INT225104

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Context Info
Confidence 0.01
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 1.41
Pain Relevance 1.14

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

cell proliferation (RETNLB) extracellular region (RETNLB) aging (CNR1)
plasma membrane (CNR1) molecular_function (RETNLB) cellular_component (RETNLB)
CNR1 (Homo sapiens)
RETNLB (Homo sapiens)
Pain Link Frequency Relevance Heat
Cannabinoid receptor 18 100.00 Very High Very High Very High
Inflammation 13 100.00 Very High Very High Very High
cytokine 10 99.96 Very High Very High Very High
Endocannabinoid 24 97.16 Very High Very High Very High
chemokine 3 94.84 High High
Chronic pancreatitis 31 85.16 High High
Pain 4 83.76 Quite High
fibrosis 12 80.80 Quite High
Cannabinoid 26 65.56 Quite High
antagonist 23 51.92 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 14 100.00 Very High Very High Very High
Primary Sclerosing Cholangitis 44 98.36 Very High Very High Very High
Cirrhosis 15 90.08 High High
Pancreatitis 32 85.16 High High
Pain 2 83.76 Quite High
Fibrosis 11 80.80 Quite High
Complex Regional Pain Syndromes 2 80.36 Quite High
Apoptosis 11 79.84 Quite High
Disease 6 39.84 Quite Low
Necrosis 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, we also observed that cannabinoid receptor-1 antagonism induced production of the pro-inflammatory cytokine IL-6 and induced a more motile PSC phenotype, as judged by a trend toward increased invasiveness and a longitudinally stretched appearance.
cannabinoid receptor-1 Positive_regulation (induced) of Gene_expression (production) of pro-inflammatory associated with inflammation, cannabinoid receptor, primary sclerosing cholangitis and cytokine
1) Confidence 0.01 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2253501 Disease Relevance 1.41 Pain Relevance 1.14

General Comments

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