INT280943

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Context Info
Confidence 0.04
First Reported 2009
Last Reported 2009
Negated 0
Speculated 2
Reported most in Body
Documents 1
Total Number 6
Disease Relevance 5.59
Pain Relevance 1.70

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
precursor cells 1
stem 1
microglia 1
neurogenic regions 1
Inhbe (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 450 99.76 Very High Very High Very High
Hippocampus 210 98.64 Very High Very High Very High
Central nervous system 126 82.88 Quite High
Spinal cord 6 81.28 Quite High
cINOD 156 80.96 Quite High
Inflammatory response 60 73.60 Quite High
Inflammatory stimuli 6 58.16 Quite High
antagonist 48 51.76 Quite High
cytokine 84 44.16 Quite Low
Intracerebroventricular 24 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Neurodegenerative Disease 768 99.76 Very High Very High Very High
INFLAMMATION 534 99.76 Very High Very High Very High
Gliosis 138 94.96 High High
Injury 60 93.44 High High
Convulsion 12 81.96 Quite High
Frailty 6 81.56 Quite High
Disease 42 80.76 Quite High
Hypertrophy 24 34.00 Quite Low
Stroke 12 31.36 Quite Low
Death 24 9.04 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In other words, it appears that interactions in the cellular microenvironment critically define the effect of activin A on neurogenesis.
Regulation (effect) of activin associated with neurodegenerative disease
1) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.95 Pain Relevance 0.19
We also investigated the effect of activin A on microglial populations in animals that received no KA.
Spec (investigated) Regulation (effect) of activin
2) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.17 Pain Relevance 0.16
We, therefore, investigated the effects of activin A on microglial responses in the neurogenic regions, the DG and pPV, 42 days after the KA-induced neurodegeneration (Fig. 4A, 4B).
Spec (investigated) Regulation (effects) of activin in neurogenic regions
3) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 0.62 Pain Relevance 0.18
However, although this would be important in terms of facilitating the neurogenesis after neurodegeneration, the data shown in Figure 7G make it clear that a direct effect of activin A on stem/precursor cells is not an essential requirement for neurogenesis after neurodegeneration.
Regulation (effect) of activin in precursor cells associated with neurodegenerative disease
4) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 1.34 Pain Relevance 0.31
Given the evidence for TLR4 activation in degenerative conditions [26, 29, 36, 37], it is feasible that the effect of activin A on inflammation following excitotoxic neurodegeneration may also result from inhibition of TLR4-mediated signaling in microglia.
Regulation (effect) of activin in microglia associated with inflammation
5) Confidence 0.04 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 1.17 Pain Relevance 0.55
However, although this would be important in terms of facilitating the neurogenesis after neurodegeneration, the data shown in Figure 7G make it clear that a direct effect of activin A on stem/precursor cells is not an essential requirement for neurogenesis after neurodegeneration.
Regulation (effect) of activin in stem associated with neurodegenerative disease
6) Confidence 0.01 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733378 Disease Relevance 1.34 Pain Relevance 0.31

General Comments

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