INT124299

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Context Info
Confidence 0.53
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 15
Total Number 21
Disease Relevance 13.80
Pain Relevance 1.51

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

mitochondrion (Sod2) oxidoreductase activity (Sod2) mitochondrion organization (Sod2)
DNA binding (Sod2) response to stress (Sod2) cytoplasm (Sod2)
Anatomy Link Frequency
bladder 12
blood 4
embryos 4
neuronal 2
liver 2
Sod2 (Mus musculus)
Pain Link Frequency Relevance Heat
Central nervous system 16 98.56 Very High Very High Very High
amygdala 5 93.16 High High
Inflammatory response 17 92.96 High High
Hippocampus 50 92.64 High High
cINOD 6 84.64 Quite High
Inflammation 31 83.52 Quite High
ischemia 65 81.68 Quite High
imagery 116 80.48 Quite High
cytokine 25 77.88 Quite High
anesthesia 21 77.72 Quite High
Disease Link Frequency Relevance Heat
Stress 179 100.00 Very High Very High Very High
Targeted Disruption 115 100.00 Very High Very High Very High
Injury 100 99.08 Very High Very High Very High
Apoptosis 276 99.00 Very High Very High Very High
Overactive Bladder 84 98.64 Very High Very High Very High
Peptic Ulcer 6 98.44 Very High Very High Very High
Gestational Diabetes 18 98.28 Very High Very High Very High
Alzheimer's Dementia 30 95.28 Very High Very High Very High
Heart Disease 10 94.72 High High
Diabetes Mellitus 126 93.44 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
For example, using mutant mice with reduced expression of SOD-2, Wenzel and colleagues demonstrated an increased oxidative stress with disrupted vascular function in these animals in relation to cardiac disease [34].
Negative_regulation (reduced) of Gene_expression (expression) of SOD-2 associated with stress and heart disease
1) Confidence 0.53 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 1.05 Pain Relevance 0
Last, we hypothesize that reduction of oxidative stress through the overexpression of SOD2 should ameliorate these effects.
Negative_regulation (reduction) of Gene_expression (overexpression) of SOD2 associated with stress
2) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 1.18 Pain Relevance 0.17
Upon SOD2 overexpression, the deficits in axonal transport recovered in association with restoration of levels of phosphorylated p38 MAPK and tau protein.
Negative_regulation (recovered) of Gene_expression (overexpression) of SOD2
3) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956689 Disease Relevance 0.91 Pain Relevance 0.09
To confirm the knockdown of Sod2 gene expression, we examined the in vivo consequence of SOD2 deficiency.
Negative_regulation (knockdown) of Gene_expression (expression) of Sod2
4) Confidence 0.42 Published 2006 Journal PLoS Genet Section Body Doc Link PMC1358942 Disease Relevance 0.31 Pain Relevance 0
The ribozyme suppressing SOD2 gene expression increased myelin fiber injury by 27%.
Negative_regulation (suppressing) of Gene_expression (expression) of SOD2
5) Confidence 0.42 Published 2007 Journal Invest. Ophthalmol. Vis. Sci. Section Body Doc Link 17251466 Disease Relevance 0.12 Pain Relevance 0
have already begun to increase but prior to plaque depostion, revealed the same pattern of blood flow deficits in Tg2576 mice that was recovered upon overexpression of SOD-2 (overall p?
Negative_regulation (recovered) of Gene_expression (overexpression) of SOD-2 in blood
6) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.51 Pain Relevance 0.04
Moreover, overexpression of SOD-2 in the Tg2576 mice reduced the levels of phospho-eNOS back to those in wild-type mice (Figure 2), which corresponded with the recovered blood flow deficits in these same mice.


Negative_regulation (reduced) of Gene_expression (overexpression) of SOD-2 in blood
7) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.20 Pain Relevance 0.08
This increase was recovered back to wildtype levels upon SOD-2 overexpression (Figure 4), coinciding with the recovery from axonal transport deficits in these animals.


Negative_regulation (recovered) of Gene_expression (overexpression) of SOD-2
8) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.17 Pain Relevance 0
This increase was recovered back to wildtype levels upon SOD-2 overexpression, suggesting that mitochondrial superoxide contributes to tau pathology not only in the olfactory bulb, but also extends to the learning and memory centers of the brain.
Negative_regulation (recovered) of Gene_expression (overexpression) of SOD-2 in brain
9) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.44 Pain Relevance 0.09
Such aberrant mitochondrial localization was accompanied by decreased mitochondrial manganese superoxide dismutase (Mn-SOD) activity, cytochrome c release into the cytosol, caspase-3 activation, and DNA fragmentation, most predominantly in hippocampal neuronal cells.
Negative_regulation (decreased) of Gene_expression (activation) of manganese superoxide dismutase in neuronal
10) Confidence 0.33 Published 2005 Journal Neurosci. Lett. Section Abstract Doc Link 15644272 Disease Relevance 0.62 Pain Relevance 0.08
was partially decreased after external carotid artery ligation in transgenic mice overexpressing SOD2, the mitochondrial isoform of SOD (Fig. 3 c).
Negative_regulation (decreased) of Gene_expression (overexpressing) of SOD2 in external carotid artery associated with targeted disruption
11) Confidence 0.30 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2605224 Disease Relevance 0.26 Pain Relevance 0.13
In our study, western blot analysis showed decreased MnSOD expression was parallel to bladder apoptosis.
Negative_regulation (decreased) of Gene_expression (expression) of MnSOD in bladder associated with apoptosis
12) Confidence 0.27 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2967004 Disease Relevance 0.80 Pain Relevance 0
In conclusion, the results of the present study provide evidence that bladder apoptosis induced by AUR after acute BOO and subsequent bladder emptying is associated with decreased MnSOD expression, increased PARP activity and imbalance between pro- and anti-apoptotic factors.
Negative_regulation (decreased) of Gene_expression (expression) of MnSOD in bladder associated with overactive bladder and apoptosis
13) Confidence 0.27 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2967004 Disease Relevance 1.05 Pain Relevance 0
Expression of MnSOD significantly decreased in the I/R group at 30 min, 60 min, and 120 min after bladder emptying compare to the control group, and began to recover thereafter.
Negative_regulation (decreased) of Gene_expression (Expression) of MnSOD in bladder
14) Confidence 0.24 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2967004 Disease Relevance 0.08 Pain Relevance 0.03
It also blocked oxidative stress via inhibition of protein oxidation, lipid peroxidation, (*)OH generation and SOD-2 expression.
Negative_regulation (inhibition) of Gene_expression (expression) of SOD-2 associated with stress
15) Confidence 0.23 Published 2009 Journal J. Pineal Res. Section Abstract Doc Link 19522738 Disease Relevance 0.84 Pain Relevance 0.64
These results indicate that bladder apoptosis, induced by acute BOO and subsequent emptying, is associated with decreased MnSOD expression, increased PARP activity and imbalance in apoptosis pathways.



Negative_regulation (decreased) of Gene_expression (expression) of MnSOD in bladder associated with apoptosis
16) Confidence 0.20 Published 2010 Journal Journal of Korean Medical Science Section Abstract Doc Link PMC2967004 Disease Relevance 0.81 Pain Relevance 0.03
Another important finding was that bladder apoptosis induced by AUR after acute BOO and subsequent bladder emptying was associated with decreased MnSOD expression, increased PARP activity and imbalance between proand anti-apoptotic factors.
Negative_regulation (decreased) of Gene_expression (expression) of MnSOD in bladder associated with overactive bladder and apoptosis
17) Confidence 0.20 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2967004 Disease Relevance 1.59 Pain Relevance 0.07
These results indicate that downregulation of MnSOD expression and imbalance of Bcl-2 family proteins expression play a critical role in the development of bladder apoptosis following AUR and subsequent reperfusion.
Negative_regulation (downregulation) of Gene_expression (expression) of MnSOD in bladder associated with overactive bladder and apoptosis
18) Confidence 0.20 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2967004 Disease Relevance 0.88 Pain Relevance 0
Numerous studies have shown that MnSOD was essential for life, because homozygous MnSOD knockout mice exhibited myocardial and liver injury and endothelial dysfunction (21-23), whereas overexpression of MnSOD reduced I/R-related damage (24, 25).
Negative_regulation (reduced) of Gene_expression (overexpression) of MnSOD in liver associated with targeted disruption and injury
19) Confidence 0.20 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2967004 Disease Relevance 1.06 Pain Relevance 0.06
Thus, expression of copper zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), and sonic hedgehog homolog (Shh) were decreased, and bone morphogenetic protein-4 (Bmp-4) was increased, in the MD embryos compared with the N embryos.
Negative_regulation (decreased) of Gene_expression (expression) of manganese superoxide dismutase in embryos
20) Confidence 0.17 Published 2008 Journal Diabetes Section Abstract Doc Link PMC2584142 Disease Relevance 0.67 Pain Relevance 0

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