INT10612

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Context Info
Confidence 0.78
First Reported 1981
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 13
Total Number 13
Disease Relevance 8.91
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.

cytosol (NLRP3) signal transduction (NLRP3) cytoplasm (NLRP3)
Anatomy Link Frequency
liver 1
endothelial cell 1
sympathetic 1
sympathetic nervous system 1
T cells 1
NLRP3 (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 15 99.68 Very High Very High Very High
narcan 2 99.28 Very High Very High Very High
Opioid 4 98.48 Very High Very High Very High
tetrodotoxin 1 96.60 Very High Very High Very High
Enkephalin 4 95.68 Very High Very High Very High
Neurotransmitter 1 95.28 Very High Very High Very High
MU agonist 1 94.60 High High
Action potential 3 90.76 High High
cytokine 47 89.40 High High
Inflammation 99 89.00 High High
Disease Link Frequency Relevance Heat
Shock 14 100.00 Very High Very High Very High
Syndrome 25 98.56 Very High Very High Very High
Tumor Necrosis Factor Receptor-associated Periodic Syndrome 3 96.44 Very High Very High Very High
Stress 68 96.40 Very High Very High Very High
Heart Rate Under Development 4 95.44 Very High Very High Very High
Cryopyrin-associated Periodic Syndromes 3 95.44 Very High Very High Very High
Atherosclerosis 28 95.40 Very High Very High Very High
Castlemans Disease 3 92.48 High High
Glioma 1 90.16 High High
Hyperplasia 4 90.04 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results suggest the etiologic possibility that the patients have a decreased dopaminergic inhibition of prostaglandin E2-mediated norepinephrine secretion, which causes periodic discharge of norepinephrine and concomitant release of ACTH and AVP.
Localization (release) of AVP
1) Confidence 0.78 Published 1988 Journal Acta Endocrinol. Section Abstract Doc Link 2837885 Disease Relevance 0.50 Pain Relevance 0.23
Mutations were not found in the coding regions of MVK, TNFRSF1A, and NLRP3 (previously NALP3/CIAS1) making the diagnoses of Hyper IgD syndrome, TNF receptor associated periodic syndrome (TRAPS), and Muckle Wells/Familial Cold Urticaria all unlikely.
Localization (regions) of CIAS1 associated with cryopyrin-associated periodic syndromes, tumor necrosis factor receptor-associated periodic syndrome and syndrome
2) Confidence 0.73 Published 2008 Journal Cases J Section Body Doc Link PMC2612653 Disease Relevance 1.80 Pain Relevance 0.18
Using western blotting technique, we aimed to detect the presence of Nalp1 and Nalp3 proteins in the HCE-T cells.
Localization (presence) of Nalp3 in T cells
3) Confidence 0.70 Published 2008 Journal Molecular Vision Section Body Doc Link PMC2526096 Disease Relevance 0 Pain Relevance 0
The cells responded to factors known to stimulate ACTH release, including high K+, CRF, and angiotensin II (AII).
Localization (release) of AII
4) Confidence 0.58 Published 1987 Journal Endocrinology Section Abstract Doc Link 3036472 Disease Relevance 0.31 Pain Relevance 0.14
Mutations were not found in the coding regions of MVK, TNFRSF1A, and NLRP3 (previously NALP3/CIAS1) making the diagnoses of Hyper IgD syndrome, TNF receptor associated periodic syndrome (TRAPS), and Muckle Wells/Familial Cold Urticaria all unlikely.
Localization (regions) of NLRP3 associated with cryopyrin-associated periodic syndromes, tumor necrosis factor receptor-associated periodic syndrome and syndrome
5) Confidence 0.46 Published 2008 Journal Cases J Section Body Doc Link PMC2612653 Disease Relevance 1.79 Pain Relevance 0.18
-H2AX foci can be decreased similarly by heat shock and MWs from mobile telephones.
Localization (decreased) of MWs associated with shock
6) Confidence 0.43 Published 2005 Journal Environ Health Perspect Section Body Doc Link PMC1280397 Disease Relevance 0.45 Pain Relevance 0
For example, nigericin does not evoke any dye uptake but is well known to activate NLRP3 inflammasome release of IL-1?
Localization (release) of NLRP3
7) Confidence 0.30 Published 2009 Journal Purinergic Signal Section Body Doc Link PMC2686830 Disease Relevance 0 Pain Relevance 0
Angiotensin II (AII) at concentrations of 0.1 and 1 microM mobilized free Ca2+ from an intracellular pool, and this effect was antagonized by the AII receptor antagonist saralasin.
Localization (mobilized) of AII associated with antagonist
8) Confidence 0.28 Published 1992 Journal Neuropeptides Section Abstract Doc Link 1508324 Disease Relevance 0.18 Pain Relevance 0.76
Mutations were not found in the coding regions of MVK, TNFRSF1A, and NLRP3 (previously NALP3/CIAS1) making the diagnoses of Hyper IgD syndrome, TNF receptor associated periodic syndrome (TRAPS), and Muckle Wells/Familial Cold Urticaria all unlikely.
Localization (regions) of NALP3 associated with cryopyrin-associated periodic syndromes, tumor necrosis factor receptor-associated periodic syndrome and syndrome
9) Confidence 0.20 Published 2008 Journal Cases J Section Body Doc Link PMC2612653 Disease Relevance 1.79 Pain Relevance 0.18
We investigated the possibility that this is due in part to alterations in activation of either release-inhibiting alpha 2-adrenoceptors or release-enhancing angiotensin II (AII) receptors at postganglionic sympathetic nerve endings.
Localization (release-inhibiting) of AII in sympathetic
10) Confidence 0.20 Published 1994 Journal J. Cardiovasc. Pharmacol. Section Abstract Doc Link 7515988 Disease Relevance 0.36 Pain Relevance 0.05
The endothelial cell releases angiotensin-II (AII) as an antagonist of NO by means of hydrolyzing angiotensin-I by angiotensine converting enzyme (ACE).
Localization (releases) of AII in endothelial cell associated with antagonist
11) Confidence 0.16 Published 2006 Journal Cardiovasc Diabetol Section Body Doc Link PMC1434727 Disease Relevance 1.31 Pain Relevance 0.31
The renin, produced by the kidney, acts on the angiotensinogen, produced by the liver degrading it to AI, which in turn will be acted on by circulating or tissue ACE and hydrolyzed to AII.
Localization (hydrolyzed) of AII in liver
12) Confidence 0.13 Published 2006 Journal Cardiovasc Diabetol Section Body Doc Link PMC1434727 Disease Relevance 0.43 Pain Relevance 0.24
It is concluded that the depressor response to AII in the conscious chicken is due to release of vasotocin, the avian equivalent to vasopressin, and the subsequent pressor response to AII is due to activation of the sympathetic nervous system.
Localization (release) of AII in sympathetic nervous system
13) Confidence 0.13 Published 1981 Journal Res. Commun. Chem. Pathol. Pharmacol. Section Abstract Doc Link 7268192 Disease Relevance 0 Pain Relevance 0

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