INT162835

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Context Info
Confidence 0.68
First Reported 2006
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 38
Total Number 38
Disease Relevance 16.09
Pain Relevance 3.02

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) oxidoreductase activity (Cybb)
Golgi apparatus (Cybb) endoplasmic reticulum (Cybb) plasma membrane (Cybb)
Anatomy Link Frequency
brain 6
macrophages 3
microglial cells 2
neuronal 2
neurons 2
Cybb (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammatory response 14 100.00 Very High Very High Very High
ketamine 69 99.80 Very High Very High Very High
cva 27 98.80 Very High Very High Very High
nMDA receptor 17 98.62 Very High Very High Very High
cytokine 217 98.04 Very High Very High Very High
GABAergic 153 96.84 Very High Very High Very High
imagery 104 96.52 Very High Very High Very High
tolerance 57 95.96 Very High Very High Very High
Hippocampus 224 95.36 Very High Very High Very High
interneuron 85 95.00 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 203 100.00 Very High Very High Very High
Brain Injury 478 99.72 Very High Very High Very High
Apoptosis 939 99.52 Very High Very High Very High
Cv General 4 Under Development 18 99.36 Very High Very High Very High
Injury 55 99.24 Very High Very High Very High
Stress 95 98.20 Very High Very High Very High
Infection 479 97.60 Very High Very High Very High
Cognitive Disorder 603 97.12 Very High Very High Very High
Mycobacterial Infection 987 97.00 Very High Very High Very High
Cancer 38 96.36 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Finally, we demonstrate in a BV-2 microglial cell line that gp91phox and/or NADPH oxidase are increased in classically activated microglial cells which are activated by IFN?.
Positive_regulation (increased) of gp91phox in microglial cells
1) Confidence 0.68 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.68 Pain Relevance 0
Some recent studies have demonstrated that expression of gp91phox increases in brain after intracerebral hemorrhage, resulting in enhanced lipid peroxidation [24,41].
Positive_regulation (increases) of gp91phox in brain associated with cv general 4 under development and cva
2) Confidence 0.68 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.86 Pain Relevance 0.23
Classically activated BV-2 increased gp91phox and p22phox
Positive_regulation (increased) of gp91phox
3) Confidence 0.68 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.16 Pain Relevance 0
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.
Positive_regulation (increased) of Nox2 protein in brain
4) Confidence 0.65 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.13 Pain Relevance 0.04
To confirm that elevation of brain IL-6 and induction of Nox2 described above led to increased Nox2-dependent superoxide production in vivo, we assessed superoxide levels using confocal imaging of dihydroethidium (DHE) oxidation to its fluorescent product (ox-DHE) in fixed brain slices prepared from DHE-injected young mice, and from DHE-injected old mice that had been treated for 7 days prior to DHE with either no drug, or with the NADPH oxidase inhibitor, apocynin, in their drinking water.
Positive_regulation (induction) of Nox2 in brain associated with imagery
5) Confidence 0.65 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0 Pain Relevance 0.11
Moreover, two chemically distinct Nox inhibitors, apocynin and AEBSF, fully blocked the age-related increase in Nox2 activity (O2 consumption) in synaptosomes prepared from old animals, and apocynin reduced synaptosomal superoxide production to levels in young synaptosomes, as well.
Positive_regulation (increase) of Nox2
6) Confidence 0.65 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.11 Pain Relevance 0.10
In addition, as predicted by our results showing that injected IL-6 induces brain Nox2, and that IL-6-/- mice lack induction of Nox2, there was preservation of these interneurons in aged IL-6-/- mice which was highly significant for CA3, and approached significance for CA1.
Positive_regulation (induction) of Nox2 in interneurons
7) Confidence 0.65 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.35 Pain Relevance 0.12
A substantial increase in Nox2 protein was observed in extracts prepared from old wild-type mice, which was absent in similar age IL-6-deficient animals (Fig. 1d, e).


Positive_regulation (increase) of Nox2 protein
8) Confidence 0.65 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.06 Pain Relevance 0.06
Collectively, these results suggest that synaptic Nox2 activity is significantly and specifically increased in aged mice.
Positive_regulation (increased) of Nox2
9) Confidence 0.65 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0 Pain Relevance 0
Several homologs of the catalytic subunit of the enzyme, gp91phox, also termed NOX2, exist (NOX1 through NOX5) [11,12].
Positive_regulation (termed) of NOX2
10) Confidence 0.49 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.55 Pain Relevance 0
Classically activated BV-2 increased gp91phox and p22phox
Positive_regulation (increased) of gp91phox
11) Confidence 0.49 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.16 Pain Relevance 0
B to induce Nox2 or p22phox has not been previously addressed.
Positive_regulation (induce) of Nox2
12) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.17 Pain Relevance 0.08
To confirm that elevation of brain IL-6 and induction of Nox2 described above led to increased Nox2-dependent superoxide production in vivo, we assessed superoxide levels using confocal imaging of dihydroethidium (DHE) oxidation to its fluorescent product (ox-DHE) in fixed brain slices prepared from DHE-injected young mice, and from DHE-injected old mice that had been treated for 7 days prior to DHE with either no drug, or with the NADPH oxidase inhibitor, apocynin, in their drinking water.
Positive_regulation (increased) of Nox2 in brain associated with imagery
13) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0 Pain Relevance 0.11
The specificity of SN50 has previously been confirmed in these same cultures by EMSA using an inactive peptide, SN50M.[37] These results suggest that Nox2 activation/induction is dependent on NF?
Positive_regulation (induction) of Nox2
14) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.14 Pain Relevance 0.12
B and the activation of superoxide production by Nox2, we utilized a primary neuronal culture system we previously described as responding to ketamine with IL-6-dependent induction and activation of Nox2[15].
Positive_regulation (induction) of Nox2 in neuronal associated with ketamine
15) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.05 Pain Relevance 0.11
We have recently reported that blockade of NMDA receptors by the drug-of-abuse, and dissociative anesthetic ketamine leads to increased Nox2 activity in brain, and is associated with damage to parvalbumin-positive (PV) GABAergic inhibitory interneurons[18].
Positive_regulation (increased) of Nox2 in inhibitory interneurons associated with ketamine, gabaergic and nmda receptor
16) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.25 Pain Relevance 0.27
The role of IL-6 in mediating age-related induction of neuronal Nox2 was then examined in old IL-6-/- mice, and in wild-type mice treated directly with IL-6.
Positive_regulation (induction) of Nox2 in neuronal
17) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.06 Pain Relevance 0
Gp91phox is upregulated in the peri-contusional region after traumatic brain injury
Positive_regulation (upregulated) of Gp91phox in brain associated with brain injury
18) Confidence 0.45 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.51 Pain Relevance 0
The data indicate that gp91phox increased in the ipsilateral hemisphere following TBI stress.
Positive_regulation (increased) of gp91phox associated with stress and brain injury
19) Confidence 0.45 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.89 Pain Relevance 0
Protein levels of gp91phox were not increased after TBI in the contralateral hemisphere of Wt mice.
Neg (not) Positive_regulation (increased) of gp91phox associated with brain injury
20) Confidence 0.45 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.73 Pain Relevance 0

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