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Context Info
Confidence 0.09
First Reported 2007
Last Reported 2008
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 1.51
Pain Relevance 0.98

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

mitochondrion (CPOX) small molecule metabolic process (CPOX) oxidoreductase activity (CPOX)
cytoplasm (CPOX)
Anatomy Link Frequency
CPOX (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 13 93.84 High High
Inflammation 51 91.76 High High
cINOD 8 87.04 High High
COX-2 inhibitor 2 86.00 High High
Inflammatory response 5 79.92 Quite High
Analgesic 1 72.92 Quite High
Spinal cord 12 69.92 Quite High
Pain 1 69.88 Quite High
Inflammatory stimuli 1 61.88 Quite High
COX2 1 50.00 Quite Low
Disease Link Frequency Relevance Heat
Cancer 68 99.64 Very High Very High Very High
Neuroblastoma 22 99.60 Very High Very High Very High
Metastasis 4 93.04 High High
INFLAMMATION 61 91.76 High High
Colon Cancer 4 81.68 Quite High
Pain 1 69.88 Quite High
Hypoxia 6 5.00 Very Low Very Low Very Low
Disease 5 5.00 Very Low Very Low Very Low
Ovarian Cancer 4 5.00 Very Low Very Low Very Low
Hyperalgesia 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The aim of the present work was to examine the mechanisms involved in ATRA-induced COX-2 up-regulation in human neuroblastoma SH-SY5Y.
Spec (examine) Positive_regulation (induced) of Spec (examine) Regulation (regulation) of COX in SH-SY5Y associated with neuroblastoma
1) Confidence 0.09 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC1769480 Disease Relevance 0.10 Pain Relevance 0.19
display elevated COX-2 expression and studies in COX-2 null mice have demonstrated the role of this enzyme in
Positive_regulation (elevated) of Regulation (studies) of COX
2) Confidence 0.03 Published 2008 Journal PPAR Research Section Body Doc Link PMC2490577 Disease Relevance 1.41 Pain Relevance 0.80

General Comments

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