INT119446

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.58
First Reported 2005
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 7
Disease Relevance 6.47
Pain Relevance 3.72

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

signal transduction (Gnb5) plasma membrane (Gnb5) nucleus (Gnb5)
signal transducer activity (Gnb5)
Anatomy Link Frequency
PAG 2
plasma 1
peripheral nerves 1
striatum 1
Gnb5 (Mus musculus)
Pain Link Frequency Relevance Heat
Morphine 21 98.80 Very High Very High Very High
Thalamus 9 97.92 Very High Very High Very High
Central grey 3 97.52 Very High Very High Very High
Opioid 12 96.60 Very High Very High Very High
Demyelination 5 81.04 Quite High
Analgesic 3 79.64 Quite High
tolerance 6 78.96 Quite High
Intracerebroventricular 3 76.48 Quite High
addiction 3 64.40 Quite High
Neuritis 8 51.00 Quite High
Disease Link Frequency Relevance Heat
Syndrome 167 100.00 Very High Very High Very High
Infection 23 99.72 Very High Very High Very High
Urological Neuroanatomy 12 99.04 Very High Very High Very High
Immunization 8 98.56 Very High Very High Very High
Neuropathy 58 95.48 Very High Very High Very High
Guillain-barre Syndrome 19 94.16 High High
Disease 43 89.84 High High
Neuropathic Pain 24 89.68 High High
Paralysis 10 87.92 High High
Demyelinating Disease 9 81.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In post-dependent mice, the increases in RGS-R7 and Gbeta5 mRNA still persisted in the PAG and striatum at 8 and 16 days after starting the chronic opioid treatment.
Positive_regulation (increases) of Gbeta5 mRNA in PAG associated with urological neuroanatomy and opioid
1) Confidence 0.58 Published 2005 Journal Neuropsychopharmacology Section Abstract Doc Link 15199376 Disease Relevance 0.38 Pain Relevance 1.25
At 2 days after commencing sustained morphine treatment, the levels of mRNA for RGS7, RGS9-2, RGS11, and Gbeta5 increased in most of the brain structures studied (striatum, thalamus, periaqueductal gray matter (PAG), and cortex).
Positive_regulation (increased) of Gbeta5 in gray matter associated with urological neuroanatomy, thalamus, central grey and morphine
2) Confidence 0.42 Published 2005 Journal Neuropsychopharmacology Section Abstract Doc Link 15199376 Disease Relevance 0.35 Pain Relevance 1.07
In post-dependent mice, the increases in RGS-R7 and Gbeta5 mRNA still persisted in the PAG and striatum at 8 and 16 days after starting the chronic opioid treatment.
Positive_regulation (increases) of Gbeta5 mRNA in striatum associated with urological neuroanatomy and opioid
3) Confidence 0.20 Published 2005 Journal Neuropsychopharmacology Section Abstract Doc Link 15199376 Disease Relevance 0.38 Pain Relevance 1.25
There is convincing evidence that GBS at least in some patients is caused by an infection-induced aberrant immune response that damages the peripheral nerves.
Positive_regulation (caused) of GBS in peripheral nerves associated with syndrome and infection
4) Confidence 0.06 Published 2010 Journal J Clin Immunol Section Body Doc Link PMC2883091 Disease Relevance 1.42 Pain Relevance 0
An experimental animal model of GBS induced by inoculation of GM1 ganglioside confirms the role of anti-GM1 antibodies in the immunopathogenesis of GBS [12].
Positive_regulation (induced) of GBS associated with syndrome
5) Confidence 0.04 Published 2010 Journal J Med Case Reports Section Body Doc Link PMC2852392 Disease Relevance 1.22 Pain Relevance 0.03
Autoantibodies are considered to be the pathogenic components which trigger GBS because plasma exchange is proven to be an effective treatment in GBS [9].
Positive_regulation (trigger) of GBS in plasma associated with syndrome
6) Confidence 0.02 Published 2011 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC3010740 Disease Relevance 1.74 Pain Relevance 0.05
The most straightforward way of verifying that molecular mimicry between microbes and autoantigens cause GBS is to establish a GBS model by the immunization of animals with components of antecedent infectious agents.
Positive_regulation (cause) of GBS associated with syndrome and immunization
7) Confidence 0.02 Published 2011 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC3010740 Disease Relevance 0.98 Pain Relevance 0.07

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox