INT288911

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Context Info
Confidence 0.07
First Reported 2009
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 3
Disease Relevance 2.96
Pain Relevance 0.28

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

mitochondrion (CYBB) small molecule metabolic process (AGT) aging (AGT)
extracellular matrix organization (AGT) cytoplasm (CYBB) cell-cell signaling (AGT)
Anatomy Link Frequency
blood 1
AGT (Homo sapiens)
CYBB (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 4 99.72 Very High Very High Very High
fibrosis 2 86.08 High High
Inflammatory response 1 84.96 Quite High
cytokine 2 77.04 Quite High
chemokine 3 70.24 Quite High
noradrenaline 2 28.88 Quite Low
adenocard 21 7.76 Low Low
antagonist 28 5.00 Very Low Very Low Very Low
beta blocker 10 5.00 Very Low Very Low Very Low
Dopamine 10 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 8 100.00 Very High Very High Very High
Syndrome 91 99.84 Very High Very High Very High
Vasculitis 1 99.72 Very High Very High Very High
Pressure And Volume Under Development 24 98.34 Very High Very High Very High
Increased Venous Pressure Under Development 17 97.40 Very High Very High Very High
Atherosclerosis 5 92.48 High High
Hyperemia 12 87.80 High High
Heart Rate Under Development 31 86.64 High High
Hypertrophy 6 86.60 High High
Fibrosis 2 86.08 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Angiotensin II raises blood pressure (BP) through direct vasoconstriction mediated by AT1 receptor stimulation, and sodium and water retention mostly mediated by the stimulation of the synthesis of aldosterone.6 In addition, angiotensin II enhances oxidative stress by stimulating NADPH oxidase, with consequent generation of reactive oxygen species.7,8 Reactive oxygen species, by enhancing inactivation of nitric oxide produced by endothelial cells, accelerate the progression of atherosclerosis and induce plaque destabilization.7,8 Moreover, angiotensin II may trigger intracellular reactions leading to myocite and vascular hypertrophy, fibrosis and apoptosis.
angiotensin II Positive_regulation (stimulating) of NADPH oxidase in blood associated with stress, fibrosis, hypertrophy, pressure and volume under development, atherosclerosis, apoptosis and increased venous pressure under development
1) Confidence 0.07 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2788599 Disease Relevance 0.97 Pain Relevance 0.04
Besides vasoconstriction and sodium retention that lead to increased preload and afterload, one of the most deleterious actions of the RAAS in CRS is the activation of NADPH-oxidase by angiotensin II.
angiotensin II Positive_regulation (activation) of NADPH-oxidase associated with syndrome and increased venous pressure under development
2) Confidence 0.03 Published 2011 Journal International Journal of Nephrology Section Body Doc Link PMC3010630 Disease Relevance 0.87 Pain Relevance 0.11
Angiotensin II activates both NADH-oxidase and NADPH-oxidase [36], which then generates reactive oxygen species.
Angiotensin II Positive_regulation (activates) of NADPH-oxidase
3) Confidence 0.00 Published 2011 Journal International Journal of Nephrology Section Body Doc Link PMC2989717 Disease Relevance 1.12 Pain Relevance 0.12

General Comments

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