INT84704

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Context Info
Confidence 0.70
First Reported 1999
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 18
Total Number 19
Disease Relevance 18.64
Pain Relevance 5.65

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

cytosol (Nqo1) oxidoreductase activity (Nqo1) cytoplasm (Nqo1)
Anatomy Link Frequency
T cells 3
liver 1
B cells 1
spinal cord 1
muscle 1
Nqo1 (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 18 99.92 Very High Very High Very High
Spinal cord 304 99.76 Very High Very High Very High
potassium channel 13 98.72 Very High Very High Very High
anesthesia 3 98.48 Very High Very High Very High
Neuropathic pain 6 98.20 Very High Very High Very High
isoflurane 1 98.04 Very High Very High Very High
Neuritis 253 97.36 Very High Very High Very High
Central nervous system 610 94.96 High High
ischemia 5 94.80 High High
Inflammation 193 92.48 High High
Disease Link Frequency Relevance Heat
Neuromyelitis Optica 2207 100.00 Very High Very High Very High
Disease 592 99.96 Very High Very High Very High
Dengue 20 99.84 Very High Very High Very High
Virus Diseases 10 99.80 Very High Very High Very High
Neuropathic Pain 11 98.20 Very High Very High Very High
Sprains And Strains 11 97.76 Very High Very High Very High
Infection 193 97.64 Very High Very High Very High
Transverse Myelitis 140 97.54 Very High Very High Very High
Optic Neuritis 243 97.36 Very High Very High Very High
Apoptosis 110 97.36 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The increase in NADPH diaphorase activity in the spinal cord associated with neuropathic pain was also blocked by these extracts.
Positive_regulation (increase) of NADPH diaphorase in spinal cord associated with neuropathic pain and spinal cord
1) Confidence 0.70 Published 2004 Journal Neurosci. Lett. Section Abstract Doc Link 15488309 Disease Relevance 0.99 Pain Relevance 1.36
Hepatotoxic doses of APAP and CCl4 increased Ho-1 and Nqo1 mRNA levels by 22- and 2.5-fold, respectively, and reduced Oatp1a1, 1a4, and Ntcp mRNA levels in liver.
Positive_regulation (increased) of Nqo1 in liver
2) Confidence 0.66 Published 2005 Journal Toxicol. Sci. Section Abstract Doc Link 15496496 Disease Relevance 0.15 Pain Relevance 0.22
The elevated ganglionic NADPH-diaphorase and diminished CO labeling in the DRG of hyperglycemic mice is consistent with previously proposed inhibition of CO activity [24] by the product of nitric oxide synthase, nitric oxide.
Positive_regulation (elevated) of NADPH-diaphorase
3) Confidence 0.32 Published 2007 Journal J Brachial Plex Peripher Nerve Inj Section Body Doc Link PMC1865541 Disease Relevance 0.19 Pain Relevance 0.26
These results suggest that ethanol inhibited not only the microsomal (CYP2E1 mediated) formation of a toxic quinone metabolite from APAP, but also accelerated the conversion of the toxic quinone metabolite produced back to APAP by stimulating cytoplasmic QR activity.
Positive_regulation (stimulating) of QR associated with paracetamol
4) Confidence 0.30 Published 1999 Journal Biochem. Pharmacol. Section Abstract Doc Link 10535745 Disease Relevance 0.20 Pain Relevance 0.96
Increased NADPH diaphorase activity and NOS immunoreactivity were histochemically detected in the cells of muscle that had been subjected to I/R.
Positive_regulation (Increased) of NADPH diaphorase in muscle
5) Confidence 0.26 Published 2003 Journal Leg Med (Tokyo) Section Abstract Doc Link 12935594 Disease Relevance 0.39 Pain Relevance 0.28
The enhancement of NADPH-diaphorase staining by NOR3 was significantly inhibited by CPTIO, an NO scavenger, ODQ, a soluble guanylate cyclase inhibitor, and KT5823, an inhibitor of cGMP-dependent protein kinase.
Positive_regulation (enhancement) of NADPH-diaphorase
6) Confidence 0.19 Published 2007 Journal Nitric Oxide Section Abstract Doc Link 17548218 Disease Relevance 0.08 Pain Relevance 0.46
Increased activity of antioxidants such as catalase, glutathione peroxidase and DT-diaphorase, and increase in glutathione level, are associated with the onset of resistance in Chinese hamster cells chronically exposed to menadione [117].
Positive_regulation (increase) of DT-diaphorase
7) Confidence 0.04 Published 2006 Journal Theor Biol Med Model Section Body Doc Link PMC1508139 Disease Relevance 0.60 Pain Relevance 0
A small animal model of NMO is essential to demonstrate whether AQP4 is indeed the incipient autoantigen capable of inducing NMO-IgG formation and NMO.
Positive_regulation (inducing) of NMO associated with neuromyelitis optica
8) Confidence 0.03 Published 2008 Journal J Neuroinflammation Section Abstract Doc Link PMC2427020 Disease Relevance 1.86 Pain Relevance 0.32
It seems clear that AQP4-specific T cells are activated in NMO.
Positive_regulation (activated) of NMO in T cells associated with neuromyelitis optica
9) Confidence 0.03 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2427020 Disease Relevance 0.94 Pain Relevance 0.05
Thus there are at least two possible incipient antigens that might be primary in the induction of NMO.
Positive_regulation (induction) of NMO associated with neuromyelitis optica
10) Confidence 0.03 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2427020 Disease Relevance 1.21 Pain Relevance 0.25
Although it has been suggested that AQP4 autoantibodies cause NMO, probably by inhibiting AQP4, [59, 64] other authors [87] keep a more skeptical view pondering that this causality still lacks definite proof, as NMO has not been produced in experimental animals through administration of the antibody.
Positive_regulation (cause) of NMO associated with neuromyelitis optica
11) Confidence 0.02 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923365 Disease Relevance 0.72 Pain Relevance 0.11
If the autoantibodies are not pathogenic per se, it may be that the ability of self-reactive B cells to capture their cognate antigen and, in the case of AQP4 or MOG, present antigen to normally non-reactive MOG or AQP4-specific T cells, instigates NMO.
Positive_regulation (instigates) of NMO in T cells associated with neuromyelitis optica
12) Confidence 0.02 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2427020 Disease Relevance 0.94 Pain Relevance 0.27
It is important to initiate development of an AQP4-based animal model of NMO to determine whether AQP4 is the autoantigen required for NMO, either due to AQP4-specific T and B cells, specific AQP4 antibody or both cellular and soluble effectors.
Spec (whether) Positive_regulation (required) of NMO in B cells associated with neuromyelitis optica
13) Confidence 0.02 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2427020 Disease Relevance 1.42 Pain Relevance 0
The other advantage of the BN strain for the basis of an AQP4 NMO model is the disease manifests (60%) within weeks of inoculation and importantly, NMO-like pathology can be induced by the naive B and T cell repertoire.


Positive_regulation (induced) of NMO-like in T cell associated with neuromyelitis optica, disease and sprains and strains
14) Confidence 0.02 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2427020 Disease Relevance 1.57 Pain Relevance 0.34
It would be interesting to know if ON and LETM patients who do not go on to develop NMO have a different AQP4-specific TCR and T helper (Th) cell profile than those who develop NMO.


Positive_regulation (develop) of NMO associated with neuromyelitis optica, transverse myelitis and neuritis
15) Confidence 0.02 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2427020 Disease Relevance 1.26 Pain Relevance 0.34
Currently there are no animal models that feature AQP4 as the autoantigen that induces NMO-like pathology.
Positive_regulation (induces) of NMO-like associated with neuromyelitis optica
16) Confidence 0.02 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2427020 Disease Relevance 1.61 Pain Relevance 0
It would be interesting to determine if antibodies to Kir4.1, an inward-rectifying potassium channel co-localized with AQP4 on astrocyte foot processes are able to cause NMO-like disease.


Positive_regulation (cause) of NMO-like in foot associated with neuromyelitis optica, potassium channel and disease
17) Confidence 0.02 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2427020 Disease Relevance 0.78 Pain Relevance 0.24
Another viral disease that can precede NMO is dengue fever, which is prevalent in Brazil.
Positive_regulation (precede) of NMO associated with virus diseases, neuromyelitis optica and dengue
18) Confidence 0.02 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2427020 Disease Relevance 2.62 Pain Relevance 0.14
and oxLDLs trigger nSMase activation, SM hydrolysis, and ceramide generation, potentially involved in apoptotic signaling.
Positive_regulation (activation) of oxLDLs associated with apoptosis
19) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2843740 Disease Relevance 1.11 Pain Relevance 0.05

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