INT209937

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Context Info
Confidence 0.24
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 1.15
Pain Relevance 0.32

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

cytosol (IL1B) signal transduction (IL1B) extracellular space (IL1B)
aging (IL1B) extracellular region (IL1B) cell-cell signaling (IL1B)
Anatomy Link Frequency
cartilage 2
IL1B (Homo sapiens)
Pain Link Frequency Relevance Heat
Osteoarthritis 67 92.36 High High
Inflammation 87 91.32 High High
Arthritis 7 62.64 Quite High
cytokine 12 50.24 Quite High
Pain 22 50.00 Quite Low
fibrosis 1 35.12 Quite Low
metalloproteinase 5 22.36 Low Low
Inflammatory mediators 6 10.56 Low Low
aspirin 9 6.08 Low Low
cINOD 35 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Osteoarthritis 67 92.36 High High
INFLAMMATION 98 91.32 High High
Disease 17 90.36 High High
Arthritis 13 90.04 High High
Cancer 6 85.96 High High
Obesity 2 78.44 Quite High
Peptic Ulcer 1 72.12 Quite High
Pain 22 50.00 Quite Low
Neurodegenerative Disease 2 46.40 Quite Low
Colitis 1 44.96 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
activators prevents IL-1-induced proteoglycan degradation [13].
Negative_regulation (prevents) of Protein_catabolism (degradation) of IL-1
1) Confidence 0.24 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906809 Disease Relevance 0.46 Pain Relevance 0.15
Epigallocatechin-3 galate inhibits IL-1–induced proteoglycan release and type 2 collagen degradation in cartilage explants.[44] In human in vitro models, it also suppresses IL-1b and attenuates activation of the transcription factor NF-kB.
Negative_regulation (inhibits) of Protein_catabolism (degradation) of IL-1 in cartilage
2) Confidence 0.05 Published 2010 Journal Surgical Neurology International Section Body Doc Link PMC3011108 Disease Relevance 0.69 Pain Relevance 0.17

General Comments

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