INT280945

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Context Info
Confidence 0.06
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 8
Disease Relevance 7.07
Pain Relevance 2.31

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
bars 2
neurons 2
astrocytes 2
Inhbe (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 600 100.00 Very High Very High Very High
Hippocampus 280 100.00 Very High Very High Very High
cINOD 208 97.24 Very High Very High Very High
antagonist 64 96.96 Very High Very High Very High
ischemia 8 96.40 Very High Very High Very High
cytokine 112 96.32 Very High Very High Very High
Pyramidal cell 16 71.60 Quite High
Central nervous system 168 65.12 Quite High
Intracerebroventricular 32 53.68 Quite High
Inflammatory response 80 47.12 Quite Low
Disease Link Frequency Relevance Heat
Neurodegenerative Disease 1024 100.00 Very High Very High Very High
INFLAMMATION 712 100.00 Very High Very High Very High
Transient Ischemic Attack 8 97.16 Very High Very High Very High
Hypoxia 8 95.88 Very High Very High Very High
Death 32 92.48 High High
Gliosis 184 81.88 Quite High
Injury 80 81.48 Quite High
Nervous System Inflammation 8 64.48 Quite High
Disease 56 46.20 Quite Low
Chronic Disease 16 33.92 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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 Gene_expression (expression) of activin in neurons associated with transient ischemic attack, hypoxia, ischemia and hippocampus
1) Confidence 0.06 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.98 Pain Relevance 0.26
In summary, neurogenesis after neurodegeneration requires expression of activin A (Fig. 7H).
Positive_regulation (requires) of Gene_expression (expression) of activin associated with neurodegenerative disease
2) Confidence 0.06 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 1.15 Pain Relevance 0.49
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 Gene_expression (expression) of activin in astrocytes associated with inflammation
3) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 1.03 Pain Relevance 0.56
Thus, progression of neurogenesis after neurodegeneration requires the presence of an anti-inflammatory agent, either endogeneously expressed activin A or, in its absence, an exogenously administered anti-inflammatory agent.
Positive_regulation (requires) of Gene_expression (expressed) of activin associated with inflammation and neurodegenerative disease
4) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 1.29 Pain Relevance 0.38
We confirmed that KA-induced neurodegeneration leads to expression of activin A.
Positive_regulation (leads) of Gene_expression (expression) of activin
5) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 1.19 Pain Relevance 0.32
We show for the first time that this activin A expression is essential for neurogenesis to proceed following neurodegeneration.
Positive_regulation (essential) of Gene_expression (expression) of activin associated with neurodegenerative disease
6) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Abstract Doc Link PMC2733378 Disease Relevance 0.62 Pain Relevance 0.13
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 (up) of Gene_expression (makes) of activin
7) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.37 Pain Relevance 0.06
(D): There was, however, increased neurogenesis in the DG, CA3, and CA1 regions of the dorsal intact hippocampus in activin A-treated animals (n = 10, gray bars), whereas (FS-288)-treated animals had no effect on neurogenesis (n = 10, black bars) compared to controls (n = 10, white bars).
Positive_regulation (increased) of Gene_expression (regions) of activin in bars associated with hippocampus and neurodegenerative disease
8) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.44 Pain Relevance 0.11

General Comments

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