INT27492

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.50
First Reported 1989
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 5
Disease Relevance 2.07
Pain Relevance 0.68

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

Anatomy Link Frequency
dorsal 1
neurons 1
Swd1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Pyramidal cell 1 99.76 Very High Very High Very High
depression 5 98.86 Very High Very High Very High
Glutamate receptor 8 95.40 Very High Very High Very High
sodium channel 2 94.68 High High
Pain 4 92.12 High High
Hippocampus 2 90.72 High High
Glutamate 4 74.64 Quite High
Thalamus 26 65.84 Quite High
GABA receptor 2 53.72 Quite High
antagonist 4 52.56 Quite High
Disease Link Frequency Relevance Heat
Hypersomnia 174 99.64 Very High Very High Very High
Depression 5 98.86 Very High Very High Very High
Sprains And Strains 40 98.50 Very High Very High Very High
Congenital Anomalies 8 96.64 Very High Very High Very High
Absence Epilepsy 30 96.58 Very High Very High Very High
Pain 3 92.12 High High
Sleep Disorders 106 90.56 High High
Apnoea 88 72.12 Quite High
Convulsion 10 55.72 Quite High
Targeted Disruption 18 53.72 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In this report we show that a prolonged and substantial depression of the dorsal hippocampal CA1 pyramidal cell population spike is produced by a brief but intense noxious stimulus applied to the tail of lightly anaesthetized rats.
Gene_expression (produced) of spike in dorsal associated with depression and pyramidal cell
1) Confidence 0.50 Published 1989 Journal Pain Section Abstract Doc Link 2616183 Disease Relevance 0.28 Pain Relevance 0.36
SWD studies
Gene_expression (studies) of SWD
2) Confidence 0.04 Published 2008 Journal Drug design, development and therapy Section Body Doc Link PMC2761173 Disease Relevance 0.36 Pain Relevance 0
In the SWD studies, men and women (18–60 years) who were diagnosed with SWD and had excessive sleepiness during the night shift were eligible.
Gene_expression (diagnosed) of SWD associated with hypersomnia
3) Confidence 0.04 Published 2008 Journal Drug design, development and therapy Section Body Doc Link PMC2761173 Disease Relevance 0.78 Pain Relevance 0
We expect that increased excitation in the thalamic reticular nucleus increases the ability of the thalamocortical circuit to activate the reticular neurons, thus producing the powerful inhibitory drive necessary for SWD generation.
Gene_expression (generation) of SWD in neurons
4) Confidence 0.02 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.13 Pain Relevance 0.14
The function or expression of other ion channels, including sodium channels, and ionotropic glutamate receptors, may be altered in other rodent models of absence epilepsy, such as the GAERS and WAG/Rij rats (16), but they are not known to be mutated in these strains, in which the SWD have a polygenic etiology (17,18) and their role in the generation of SWD is unknown.
Gene_expression (generation) of SWD associated with glutamate receptor, sodium channel, sprains and strains and absence epilepsy
5) Confidence 0.02 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.52 Pain Relevance 0.17

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox