INT181886

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.64
First Reported 2003
Last Reported 2010
Negated 4
Speculated 0
Reported most in Body
Documents 40
Total Number 41
Disease Relevance 40.53
Pain Relevance 4.56

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
plasma 2
liver 2
intestines 2
macrophages 1
synovial fluid 1
Apoa1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 382 100.00 Very High Very High Very High
agonist 345 99.72 Very High Very High Very High
Bile 114 99.64 Very High Very High Very High
rheumatoid arthritis 213 99.12 Very High Very High Very High
alcohol 194 98.96 Very High Very High Very High
methotrexate 17 93.48 High High
cytokine 93 91.04 High High
Arthritis 27 91.04 High High
antagonist 16 86.40 High High
ischemia 39 84.44 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 404 100.00 Very High Very High Very High
Repression 19 100.00 Very High Very High Very High
Disorder Of Lipid Metabolism 5715 99.92 Very High Very High Very High
Targeted Disruption 207 99.84 Very High Very High Very High
Coronary Artery Disease 117 99.84 Very High Very High Very High
Psoriasis 318 99.64 Very High Very High Very High
Rheumatoid Arthritis 228 99.12 Very High Very High Very High
Hyperlipidemia 55 98.88 Very High Very High Very High
Disease 297 98.80 Very High Very High Very High
Myocardial Infarction 372 98.12 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These studies suggest that variations of apoA-I levels may inversely correlate with disease activity.
Gene_expression (levels) of apoA-I associated with disease
1) Confidence 0.64 Published 2004 Journal Arthritis Res Ther Section Body Doc Link PMC1064871 Disease Relevance 1.19 Pain Relevance 0.38
The elevation of apoA-I levels in synovial fluid of RA patients correlated with a rise in cholesterol, suggesting infiltration of HDL particles into the inflamed joint.
Gene_expression (levels) of apoA-I in synovial fluid associated with rheumatoid arthritis and disorder of lipid metabolism
2) Confidence 0.64 Published 2004 Journal Arthritis Res Ther Section Body Doc Link PMC1064871 Disease Relevance 1.25 Pain Relevance 0.37
Apo A-1 overexpression in transgenic mice and rabbits has been demonstrated to increase the number of circulating HDL particles and confer protection from the development of diet- or gene-induced atherosclerosis.
Gene_expression (overexpression) of Apo A-1 associated with targeted disruption, atherosclerosis and disorder of lipid metabolism
3) Confidence 0.58 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2988622 Disease Relevance 1.29 Pain Relevance 0.03
Specific apoA-I staining was present in all samples.
Gene_expression (present) of apoA-I
4) Confidence 0.57 Published 2004 Journal Arthritis Res Ther Section Body Doc Link PMC1064871 Disease Relevance 0.71 Pain Relevance 0.48
ApoA-I was not present in synovium from patients in apparent remission, suggesting that it has a specific role during phases of disease activity.
Neg (not) Gene_expression (present) of ApoA-I in synovium associated with disease
5) Confidence 0.57 Published 2004 Journal Arthritis Res Ther Section Abstract Doc Link PMC1064871 Disease Relevance 0.79 Pain Relevance 0.28
As determined by immunohistochemistry, apoA-I was consistently present in inflamed synovial tissue that contained infiltrating T cells and macrophages, but it was absent from noninflamed tissue samples obtained from treated patients and from normal subjects.
Neg (absent) Gene_expression (present) of apoA-I in macrophages
6) Confidence 0.57 Published 2004 Journal Arthritis Res Ther Section Abstract Doc Link PMC1064871 Disease Relevance 0.96 Pain Relevance 0.33
Since apoA-I is virtually absent from the synovial tissue of patients with inactive RA (Fig. 1c), its presence in actively inflamed tissue suggests that its infiltration during a flare-up may represent a physiologic mechanism that inhibits proinflammatory cytokine production and limits disease recurrence.
Neg (absent) Gene_expression (absent) of apoA-I associated with rheumatoid arthritis, disease, recurrence and cytokine
7) Confidence 0.57 Published 2004 Journal Arthritis Res Ther Section Body Doc Link PMC1064871 Disease Relevance 0.67 Pain Relevance 0.22
It was also reported that apoA1 sequestration in the inflamed tissues might lead to reduced HDL-C serum levels and thus increase the risk of cardiovascular disease in psoriatic patients [81].
Gene_expression (sequestration) of apoA1 associated with psoriasis, cardiovascular disease and disorder of lipid metabolism
8) Confidence 0.35 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2914266 Disease Relevance 1.15 Pain Relevance 0.03
Many authors did not show any differences in apoA1, apoA2, and apoB levels between psoriatic patients and the control group [10, 76, 80].
Gene_expression (levels) of apoA1 associated with psoriasis
9) Confidence 0.35 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2914266 Disease Relevance 1.22 Pain Relevance 0.03
Similar results have been demonstrated in balloon injured arteries in hypercholesterolemic rabbits, Apo E-deficient mice, and in transgenic mouse models of Apo AI over-expression (Rubin et al 1991; Shah et al 1998).
Gene_expression (over) of Apo AI associated with targeted disruption
10) Confidence 0.33 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 0.87 Pain Relevance 0
Mechanisms by which alcohol consumption increases HDL-C may involve changes in Apo AI synthesis and transportation, inhibition of CETP activity and stimulation of early steps in RCT (Van der Gaag et al 2001).
Gene_expression (synthesis) of Apo AI associated with disorder of lipid metabolism and alcohol
11) Confidence 0.33 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 1.06 Pain Relevance 0.24
Similar findings have been reported in animal models of Apo AI gene over-expression (Dimayuga et al 1999).
Gene_expression (over) of Apo AI
12) Confidence 0.33 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 1.47 Pain Relevance 0
Apo AI is produced by the liver and intestines and constitutes 70% of HDL-C protein content.
Gene_expression (produced) of Apo AI in liver associated with disorder of lipid metabolism
13) Confidence 0.33 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 1.54 Pain Relevance 0
and by enhancing expression of Apo AI and AII, LL, and ABCA1, which collectively enhance RCT (Tilly-Kiesi et al 1992).
Gene_expression (expression) of Apo AI
14) Confidence 0.33 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 1.10 Pain Relevance 0.03
In most studies, elevated levels of apoA1, apoB [16, 43], apoC3, and apoE [41, 76–78] were detected in the serum of psoriatic patients compared to the healthy control group.
Gene_expression (levels) of apoA1 associated with psoriasis
15) Confidence 0.31 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2914266 Disease Relevance 1.08 Pain Relevance 0.03
The PI3K/Akt pathway has been implicated in many of the effects of HDL on the endothelium; furthermore, mice overexpressing ApoA-I present an increased Akt phosphorylation in the arterial wall (Norata et al 2005) and mice lacking one of the lysosphingolipid receptors show a reduced Akt phosphorylation in the arterial wall (Nofer et al 2004).
Gene_expression (overexpressing) of ApoA-I in endothelium associated with disorder of lipid metabolism
16) Confidence 0.29 Published 2005 Journal Vascular Health and Risk Management Section Body Doc Link PMC1993938 Disease Relevance 1.11 Pain Relevance 0.07
Exogenous HDL-C or Apo AI administration also enhance fecal steroid excretion, increase serum pre-?
Gene_expression (administration) of Apo AI associated with disorder of lipid metabolism
17) Confidence 0.29 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 0.84 Pain Relevance 0
While measuring HDL-C subfractions are not recommended at present, recent data suggests that increased Apo AI plasma levels and Apo AI:Apo B ratios correlate with a reduced risk of myocardial infarction and stroke (Qureshi et al 2002).
Gene_expression (levels) of Apo AI in plasma associated with stroke, myocardial infarction and disorder of lipid metabolism
18) Confidence 0.29 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 1.42 Pain Relevance 0.08
Emerging therapies such as Apo AI mimetics (Eriksson et al 1999) and LXR agonists (Plosch et al 2002) increase fecal sterol excretion (FSE), while CETP inhibition with torcetrapib fails to affect fecal sterol content (Brousseau et al 2005).
Gene_expression (mimetics) of Apo AI associated with agonist
19) Confidence 0.29 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 1.17 Pain Relevance 0.10
Conversely, over expression of human LCAT in transgenic animal models correlates with a 7-fold increase in serum HDL-C, increases in Apo AI levels, and a marked reduction in atheromatous plaque burden (Francone et al 1990).
Gene_expression (levels) of Apo AI in plaque associated with targeted disruption and disorder of lipid metabolism
20) Confidence 0.29 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2464766 Disease Relevance 1.61 Pain Relevance 0.03

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox