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Context Info
Confidence 0.66
First Reported 1997
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 5
Disease Relevance 3.79
Pain Relevance 0.58

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

peptidase activity (F2) extracellular space (F2) extracellular region (F2)
Anatomy Link Frequency
platelets 4
muscle 2
F2 (Mus musculus)
Pain Link Frequency Relevance Heat
tetrodotoxin 4 96.16 Very High Very High Very High
Kinase C 225 88.96 High High
imagery 3 67.84 Quite High
antagonist 3 58.04 Quite High
cva 3 55.88 Quite High
Inflammation 1 24.00 Low Low
Pain 4 22.56 Low Low
Bioavailability 2 14.76 Low Low
Potency 4 5.00 Very Low Very Low Very Low
agonist 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hemolytic Anemia 11 98.68 Very High Very High Very High
Thrombophilia 6 94.72 High High
Sickle Cell Anemia 27 92.80 High High
Hypertension 62 92.52 High High
Myocardial Infarction 2 91.92 High High
Hemolysis 16 91.72 High High
Thalassemia 25 90.00 High High
Stroke 2 89.92 High High
Atherosclerotic Plaque 1 88.24 High High
Rupture 1 87.08 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The application of ACh to electrically blocked muscle cultures resulted in a 2.5-fold increase in thrombin activity released into the medium and a 2-fold increase in prothrombin gene expression.
Positive_regulation (increase) of Gene_expression (expression) of prothrombin in muscle
1) Confidence 0.66 Published 1997 Journal Brain Res. Dev. Brain Res. Section Abstract Doc Link 9125468 Disease Relevance 0 Pain Relevance 0.39
Setty et al. [19] has reported increased tissue factor expression and thrombin generation induced by free heme.
Positive_regulation (increased) of Gene_expression (expression) of thrombin
2) Confidence 0.16 Published 2010 Journal F1000 Med Rep Section Body Doc Link PMC2948405 Disease Relevance 2.44 Pain Relevance 0
In vitro studies indicate that platelets mediate thrombin generation and coagulation by exposing phosphatidylserine (PS) on their membrane surface following prolonged increases in cytosolic Ca2+ [7], [8], [9].
Positive_regulation (mediate) of Gene_expression (generation) of thrombin in platelets
3) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2861630 Disease Relevance 0.31 Pain Relevance 0.03
It dissociates from vWF, interacts with negatively charged phospholipids on the surface of activated platelets, and acts as a cofactor for factor IXa in the activation of factor X.1 This in turn leads to the generation of substantial amounts of thrombin, the key enzyme in the coagulation cascade, and to the generation of a hemostatic plug.
Positive_regulation (leads) of Gene_expression (generation) of thrombin in platelets
4) Confidence 0.06 Published 2010 Journal Int J Nanomedicine Section Body Doc Link PMC2939703 Disease Relevance 0.60 Pain Relevance 0.03
In addition, sustained intracellular calcium signaling induces phosphatidylserine (PS)4 exposure, which accelerates thrombin generation and coagulation.
Positive_regulation (accelerates) of Gene_expression (generation) of thrombin
5) Confidence 0.06 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2906332 Disease Relevance 0.44 Pain Relevance 0.12

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