INT91594

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Context Info
Confidence 0.78
First Reported 2000
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 12
Total Number 14
Disease Relevance 5.39
Pain Relevance 2.02

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

small molecule metabolic process (NOS3) aging (NOS3) Golgi apparatus (NOS3)
mitochondrion organization (NOS3) cytoplasm (NOS3) cytosol (NOS3)
Anatomy Link Frequency
neuronal 2
myocyte 2
endothelial cells 2
smooth muscles 1
odontoblasts 1
NOS3 (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 8 99.68 Very High Very High Very High
pulpitis 4 99.60 Very High Very High Very High
bradykinin 52 99.30 Very High Very High Very High
agonist 71 98.58 Very High Very High Very High
Inflammation 97 96.56 Very High Very High Very High
Angina 7 95.56 Very High Very High Very High
cytokine 14 90.68 High High
Central nervous system 17 79.04 Quite High
Inflammatory mediators 2 78.40 Quite High
ischemia 1 68.44 Quite High
Disease Link Frequency Relevance Heat
Pulpitis 4 99.60 Very High Very High Very High
Diabetes Mellitus 79 99.28 Very High Very High Very High
Increased Venous Pressure Under Development 86 99.00 Very High Very High Very High
Atherosclerosis 7 97.88 Very High Very High Very High
Pre-eclampsia 33 97.08 Very High Very High Very High
Disease 35 96.92 Very High Very High Very High
INFLAMMATION 109 96.56 Very High Very High Very High
Cv General 3 Under Development 7 95.56 Very High Very High Very High
Acute Coronary Syndrome 5 95.28 Very High Very High Very High
Targeted Disruption 12 94.64 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We have localized the eNOS and iNOS by immunohistochemistry and have tested their mRNA expression by RT-PCR and protein levels by Western blots. eNOS is present in the endothelial cells and odontoblasts of the healthy pulp, but an elevation of eNOS mRNA and protein levels with a concomitant dilation of vessels was characteristic under pathological conditions.
Localization (localized) of eNOS in endothelial cells
1) Confidence 0.78 Published 2004 Journal J. Dent. Res. Section Abstract Doc Link 15044505 Disease Relevance 0.26 Pain Relevance 0.22
In fact, direct in vivo evidence that a continuous eNOS-dependent local release of NO modulates basal vascular tone is lacking.
Localization (release) of eNOS
2) Confidence 0.54 Published 2009 Journal Trends in Cardiovascular Medicine Section Body Doc Link PMC2984617 Disease Relevance 0.24 Pain Relevance 0.09
Because l-NMMA reduces basal NO production by cultured endothelial cells and induces vasoconstriction in isolated vascular rings, and eNOS-derived NO is involved in agonist-induced vasodilation, it has generally been considered that sustained release of NO by eNOS is the underlying mechanism for “tonic vasodilatation” observed in vivo (Moncada et al. 1993, 2006).
Localization (release) of eNOS in endothelial cells associated with agonist and increased venous pressure under development
3) Confidence 0.54 Published 2009 Journal Trends in Cardiovascular Medicine Section Body Doc Link PMC2984617 Disease Relevance 0.58 Pain Relevance 0.05
In the human endometrium, eNOS have been localized in the glandular epithelium and in endometrial microvascular endothelium, primarily during the luteal phase. iNOS has been found in the endometrial epithelium during menstruation, in immunocompetent endometrial cells, and in decidualized stromal cells.
Localization (localized) of eNOS in epithelium
4) Confidence 0.51 Published 2000 Journal Hum. Reprod. Section Abstract Doc Link 11041226 Disease Relevance 0.22 Pain Relevance 0.08
Although three distinct isoforms of NO synthase (NOS)—endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS—may generate NO with the use of l-arginine as substrate, it has generally been accepted that the local regulation of vascular tone in health is primarily dependent upon the release of NO from eNOS (Deanfield et al. 2007, Moncada and Higgs 2006).
Localization (release) of eNOS in neuronal
5) Confidence 0.51 Published 2009 Journal Trends in Cardiovascular Medicine Section Body Doc Link PMC2984617 Disease Relevance 0.18 Pain Relevance 0
Myatt et al. comparing the presence and localization of eNOS and nitrotyrosine (a marker of peroxynitrite formed by interaction of NO and superoxide) in placental villi from normotensive pregnancies and pregnancies complicated by preeclampsia, found that the later displays greater nitrotyrosine immunostaining in vascular endothelium, in the surrounding vascular smooth muscles and in villous stroma[116].
Localization (localization) of eNOS in smooth muscles associated with pre-eclampsia
6) Confidence 0.36 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2739214 Disease Relevance 0.27 Pain Relevance 0
EPCs by a mechanism independent of eNOS [94]; however, further studies based on
Localization (mechanism) of eNOS
7) Confidence 0.31 Published 2008 Journal PPAR Research Section Body Doc Link PMC2366048 Disease Relevance 0.30 Pain Relevance 0
We have localized the eNOS and iNOS by immunohistochemistry and have tested their mRNA expression by RT-PCR and protein levels by Western blots. eNOS is present in the endothelial cells and odontoblasts of the healthy pulp, but an elevation of eNOS mRNA and protein levels with a concomitant dilation of vessels was characteristic under pathological conditions.
Localization (localized) of eNOS in odontoblasts
8) Confidence 0.27 Published 2004 Journal J. Dent. Res. Section Abstract Doc Link 15044505 Disease Relevance 0.26 Pain Relevance 0.22
In the heart, endothelial NOS (eNOS) is localized n caveolin-enriched myocyte membrane fractions and it has been shown that lipid draft-disrupting agents severely compromise NO-dependent inhibition of adenylyl cyclase types 5 and 6 [35].
Localization (localized) of eNOS in myocyte
9) Confidence 0.19 Published 2005 Journal BMC Cell Biol Section Body Doc Link PMC1090567 Disease Relevance 0.05 Pain Relevance 0.03
In the heart, endothelial NOS (eNOS) is localized n caveolin-enriched myocyte membrane fractions and it has been shown that lipid draft-disrupting agents severely compromise NO-dependent inhibition of adenylyl cyclase types 5 and 6 [35].
Localization (localized) of endothelial NOS in myocyte
10) Confidence 0.19 Published 2005 Journal BMC Cell Biol Section Body Doc Link PMC1090567 Disease Relevance 0.05 Pain Relevance 0.03
BKmig derived from H PBMC generated NO in response to BK stimulation through a mechanism involving both kinin receptors (being similarly blunted by B1R antagonist LdA-BK and B2R antagonist icatibant) and eNOS (being totally blocked by L-NIO), while T1D BKmig did not (Fig. 7A).
Neg (blocked) Localization (blocked) of eNOS associated with diabetes mellitus, antagonist and bradykinin
11) Confidence 0.19 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2887352 Disease Relevance 0.61 Pain Relevance 0.40
In situ RT-PCR was also carried out to co-localize the eNOS messengers and the VSMC phenotype.
Localization (localize) of eNOS
12) Confidence 0.17 Published 2005 Journal Eur J Histochem Section Abstract Doc Link 15823793 Disease Relevance 1.08 Pain Relevance 0.36
Recent publications suggest that endothelial-derived NO is required for Ang1-induced angiogenesis and that the PI3-kinase signaling mediates the activation of eNOS and NO release in response to Ang1 [11].
Neg (NO) Localization (release) of eNOS
13) Confidence 0.11 Published 2006 Journal BMC Cell Biol Section Body Doc Link PMC1456963 Disease Relevance 0.45 Pain Relevance 0.09
Nitric oxide (NO), a gaseous free radical, is released by a family of enzymes, including endothelia NOS (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS), with the formation of stoichiometric amounts of L-citrulline from L-arginine.59 Excessive and prolonged iNOS-mediated NO generation has attracted attention because of its relevance to inflammation.
Localization (released) of eNOS in neuronal associated with inflammation
14) Confidence 0.05 Published 2005 Journal Yonsei Medical Journal Section Body Doc Link PMC2562783 Disease Relevance 0.83 Pain Relevance 0.45

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