INT116242

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.57
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 13
Disease Relevance 8.57
Pain Relevance 1.24

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
macrophages 1
microglia 1
respiratory 1
phagocyte 1
Cybb (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 14 99.46 Very High Very High Very High
metalloproteinase 19 94.48 High High
cva 9 87.96 High High
Inflammation 126 62.72 Quite High
GABAergic 18 50.00 Quite Low
Hippocampus 26 44.80 Quite Low
imagery 12 29.92 Quite Low
cytokine 59 17.52 Low Low
fibrosis 4 16.44 Low Low
chemokine 20 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Brain Injury 159 99.20 Very High Very High Very High
Toxicity 13 99.12 Very High Very High Very High
Bacterial Infection 5 98.88 Very High Very High Very High
Infection 332 98.44 Very High Very High Very High
Death 72 98.44 Very High Very High Very High
Contusions 15 97.84 Very High Very High Very High
Ulcers 10 95.44 Very High Very High Very High
Neutrophil Disorders 15 95.36 Very High Very High Very High
Targeted Disruption 26 94.52 High High
Apoptosis 664 94.40 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Gp91phox inhibition reduces the severity of TBI in vivo
Negative_regulation (inhibition) of Gp91phox associated with brain injury
1) Confidence 0.57 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 1.03 Pain Relevance 0
Our findings indicate that gp91phox inhibition and control of microglial classically-activation might provide a new therapeutic option by suppressing ROS generation after TBI.
Negative_regulation (inhibition) of gp91phox associated with brain injury
2) Confidence 0.42 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 1.20 Pain Relevance 0.11
In gp91phox-/- mice, in situ generation of O2-and an ONOO- metabolite, 3-NT, were suppressed in microglia after TBI.
Negative_regulation (suppressed) of gp91phox in microglia associated with brain injury
3) Confidence 0.42 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2917406 Disease Relevance 0.87 Pain Relevance 0
No significant differences in toxicity (serum transaminase levels or histopathology) were observed between wild-type and mice deficient in gp91phox.
Negative_regulation (deficient) of gp91phox associated with toxicity
4) Confidence 0.40 Published 2003 Journal Free Radic. Res. Section Abstract Doc Link 14753753 Disease Relevance 0.65 Pain Relevance 0.38
In the present study, we examined the significance of superoxide produced by macrophages by comparing the toxicity of acetaminophen in wild-type mice to mice deficient in gp91phox, a critical subunit of NADPH oxidase that is the primary source of phagocytic superoxide.
Negative_regulation (deficient) of gp91phox in macrophages associated with toxicity and paracetamol
5) Confidence 0.40 Published 2003 Journal Free Radic. Res. Section Abstract Doc Link 14753753 Disease Relevance 0.54 Pain Relevance 0.36
Effects of IL-6 and IL-6 deficiency on Nox2 activity: oximetry and EPR spectroscopy in synaptosomes from IL-6-treated and IL-6-/- mice
Negative_regulation (deficiency) of Nox2
6) Confidence 0.40 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.09 Pain Relevance 0
However, there are also several recent studies supporting efficacy of apocynin as a Nox2 inhibitor[30], [41], reviewed in [42], with the use of appropriate controls.
Negative_regulation (inhibitor) of Nox2
7) Confidence 0.40 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.08 Pain Relevance 0
The classical respiratory burst is transient, since this generates sufficient amounts ROS to kill susceptible bacteria and thus reduce NOX2 activity.
Negative_regulation (reduce) of NOX2 in respiratory
8) Confidence 0.18 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2858756 Disease Relevance 0.49 Pain Relevance 0
One approach is to directly inhibit NOX2 activity by either perturbing the recruitment of the subunits to the phagosome[3], [52] or by decreasing the steady state levels of NOX2 complex subunits[7], [8].
Negative_regulation (inhibit) of NOX2
9) Confidence 0.13 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2858756 Disease Relevance 0.78 Pain Relevance 0
One approach is to directly inhibit NOX2 activity by either perturbing the recruitment of the subunits to the phagosome[3], [52] or by decreasing the steady state levels of NOX2 complex subunits[7], [8].
Negative_regulation (decreasing) of NOX2
10) Confidence 0.13 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2858756 Disease Relevance 0.72 Pain Relevance 0
Correspondingly, mice deficient in the NOX2 subunits are much more susceptible to infections with bacterial pathogens such as Salmonella typhimurium for example [3], [5].
Negative_regulation (deficient) of NOX2 associated with infection
11) Confidence 0.13 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2858756 Disease Relevance 0.73 Pain Relevance 0
induction might be mediated via ROS generated in mitochondria which would be inhibited by glutathione and DPI but not by deletion of NOX2.
Negative_regulation (deletion) of NOX2
12) Confidence 0.13 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2858756 Disease Relevance 0.84 Pain Relevance 0
However, a recent study showed that mice lacking gp91phox, a phagocyte-specific component of the NADPH oxidase, developed extensive, spontaneous emphysematous destruction of their peripheral air spaces (Kassim et al 2005).
Negative_regulation (lacking) of gp91phox in phagocyte
13) Confidence 0.07 Published 2007 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2695202 Disease Relevance 0.55 Pain Relevance 0.38

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox