INT269064

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Context Info
Confidence 0.75
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 5
Disease Relevance 0.79
Pain Relevance 0.31

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

transport (Cybb) mitochondrion (Cybb) Golgi apparatus (Cybb)
endoplasmic reticulum (Cybb) intracellular (Cybb) cytoplasm (Cybb)
Anatomy Link Frequency
brain 8
interneurons 2
Il6 (Mus musculus)
Cybb (Mus musculus)
Pain Link Frequency Relevance Heat
GABAergic 45 97.36 Very High Very High Very High
imagery 30 96.08 Very High Very High Very High
ketamine 20 88.20 High High
Hippocampus 65 59.28 Quite High
cytokine 45 39.32 Quite Low
Inflammation 30 38.96 Quite Low
interneuron 25 5.00 Very Low Very Low Very Low
long-term potentiation 15 5.00 Very Low Very Low Very Low
anesthesia 15 5.00 Very Low Very Low Very Low
Central nervous system 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Schizophrenia 10 98.16 Very High Very High Very High
Aging 115 79.52 Quite High
Stress 5 50.56 Quite High
Cognitive Disorder 175 50.00 Quite Low
Cancer 10 42.36 Quite Low
Urological Neuroanatomy 10 39.80 Quite Low
INFLAMMATION 30 38.96 Quite Low
Disease 30 5.00 Very Low Very Low Very Low
Hypertension 10 5.00 Very Low Very Low Very Low
Diabetes Mellitus 10 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Moreover, we recently demonstrated that IL-6 can directly induce and activate Nox2 protein expression in cultured neurons[15], but in that study in young mice, acute peripheral injection of IL-6 failed to induce brain Nox2 expression.
IL-6 Positive_regulation (induce) of Gene_expression (expression) of Nox2 protein in brain
1) Confidence 0.75 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.24 Pain Relevance 0.05
Consistent with a direct effect of IL-6 on Nox2 expression, direct systemic injection of IL-6 into mice increased Nox2 protein and activity, confirming the ability of peripheral IL-6 to mediate increased Nox2 expression and superoxide production in brain.
IL-6 Positive_regulation (mediate) of Gene_expression (expression) of Nox2 in brain
2) Confidence 0.75 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.20 Pain Relevance 0.05
B-mediated transcriptional events completely prevented IL-6-mediated induction of Nox2 expression and superoxide production (Fig. 5b, c) and prevented the loss of GABAergic phenotype of PV-interneurons (Fig. 5d, e), as demonstrated by loss of PV and GAD67 immunoreactivity.
IL-6-mediated Positive_regulation (induction) of Gene_expression (expression) of Nox2 in interneurons associated with gabaergic
3) Confidence 0.54 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.06 Pain Relevance 0.12
Moreover, we recently demonstrated that IL-6 can directly induce and activate Nox2 protein expression in cultured neurons[15], but in that study in young mice, acute peripheral injection of IL-6 failed to induce brain Nox2 expression.
IL-6 Positive_regulation (activate) of Gene_expression (expression) of Nox2 protein in brain
4) Confidence 0.50 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.24 Pain Relevance 0.05
We next determined that increasing plasma IL-6 levels by direct peripheral injection of IL-6 enhances Nox2 expression and superoxide production in brain.
IL-6 Positive_regulation (enhances) of Gene_expression (expression) of Nox2 in brain
5) Confidence 0.50 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.06 Pain Relevance 0.03

General Comments

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