponding diols, dihydroxyeicosatrienoic acid (DHET) and dihydroxyoctadecenoic acid (DiHOME), respectively.
Regulation (metabolize) of sEH
1) Confidence 0.45 Published 2010 Journal Curr Atheroscler Rep Section Body Doc Link PMC2857794 Disease Relevance 0.68 Pain Relevance 0.16
Thus, chronic renal failure as a possible drug target for sEH inhibitors should be reconsidered.



Spec (possible) Regulation (target) of sEH associated with chronic renal failure
2) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2915917 Disease Relevance 0.46 Pain Relevance 0.07
Given the low plasma concentrations of EETs, it is however difficult to imagine that the somewhat modest increase in response to sEH inhibition or renal failure is sufficient to induce a significant product inhibition of the CYP enzymes, although other observations supporting the complex crosstalk have been published for inflammatory models [45].
Regulation (response) of sEH in plasma associated with inflammation and renal failure
3) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2915917 Disease Relevance 0.58 Pain Relevance 0.08
In order to understand the underlying mechanisms of differences in sEH in these rat strains, the authors hypothesized that single nucleotide polymorphisms (SNPs) may be responsible for the differences in sEH as well as blood pressure in these animals.
Spec (may) Regulation (responsible) of sEH in blood associated with sprains and strains
4) Confidence 0.39 Published 2010 Journal Curr Atheroscler Rep Section Body Doc Link PMC2857794 Disease Relevance 0.65 Pain Relevance 0

General Comments

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