INT320993

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Context Info
Confidence 0.18
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 1.11
Pain Relevance 0.30

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 (C3ar1) plasma membrane (C3ar1) signal transducer activity (C3ar1)
Anatomy Link Frequency
heart 1
C3ar1 (Mus musculus)
Pain Link Frequency Relevance Heat
ischemia 20 98.72 Very High Very High Very High
Inflammation 28 92.64 High High
antagonist 17 89.88 High High
rheumatoid arthritis 4 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
Inflammatory response 2 5.00 Very Low Very Low Very Low
isoflurane 2 5.00 Very Low Very Low Very Low
Arthritis 2 5.00 Very Low Very Low Very Low
cytokine 1 5.00 Very Low Very Low Very Low
Central nervous system 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Coronary Artery Disease 7 99.16 Very High Very High Very High
Reperfusion Injury 2 98.20 Very High Very High Very High
Death 4 95.08 Very High Very High Very High
INFLAMMATION 27 92.64 High High
Injury 37 91.68 High High
Cv Unclassified Under Development 16 75.60 Quite High
Neutropenia 9 65.60 Quite High
Myocarditis 2 48.40 Quite Low
Disease 10 5.00 Very Low Very Low Very Low
Myocardial Infarction 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Role of the complement components C5 and C3a in a mouse model of myocardial ischemia and reperfusion injury

Objective: Ischemic heart disease is the leading cause of death worldwide.

Regulation (Role) of C3a in heart associated with reperfusion injury, coronary artery disease, ischemia and death
1) Confidence 0.18 Published 2010 Journal GMS German Medical Science Section Title Doc Link PMC2940219 Disease Relevance 1.11 Pain Relevance 0.21
Dark areas indicate controlFig. 2Cell proliferation induced by C5a. [3H]-thymidine incorporation was measured with a liquid scintillation counter 48 h after adding the various concentrations of C5a, C5, or C3a to the HMEC-1 suspension. a C5a increased HMEC-1 proliferation in a dose-dependent manner, whereas C5 (b) and C3a (c) did not induce proliferation. d HMEC-1 was stimulated with either 10 nM C5a in the presence of various concentrations of C5a receptor antagonist W-54011 (closed column) or W-54011 alone (open column).
Regulation (concentrations) of C3a associated with antagonist
2) Confidence 0.01 Published 2010 Journal Inflamm Res Section Body Doc Link PMC2902742 Disease Relevance 0 Pain Relevance 0.09

General Comments

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