INT140659

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Context Info
Confidence 0.49
First Reported 2007
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 3
Total Number 3
Disease Relevance 0.68
Pain Relevance 2.18

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

cytosol (Trpv1) nucleoplasm (Phax) RNA binding (Phax)
plasma membrane (Trpv1) nucleus (Phax) lipid metabolic process (Trpv1)
Anatomy Link Frequency
nerve 2
synapse 1
Phax (Rattus norvegicus)
Trpv1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
qutenza 39 100.00 Very High Very High Very High
Glutamate 2 100.00 Very High Very High Very High
Analgesic 3 99.76 Very High Very High Very High
substantia gelatinosa 4 99.68 Very High Very High Very High
agonist 7 99.04 Very High Very High Very High
Inflammation 17 97.92 Very High Very High Very High
tetrodotoxin 1 94.80 High High
antagonist 8 93.92 High High
dorsal root ganglion 25 90.44 High High
Cancer pain 1 87.80 High High
Disease Link Frequency Relevance Heat
Hypersensitivity 11 98.92 Very High Very High Very High
INFLAMMATION 18 97.92 Very High Very High Very High
Ganglion Cysts 27 90.44 High High
Bone Cancer 3 87.60 High High
Inflammatory Pain 1 85.44 High High
Pain 10 83.32 Quite High
Paralysis 1 54.60 Quite High
Nociception 9 5.00 Very Low Very Low Very Low
Death 4 5.00 Very Low Very Low Very Low
Depression 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
RTX enhances the spontaneous release of L-glutamate from nerve terminals with similar efficacy as capsaicin and produces a membrane depolarization by activating TRPV1 in the SG, with fast desensitization and slow recovery from desensitization.
RTX Positive_regulation (activating) of TRPV1 in nerve associated with substantia gelatinosa, glutamate and qutenza
1) Confidence 0.49 Published 2009 Journal Neuroscience Section Abstract Doc Link 19778582 Disease Relevance 0 Pain Relevance 1.04
However, when TRPV1 containing nerve endings were initially activated by RTX, the release of mediators may have affected SAR discharges.
RTX Positive_regulation (activated) of TRPV1 in nerve
2) Confidence 0.12 Published 2007 Journal Auton Neurosci Section Abstract Doc Link 17169618 Disease Relevance 0.05 Pain Relevance 0.03
The analgesic effects of RTX treatment arise from its ability to activate TRPV1 in a slow and sustained manner, leading to block of transmission at the first sensory synapse in the short-term and nerve terminal ablation in the long-term.


RTX Positive_regulation (activate) of TRPV1 in synapse associated with analgesic
3) Confidence 0.08 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2737142 Disease Relevance 0.62 Pain Relevance 1.12

General Comments

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