INT129910

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Context Info
Confidence 0.05
First Reported 2005
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 5
Disease Relevance 3.84
Pain Relevance 1.07

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

extracellular region (Inhbe)
Anatomy Link Frequency
neurons 1
astrocytes 1
Inhbe (Mus musculus)
Pain Link Frequency Relevance Heat
addiction 1 100.00 Very High Very High Very High
Hippocampus 140 98.84 Very High Very High Very High
Inflammation 300 97.84 Very High Very High Very High
ischemia 4 96.40 Very High Very High Very High
cytokine 56 96.32 Very High Very High Very High
cINOD 104 77.12 Quite High
Pyramidal cell 8 71.60 Quite High
pain pelvic 2 67.16 Quite High
antagonist 32 54.72 Quite High
endometriosis 1 50.68 Quite High
Disease Link Frequency Relevance Heat
Injury 40 100.00 Very High Very High Very High
Neurodegenerative Disease 512 99.80 Very High Very High Very High
Disease 29 99.12 Very High Very High Very High
Targeted Disruption 2 98.70 Very High Very High Very High
INFLAMMATION 356 97.84 Very High Very High Very High
Transient Ischemic Attack 4 97.16 Very High Very High Very High
Hypoxia 4 95.88 Very High Very High Very High
Cyst 3 90.00 High High
Death 16 83.12 Quite High
Gliosis 92 81.88 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A second transgenic mouse model that causes loss of activin action (inhibin alpha-subunit transgenic mice) develops similar cystic structures, supporting a TGF-beta/activin/Smad2 dependence in the onset of this disease.
Positive_regulation (dependence) of activin associated with targeted disruption, addiction and disease
1) Confidence 0.05 Published 2005 Journal Endocrinology Section Abstract Doc Link 16141389 Disease Relevance 0.83 Pain Relevance 0.14
However, increased activin A expression from surviving neurons is a potent anti-inflammatory agent that inhibits proliferation and activation of microglia and either directly and/or indirectly inhibits the gliotic response by astrocytes.
Positive_regulation (increased) of activin in astrocytes associated with inflammation
2) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 1.03 Pain Relevance 0.56
Activin A is, however, expressed more than 48 hours after KA injury (supporting information Table 1) and, as shown in Figures 1 and 2, is required for neurogenesis after neurodegeneration occurs.
Positive_regulation (required) of Activin associated with injury and neurodegenerative disease
3) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.64 Pain Relevance 0.05
A number of studies have shown that activin A expression is increased in principal neurons in the hippocampus of adult rodents in models of transient cerebral ischemia and hypoxia and also after KA treatment [11–14].
Positive_regulation (increased) of activin in neurons associated with transient ischemic attack, hypoxia, ischemia and hippocampus
4) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.98 Pain Relevance 0.26
A subunit that makes up activin A increased almost 24-fold in KA-treated hippocampi compared to that in hippocampi that received a control injection, although there were essentially no changes in the expression of mRNAs encoding the ?
Positive_regulation (increased) of activin
5) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.37 Pain Relevance 0.06

General Comments

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