INT328302

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Context Info
Confidence 0.03
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.17
Pain Relevance 0.08

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 (GH1) extracellular region (GH1)
Anatomy Link Frequency
fat 2
neurons 1
GHS (Homo sapiens)
GH1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Somatostatin 7 84.80 Quite High
adenocard 1 45.80 Quite Low
antagonist 19 5.00 Very Low Very Low Very Low
agonist 17 5.00 Very Low Very Low Very Low
Inflammation 10 5.00 Very Low Very Low Very Low
medulla 4 5.00 Very Low Very Low Very Low
cytokine 4 5.00 Very Low Very Low Very Low
tolerance 4 5.00 Very Low Very Low Very Low
Neuropeptide 3 5.00 Very Low Very Low Very Low
vagus nerve 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Growth Problems 5 99.50 Very High Very High Very High
Pancreatic Cancer 1 66.44 Quite High
Appetite Loss 13 5.20 Low Low
Targeted Disruption 17 5.00 Very Low Very Low Very Low
Obesity 15 5.00 Very Low Very Low Very Low
INFLAMMATION 12 5.00 Very Low Very Low Very Low
Stress 10 5.00 Very Low Very Low Very Low
Apoptosis 8 5.00 Very Low Very Low Very Low
Cancer 6 5.00 Very Low Very Low Very Low
Repression 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Mutational disruption of constitutive GHS-R1a activity is associated with short stature in humans [27], whereas overexpression of GHS-R1a on GHRH neurons augments postweaning growth, reduces fat mass, and augments GHRH and GH gene expression in mice [28].
Gene_expression (overexpression) of GHS in neurons Positive_regulation (augments) of Gene_expression (expression) of GH gene in fat associated with growth problems
1) Confidence 0.03 Published 2010 Journal International Journal of Peptides Section Body Doc Link PMC2925380 Disease Relevance 0.17 Pain Relevance 0.08

General Comments

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