INT207444

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Context Info
Confidence 0.71
First Reported 2007
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 8
Total Number 17
Disease Relevance 11.31
Pain Relevance 3.18

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

extracellular space (PLA2G7) extracellular region (PLA2G7)
Anatomy Link Frequency
plasma 6
plaque 5
macrophages 1
monocytes 1
PLA2G7 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 129 100.00 Very High Very High Very High
rheumatoid arthritis 504 99.84 Very High Very High Very High
addiction 9 99.84 Very High Very High Very High
Inflammatory response 8 89.60 High High
Angina 17 87.00 High High
methotrexate 27 70.48 Quite High
corticosteroid 9 44.24 Quite Low
Inflammatory marker 26 5.00 Very Low Very Low Very Low
imagery 8 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 163 100.00 Very High Very High Very High
Rheumatoid Arthritis 504 99.84 Very High Very High Very High
Atherosclerotic Plaque 24 99.84 Very High Very High Very High
Increased Venous Pressure Under Development 144 99.72 Very High Very High Very High
Necrosis 9 98.86 Very High Very High Very High
Atherosclerosis 72 98.84 Very High Very High Very High
Cancer 65 98.68 Very High Very High Very High
Disorder Of Lipid Metabolism 515 96.88 Very High Very High Very High
Acute Coronary Syndrome 9 95.48 Very High Very High Very High
Disease 125 93.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Most of the proinflammatory mediators (lipopolysaccharide, tumor necrosis factor alpha, IL-1, IL-8, and interferon gamma) inhibit Lp-PLA2 expression by macrophages in vitro [13].
Gene_expression (expression) of Lp-PLA2 in macrophages associated with necrosis and cancer
1) Confidence 0.71 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1860077 Disease Relevance 0.89 Pain Relevance 0.28
439 participants who were initially healthy or had a history of stable vascular disease at baseline, Lp-PLA2 activity was available in 57?
Gene_expression (activity) of Lp-PLA2 associated with increased venous pressure under development
2) Confidence 0.68 Published 2010 Journal Lancet Section Body Doc Link PMC2864403 Disease Relevance 0.63 Pain Relevance 0
However, because data for serial Lp-PLA2 measurements were sparse and apparently divergent, we could not reliably correct for regression dilution.23 If, for example, the true correlation of Lp-PLA2 concentrations taken a few years apart in the same people is about 0ยท5, then the degree of underestimation of RRs could be as large as two-fold.
Gene_expression (measurements) of Lp-PLA2
3) Confidence 0.68 Published 2010 Journal Lancet Section Body Doc Link PMC2864403 Disease Relevance 0.26 Pain Relevance 0
931 participants from 18 studies and Lp-PLA2 mass in 58?
Gene_expression (mass) of Lp-PLA2
4) Confidence 0.68 Published 2010 Journal Lancet Section Body Doc Link PMC2864403 Disease Relevance 0.61 Pain Relevance 0
The cellular expression of plasma Lp-PLA2 is regulated by various factors, including the differentiation state of the cell and the degree of activation by proinflammatory mediators [13,32].
Gene_expression (expression) of plasma Lp-PLA2 in plasma
5) Confidence 0.62 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1860077 Disease Relevance 0.70 Pain Relevance 0.22
Lipoprotein-associated phospholipase A2 (Lp-PLA2), an enzyme expressed by inflammatory cells in atherosclerotic plaques,1,2 is carried in the circulation bound predominantly to LDL.3 Lp-PLA2 and other human A2 phospholipases (such as secretory phospholipase A2)4 propagate inflammation by producing precursors of arachidonic acid from membrane glycerophospholipids.5 Lp-PLA2 (also called platelet-activating factor acetylhydrolase) hydrolyses oxidised phospholipids to yield pro-inflammatory products that are implicated in endothelial dysfunction, plaque inflammation, and formation of necrotic core in plaque,6,7 and is postulated to link oxidative modification of LDL and development of inflammatory responses in the arterial intima.8,9
Gene_expression (producing) of Lp-PLA2 in plaque associated with atherosclerotic plaque, inflammatory response and inflammation
6) Confidence 0.60 Published 2010 Journal Lancet Section Body Doc Link PMC2864403 Disease Relevance 0.62 Pain Relevance 0.24
Lipoprotein-associated phospholipase A2 (Lp-PLA2), an inflammatory enzyme expressed in atherosclerotic plaques, is a therapeutic target being assessed in trials of vascular disease prevention.
Gene_expression (expressed) of Lipoprotein-associated phospholipase A2 in plaques associated with atherosclerotic plaque, inflammation and increased venous pressure under development
7) Confidence 0.60 Published 2010 Journal Lancet Section Abstract Doc Link PMC2864403 Disease Relevance 0.66 Pain Relevance 0.05
Lipoprotein-associated phospholipase A2 (Lp-PLA2), an enzyme expressed by inflammatory cells in atherosclerotic plaques,1,2 is carried in the circulation bound predominantly to LDL.3 Lp-PLA2 and other human A2 phospholipases (such as secretory phospholipase A2)4 propagate inflammation by producing precursors of arachidonic acid from membrane glycerophospholipids.5 Lp-PLA2 (also called platelet-activating factor acetylhydrolase) hydrolyses oxidised phospholipids to yield pro-inflammatory products that are implicated in endothelial dysfunction, plaque inflammation, and formation of necrotic core in plaque,6,7 and is postulated to link oxidative modification of LDL and development of inflammatory responses in the arterial intima.8,9
Gene_expression (producing) of platelet-activating factor acetylhydrolase in plaque associated with atherosclerotic plaque, inflammatory response and inflammation
8) Confidence 0.60 Published 2010 Journal Lancet Section Body Doc Link PMC2864403 Disease Relevance 0.63 Pain Relevance 0.24
Lipoprotein-associated phospholipase A2 (Lp-PLA2), an enzyme expressed by inflammatory cells in atherosclerotic plaques,1,2 is carried in the circulation bound predominantly to LDL.3 Lp-PLA2 and other human A2 phospholipases (such as secretory phospholipase A2)4 propagate inflammation by producing precursors of arachidonic acid from membrane glycerophospholipids.5 Lp-PLA2 (also called platelet-activating factor acetylhydrolase) hydrolyses oxidised phospholipids to yield pro-inflammatory products that are implicated in endothelial dysfunction, plaque inflammation, and formation of necrotic core in plaque,6,7 and is postulated to link oxidative modification of LDL and development of inflammatory responses in the arterial intima.8,9
Gene_expression (expressed) of Lp-PLA2 in plaque associated with atherosclerotic plaque, inflammatory response and inflammation
9) Confidence 0.60 Published 2010 Journal Lancet Section Body Doc Link PMC2864403 Disease Relevance 0.53 Pain Relevance 0.22
Lipoprotein-associated phospholipase A2 (Lp-PLA2), an inflammatory enzyme expressed in atherosclerotic plaques, is a therapeutic target being assessed in trials of vascular disease prevention.
Gene_expression (expressed) of Lp-PLA2 in plaques associated with atherosclerotic plaque, inflammation and increased venous pressure under development
10) Confidence 0.60 Published 2010 Journal Lancet Section Abstract Doc Link PMC2864403 Disease Relevance 0.66 Pain Relevance 0.05
The aim of the present study was to investigate the plasma levels of oxLDL and Lp-PLA2 activity as well as the autoantibody titers against various types of mildly oxidized LDL in patients with early rheumatoid arthritis (ERA).
Spec (investigate) Gene_expression (levels) of Lp-PLA2 in plasma associated with rheumatoid arthritis
11) Confidence 0.55 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1860077 Disease Relevance 0.93 Pain Relevance 0.31
It is well established that the main cellular source of the plasma form of Lp-PLA2 is monocytes, which secrete this enzyme during their differentiation into macrophages [31].
Gene_expression (source) of Lp-PLA2 in monocytes
12) Confidence 0.55 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1860077 Disease Relevance 0.79 Pain Relevance 0.28
A factor that could also influence the plasma Lp-PLA2 levels in ERA patients is Lp(a).
Gene_expression (levels) of plasma Lp-PLA2 in plasma associated with rheumatoid arthritis
13) Confidence 0.54 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1860077 Disease Relevance 0.72 Pain Relevance 0.31
The dependence of the plasma Lp-PLA2 levels from the LDL-cholesterol levels could also explain our results showing that therapy with DMARDs did not affect either the plasma LDL-cholesterol levels or the plasma Lp-PLA2 activity.
Gene_expression (levels) of plasma Lp-PLA2 in plasma associated with addiction
14) Confidence 0.54 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1860077 Disease Relevance 0.73 Pain Relevance 0.32
The dependence of the plasma Lp-PLA2 levels from the LDL-cholesterol levels could also explain our results showing that therapy with DMARDs did not affect either the plasma LDL-cholesterol levels or the plasma Lp-PLA2 activity.
Gene_expression (levels) of plasma Lp-PLA2 in plasma associated with addiction
15) Confidence 0.54 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1860077 Disease Relevance 0.72 Pain Relevance 0.30
Determination of lipoprotein-associated phospholipase A2 activity
Gene_expression (activity) of lipoprotein-associated phospholipase A2
16) Confidence 0.54 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1860077 Disease Relevance 0.24 Pain Relevance 0.03
We investigated the plasma levels of oxLDL and Lp-PLA2 activity as well as the autoantibody titers against mildly oxLDL in patients with early rheumatoid arthritis (ERA).
Spec (investigated) Gene_expression (levels) of Lp-PLA2 in plasma associated with rheumatoid arthritis
17) Confidence 0.24 Published 2007 Journal Arthritis Res Ther Section Abstract Doc Link PMC1860077 Disease Relevance 0.98 Pain Relevance 0.34

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