INT172142

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Context Info
Confidence 0.03
First Reported 2000
Last Reported 2007
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 1.69
Pain Relevance 0.68

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

cell-cell signaling (IL10, IL1B) extracellular space (IL10, IL1B) extracellular region (IL10, IL1B)
aging (IL1B) intracellular (IL10) response to stress (IL10)
IL10 (Homo sapiens)
IL1B (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 88 96.76 Very High Very High Very High
rheumatoid arthritis 175 93.20 High High
Arthritis 67 83.04 Quite High
cytokine 96 81.92 Quite High
antagonist 14 25.36 Quite Low
aspirin 3 19.72 Low Low
chemokine 16 5.00 Very Low Very Low Very Low
metalloproteinase 7 5.00 Very Low Very Low Very Low
corticosteroid 6 5.00 Very Low Very Low Very Low
methotrexate 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 90 96.76 Very High Very High Very High
Rheumatoid Arthritis 178 93.20 High High
Arthritis 59 91.40 High High
Experimental Arthritis 19 84.08 Quite High
Apoptosis 13 64.76 Quite High
Pressure And Volume Under Development 3 59.92 Quite High
Adhesions 8 58.04 Quite High
Disease 40 56.00 Quite High
Death 2 51.68 Quite High
Herpes Simplex Virus 2 48.56 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Unlike IL-4, IL-10 can also enhance degradation of the mRNA for IL-1 and TNF-?
IL-10 Positive_regulation (enhance) of Protein_catabolism (degradation) of IL-1
1) Confidence 0.03 Published 2000 Journal Arthritis Res Section Body Doc Link PMC130001 Disease Relevance 0.86 Pain Relevance 0.31
Unlike IL-4, IL-10 can also enhance degradation of the mRNA for IL-1 and TNF-?
IL-10 Positive_regulation (enhance) of Protein_catabolism (degradation) of IL-1
2) Confidence 0.02 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2246244 Disease Relevance 0.82 Pain Relevance 0.37

General Comments

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