INT49172

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Context Info
Confidence 0.52
First Reported 1995
Last Reported 2011
Negated 3
Speculated 7
Reported most in Body
Documents 43
Total Number 50
Disease Relevance 27.53
Pain Relevance 23.66

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

cytosol (Nos1) mitochondrion (Nos1) oxidoreductase activity (Nos1)
plasma membrane (Nos1) cytoskeleton (Nos1) nucleus (Nos1)
Anatomy Link Frequency
spinal cord 8
neuronal 7
nerve 3
brainstem 2
sciatic nerve 2
Nos1 (Mus musculus)
Pain Link Frequency Relevance Heat
opioid receptor 255 100.00 Very High Very High Very High
nMDA receptor 95 100.00 Very High Very High Very High
intrathecal 64 100.00 Very High Very High Very High
Neuronal nitric oxide synthase 40 100.00 Very High Very High Very High
anesthesia 34 100.00 Very High Very High Very High
agonist 29 100.00 Very High Very High Very High
Enkephalin 7 100.00 Very High Very High Very High
Antinociceptive 25 99.98 Very High Very High Very High
Neurotransmitter 42 99.96 Very High Very High Very High
Kinase C 126 99.92 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 649 100.00 Very High Very High Very High
Neuropathic Pain 404 99.84 Very High Very High Very High
Nervous System Injury 467 99.82 Very High Very High Very High
Injury 198 99.66 Very High Very High Very High
Pain 273 99.64 Very High Very High Very High
Hypoxia 15 99.52 Very High Very High Very High
Herpes Simplex Virus Infection 11 99.40 Very High Very High Very High
Disease 117 99.32 Very High Very High Very High
Aggression 10 99.10 Very High Very High Very High
Shock 18 99.04 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Whether importins are involved in the rapid up-regulation of nNOS (neuronal-nitric oxide synthase) activity following nerve injury is unclear (Yu, 2002).
Regulation (regulation) of neuronal-nitric oxide synthase in nerve associated with nervous system injury
1) Confidence 0.52 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2954441 Disease Relevance 0.25 Pain Relevance 0.19
Whether importins are involved in the rapid up-regulation of nNOS (neuronal-nitric oxide synthase) activity following nerve injury is unclear (Yu, 2002).
Regulation (regulation) of nNOS in nerve associated with nervous system injury
2) Confidence 0.52 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2954441 Disease Relevance 0.25 Pain Relevance 0.19
To clarify whether NO itself affected nNOS activity in the spinal cord as a retrograde messenger, we examined the involvement of the NO/cGMP signaling pathway in the regulation of nNOS activity by NADPH-diaphorase histochemistry.
Spec (whether) Regulation (affected) of nNOS in spinal cord associated with spinal cord
3) Confidence 0.51 Published 2007 Journal Nitric Oxide Section Abstract Doc Link 17548218 Disease Relevance 0.10 Pain Relevance 0.34
These results suggest that NO may regulate nNOS activity as a retrograde messenger in the spinal cord via activation of NMDA receptor containing GluRepsilon1 and GluRepsilon2 subunits.
Spec (may) Regulation (regulate) of nNOS in spinal cord associated with nmda receptor and spinal cord
4) Confidence 0.51 Published 2007 Journal Nitric Oxide Section Abstract Doc Link 17548218 Disease Relevance 0.06 Pain Relevance 0.45
In the postsynapse, the regulation of nNOS is dependent on the balance between activating and inactivating phosphorylation.
Regulation (regulation) of nNOS
5) Confidence 0.45 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0 Pain Relevance 0.25
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 NOS1 associated with pain, herpes simplex virus infection and postherpetic neuralgia
6) Confidence 0.45 Published 2007 Journal Neuroscience Section Abstract Doc Link 17997045 Disease Relevance 1.57 Pain Relevance 1.08
To clarify whether NO itself affected nNOS activity in the spinal cord as a retrograde messenger, we examined the involvement of the NO/cGMP signaling pathway in the regulation of nNOS activity by NADPH-diaphorase histochemistry.
Regulation (regulation) of nNOS in spinal cord associated with spinal cord
7) Confidence 0.43 Published 2007 Journal Nitric Oxide Section Abstract Doc Link 17548218 Disease Relevance 0.09 Pain Relevance 0.34
These results indicated that the compensatory changes in the spinal cord expression of NOS3 in NOS1-KO under basal conditions does not fully compensate for NOS1 function in neuropathic pain, which is mainly produced by NOS2.
Neg (not) Regulation (compensate) of NOS1 in spinal cord associated with targeted disruption, neuropathic pain and spinal cord
8) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001461 Disease Relevance 1.04 Pain Relevance 0.90
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 NOS1 associated with targeted disruption and allodynia
9) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001461 Disease Relevance 1.56 Pain Relevance 1.03
However, in the clinical setup, the heart may be subjected to stresses that can result in the expression of the inducible NOS (iNOS) and it would be important to elucidate the role of the constitutive NOS isoforms, nNOS and eNOS, in the pathophysiology of ischemia/reperfusion-induced injury under such conditions.
Regulation (role) of nNOS in heart associated with stress, ischemia and injury
10) Confidence 0.42 Published 2010 Journal BMC Physiol Section Body Doc Link PMC2927582 Disease Relevance 0.50 Pain Relevance 0.12
We further studied the role of NO on acute inflammatory pain by measuring the change in gene expression of the 3 NOS isoforms using qRT-PCR. nNOS was significantly down-regulated in both the placebo group (2.4 fold; p = 0.02; paired t-test) and the ketorolac treatment group (3.4 fold; p = 0.0003; paired t-test).
Regulation (regulated) of nNOS associated with eae and acular
11) Confidence 0.40 Published 2010 Journal Mol Pain Section Body Doc Link PMC2949722 Disease Relevance 0.33 Pain Relevance 0.54
Peripheral antinociceptive effects of mu- and delta-opioid receptor agonists in NOS2 and NOS1 knockout mice during chronic inflammatory pain.
Regulation (effects) of NOS1 associated with targeted disruption, analgesic, ipn, agonist, opioid receptor and antinociceptive
12) Confidence 0.39 Published 2009 Journal Eur. J. Pharmacol. Section Title Doc Link 19041302 Disease Relevance 1.20 Pain Relevance 1.89
Effect of intrathecal injection of nonspecific and specific nNOS inhibitors on nerve injury-induced mechanical hypersensitivity
Regulation (Effect) of nNOS in nerve associated with nervous system injury, hypersensitivity and intrathecal
13) Confidence 0.39 Published 2007 Journal Mol Pain Section Body Doc Link PMC2089056 Disease Relevance 1.22 Pain Relevance 0.41
The present study combined a genetic strategy with a pharmacologic approach to examine the effects of genetic knockout and pharmacologic inhibition of nNOS on neuropathic pain induced by unilateral fifth lumbar spinal nerve injury in mice.
Spec (examine) Regulation (effects) of nNOS in spinal nerve associated with targeted disruption, nervous system injury and neuropathic pain
14) Confidence 0.39 Published 2007 Journal Mol Pain Section Abstract Doc Link PMC2089056 Disease Relevance 1.28 Pain Relevance 0.49
Although it has been reported that spinal eNOS is upregulated in nNOS KO mice [5], it appears that this upregulation does not fully compensate for nNOS function in neuropathic pain.
Neg (not) Spec (appears) Regulation (compensate) of nNOS in spinal associated with neuropathic pain
15) Confidence 0.39 Published 2007 Journal Mol Pain Section Body Doc Link PMC2089056 Disease Relevance 1.32 Pain Relevance 0.61
These results agree with previous data and suggest that the down-regulation of nNOS activity at an early age is causally linked with accelerated brain aging in SAMP8.
Regulation (regulation) of nNOS in brain associated with aging
16) Confidence 0.38 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1766358 Disease Relevance 0.38 Pain Relevance 0.24
By contrast, it appears that delayed IP (72 hours) is dependent on nNOS in the rabbit [12], whereas the deficit of nNOS reduces cerebral ischemic injury in mice [13].
Spec (appears) Regulation (dependent) of nNOS associated with injury
17) Confidence 0.37 Published 2010 Journal BMC Physiol Section Body Doc Link PMC2927582 Disease Relevance 0.44 Pain Relevance 0.07
In this connection, other investigators have also reported in an infarct size model that nNOS plays an opposite role in ischemia/reperfusion and IP [23] and that the protection of delayed IP in the rabbit heart is dependent on nNOS [12].
Regulation (dependent) of nNOS in heart associated with ischemia
18) Confidence 0.37 Published 2010 Journal BMC Physiol Section Body Doc Link PMC2927582 Disease Relevance 0.81 Pain Relevance 0.16
However, the gene expression results suggest a relatively low level of NO at the site of injury, given the down regulation of nNOS and insignificant change of the other two isoforms.
Regulation (regulation) of nNOS associated with injury
19) Confidence 0.35 Published 2010 Journal Mol Pain Section Body Doc Link PMC2949722 Disease Relevance 0.62 Pain Relevance 0.59
The down-regulation of nNOS in both treatment groups seen here is an interesting finding that may reflect a feedback effect to the higher NO levels at earlier time points.
Regulation (regulation) of nNOS
20) Confidence 0.35 Published 2010 Journal Mol Pain Section Body Doc Link PMC2949722 Disease Relevance 0.62 Pain Relevance 0.50

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