INT261373

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Context Info
Confidence 0.10
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 2.05
Pain Relevance 0.19

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

oxidoreductase activity (Nsdhl) structural molecule activity (Gfap) endoplasmic reticulum (Nsdhl)
extracellular matrix organization (Gfap) cytoplasm (Gfap)
Anatomy Link Frequency
glial cells 2
brain 2
Nsdhl (Mus musculus)
Gfap (Rattus norvegicus)
Pain Link Frequency Relevance Heat
antagonist 4 96.96 Very High Very High Very High
cytokine 4 95.02 Very High Very High Very High
Glutamate 6 69.44 Quite High
Anterior cingulate cortex 2 49.04 Quite Low
Hippocampus 10 34.96 Quite Low
Dopamine 70 9.88 Low Low
gABA 32 5.00 Very Low Very Low Very Low
Locus ceruleus 20 5.00 Very Low Very Low Very Low
midbrain 12 5.00 Very Low Very Low Very Low
Pain 12 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disease 52 99.64 Very High Very High Very High
Schizophrenia 440 99.32 Very High Very High Very High
Autoimmune Disease 8 96.90 Very High Very High Very High
Leukemia 2 90.88 High High
Congenital Anomalies 88 69.68 Quite High
Toxicity 8 68.64 Quite High
Alzheimer's Dementia 2 37.48 Quite Low
Attention Deficit Hyperactivity Disorder 20 16.92 Low Low
Autism 16 16.60 Low Low
Stress 28 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The increase of GFAP expression by BPA is important to schizophrenia because treatment of rat brain with the NMDA antagonist, MK-801, also increases GFAP-positive astroglial cells that are believed to play a role in schizophrenia pathology.
BPA Positive_regulation (increase) of Gene_expression (expression) of GFAP in brain associated with antagonist and schizophrenia
1) Confidence 0.10 Published 2009 Journal Schizophrenia Bulletin Section Body Doc Link PMC2643957 Disease Relevance 0.94 Pain Relevance 0.12
In a schizophrenia animal model, leukemia inhibitory factor (LIF)–treated rats have decreased motor activity and prepulse inhibition in the acoustic startle test at adolescence, an abnormality that may involve glial cells.118 LIF is a IL-6 cytokine, a class that is elevated in schizophrenia, Alzheimer's disease (AD), and autoimmune diseases.118–122 When astrocyte progenitor cells are exposed to LIF, then treated with BPA, the expression of glial fibrillary acid protein (GFAP) is enhanced.123 BPA treatment of LIF-stimulated cells enhances GFAP expression through activation of excessive “signal transducer and activator of transcription 3” (STAT3) and “mothers against decapentaplegic homolog 1” (Smad1).124 This effect on GFAP may be due to the “cross-talk” reported between STAT3 and estrogen receptor (ER) signaling.125 LIF, like BPA, also induces STAT3 phosphorylation and increases GFAP.118 A cross-talk also exists between Smad proteins and MAPKs (mentioned above under the section on cell growth) that has been linked with the pathogenesis of AD.126
BPA Positive_regulation (enhances) of Gene_expression (expression) of GFAP in glial cells associated with leukemia, autoimmune disease, disease, schizophrenia and cytokine
2) Confidence 0.10 Published 2009 Journal Schizophrenia Bulletin Section Body Doc Link PMC2643957 Disease Relevance 1.11 Pain Relevance 0.07

General Comments

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