INT152876

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Context Info
Confidence 0.34
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Abstract
Documents 1
Total Number 1
Disease Relevance 0.28
Pain Relevance 0.87

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

Golgi apparatus (Cav2) mitochondrion organization (Cav2) intracellular (Cav2)
protein complex (Cav2) cytoplasm (Cav2) cytosol (Cav2)
Anatomy Link Frequency
spinal cord 1
Cav2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
nav1.8 1 100.00 Very High Very High Very High
Nav1.7 1 100.00 Very High Very High Very High
nav1.3 1 100.00 Very High Very High Very High
substance P 1 98.16 Very High Very High Very High
Neuropathic pain 3 97.94 Very High Very High Very High
Spinal cord 1 97.16 Very High Very High Very High
nMDA receptor 1 96.12 Very High Very High Very High
Preemptive analgesia 1 71.56 Quite High
Analgesic 3 53.04 Quite High
Pain 1 52.08 Quite High
Disease Link Frequency Relevance Heat
Neuropathic Pain 3 97.94 Very High Very High Very High
Pain 3 52.08 Quite High
Nervous System Injury 1 43.32 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Suppression of neuropathic pain-related behavior was likely caused by a combination of mechanisms reported for ralfinamide, including inhibition of Na+ and Ca++ currents in Nav1.3, Nav1.7, Nav1.8, and Cav2.2 channels in rat DRG neurons, inhibition of substance P release from spinal cord synaptosomes, NMDA receptor antagonism and neuroprotection.
Negative_regulation (inhibition) of Cav2 in spinal cord associated with nav1.3, nmda receptor, neuropathic pain, nav1.8, nav1.7, spinal cord and substance p
1) Confidence 0.34 Published 2008 Journal Pain Section Abstract Doc Link 18583049 Disease Relevance 0.28 Pain Relevance 0.87

General Comments

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