INT134888

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Context Info
Confidence 0.24
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Abstract
Documents 1
Total Number 1
Disease Relevance 0.38
Pain Relevance 0.33

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

signal transduction (TNFRSF11A, CCL2) aging (CCL2) cytoplasm (CCL2)
cell-cell signaling (TNFRSF11A) extracellular space (CCL2) extracellular region (CCL2)
Anatomy Link Frequency
endothelial cells 3
TNFRSF11A (Homo sapiens)
CCL2 (Homo sapiens)
Pain Link Frequency Relevance Heat
aspirin 6 97.00 Very High Very High Very High
cINOD 1 66.44 Quite High
Inflammation 1 64.08 Quite High
chemokine 1 55.16 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 2 66.20 Quite High
Disease 1 63.04 Quite High
Diabetes Mellitus 1 62.32 Quite High
Increased Venous Pressure Under Development 2 60.84 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The results showed that (i) aspirin, fenofibrate and clofibrate decrease significantly the MCP-1 expression and secretion in human endothelial cells; (ii) the high glucose up-regulated expression of MCP-1 in endothelial cells was significantly reduced by inhibitors of NF-kB and reactive oxygen species; (iii) all drugs notably decrease the level of the reactive oxygen species and activation of NF-kB and AP-1.
Negative_regulation (inhibitors) of NF-kB in endothelial cells Negative_regulation (reduced) of Gene_expression (expression) of MCP-1 in endothelial cells associated with aspirin
1) Confidence 0.24 Published 2006 Journal Vascul. Pharmacol. Section Abstract Doc Link 16600694 Disease Relevance 0.38 Pain Relevance 0.33

General Comments

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