INT323480

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Context Info
Confidence 0.36
First Reported 2010
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 6
Disease Relevance 0.90
Pain Relevance 2.06

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 (Ghsr) plasma membrane (Ghsr) signal transducer activity (Ghsr)
Anatomy Link Frequency
plasma 1
pancreas 1
midbrain 1
dopamine neurons 1
Ghsr (Mus musculus)
Pain Link Frequency Relevance Heat
antagonist 174 100.00 Very High Very High Very High
Ventral tegmentum 204 99.98 Very High Very High Very High
Dopamine 219 99.36 Very High Very High Very High
tolerance 54 99.00 Very High Very High Very High
midbrain 3 97.88 Very High Very High Very High
Eae 54 96.60 Very High Very High Very High
agonist 6 81.16 Quite High
cocaine 6 74.64 Quite High
alcohol 21 66.96 Quite High
Opioid 24 59.28 Quite High
Disease Link Frequency Relevance Heat
Impaired Glucose Tolerance 60 99.00 Very High Very High Very High
Targeted Disruption 162 91.16 High High
Body Weight 33 84.72 Quite High
Sprains And Strains 3 51.08 Quite High
Hyperinsulinism 30 46.56 Quite Low
Obesity 150 38.44 Quite Low
Diabetes Mellitus 90 5.00 Very Low Very Low Very Low
Insulin Resistance 54 5.00 Very Low Very Low Very Low
Disease 18 5.00 Very Low Very Low Very Low
Appetite Loss 15 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Furthermore, GHSR blockade increased plasma insulin concentrations in gastrectomized and normal rats to a similar extent [91].
Negative_regulation (blockade) of GHSR in plasma
1) Confidence 0.36 Published 2010 Journal International Journal of Peptides Section Body Doc Link PMC2911604 Disease Relevance 0 Pain Relevance 0.03
The dose of BIM28163 (Ipsen Biomeasure Inc, Milford, MA, USA), a GHS-R1A antagonist, has also been determined previously (Halem et al. 2004; Jerlhag et al. 2009).
Negative_regulation (antagonist) of GHS-R1A associated with antagonist
2) Confidence 0.35 Published 2011 Journal Addiction Biology Section Body Doc Link PMC3015055 Disease Relevance 0.14 Pain Relevance 0.31
Mice deficient in either ghrelin, GHSR, or both showed lower glucose peak levels at a single time point (15 minutes after the injection) suggesting a slightly faster release of insulin.
Negative_regulation (deficient) of GHSR
3) Confidence 0.35 Published 2010 Journal International Journal of Peptides Section Body Doc Link PMC2911604 Disease Relevance 0.77 Pain Relevance 0.09
It was observed that the glucose-induced insulin release from the rat-perfused pancreas was markedly enhanced by blockade of GHSR and immunoneutralization of endogenous ghrelin.
Negative_regulation (blockade) of GHSR in pancreas
4) Confidence 0.35 Published 2010 Journal International Journal of Peptides Section Body Doc Link PMC2911604 Disease Relevance 0 Pain Relevance 0.03
The activation of the mesolimbic dopamine system by ghrelin may be due to the reported ability of the GHS-R1A to dimerize with the dopamine D1 receptor, both receptors expressed on dopamine neurons in the VTA, and thereby amplifies the dopamine signalling (Jiang, Betancourt & Smith 2006).
Negative_regulation (ability) of GHS-R1A in dopamine neurons associated with ventral tegmentum and dopamine
5) Confidence 0.35 Published 2011 Journal Addiction Biology Section Body Doc Link PMC3015055 Disease Relevance 0 Pain Relevance 0.75
In the present study, it was demonstrated that the actions of peripheral ghrelin on the midbrain dopamine system, reflected by locomotor stimulation and accumbal dopamine release, can be blocked by VTA administration of a GHS-R1A antagonist.
Negative_regulation (administration) of GHS-R1A in midbrain associated with ventral tegmentum, dopamine, antagonist and midbrain
6) Confidence 0.35 Published 2011 Journal Addiction Biology Section Body Doc Link PMC3015055 Disease Relevance 0 Pain Relevance 0.85

General Comments

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