INT73809

From wiki-pain
Revision as of 01:08, 22 September 2012 by Daniel (Talk | contribs)

(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to: navigation, search
Context Info
Confidence 0.45
First Reported 1998
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 18
Total Number 18
Disease Relevance 10.05
Pain Relevance 2.27

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
blood 3
sciatic nerve 1
retinas 1
endothelial cell 1
heart 1
Nos3 (Mus musculus)
Pain Link Frequency Relevance Heat
cINOD 8 99.84 Very High Very High Very High
Bioavailability 13 99.32 Very High Very High Very High
Tetrahydrobiopterin 26 99.14 Very High Very High Very High
ischemia 31 98.88 Very High Very High Very High
Spinal cord 53 98.80 Very High Very High Very High
Sciatic nerve 77 98.12 Very High Very High Very High
aspirin 1 96.20 Very High Very High Very High
Pain 53 93.04 High High
acular 25 80.04 Quite High
Analgesic 19 79.84 Quite High
Disease Link Frequency Relevance Heat
Disease 264 99.48 Very High Very High Very High
Aging 147 99.32 Very High Very High Very High
Cv Unclassified Under Development 34 98.88 Very High Very High Very High
Obesity 176 98.72 Very High Very High Very High
Acute Coronary Syndrome 45 98.28 Very High Very High Very High
Coronary Artery Disease 77 97.96 Very High Very High Very High
Stress 153 97.88 Very High Very High Very High
Injury 45 97.72 Very High Very High Very High
Hypertension 206 96.96 Very High Very High Very High
Diabetes Mellitus 235 96.76 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Accumulating evidence, including findings of elevation of arterial blood pressure in mice lacking the endothelial nitric oxide synthase (eNOS) gene, strongly suggests that alteration in NO metabolism is implicated in hypertension.
Regulation (lacking) of eNOS in blood associated with hypertension
1) Confidence 0.45 Published 1998 Journal Hypertension Section Abstract Doc Link 9674630 Disease Relevance 0.69 Pain Relevance 0.07
Accumulating evidence, including findings of elevation of arterial blood pressure in mice lacking the endothelial nitric oxide synthase (eNOS) gene, strongly suggests that alteration in NO metabolism is implicated in hypertension.
Regulation (lacking) of endothelial nitric oxide synthase in blood associated with hypertension
2) Confidence 0.45 Published 1998 Journal Hypertension Section Abstract Doc Link 9674630 Disease Relevance 0.69 Pain Relevance 0.07
The effect of mitochondrial superoxide on eNOS function in AD
Regulation (effect) of eNOS associated with disease
3) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.31 Pain Relevance 0.03
A possible mechanism by which mitochondrial superoxide could modulate blood flow is through modulation of eNOS function.
Regulation (modulation) of eNOS in blood
4) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.24 Pain Relevance 0
The down regulation of eNOS by NSAIDs, on the other hand, is in line with the suppression of eNOS expression by high-dose aspirin or meloxicam, in retinas of diabetic rats [36].
Regulation (regulation) of eNOS in retinas associated with aspirin, diabetes mellitus and cinod
5) Confidence 0.37 Published 2010 Journal Mol Pain Section Body Doc Link PMC2949722 Disease Relevance 0.59 Pain Relevance 0.85
In the present study, we sought to evaluate the effects of the eNOS T-786C polymorphism on the development of ACS and CHD.


Regulation (effects) of eNOS associated with acute coronary syndrome and coronary artery disease
6) Confidence 0.35 Published 2008 Journal Lipids Health Dis Section Body Doc Link PMC2267783 Disease Relevance 1.47 Pain Relevance 0.13
Statins restore NO production by several mechanisms, including up-regulation of eNOS mRNA and protein levels and preservation of NO inactivation by reactive oxygen species.
Regulation (regulation) of eNOS
7) Confidence 0.35 Published 2010 Journal The Open Neurology Journal Section Body Doc Link PMC2923338 Disease Relevance 0.21 Pain Relevance 0.08
Its activity, however, has not yet been measured. eNOS activity is regulated mainly via phosphorylation, with two most prominent regulatory sites: threonine 495, which is inhibitory [45] and serine 1177, which is permissive [46].
Regulation (regulated) of eNOS
8) Confidence 0.31 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 0.39 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.
Regulation (influence) of endothelial nitric oxide synthase
9) Confidence 0.25 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2982841 Disease Relevance 0.33 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.
Regulation (influence) of eNOS
10) Confidence 0.25 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2982841 Disease Relevance 0.33 Pain Relevance 0
This uncoupling of eNOS plays an important role in endothelial cell dysfunction and increased oxidative stress. [47] Hyperglycemia and peroxynitrite (ONOO') also induce eNOS uncoupling with increases in O2' production. [48] Just published, Verma S and colleagues reported that CRP caused a marked down regulation of eNOS mRNA and protein expression with subsequent lower eNO production.
Regulation (regulation) of eNOS in endothelial cell associated with hyperglycemia and stress
11) Confidence 0.24 Published 2002 Journal Cardiovasc Diabetol Section Body Doc Link PMC140143 Disease Relevance 0.84 Pain Relevance 0.10
Changes in the expression (mRNA and protein levels) of NOS1, NOS2 and NOS3 in the lumbar section of the spinal cord from sciatic nerve-injured or sham-operated WT, NOS1-KO and NOS2-KO mice at 21 days after surgery were analyzed by using a two-way ANOVA (genotype and surgery as between factors of variation), followed by a one-way ANOVA when required.
Spec (analyzed) Regulation (Changes) of NOS3 in sciatic nerve associated with targeted disruption, sciatic nerve and spinal cord
12) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001461 Disease Relevance 0.63 Pain Relevance 0.31
By contrast, topical superfusion of 7-NI (100 microM) attenuated the ACh response in eNOS mutants only (66%, P < 0.05, and 25% decrease, P < 0.05, at 1 and 10 microM ACh, respectively).
Regulation (response) of eNOS
13) Confidence 0.23 Published 1998 Journal Am. J. Physiol. Section Abstract Doc Link 9486242 Disease Relevance 0.17 Pain Relevance 0.11
The data suggest that GSNO-R activity is modulated by both estrogens and androgens in conjunction with hormonal regulation of eNOS to maintain S-nitrosothiol homeostasis.
Regulation (regulation) of eNOS
14) Confidence 0.22 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2982841 Disease Relevance 0.31 Pain Relevance 0
Secondary prevention that involves factors which influence eNOS function and NO bioavailability may be of even more benefit among patients with T2DM, especially in women.
Regulation (influence) of eNOS associated with diabetes mellitus and bioavailability
15) Confidence 0.20 Published 2008 Journal BMC Cardiovasc Disord Section Body Doc Link PMC2636751 Disease Relevance 1.01 Pain Relevance 0.09
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 eNOS in heart associated with stress, ischemia and injury
16) Confidence 0.17 Published 2010 Journal BMC Physiol Section Body Doc Link PMC2927582 Disease Relevance 0.50 Pain Relevance 0.12
A number of signaling molecules have been shown to participate in obesity and
                   aging-induced biological responses and regulation of cardiac function, including
                   Akt, the Akt downstream signal eNOS and the cellular fuel AMPK [29], [30]. 
Regulation (regulation) of eNOS associated with aging and obesity
17) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852499 Disease Relevance 0.95 Pain Relevance 0
Tetrahydrobiopterin (BH4) is an essential cofactor that critically controls the assembly and activity of eNOS.
Regulation (controls) of eNOS associated with tetrahydrobiopterin
18) Confidence 0.10 Published 2010 Journal Curr Hypertens Rep Section Body Doc Link PMC2910890 Disease Relevance 0.39 Pain Relevance 0.31

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox