INT34770

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Context Info
Confidence 0.41
First Reported 1986
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 16
Total Number 17
Disease Relevance 8.52
Pain Relevance 5.21

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

plasma membrane (PTGIR) cell-cell signaling (PTGIR) signal transducer activity (PTGIR)
Anatomy Link Frequency
platelet 3
endothelial cells 1
osteoblasts 1
vessels 1
PTGIR (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 292 99.32 Very High Very High Very High
Inflammation 153 98.80 Very High Very High Very High
agonist 58 98.60 Very High Very High Very High
COX-2 inhibitor 45 98.36 Very High Very High Very High
IPN 9 95.36 Very High Very High Very High
diclofenac 175 92.48 High High
antagonist 9 92.40 High High
Inflammatory response 19 90.96 High High
aspirin 108 90.20 High High
licofelone 8 87.76 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 223 98.80 Very High Very High Very High
Stress 22 98.80 Very High Very High Very High
Atherosclerosis 17 98.52 Very High Very High Very High
Pre-eclampsia 5 98.16 Very High Very High Very High
Myocardial Infarction 54 97.12 Very High Very High Very High
Cough 61 97.08 Very High Very High Very High
Pressure And Volume Under Development 87 97.04 Very High Very High Very High
Asthma 33 96.72 Very High Very High Very High
Hemorrhage 42 96.40 Very High Very High Very High
Increased Venous Pressure Under Development 19 95.80 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In preeclampsia this equilibrium, which is particularly marked in the placenta and region of the foetal vessels, is disturbed with decreasing PGI2.
Negative_regulation (decreasing) of PGI2 in vessels associated with pre-eclampsia
1) Confidence 0.41 Published 1986 Journal Geburtshilfe Frauenheilkd Section Abstract Doc Link 3082707 Disease Relevance 0.75 Pain Relevance 0.06
These findings suggest that inhibition of COX-2-dependent prostacyclin might contribute to acceleration of atherogenesis in patients taking traditional nonsteroidal antiinflammatory drugs (NSAIDs) and NSAIDs selective for COX-2 through downregulation of HO-1, which halts TNF-alpha generation in human endothelial cells.
Negative_regulation (inhibition) of prostacyclin in endothelial cells associated with inflammation, atherosclerosis and cinod
2) Confidence 0.17 Published 2009 Journal Circ. Res. Section Abstract Doc Link 19122175 Disease Relevance 0.83 Pain Relevance 0.37
The use of these biochemical markers together with genetic biomarkers will help to select patients uniquely susceptible to developing CV risk through inhibition of COX-2-dependent-prostacyclin when exposed to NSAIDs.
Negative_regulation (inhibition) of prostacyclin associated with cinod
3) Confidence 0.14 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2621416 Disease Relevance 0 Pain Relevance 0.42
Similarly to inhibition of prostacyclin biosynthesis or activity, the novel imidazole-based HO-1 inhibitor QC15 reversed TNF-alpha reduction by LSS.
Negative_regulation (inhibition) of prostacyclin associated with stress
4) Confidence 0.12 Published 2009 Journal Circ. Res. Section Abstract Doc Link 19122175 Disease Relevance 0.84 Pain Relevance 0.37
Overall, our data support the conclusion that inhibition of PGI2 formation or action may be a novel treatment for chronic non-productive cough in asthmatic airway, especially in cough variant asthma or cough predominant asthma with normal baseline pulmonary function.
Negative_regulation (inhibition) of PGI2 associated with asthma and cough
5) Confidence 0.12 Published 2007 Journal Cough Section Body Doc Link PMC1781075 Disease Relevance 1.57 Pain Relevance 0.03
Moreover adult osteoblasts lose the IP receptor when these cells are trapped in the bone matrix.
Negative_regulation (lose) of IP receptor in osteoblasts
6) Confidence 0.11 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2592809 Disease Relevance 0.62 Pain Relevance 0.30
The increased incidence of thrombotic events associated with profound inhibition of COX-2-dependent prostacyclin can be mitigated, even if not removed, by a complete suppression of platelet COX-1 activity.
Negative_regulation (inhibition) of prostacyclin in platelet
7) Confidence 0.11 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2621416 Disease Relevance 0.16 Pain Relevance 0.28
A plausible mechanism in increased risk of vascular events in individuals treated with NSAIDs selective for COX-2 and some tNSAIDs is the inhibition of COX-2-dependent prostacyclin unaccompanied by inhibition of COX-1-dependent TXA2 at functional range, ie >95%.
Negative_regulation (inhibition) of prostacyclin associated with cinod
8) Confidence 0.11 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2621416 Disease Relevance 0.26 Pain Relevance 0.23
In this context, even an incomplete inhibition of COX-1 might attenuate the functional effect derived from inhibition of COX-2-dependent prostacyclin.
Negative_regulation (inhibition) of prostacyclin
9) Confidence 0.11 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2621416 Disease Relevance 0.34 Pain Relevance 0.35
A linear relationship exists between the extent of inhibition of COX-2 and that of prostacyclin in vivo (Patrignani et al 2008a).
Negative_regulation (inhibition) of prostacyclin
10) Confidence 0.11 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2621416 Disease Relevance 0.37 Pain Relevance 0.37
The increased incidence of thrombotic events associated with profound inhibition of COX-2-dependent prostacyclin by coxibs and tNSAIDs can be mitigated, even if not obliterated, by a complete suppression of platelet COX-1 activity.
Negative_regulation (inhibition) of prostacyclin in platelet
11) Confidence 0.11 Published 2008 Journal Therapeutics and Clinical Risk Management Section Abstract Doc Link PMC2621416 Disease Relevance 0.24 Pain Relevance 0.38
Thus, naproxen is associated with profound inhibition of prostacyclin but the possible CV hazard associated with this effect may be mitigated by a parallel profound and persistent suppression of platelet TXA2 (Capone et al 2004), which translates into a small CV protection or neutral effect (Hernández-Díaz et al 2006; Kearney et al 2006).
Negative_regulation (inhibition) of prostacyclin in platelet
12) Confidence 0.11 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2621416 Disease Relevance 0.13 Pain Relevance 0.36
Cardiovascular side effects have been found in selective COX-2 inhibitors (Rahman and Khan, 2004; Singh, 2004; Solomon et al, 2005), presumably due to the decrease in PGI2/TXA2.
Negative_regulation (decrease) of PGI2 associated with cox-2 inhibitor
13) Confidence 0.08 Published 2008 Journal Mol Syst Biol Section Body Doc Link PMC2673713 Disease Relevance 0.44 Pain Relevance 0.45
In our simulation, the value of PGI2/TXA2 was observed to decrease.
Negative_regulation (value) of PGI2
14) Confidence 0.06 Published 2008 Journal Mol Syst Biol Section Body Doc Link PMC2673713 Disease Relevance 0.46 Pain Relevance 0.34
isoforms suggest that such inhibitory responses of prostacyclin and NO are mediated, at least in part, directly at the level of TP?
Negative_regulation (responses) of prostacyclin
15) Confidence 0.03 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.08
isoforms, respectively, suggest that such inhibitory responses of prostacyclin and NO are mediated, at least in part, at the interface of the stimulatory GPCR (i.e. the TP).
Negative_regulation (responses) of prostacyclin
16) Confidence 0.03 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.03
Moreover, animal models lacking the PGE2 prostaglandin receptor demonstrate a reduced algesic response indicating the importance of prostanoids in the signaling and perception of inflammatory pain [3].
Negative_regulation (lacking) of prostaglandin receptor associated with ipn
17) Confidence 0.02 Published 2005 Journal Cell Commun Signal Section Body Doc Link PMC1198236 Disease Relevance 1.50 Pain Relevance 0.79

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