INT73431

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Context Info
Confidence 0.65
First Reported 1998
Last Reported 2010
Negated 3
Speculated 2
Reported most in Body
Documents 82
Total Number 84
Disease Relevance 53.22
Pain Relevance 11.61

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

mitochondrion (Nos3) Golgi apparatus (Nos3) cytoplasm (Nos3)
signal transduction (Nos3) oxidoreductase activity (Nos3) nucleolus (Nos3)
Anatomy Link Frequency
endothelial cells 5
lung 4
peritoneum 3
blood 3
vasculature 3
Nos3 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 684 99.60 Very High Very High Very High
Pain 99 99.52 Very High Very High Very High
Thermal hyperalgesia 44 99.46 Very High Very High Very High
Bioavailability 24 99.36 Very High Very High Very High
ischemia 72 99.28 Very High Very High Very High
Serotonin 35 99.24 Very High Very High Very High
bradykinin 31 99.02 Very High Very High Very High
cytokine 229 98.24 Very High Very High Very High
Dorsal horn 13 97.36 Very High Very High Very High
cINOD 23 97.04 Very High Very High Very High
Disease Link Frequency Relevance Heat
Disorder Of Lipid Metabolism 1476 99.98 Very High Very High Very High
Targeted Disruption 456 99.96 Very High Very High Very High
Peritonitis 432 99.76 Very High Very High Very High
Hypoxia 368 99.76 Very High Very High Very High
Stress 377 99.66 Very High Very High Very High
INFLAMMATION 807 99.60 Very High Very High Very High
Pain 98 99.52 Very High Very High Very High
Hyperalgesia 77 99.46 Very High Very High Very High
Hyperglycemia 33 99.36 Very High Very High Very High
Brain Hemorrhage 12 99.28 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We conclude that, regardless of the state of alertness, -/- mice develop salt-sensitive hypertension after prolonged feeding on HS, in part due to their inability to reduce PRA, whereas the specific renal upregulation of ecNOS and ET-1 in response to HS intake may be an ANP-independent adaptive adjustment aimed at improving kidney function and counteracting the pressor effect of salt.
Positive_regulation (upregulation) of ecNOS in kidney associated with hypertension
1) Confidence 0.65 Published 1998 Journal Am. J. Physiol. Section Abstract Doc Link 9458926 Disease Relevance 0.25 Pain Relevance 0.06
This may be related to the uneven effect of LPS on the specific NOS regulation: the 2.5-fold increase in eNOS is below the induction of iNOS (normally absent from the peritoneum) and the >10-fold increase in nNOS.
Positive_regulation (increase) of eNOS in peritoneum
2) Confidence 0.57 Published 2010 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2796899 Disease Relevance 0.64 Pain Relevance 0.16
This important difference illustrates the fact that eNOS, initially described as a constitutive isoform, can actually be induced by a variety of stimuli including growth factors, cytokines and bacterial LPS [2,34].
Positive_regulation (induced) of eNOS associated with cytokine
3) Confidence 0.57 Published 2010 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2796899 Disease Relevance 0.60 Pain Relevance 0.25
At any rate, the upregulation of eNOS is critical to regulate transport parameters in the early phase of peritonitis, which emphasizes the therapeutic potential of selective inhibitors targeting this isoform.
Positive_regulation (upregulation) of eNOS associated with peritonitis
4) Confidence 0.57 Published 2010 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2796899 Disease Relevance 0.65 Pain Relevance 0.25
Immunoblotting studies (Figure 4) demonstrated that LPS-induced peritonitis was associated with a major upregulation of nNOS (155 kD) and eNOS (140 kD), and the induction of iNOS (130 kD) in the peritoneum (Figure 4A).
Positive_regulation (upregulation) of eNOS in peritoneum associated with peritonitis
5) Confidence 0.57 Published 2010 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2796899 Disease Relevance 0.47 Pain Relevance 0.04
At variance with the 6-day catheter peritonitis model, the upregulation of eNOS 18 h after LPS does not reflect a significant vascular proliferation in the peritoneum.
Positive_regulation (upregulation) of eNOS in peritoneum associated with peritonitis
6) Confidence 0.57 Published 2010 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2796899 Disease Relevance 0.53 Pain Relevance 0.23
Immunostaining (Figure 3) showed that LPS-induced acute peritonitis was associated with the increased eNOS signal in the endothelium lining peritoneal blood vessels (Figure 3A,B) and increased immunoreactivity for nNOS in endothelial and perivascular inflammatory cells including macrophages, and nerve sections (Figure 3C–F).
Positive_regulation (increased) of eNOS in endothelium associated with inflammation and peritonitis
7) Confidence 0.57 Published 2010 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2796899 Disease Relevance 0.78 Pain Relevance 0.15
Thus, GSNO-R might protect against nitrosative stress, which would be anticipated to be greater in female mice than in males because of the estrogen-mediated increase in eNOS activity.
Positive_regulation (increase) of eNOS associated with stress
8) Confidence 0.56 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2982841 Disease Relevance 0.36 Pain Relevance 0
Theoretically, increased eNOS levels produce an increase in S-nitrosylated proteins.
Positive_regulation (increased) of eNOS
9) Confidence 0.56 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2982841 Disease Relevance 0.45 Pain Relevance 0
To determine if the increase in GSNO-R activity in the lungs of female animals is due to estrogen-induced increases in eNOS activity, murine pulmonary endothelial cells isolated from female mice were treated with 10 nM estrogen in the absence or presence of L-NAME.
Positive_regulation (increases) of eNOS in lungs
10) Confidence 0.56 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2982841 Disease Relevance 0 Pain Relevance 0
This increase in eNOS protein/activity levels is thought to be responsible for the protective effects on the vasculature.
Positive_regulation (increase) of eNOS in vasculature
11) Confidence 0.56 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2982841 Disease Relevance 0.59 Pain Relevance 0
The vasoregulatory molecules iNOS, eNOS, HO-1 and COX-2 were upregulated in the kidneys.
Positive_regulation (upregulated) of eNOS
12) Confidence 0.52 Published 2007 Journal Nephron Exp. Nephrol. Section Body Doc Link 17220637 Disease Relevance 0 Pain Relevance 0
Two factors that modulate the development of cardiovascular diseases are HDL and estradiol [33,34], both which also can promote the stimulation of eNOS and generation of nitric oxide [35,36].
Positive_regulation (stimulation) of eNOS associated with cardiovascular disease and disorder of lipid metabolism
13) Confidence 0.51 Published 2008 Journal BMC Cardiovasc Disord Section Body Doc Link PMC2636751 Disease Relevance 1.53 Pain Relevance 0
Endothelial nitric oxide synthase increases GSNO-R Activity
Positive_regulation (increases) of Endothelial nitric oxide synthase
14) Confidence 0.47 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2982841 Disease Relevance 0 Pain Relevance 0
To further evaluate the role of androgens in the activation of GSNO-R, eNOS?
Positive_regulation (activation) of eNOS
15) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2982841 Disease Relevance 0.05 Pain Relevance 0
Estrogen has been shown to influence the expression and activity of endothelial nitric oxide synthase (eNOS) which is associated with increased S-nitrosothiol production.
Positive_regulation (activity) of eNOS
16) Confidence 0.43 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2982841 Disease Relevance 0.32 Pain Relevance 0
Because eNOS activity is elevated in the female mouse lung, it is possible that GSNO-R opposes protein S-nitrosylation by eNOS through its de-nitrosylating activity.
Positive_regulation (elevated) of eNOS in lung
17) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2982841 Disease Relevance 0.22 Pain Relevance 0
Estrogen has been shown to influence the expression and activity of endothelial nitric oxide synthase (eNOS) which is associated with increased S-nitrosothiol production.
Positive_regulation (activity) of endothelial nitric oxide synthase
18) Confidence 0.43 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2982841 Disease Relevance 0.32 Pain Relevance 0
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.
Positive_regulation (upregulated) of eNOS in spinal associated with neuropathic pain
19) Confidence 0.41 Published 2007 Journal Mol Pain Section Body Doc Link PMC2089056 Disease Relevance 1.31 Pain Relevance 0.56
However, studies performed on knockout mice as well as those using different selective and non-selective NOS inhibitors point to a possible role for eNOS isoform in pain processing [16,17].
Spec (possible) Positive_regulation (role) of eNOS associated with targeted disruption and pain
20) Confidence 0.41 Published 2010 Journal Mol Pain Section Body Doc Link PMC2949722 Disease Relevance 1.61 Pain Relevance 1.47

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