INT89854

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Context Info
Confidence 0.61
First Reported 2000
Last Reported 2010
Negated 9
Speculated 11
Reported most in Body
Documents 49
Total Number 66
Disease Relevance 42.58
Pain Relevance 24.10

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

cytosol (Nos2) signal transduction (Nos2) extracellular space (Nos2)
oxidoreductase activity (Nos2) peroxisome (Nos2) nucleus (Nos2)
Anatomy Link Frequency
macrophages 4
spinal cord 4
sciatic nerve 4
RAW 264 3
motoneurons 2
Nos2 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 404 100.00 Very High Very High Very High
COX2 62 100.00 Very High Very High Very High
agonist 47 100.00 Very High Very High Very High
tetrodotoxin 14 100.00 Very High Very High Very High
Neuronal nitric oxide synthase 7 100.00 Very High Very High Very High
opioid receptor 3 100.00 Very High Very High Very High
Antinociceptive 9 99.98 Very High Very High Very High
Eae 30 99.96 Very High Very High Very High
Paracetamol 14 99.84 Very High Very High Very High
lidocaine 32 99.80 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 1054 100.00 Very High Very High Very High
INFLAMMATION 493 100.00 Very High Very High Very High
Neuropathic Pain 617 99.82 Very High Very High Very High
Nervous System Injury 297 99.82 Very High Very High Very High
Parkinson's Disease 111 99.76 Very High Very High Very High
Influenza Virus Infection 56 99.68 Very High Very High Very High
Toxicity 35 99.64 Very High Very High Very High
Diabetes Mellitus 245 99.60 Very High Very High Very High
Pain 198 99.58 Very High Very High Very High
Polyps 3 99.46 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
More recently, a calcineurin/NFAT (nuclear factor of activated T-cells) signaling cascade has been implicated in cardiomyocyte protection through the transcriptional control of the iNos gene [45].
Regulation (control) of iNos in T-cells
1) Confidence 0.61 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2361191 Disease Relevance 0.21 Pain Relevance 0
This compensatory up-regulation of NOS2 in NOS1-KO mice suggests that the increased expression of this isoenzyme might be responsible for the thermal allodynia observed in NOS1-KO mice at 21 days after surgery.
Regulation (regulation) of NOS2 associated with targeted disruption and allodynia
2) Confidence 0.58 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001461 Disease Relevance 1.56 Pain Relevance 1.02
Indeed, sciatic nerve injury did not alter the NOS2 protein levels in the spinal cord of WT mice but significantly increased their expression in NOS1-KO mice when comparing sham-operated vs. sciatic nerve-injured animals (one way ANOVA, p<0.028).
Neg (not) Regulation (alter) of NOS2 protein in sciatic nerve associated with targeted disruption, nervous system injury, sciatic nerve and spinal cord
3) Confidence 0.58 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001461 Disease Relevance 0.73 Pain Relevance 0.62
However, clonidine did not affect iNOS mRNA stability.
Neg (not) Regulation (affect) of iNOS
4) Confidence 0.52 Published 2008 Journal J. Surg. Res. Section Body Doc Link 18262561 Disease Relevance 0 Pain Relevance 0
By using the A/NWS/33 influenza virus infected BALB/c model mouse, we were able to demonstrate that influenza virus infection leads to an up regulation of NOS-2 and astrocytes, mostly around capillary blood vessels of the hippocampus and olfactory bulb, starting at an early stage of the disease.
Regulation (regulation) of NOS-2 in olfactory bulb associated with influenza virus infection, hippocampus and disease
5) Confidence 0.51 Published 2007 Journal Neurochem Res Section Body Doc Link PMC2295255 Disease Relevance 1.42 Pain Relevance 0.22
Although CHOP (an apoptosis-associated gene correlated with the UPR) expression is elevated in response to erstressin treatment in A172 cells, the effects on iNOS expression levels or activity are not a consequence of reduced viability or programmed cell death induced by the compound.
Regulation (effects) of iNOS in A172 associated with apoptosis
6) Confidence 0.51 Published 2008 Journal Current Chemical Genomics Section Body Doc Link PMC2803434 Disease Relevance 0.25 Pain Relevance 0
Transcriptional and post-transcriptional regulation of iNOS is governed by a number of well characterized signaling pathways [2], however, additional undiscovered pathways of regulation may exist.
Regulation (regulation) of iNOS
7) Confidence 0.51 Published 2008 Journal Current Chemical Genomics Section Body Doc Link PMC2803434 Disease Relevance 0.62 Pain Relevance 0.24
However, while the disruption of NOS1 gene did not alter the mRNA or protein levels of NOS2 in sham-operated mice a significant increase in the spinal cord expression of NOS3 was further demonstrated in sham-operated NOS1-KO mice [18].
Neg (not) Regulation (alter) of NOS2 in spinal cord associated with targeted disruption and spinal cord
8) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001461 Disease Relevance 1.15 Pain Relevance 0.88
It may be worth testing the effects of NOS2 and NOS1 inhibitors on herpetic pain and postherpetic neuralgia in human subjects, respectively.
Regulation (effects) of NOS2 associated with pain, herpes simplex virus infection and postherpetic neuralgia
9) Confidence 0.44 Published 2007 Journal Neuroscience Section Abstract Doc Link 17997045 Disease Relevance 1.57 Pain Relevance 1.08
This effect was due to down-regulation of iNOS mRNA and suppression of iNOS proteins, i.e., blueberry extract may inhibit one of the primary steps in the inflammatory stress pathway [41].
Regulation (regulation) of iNOS associated with stress and inflammation
10) Confidence 0.44 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2693933 Disease Relevance 0.86 Pain Relevance 0.20
The effects of TTX on iNOS, CAT-2, and GTPCH expression were comparable to those of lidocaine.
Regulation (effects) of iNOS associated with tetrodotoxin and lidocaine
11) Confidence 0.43 Published 2006 Journal Anesth. Analg. Section Abstract Doc Link 16717319 Disease Relevance 0 Pain Relevance 1.16
As seen for iNOS protein, compound 2 had no statistical effect on iNOS mRNA levels relative to vehicle (Fig. 2C).
Neg (no) Regulation (effect) of iNOS
12) Confidence 0.43 Published 2008 Journal Current Chemical Genomics Section Body Doc Link PMC2803434 Disease Relevance 0 Pain Relevance 0.11
Our data also indicate that: i) the increased spinal cord expression of NOS1 plays a critical role in the maintenance of peripheral neuropathic pain, ii) a compensatory up-regulation of NOS2 isoform takes place in the spinal cord of sciatic nerve-injured NOS1-KO mice, and iii) the up-regulation of NOS1 in the spinal cord of sciatic nerve-injured WT mice at 21 days after surgery is modulated by NOS2.


Regulation (regulation) of NOS2 in spinal cord associated with targeted disruption, neuropathic pain, sciatic nerve and spinal cord
13) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001461 Disease Relevance 1.00 Pain Relevance 0.85
Similarly, PGE2 down regulated the activity of inducible nitric oxide synthase (iNOS), which was up regulated by APAP.
Regulation (regulated) of iNOS in PGE2
14) Confidence 0.42 Published 2010 Journal Histol. Histopathol. Section Abstract Doc Link 20503171 Disease Relevance 0.20 Pain Relevance 0.18
Inducible nitric oxide synthase (iNOS), a proinflammatory enzyme responsible for the generation of nitric oxide (NO), has been implicated in the pathogenesis of inflammatory diseases.
Regulation (responsible) of iNOS associated with inflammation and disease
15) Confidence 0.39 Published 2006 Journal Planta Med. Section Abstract Doc Link 16732525 Disease Relevance 0.48 Pain Relevance 0.21
To examine the effect of NO donor and iNOS inhibitor, C2C12 cells seeded in 35 mm-wells at 1 × 105 and allowed to adhere for at least 12 hour prior to stimulation by TNF-?
Spec (examine) Regulation (effect) of iNOS
16) Confidence 0.39 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2361191 Disease Relevance 0 Pain Relevance 0
Peripheral antinociceptive effects of mu- and delta-opioid receptor agonists in NOS2 and NOS1 knockout mice during chronic inflammatory pain.
Regulation (effects) of NOS2 associated with targeted disruption, analgesic, ipn, agonist, opioid receptor and antinociceptive
17) Confidence 0.39 Published 2009 Journal Eur. J. Pharmacol. Section Title Doc Link 19041302 Disease Relevance 1.20 Pain Relevance 1.88
It also demonstrated inhibitory activity against inducible nitric oxide synthase (iNOS)-mediated NO production at least partly by the down-regulation of iNOS.
Regulation (regulation) of iNOS
18) Confidence 0.38 Published 2009 Journal Arch. Pharm. Res. Section Abstract Doc Link 20091265 Disease Relevance 0.57 Pain Relevance 0.32
In accordance to our findings, DeAlba et al. [4] also demonstrated that the spinal cord protein levels of NOS2 did not change at 26 days after total sciatic nerve ligation, although an increase in the protein levels of NOS2 has been also demonstrated in the spinal cord of WT mice at 7 or 14 days after nerve injury [8].
Neg (not) Regulation (change) of NOS2 in nerve associated with nervous system injury, sciatic nerve and spinal cord
19) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001461 Disease Relevance 0.91 Pain Relevance 0.74
The effects of inducible nitric oxide synthase (iNOS)-derived NO in APAP toxicity are known; however, the role of endothelial nitric oxide synthase (eNOS)-derived NO is unknown.
Regulation (effects) of iNOS associated with toxicity and paracetamol
20) Confidence 0.36 Published 2006 Journal Acad Emerg Med Section Abstract Doc Link 16551773 Disease Relevance 0.55 Pain Relevance 0.59

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