INT267189

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Context Info
Confidence 0.68
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 2.49
Pain Relevance 0.03

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

nucleus (Hspb8) intracellular (Hspb8) response to stress (Hspb8)
cytoplasm (Hspb8)
Hspb8 (Mus musculus)
Pain Link Frequency Relevance Heat
fibrosis 10 52.72 Quite High
Central nervous system 2 19.12 Low Low
anesthesia 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 192 99.40 Very High Very High Very High
Coronary Heart Disease 60 94.64 High High
Muscular Atrophy 12 90.08 High High
Neurodegenerative Disease 8 84.12 Quite High
Alzheimer's Dementia 64 82.76 Quite High
Stress 12 72.48 Quite High
Toxicity 8 71.12 Quite High
Death 24 55.76 Quite High
Hypertrophy 2 54.80 Quite High
Fibrosis 10 52.72 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In contrast to NTG mice, GGA treatment markedly enhanced the induction of HSPB8 and HSPB1 in R120G TG mice (Figure 2D and E) with a slight induction of HSP70 (Figure 2D and E).
Positive_regulation (enhanced) of Positive_regulation (induction) of HSPB8 associated with targeted disruption
1) Confidence 0.68 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.54 Pain Relevance 0.03
In the model tested here, we found that long-term treatment with GGA results in HSPB8 induction and a similar level of overexpression of HSPB8 via transgenic manipulation recapitulates the protective effect of GGA in HSPB5 R120G cardiomyopathy.
Positive_regulation (results) of Positive_regulation (induction) of HSPB8 associated with targeted disruption and coronary heart disease
2) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 0.94 Pain Relevance 0

General Comments

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