INT115690

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.47
First Reported 2004
Last Reported 2005
Negated 0
Speculated 1
Reported most in Abstract
Documents 1
Total Number 3
Disease Relevance 0.72
Pain Relevance 3.63

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

nucleus (Prkcg, Fos) response to stress (Prkcg, Fos) cytosol (Prkcg)
aging (Fos) nucleolus (Fos) plasma membrane (Prkcg)
Anatomy Link Frequency
nucleus 6
Prkcg (Rattus norvegicus)
Fos (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Morphine 33 100.00 Very High Very High Very High
Kinase C 19 100.00 Very High Very High Very High
withdrawal 16 100.00 Very High Very High Very High
Glutamate receptor 2 99.20 Very High Very High Very High
medulla 6 95.08 Very High Very High Very High
antagonist 1 92.00 High High
addiction 2 88.64 High High
cerebral cortex 1 88.64 High High
Thalamus 1 78.48 Quite High
narcan 7 76.56 Quite High
Disease Link Frequency Relevance Heat
Toxocariasis 10 94.56 High High
Attention Deficit Hyperactivity Disorder 2 84.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Because activation of protein kinase C (PKC) may occur following the activation of glutamate receptors, we determined whether pharmacological inhibition of PKC would attenuate morphine-induced c-Fos expression, and whether acute administration of morphine would induce translocation of PKC.
Spec (476) Negative_regulation (inhibition) of PKC Spec (whether) Negative_regulation (attenuate) of Spec (whether) Gene_expression (expression) of c-Fos associated with kinase c, glutamate receptor and morphine
1) Confidence 0.47 Published 2004 Journal Brain Res. Bull. Section Abstract Doc Link 14709343 Disease Relevance 0 Pain Relevance 1.24
The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate morphine withdrawal-induced c-Fos expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
Negative_regulation (inhibition) of PKC in nucleus Negative_regulation (attenuate) of Gene_expression (expression) of Fos in nucleus associated with medulla, kinase c, toxocariasis, withdrawal and morphine
2) Confidence 0.43 Published 2005 Journal J. Neurochem. Section Abstract Doc Link 16190878 Disease Relevance 0.36 Pain Relevance 1.20
The present study was designed to investigate the role of protein kinase C (PKC) in this process by estimating changes in PKCalpha and PKCgamma immunoreactivity, and whether pharmacological inhibition of PKC would attenuate morphine withdrawal-induced c-Fos expression and changes in tyrosine hydroxylase (TH) immunoreactivity levels in the PVN and nucleus tractus solitarius/ ventrolateral medulla (NTS/VLM).
Negative_regulation (inhibition) of PKC in nucleus Negative_regulation (attenuate) of in PVN Gene_expression (expression) of Fos in nucleus associated with medulla, kinase c, toxocariasis, withdrawal and morphine
3) Confidence 0.15 Published 2005 Journal J. Neurochem. Section Abstract Doc Link 16190878 Disease Relevance 0.36 Pain Relevance 1.20

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox