INT181885

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Context Info
Confidence 0.35
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 7
Total Number 7
Disease Relevance 5.66
Pain Relevance 0.84

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

lipid binding (Apoa1) extracellular space (Apoa1) extracellular region (Apoa1)
nucleus (Apoa1) enzyme binding (Apoa1)
Anatomy Link Frequency
macrophages 1
endothelial cells 1
body 1
Apoa1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 51 99.64 Very High Very High Very High
cytokine 18 95.36 Very High Very High Very High
noradrenaline 14 92.68 High High
rheumatoid arthritis 60 88.80 High High
agonist 27 77.80 Quite High
Catecholamine 12 54.64 Quite High
Arthritis 6 23.20 Low Low
imagery 114 5.00 Very Low Very Low Very Low
Central nervous system 33 5.00 Very Low Very Low Very Low
alcohol 13 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Obesity 89 100.00 Very High Very High Very High
INFLAMMATION 61 99.64 Very High Very High Very High
Repression 4 99.36 Very High Very High Very High
Disorder Of Lipid Metabolism 456 98.78 Very High Very High Very High
Myocardial Infarction 22 96.48 Very High Very High Very High
Disease 42 91.64 High High
Coronary Heart Disease 33 89.24 High High
Rheumatoid Arthritis 63 88.80 High High
Glioblastoma 3 85.12 High High
Metabolic Syndrome 8 84.72 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To overcome apoA-I inhibition, A-SAA would be expected to localize in the same area.
apoA-I Neg (inhibition) Binding (inhibition) of
1) Confidence 0.35 Published 2004 Journal Arthritis Res Ther Section Body Doc Link PMC1064871 Disease Relevance 0.54 Pain Relevance 0.17
ApoA-I that binds surface factors on stimulated T cells is retained in the perivascular regions, where it may limit contact-mediated cytokine induction in monocyte–macrophages [5] and inhibit critical pathways associated with disease exacerbation.
ApoA-I Binding (binds) of in macrophages associated with disease and cytokine
2) Confidence 0.34 Published 2004 Journal Arthritis Res Ther Section Body Doc Link PMC1064871 Disease Relevance 0.84 Pain Relevance 0.30
The mechanism of HDL-C mediated eNOS activation remains unknown, however may involve an interaction between endothelial SR-B1 and Apo AI (Yuhanna et al 2001).
Apo AI Binding (interaction) of associated with disorder of lipid metabolism
3) Confidence 0.21 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 2.02 Pain Relevance 0.16
0.5, Fig. 1A) but was not related to apoA1 or body mass index (both r?
apoA1 Binding (index) of in body associated with obesity
4) Confidence 0.14 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2582480 Disease Relevance 0.95 Pain Relevance 0.15
A recent study showed that lysosphingolipids present in HDL are responsible for these effects (Nofer et al 2004), while ApoA-I is fundamental for the binding to the membrane of endothelial cells.
ApoA-I Binding (binding) of in endothelial cells associated with disorder of lipid metabolism
5) Confidence 0.13 Published 2005 Journal Vascular Health and Risk Management Section Body Doc Link PMC1993938 Disease Relevance 0.74 Pain Relevance 0.03
of rat ApoA-I and activation by PPAR?
ApoA-I Binding (rat) of
6) Confidence 0.07 Published 2008 Journal PPAR Research Section Body Doc Link PMC2435221 Disease Relevance 0.18 Pain Relevance 0.04
Further research is required to reveal the mechanisms behind the interaction between SR-B1 and apoA-1 and their possible role in enhancing the drug delivery via RME pathway.
apoA-1 Binding (interaction) of
7) Confidence 0.05 Published 2010 Journal Part Fibre Toxicol Section Body Doc Link PMC2847536 Disease Relevance 0.39 Pain Relevance 0

General Comments

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