INT50367

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Context Info
Confidence 0.57
First Reported 1995
Last Reported 2005
Negated 0
Speculated 0
Reported most in Abstract
Documents 10
Total Number 10
Disease Relevance 5.13
Pain Relevance 2.38

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

generation of precursor metabolites and energy (COX8A) mitochondrion (COX8A) small molecule metabolic process (COX8A)
Anatomy Link Frequency
blood 1
COX8A (Homo sapiens)
Pain Link Frequency Relevance Heat
opioid receptor 3 99.98 Very High Very High Very High
cINOD 22 99.48 Very High Very High Very High
headache 1 93.52 High High
cva 16 90.80 High High
Inflammation 2 89.12 High High
agonist 3 88.64 High High
opiate 3 75.00 Quite High
Angina 3 75.00 Quite High
rheumatoid arthritis 2 66.08 Quite High
COX-2 inhibitor 1 52.88 Quite High
Disease Link Frequency Relevance Heat
Targeted Disruption 2 99.96 Very High Very High Very High
INFLAMMATION 4 98.76 Very High Very High Very High
Hemorrhage 6 98.68 Very High Very High Very High
Increased Venous Pressure Under Development 2 95.68 Very High Very High Very High
Coronary Artery Disease 5 94.60 High High
Bordatella Infection 1 93.52 High High
Headache 1 93.52 High High
Thrombosis 21 93.04 High High
Heart Rate Under Development 2 92.72 High High
Disorder Of Lipid Metabolism 1 90.92 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The conventional view that the mechanism of gastrointestinal damage is principally caused by COX-1 inhibition needs to be revised in view of recent studies using selective inhibitors of the COX enzymes and COX knockout animals.
Negative_regulation (inhibitors) of COX associated with targeted disruption
1) Confidence 0.57 Published 2003 Journal Inflammopharmacology Section Abstract Doc Link 15035790 Disease Relevance 0.53 Pain Relevance 0.43
Inhibition of the COX isozymes by nonsteroidal anti-inflammatory drugs (NSAIDs) or COX-2 selective inhibitors may therefore influence hemostasis and the risk of CHD.
Negative_regulation (Inhibition) of COX associated with coronary artery disease, inflammation and cinod
2) Confidence 0.57 Published 2001 Journal Clin. Exp. Rheumatol. Section Abstract Doc Link 11695251 Disease Relevance 0.63 Pain Relevance 0.45
CONCLUSIONS: Mechanisms other than COX inhibition may also play a role in drug intolerance in patients with CU.
Negative_regulation (inhibition) of COX
3) Confidence 0.57 Published 2003 Journal J Investig Allergol Clin Immunol Section Body Doc Link 12861852 Disease Relevance 0.07 Pain Relevance 0
In addition, we show that proteins that interfere with the activity of Gbetagamma subunits (Gbetagamma scavengers) strongly attenuate the acute inhibition of AC-I and -VIII and the superactivation of AC-I, and abolish the superactivation of AC-VIII.
Negative_regulation (inhibition) of VIII
4) Confidence 0.42 Published 2005 Journal J. Mol. Neurosci. Section Abstract Doc Link 16186630 Disease Relevance 0.09 Pain Relevance 0.20
The conventional view that the mechanism of gastrointestinal damage is principally caused by COX-1 inhibition needs to be revised in view of recent studies using selective inhibitors of the COX enzymes and COX knockout animals.
Negative_regulation (inhibitors) of COX associated with targeted disruption
5) Confidence 0.42 Published 2003 Journal Inflammopharmacology Section Abstract Doc Link 15035790 Disease Relevance 0.53 Pain Relevance 0.43
Hemostatic factors included fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2 antiplasmin, euglobulin clot lysis time, tissue plasminogen activator before and after venous occlusion, and plasminogen activator inhibitor.
Negative_regulation (inhibitor) of VIII
6) Confidence 0.42 Published 1995 Journal Am. J. Cardiol. Section Abstract Doc Link 7618616 Disease Relevance 1.31 Pain Relevance 0.15
The response can be measured by shortening of the bleeding time (BT) and of partial thromboplastin time (PTT), indicating a rise of Factor (F) VIII or von Willebrand factor (vWF).
Negative_regulation (rise) of VIII associated with hemorrhage
7) Confidence 0.42 Published 1998 Journal Semin. Thromb. Hemost. Section Abstract Doc Link 10066151 Disease Relevance 1.24 Pain Relevance 0.09
However, independently of the method used to activate specific adenylyl cyclase isozymes, acute activation of the mu-opioid receptor inhibited the activity of adenylyl cyclases I, V, VI, and VIII, while types II, IV, and VII were stimulated and type III was not affected.
Negative_regulation (inhibited) of VIII associated with opioid receptor
8) Confidence 0.42 Published 1997 Journal J. Biol. Chem. Section Abstract Doc Link 9030567 Disease Relevance 0 Pain Relevance 0.27
In human whole blood, both CINODs showed inhibition, comparable to naproxen, of both COX isozymes and slowly released naproxen.
Negative_regulation (inhibition) of COX in blood
9) Confidence 0.41 Published 2005 Journal Biochem. Pharmacol. Section Abstract Doc Link 16168964 Disease Relevance 0 Pain Relevance 0.25
It inactivates factors Va and VIIIa.
Negative_regulation (inactivates) of VIIIa
10) Confidence 0.02 Published 2004 Journal Thromb J Section Body Doc Link PMC415559 Disease Relevance 0.74 Pain Relevance 0.12

General Comments

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