INT323484

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Context Info
Confidence 0.27
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0.87
Pain Relevance 0.43

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

extracellular space (Ins1) signal transduction (Ghsr) extracellular region (Ins1)
plasma membrane (Ghsr) carbohydrate metabolic process (Ins1) cytoplasm (Ins1)
Anatomy Link Frequency
pancreas 2
Ghsr (Mus musculus)
Ins1 (Mus musculus)
Pain Link Frequency Relevance Heat
tolerance 36 100.00 Very High Very High Very High
antagonist 28 100.00 Very High Very High Very High
Somatostatin 8 5.00 Very Low Very Low Very Low
Kinase C 6 5.00 Very Low Very Low Very Low
vagus nerve 4 5.00 Very Low Very Low Very Low
Neurotransmitter 2 5.00 Very Low Very Low Very Low
agonist 2 5.00 Very Low Very Low Very Low
Action potential 2 5.00 Very Low Very Low Very Low
Opioid 2 5.00 Very Low Very Low Very Low
Calcium channel 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Impaired Glucose Tolerance 40 100.00 Very High Very High Very High
Disease 12 90.40 High High
Obesity 98 84.64 Quite High
Diabetes Mellitus 60 55.60 Quite High
Insulin Resistance 36 54.48 Quite High
Hyperinsulinism 20 31.92 Quite Low
Liver Failure 4 15.20 Low Low
Targeted Disruption 108 5.00 Very Low Very Low Very Low
Body Weight 18 5.00 Very Low Very Low Very Low
Appetite Loss 10 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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.
GHSR Positive_regulation (enhanced) of Localization (release) of insulin in pancreas
1) Confidence 0.27 Published 2010 Journal International Journal of Peptides Section Body Doc Link PMC2911604 Disease Relevance 0 Pain Relevance 0.03
This result, in combination with the effect of the compound on insulin secretion, demonstrates that, at least acutely, the GHSR1a antagonist YIL-781 improves glucose tolerance by promoting insulin release rather than enhancing insulin sensitivity.
GHSR1a Positive_regulation (promoting) of Localization (release) of insulin associated with antagonist, tolerance and impaired glucose tolerance
2) Confidence 0.27 Published 2010 Journal International Journal of Peptides Section Body Doc Link PMC2911604 Disease Relevance 0.87 Pain Relevance 0.41

General Comments

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