INT97596

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Context Info
Confidence 0.78
First Reported 2001
Last Reported 2011
Negated 0
Speculated 1
Reported most in Body
Documents 94
Total Number 95
Disease Relevance 90.69
Pain Relevance 40.41

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

extracellular space (S100a8) extracellular region (S100a8) plasma membrane (S100a8)
cytoskeleton (S100a8) cytoplasm (S100a8)
Anatomy Link Frequency
macrophages 11
microglia 6
immune cells 5
neutrophils 3
neuronal 3
S100a8 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 2720 100.00 Very High Very High Very High
cytokine 1291 100.00 Very High Very High Very High
Inflammatory mediators 167 100.00 Very High Very High Very High
Pain 94 99.78 Very High Very High Very High
cINOD 500 99.70 Very High Very High Very High
imagery 38 99.58 Very High Very High Very High
chemokine 269 99.52 Very High Very High Very High
agonist 233 99.46 Very High Very High Very High
Central nervous system 314 98.84 Very High Very High Very High
ischemia 480 98.42 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 3060 100.00 Very High Very High Very High
Obesity 560 99.98 Very High Very High Very High
Stress 220 99.98 Very High Very High Very High
Cancer 524 99.84 Very High Very High Very High
Disease 1268 99.80 Very High Very High Very High
Pain 90 99.78 Very High Very High Very High
Injury 549 99.76 Very High Very High Very High
Hyperplasia 28 99.72 Very High Very High Very High
Crystal Associated Disease 71 99.62 Very High Very High Very High
Necrosis 120 99.60 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Secondly, we found a strong colocalization of S100A8/A9 with granulocytes, but not with macrophages.
Localization (colocalization) of S100A8 in granulocytes
1) Confidence 0.78 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954806 Disease Relevance 0.90 Pain Relevance 0.07
Spectral imaging was used to analyze colocalization of S100A8/A9 and with Ly6G or F4/80.
Spec (analyze) Localization (colocalization) of S100A8 in F4/80 associated with imagery
2) Confidence 0.78 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954806 Disease Relevance 0 Pain Relevance 0.09
Depletion of S100A8 inhibited S-CorNV and inflammation
Localization (Depletion) of S100A8 associated with inflammation
3) Confidence 0.74 Published 2010 Journal Molecular Vision Section Body Doc Link PMC2994359 Disease Relevance 0.49 Pain Relevance 0.13
Considering the above observation that S100A8 and S100A9 proteins are located in both neutrophils and macrophages (Figure 2), we suggest that S100A8 (and S100A9) produced by neutrophils attracted more neutrophils in turn, thus forming a positive feedback in certain stages of inflammatory CorNV.
Localization (located) of S100A8 in neutrophils associated with inflammation
4) Confidence 0.74 Published 2010 Journal Molecular Vision Section Body Doc Link PMC2994359 Disease Relevance 0.41 Pain Relevance 0.15
S100A8/A9 expression and localization
Localization (localization) of S100A8
5) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954806 Disease Relevance 0.24 Pain Relevance 0.07
Upon stress S100A8/S100A9 are released into the extracellular compartment by damaged cells or macrophages and act as danger signals activating immune cells and vascular endothelium.
Localization (released) of S100A8 in vascular endothelium associated with stress
6) Confidence 0.68 Published 2010 Journal BMC Infect Dis Section Body Doc Link PMC2915993 Disease Relevance 0.51 Pain Relevance 0.18
It had no effect on the early events of peritoneal inflammation (vascular permeability, inflammatory cell infiltration, and release of pro-inflammatory cytokines) in acetic acid or zymosan-injected mice.
Localization (release) of pro-inflammatory associated with inflammation and cytokine
7) Confidence 0.68 Published 2008 Journal Eur. J. Pharmacol. Section Abstract Doc Link 18952075 Disease Relevance 1.52 Pain Relevance 0.72
Pre-treatment, but not post-treatment, with minocycline markedly attenuated increased pro-inflammatory cytokines release and oxidative and nitrosative stress in mononeuropathic rats.
Localization (release) of pro-inflammatory associated with stress, inflammation and cytokine
8) Confidence 0.68 Published 2008 Journal Eur. J. Pharmacol. Section Abstract Doc Link 18952075 Disease Relevance 1.93 Pain Relevance 0.91
Concluding, this study clearly shows minocycline, an inhibitor of microglial activation, by inhibiting the release of pro-inflammatory mediators and reducing oxidative stress prevented the development of neuropathic pain.
Localization (release) of pro-inflammatory associated with stress, inflammatory mediators and neuropathic pain
9) Confidence 0.68 Published 2008 Journal Eur. J. Pharmacol. Section Abstract Doc Link 18952075 Disease Relevance 1.65 Pain Relevance 0.79
The precise mechanism responsible for the antinociceptive effect of the extract still remains unclear, but seems to be partly related to modulation of the release or action of pro-inflammatory mediators involved in the models of pain used.
Localization (release) of pro-inflammatory associated with pain, inflammatory mediators and antinociceptive
10) Confidence 0.60 Published 2005 Journal J. Pharm. Pharmacol. Section Abstract Doc Link 16259764 Disease Relevance 0.61 Pain Relevance 0.87
Both S100A8 and S100A9 are known to be abundant cytosolic proteins in human PMN that can be secreted and exhibit potent actions in inflammatory cell recruitment [20].
Localization (secreted) of S100A8 associated with inflammation
11) Confidence 0.57 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2268966 Disease Relevance 0.76 Pain Relevance 0.64
S100A8 and S100A9 proteins are secreted in an energy-dependent fashion by phagocytes during inflammatory processes.
Localization (secreted) of S100A8 in phagocytes associated with inflammation
12) Confidence 0.41 Published 2009 Journal J Transl Med Section Body Doc Link PMC2666642 Disease Relevance 0.50 Pain Relevance 0.13
Chronic administration of melatonin for 5 days to antigen-primed mice increased the production of pro-inflammatory cytokine IL-10 but decreased the secretion of anti-inflammatory cytokine TNF-alpha.
Localization (secretion) of anti-inflammatory cytokine TNF-alpha associated with inflammation and cytokine
13) Confidence 0.37 Published 2001 Journal Mol. Cell. Biochem. Section Abstract Doc Link 11506187 Disease Relevance 0.20 Pain Relevance 0.47
The mechanism by which the extract produced antinociception still remains unclear, but a great part of this effect seems to be related to modulation of the release or action of pro-inflammatory mediators.
Localization (release) of pro-inflammatory associated with antinociception and inflammatory mediators
14) Confidence 0.25 Published 2007 Journal J Ethnopharmacol Section Abstract Doc Link 17350194 Disease Relevance 0.77 Pain Relevance 0.84
Considering the above observation that S100A8 and S100A9 proteins are located in both neutrophils and macrophages (Figure 2), we suggest that S100A8 (and S100A9) produced by neutrophils attracted more neutrophils in turn, thus forming a positive feedback in certain stages of inflammatory CorNV.
Localization (located) of S100A8 in macrophages associated with inflammation
15) Confidence 0.25 Published 2010 Journal Molecular Vision Section Body Doc Link PMC2994359 Disease Relevance 0.41 Pain Relevance 0.15
Upon stress S100A8/S100A9 are released into the extracellular compartment by damaged cells or macrophages and act as danger signals activating immune cells and vascular endothelium.
Localization (released) of S100A8 in immune cells associated with stress
16) Confidence 0.23 Published 2010 Journal BMC Infect Dis Section Body Doc Link PMC2915993 Disease Relevance 0.51 Pain Relevance 0.18
The predominant role of the innate immune system in systemic onset disease is also underscored by the high expression and serum concentrations of the calcium-binding proteins S100A8, S100A9, and S100A12, which are specifically secreted during activation of neutrophilic granulocytes and monocytes47).
Localization (secreted) of S100A8 in immune system associated with disease
17) Confidence 0.22 Published 2010 Journal Korean Journal of Pediatrics Section Body Doc Link PMC3012271 Disease Relevance 1.08 Pain Relevance 0.24
In particular, TAS1-191 (calgranulin C) secretion by tumor necrosis factor (TNF)- stimulated granulocytes causes target cell activation that results in the upregulated expression of proinflammatory cytokines such as TNF and IL1?
Localization (secretion) of calgranulin in granulocytes associated with necrosis, cancer and cytokine
18) Confidence 0.11 Published 2008 Journal DNA Research: An International Journal for Rapid Publication of Reports on Genes and Genomes Section Body Doc Link PMC2575881 Disease Relevance 0.78 Pain Relevance 0.16
An imbalance in favour of the pro-inflammatory cytokines interleukin-1?
Localization (favour) of pro-inflammatory associated with inflammation and cytokine
19) Confidence 0.08 Published 2011 Journal Evidence-based Complementary and Alternative Medicine : eCAM Section Body Doc Link PMC2976071 Disease Relevance 1.63 Pain Relevance 0.73
Upon activation, mast cells can immediately release large amounts of pro-inflammatory cytokines that are contained in pre-formed granules [8] and can continue to synthesize and release a wide array of pro-inflammatory mediators de novo.
Localization (release) of pro-inflammatory in mast cells associated with inflammatory mediators, inflammation and cytokine
20) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2923184 Disease Relevance 0.99 Pain Relevance 0.34

General Comments

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