INT112003

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Context Info
Confidence 0.73
First Reported 2002
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 94
Total Number 94
Disease Relevance 66.32
Pain Relevance 12.16

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) plasma membrane (ROS1)
Anatomy Link Frequency
macrophages 5
neutrophils 5
lung 4
neurons 4
respiratory 3
ROS1 (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 677 100.00 Very High Very High Very High
chemokine 185 100.00 Very High Very High Very High
Inflammatory mediators 53 100.00 Very High Very High Very High
Central nervous system 143 99.96 Very High Very High Very High
addiction 58 99.92 Very High Very High Very High
antagonist 174 99.76 Very High Very High Very High
Inflammation 1743 99.74 Very High Very High Very High
Spinal cord 169 99.00 Very High Very High Very High
Glutamate 219 98.94 Very High Very High Very High
monoamine 19 98.90 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 1935 100.00 Very High Very High Very High
Apoptosis 1727 100.00 Very High Very High Very High
Disease 1127 100.00 Very High Very High Very High
Parkinson's Disease 92 100.00 Very High Very High Very High
Stress 3291 99.96 Very High Very High Very High
Injury 905 99.96 Very High Very High Very High
Adult Respiratory Distress Syndrome 22 99.84 Very High Very High Very High
Infection 347 99.76 Very High Very High Very High
Aging 164 99.52 Very High Very High Very High
Acquired Immune Deficiency Syndrome Or Hiv Infection 112 99.52 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
For example, microglia, the principal mediator of inflammation in the CNS, release a large amount of ROS/RNS upon activation (Colton and Gilbert, 1987; Moss and Bates, 2001; Liu et al., 2002; Block et al., 2007), leading to OS increases and further neuronal damage.


Localization (release) of ROS in microglia associated with stress, inflammation and central nervous system
1) Confidence 0.73 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874397 Disease Relevance 0.99 Pain Relevance 0.42
Currently available evidence shows that mitochondria isolated from CA1 neurons release more ROS than those from CA3 neurons (Mattiasson et al., 2003a).
Localization (release) of ROS in neurons
2) Confidence 0.64 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874397 Disease Relevance 0.52 Pain Relevance 0
Dysfunctional mitochondria in vulnerable neurons can release more ROS and thus maintain a vicious cycle of oxidative modification of mitochondrial proteins leading to further OS.
Localization (release) of ROS in neurons associated with stress
3) Confidence 0.64 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874397 Disease Relevance 0.38 Pain Relevance 0.08
TNF-alpha overproduction is thought to be the main contributor to increased ROS release in patients with RA.
Localization (release) of ROS associated with rheumatoid arthritis
4) Confidence 0.63 Published 2008 Journal Iran J Allergy Asthma Immunol Section Abstract Doc Link 19052348 Disease Relevance 1.45 Pain Relevance 0.43
In addition, redox-active transition metal ions that are known to increase ROS formation through the Fenton reaction, such as iron and copper, bind with high affinity to A?
Localization (formation) of ROS
5) Confidence 0.60 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874397 Disease Relevance 1.10 Pain Relevance 0
The iron levels in this brain region are high, as is the activity of monoamine oxidase, and both of these entities contribute to the generation of ROS in these neurons.
Localization (generation) of ROS in neurons associated with monoamine
6) Confidence 0.60 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874397 Disease Relevance 0.82 Pain Relevance 0.18
The data show that the copper-chloroquine complexes 1-3 inhibit neutrophil release of ROS in PMNs activated either by a phorbol ester or by phagocytosable particles.
Localization (release) of ROS in PMNs
7) Confidence 0.59 Published 2005 Journal J. Inorg. Biochem. Section Abstract Doc Link 15967505 Disease Relevance 0.07 Pain Relevance 0.09
Mitochondria isolated from the CA1 release more ROS than those from the CA3 region (Mattiasson et al., 2003a).
Localization (release) of ROS
8) Confidence 0.56 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2874397 Disease Relevance 0.81 Pain Relevance 0
The other points of generation of ROS are the cytoplasmic NADPH-oxidase, cytochrome p450 enzymes and the xanthine oxidoreductase enzymes.
Localization (generation) of ROS
9) Confidence 0.55 Published 2005 Journal Reprod Biol Endocrinol Section Body Doc Link PMC1215514 Disease Relevance 0.63 Pain Relevance 0
increase towards the late secretory phase and ROS triggers the release of prostaglandin F2 ?
Localization (phase) of ROS
10) Confidence 0.55 Published 2005 Journal Reprod Biol Endocrinol Section Body Doc Link PMC1215514 Disease Relevance 0.49 Pain Relevance 0.13
Activation of JNK by morphine led to reactive oxygen species (ROS) generation via the mitochondrial permeability transition pore, because the mPTP inhibitor cyclosporin A significantly inhibited ROS generation.
Localization (generation) of ROS in pore associated with morphine
11) Confidence 0.52 Published 2009 Journal FEBS J. Section Abstract Doc Link 19292871 Disease Relevance 0.38 Pain Relevance 0.62
Although this is very good evidence for the production of mitochondrial ROS generation by rat spermatozoa, it is uncertain as to whether mitochondria are an important source of ROS in the spermatozoa of other species, particularly the human [25].
Localization (generation) of ROS in spermatozoa
12) Confidence 0.51 Published 2005 Journal Reprod Biol Endocrinol Section Body Doc Link PMC1315356 Disease Relevance 0 Pain Relevance 0
These resident macrophages are indeed able to down-regulate under physiological conditions antigen presentation and T cell activation by releasing TNF, IL-10 and ROS.
Localization (releasing) of ROS in T cell
13) Confidence 0.49 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2584013 Disease Relevance 1.20 Pain Relevance 0.17
As an indicator of TRPV1 mediated ROS released into the supernatant, ROS metabolites 2,5-DHBA and 2,3-DHBA were trapped with salicylic acid [50] and the samples analyzed by high performance liquid chromatography with electrochemical detection (HPLC-ECD).
Localization (released) of ROS
14) Confidence 0.48 Published 2010 Journal Mol Pain Section Body Doc Link PMC2924298 Disease Relevance 0 Pain Relevance 0.11
First, only some HCV-related proteins, such as NS5A, NS3 and HCV core protein, are likely to play roles in mediating redox perturbations, which can include increased generation of both ROS and RNS, iNOS and COX-2 (NS5A and C).
Localization (generation) of ROS associated with hepatitis c virus infection
15) Confidence 0.46 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2584013 Disease Relevance 1.28 Pain Relevance 0.07
Such a discrepancy between the effects reported for ROS and HNE is likely to depend on the different mechanisms of action: although Uchida and coworkers [23,332] have proposed that, in some cells, HNE may result in mitochondrial damage and subsequent release of ROS (at high concentrations, however, such as 20 ?
Localization (reported) of ROS
16) Confidence 0.46 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2584013 Disease Relevance 0.05 Pain Relevance 0
One can envisage a scenario in which, in the presence of continuous antigen stimulation, cytokines released by lymphocytes can actively sustain Kupffer cell-mediated release of cytokines and chemokines as well as of ROS and NO, which, in turn, may contribute to the perpetuation of oxidative injury, the inflammatory response and fibrogenesis.
Localization (release) of ROS in Kupffer cell associated with fibrosis, chemokine, inflammatory response, injury and cytokine
17) Confidence 0.43 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2584013 Disease Relevance 1.32 Pain Relevance 0.31
Several relevant events for fibrosclerotic progression of CLDs may be considered relatively independent of the specific aetiology, as detailed in Figure 13; in these conditions of persisting tissue injury, ROS and other related mediators, released by damaged cells or activated inflammatory cells, are likely to play a relevant role.
Localization (released) of ROS associated with liver disease, inflammation and injury
18) Confidence 0.43 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2584013 Disease Relevance 1.05 Pain Relevance 0.05
In such a chronic scenario, ROS and other reactive intermediates or pro-oxidants (for example, HOCl) released by activated inflammatory cells, either resident (that is, Kupffer cells) or recruited from peripheral blood, may significantly contribute to injury perpetuation.
Localization (released) of ROS in blood associated with inflammation and injury
19) Confidence 0.43 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2584013 Disease Relevance 1.47 Pain Relevance 0.34
Indeed, TNF-TNFRI interaction may serve as a paradigm for describing the role of ROS (here generated mostly by mitochondria) since (see below) several conditions leading to the increased generation of ROS will converge on sustained JNK activation and its consequences.
Localization (generation) of ROS
20) Confidence 0.40 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2584013 Disease Relevance 1.02 Pain Relevance 0.04

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