INT119346

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Context Info
Confidence 0.58
First Reported 2004
Last Reported 2009
Negated 1
Speculated 0
Reported most in Body
Documents 9
Total Number 9
Disease Relevance 6.20
Pain Relevance 1.61

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
endothelial cells 2
tail 1
bladder 1
platelet 1
PTGIR (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 46 100.00 Very High Very High Very High
aspirin 25 100.00 Very High Very High Very High
cOX1 2 100.00 Very High Very High Very High
COX2 2 100.00 Very High Very High Very High
bradykinin 12 99.28 Very High Very High Very High
Pain 14 98.32 Very High Very High Very High
Inflammatory response 3 97.68 Very High Very High Very High
cINOD 52 95.24 Very High Very High Very High
agonist 22 91.24 High High
Inflammatory mediators 7 90.84 High High
Disease Link Frequency Relevance Heat
Stress 21 99.00 Very High Very High Very High
Pulmonary Hypertension 189 98.74 Very High Very High Very High
Atherosclerosis 8 98.52 Very High Very High Very High
Pressure And Volume Under Development 5 98.36 Very High Very High Very High
Pain 18 98.32 Very High Very High Very High
Cancer 9 98.28 Very High Very High Very High
Necrosis 5 98.04 Very High Very High Very High
INFLAMMATION 62 97.68 Very High Very High Very High
Increased Venous Pressure Under Development 48 97.08 Very High Very High Very High
Thrombosis 7 96.76 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Prostacyclin activation of prostanoid IP receptors may result in pain sensation, inflammatory responses, inhibition of platelet aggregation, and vasodilation in vascular tissue.
Positive_regulation (activation) of Prostacyclin in platelet associated with pain, inflammatory response and increased venous pressure under development
1) Confidence 0.58 Published 2004 Journal Eur. J. Pharmacol. Section Abstract Doc Link 15194446 Disease Relevance 0.29 Pain Relevance 0.18
Induction of prostacyclin by steady laminar shear stress suppresses tumor necrosis factor-alpha biosynthesis via heme oxygenase-1 in human endothelial cells.
Positive_regulation (Induction) of prostacyclin in endothelial cells associated with stress, aspirin, necrosis and cancer
2) Confidence 0.20 Published 2009 Journal Circ. Res. Section Title Doc Link 19122175 Disease Relevance 0.89 Pain Relevance 0.34
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.
Positive_regulation (dependent) of prostacyclin in endothelial cells associated with inflammation, atherosclerosis and cinod
3) Confidence 0.14 Published 2009 Journal Circ. Res. Section Abstract Doc Link 19122175 Disease Relevance 0.82 Pain Relevance 0.36
COX-2-dependent prostacyclin is the major pathway in vascular protection
Positive_regulation (dependent) of prostacyclin
4) Confidence 0.12 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2621416 Disease Relevance 0.48 Pain Relevance 0.06
The combination of increased prostacyclin and platelet-activating factor in the bladder circulation may result in vasodilation and increased polymorphonuclear leukocyte adherence to the endothelium and may facilitate recruitment of polymorphonuclear leukocytes to the bladder wall of patients with interstitial cystitis.
Positive_regulation (increased) of prostacyclin in bladder associated with increased venous pressure under development and interstitial cystitis
5) Confidence 0.10 Published 2005 Journal Am. J. Physiol. Renal Physiol. Section Abstract Doc Link 15561975 Disease Relevance 0.54 Pain Relevance 0.30
Even worse, it causes a cardiovascular side effect due to the induced unbalance between PGI2 and TXA2 (Wang et al, 2005).
Positive_regulation (induced) of PGI2
6) Confidence 0.06 Published 2008 Journal Mol Syst Biol Section Body Doc Link PMC2673713 Disease Relevance 0.88 Pain Relevance 0.25
In addition, the vasodilatory effect of Ang-(1–7) could be partly explained by stimulating NO or PGI2, by potentiating bradykinin via the Mas receptor [18-21], and by competing with Ang I for ACE[22]
Neg (NO) Positive_regulation (stimulating) of PGI2 associated with bradykinin
7) Confidence 0.06 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2739214 Disease Relevance 0.36 Pain Relevance 0.09
This forms the pathophysiologic basis of common treatment strategies for arterial pulmonary hypertension which attempt to achieve balance in key molecular pathways by increasing available NO and prostacyclin, or reducing the effects of endothelin-1.
Positive_regulation (increasing) of prostacyclin associated with pulmonary hypertension
8) Confidence 0.04 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2605326 Disease Relevance 1.94 Pain Relevance 0.03
is subject to regulation by both direct prostacyclin/PKA and NO/PKG-inhibition mediated through their respective phosphorylation of Ser329 and Ser331 within the unique C-tail domain of TP?
Positive_regulation (direct) of prostacyclin in tail
9) Confidence 0.02 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0

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