INT143357

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Context Info
Confidence 0.36
First Reported 2005
Last Reported 2011
Negated 2
Speculated 1
Reported most in Body
Documents 48
Total Number 49
Disease Relevance 27.76
Pain Relevance 6.00

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

cell differentiation (Ros1) cell proliferation (Ros1) signal transduction (Ros1)
plasma membrane (Ros1) kinase activity (Ros1)
Anatomy Link Frequency
CII 3
neuronal 3
neurons 3
hepatocytes 2
cartilage 2
Ros1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 498 99.76 Very High Very High Very High
Paracetamol 10 98.82 Very High Very High Very High
rheumatoid arthritis 250 98.04 Very High Very High Very High
ischemia 73 97.84 Very High Very High Very High
Osteoarthritis 246 97.68 Very High Very High Very High
metalloproteinase 33 97.24 Very High Very High Very High
potassium channel 228 97.18 Very High Very High Very High
Potency 63 93.76 High High
fibrosis 55 93.72 High High
chemokine 56 89.76 High High
Disease Link Frequency Relevance Heat
Toxicity 80 100.00 Very High Very High Very High
Lung Injury 2 99.96 Very High Very High Very High
Chronic Disease 9 99.92 Very High Very High Very High
Stress 352 99.90 Very High Very High Very High
INFLAMMATION 590 99.76 Very High Very High Very High
Alzheimer's Dementia 74 99.74 Very High Very High Very High
Aging 69 99.60 Very High Very High Very High
Arthritis 271 99.52 Very High Very High Very High
Natriuresis 1 98.68 Very High Very High Very High
Disease 594 98.56 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In fact, insulin reduces ROS generation by mononuclear cells, suppresses NADPH oxidase expression and intranuclear NF-kB binding, induces IkB expression and suppresses some inflammatory molecules [69,76].
ROS Binding (generation) of in mononuclear cells associated with inflammation
1) Confidence 0.36 Published 2005 Journal Immun Ageing Section Body Doc Link PMC1166571 Disease Relevance 1.65 Pain Relevance 0.34
The results obtained disclose the effectual role of AuNPs as an anti-oxidative agent, by inhibiting the formation of ROS, scavenging free radicals; thus increasing the anti-oxidant defense enzymes and creating a sustained control over hyperglycemic conditions which consequently evoke the potential of AuNPs as an economic therapeutic remedy in diabetic treatments and its complications.



ROS Binding (formation) of associated with diabetes mellitus
2) Confidence 0.15 Published 2010 Journal J Nanobiotechnology Section Abstract Doc Link PMC2914719 Disease Relevance 0.55 Pain Relevance 0
Through its distinctive combination of antioxidant and anti-glycating properties, carnosine can attenuate cellular oxidative stress and inhibit the intracellular formation of ROS and reactive nitrogen species.
ROS Binding (formation) of associated with stress
3) Confidence 0.13 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2970564 Disease Relevance 0.19 Pain Relevance 0
High reactive oxygen species (ROS) levels are typically associated with the aging process, where there is ROS overproduction in conjunction with a reduction in the cellular antioxidant defense [4].
ROS Binding (associated) of associated with aging
4) Confidence 0.11 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 1.16 Pain Relevance 0
has also been shown to induce the formation of ROS in mature hippocampal neurons, mediated via N-methyl-D-Aspartate (NMDA) receptors.
ROS Binding (formation) of in neurons
5) Confidence 0.11 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866668 Disease Relevance 1.22 Pain Relevance 0
It was also found that APAP selectively caused escalation in reactive oxygen species (ROS) formation and intracellular GSH (ICG) depletion in melanocytic human SK-MEL-28 and murine B16-F0 melanoma cells that express functional tyrosinase whereas it lacked significant effects on ROS formation and ICG in amelanotic C32 melanoma cells that do not express functional tyrosinase.
ROS Binding (formation) of in SK-MEL-28 associated with paracetamol and skin cancer
6) Confidence 0.11 Published 2009 Journal Int. J. Oncol. Section Abstract Doc Link 19513568 Disease Relevance 1.16 Pain Relevance 0.71
We generated ROS with 35 seconds of EL and then replaced the K-H solution for measurements after 15 minutes of equilibrium.
ROS Binding (generated) of
7) Confidence 0.10 Published 2010 Journal Korean Journal of Anesthesiology Section Body Doc Link PMC2926425 Disease Relevance 0.80 Pain Relevance 0.24
Effect of bilirubin on ROS formation was tested at concentrations of 0.25–25 ?
ROS Binding (formation) of
8) Confidence 0.09 Published 2006 Journal BMC Cardiovasc Disord Section Body Doc Link PMC1654181 Disease Relevance 0.07 Pain Relevance 0
Further study is needed to illuminate the pathway that leads from lung injury, associated with ROS and acute inflammation, to initiation of the fibrogenic process, which involves remodeling mediators such as MMPs and TIMPs.
ROS Binding (associated) of in lung associated with lung injury, inflammation and metalloproteinase
9) Confidence 0.08 Published 2005 Journal Respir Res Section Body Doc Link PMC548519 Disease Relevance 0.65 Pain Relevance 0.36
Since the applied GTN dose was low, wild type mitochondria showed no increased ROS formation in response to GTN in vivo treatment which could be best explained by antioxidant properties of the small amounts of the solvent ethanol.
ROS Neg (no) Binding (formation) of
10) Confidence 0.07 Published 2006 Journal BMC Cardiovasc Disord Section Body Doc Link PMC1654181 Disease Relevance 0.14 Pain Relevance 0.13
Mitochondria from rat heart were prepared by a similar procedure and ROS formation was detected by L-012 ECL as published [31].
ROS Binding (formation) of in heart
11) Confidence 0.07 Published 2006 Journal BMC Cardiovasc Disord Section Body Doc Link PMC1654181 Disease Relevance 0.08 Pain Relevance 0
ROS are well recognized to have primarily deleterious effects in mammalian cells.
ROS Binding (recognized) of
12) Confidence 0.07 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2361191 Disease Relevance 1.03 Pain Relevance 0
Currently, NASH pathogenesis is proposed to occur in response to fat accumulation in hepatocytes coupled with mitochondrial dysfunction, which may be manifested by disrupted fatty acid oxidation, depressed bioenergetics and increased oxidative stress arising from enhanced generation of ROS (reactive oxygen species) and RNS (reactive nitrogen species) [8].
ROS Binding (generation) of in hepatocytes associated with stress, parkinson's disease and nash(non-alcoholic steatohepatitis)
13) Confidence 0.07 Published 2008 Journal Biochemical Journal Section Body Doc Link PMC2637578 Disease Relevance 1.45 Pain Relevance 0.06
Specifically, damaged mitochondria exposed to low O2 will be under a greater reductive stress and it is under these conditions that the interaction of NO with mitochondria may be pathologic, because ROS and RNS formation is enhanced and ATP production is compromised [19].
ROS Binding (formation) of associated with stress
14) Confidence 0.07 Published 2008 Journal Biochemical Journal Section Body Doc Link PMC2637578 Disease Relevance 0.73 Pain Relevance 0
expression and this is correlated with COX-2 expression and formation of ROS (as indicated by HE intensity).
ROS Binding (formation) of
15) Confidence 0.07 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2923122 Disease Relevance 0.83 Pain Relevance 0.16
In summary, previous studies have proposed that the interaction of NO with cytochrome c oxidase is a regulated and physiologically relevant pathway that functions to control ROS formation for redox signalling and maintain O2 gradients in tissues [19].
ROS Binding (formation) of
16) Confidence 0.06 Published 2008 Journal Biochemical Journal Section Body Doc Link PMC2637578 Disease Relevance 0.38 Pain Relevance 0
For example, alterations in shear stress can lead to ROS-dependent NF-?
ROS Binding (lead) of associated with stress
17) Confidence 0.06 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2605224 Disease Relevance 0.45 Pain Relevance 0.26
Besides endogenous vascular cell production of superoxide, infiltrating macrophages within the arterial wall may also represent a source of ROS which can diffuse into the extracellular matrix and activate matrix metalloproteinases that are essential for vascular remodeling (14).
ROS Binding (source) of in macrophages associated with metalloproteinase
18) Confidence 0.06 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2605224 Disease Relevance 0.16 Pain Relevance 0.18
Assay for reactive oxygen species (ROS)
ROS Binding (Assay) of
19) Confidence 0.06 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2413210 Disease Relevance 0.07 Pain Relevance 0.06
Whereas the latter would be predicted to decrease ROS formation as outlined above, there is evidence to suggest than an increase pH gradient or matrix pH can increase ROS formation from complex 1 [254].
ROS Binding (formation) of
20) Confidence 0.05 Published 2007 Journal Biochimica et Biophysica Acta Section Body Doc Link PMC2212780 Disease Relevance 0 Pain Relevance 0.08

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