INT178711

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Context Info
Confidence 0.84
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 15
Total Number 15
Disease Relevance 6.75
Pain Relevance 3.19

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

signal transduction (Tlr4) plasma membrane (Tlr4) intracellular (Tlr4)
cytoplasm (Tlr4)
Anatomy Link Frequency
blood 1
Nasal 1
respiratory 1
Tlr4 (Mus musculus)
Pain Link Frequency Relevance Heat
Thoracotomy 46 100.00 Very High Very High Very High
Inflammation 260 99.90 Very High Very High Very High
Inflammatory stimuli 8 99.88 Very High Very High Very High
cytokine 121 98.72 Very High Very High Very High
ketamine 6 97.68 Very High Very High Very High
ischemia 154 97.60 Very High Very High Very High
tolerance 255 93.60 High High
Dopamine 66 93.16 High High
isoflurane 13 92.24 High High
anesthesia 16 91.36 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 295 99.90 Very High Very High Very High
Injury 77 97.92 Very High Very High Very High
Cv Unclassified Under Development 129 97.60 Very High Very High Very High
Endotoxemia 7 97.36 Very High Very High Very High
Parkinson's Disease 6 96.80 Very High Very High Very High
Body Weight 12 96.64 Very High Very High Very High
Death 42 93.80 High High
Brain Hemorrhage 10 91.68 High High
Sepsis 23 91.20 High High
Atelectasis 20 89.64 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The factors liberated from necrotic cells could trigger inflammation and damage through Tlr4–NF-?
Protein_catabolism (damage) of Tlr4 associated with inflammation
1) Confidence 0.84 Published 2010 Journal Molecular Vision Section Body Doc Link PMC2956702 Disease Relevance 0.94 Pain Relevance 0.27
Effect of LPS administration on intestinal transit
Protein_catabolism (administration) of LPS
2) Confidence 0.75 Published 2005 Journal BMC Gastroenterol Section Body Doc Link PMC1177942 Disease Relevance 0.17 Pain Relevance 0
After 10 minutes of monitoring to ensure stability of pressure and respiratory rate, LPS (25 ?
Protein_catabolism (stability) of LPS in respiratory
3) Confidence 0.75 Published 2005 Journal BMC Gastroenterol Section Body Doc Link PMC1177942 Disease Relevance 0.09 Pain Relevance 0.04
LPS administration
Protein_catabolism (administration) of LPS
4) Confidence 0.65 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2409311 Disease Relevance 0.14 Pain Relevance 0.05
This was not the result of widespread nonspecific degradation of TLR4-responsive kinases because endogenous levels of the TLR-responsive MAPK p38 were not reduced, even at the highest levels of transfected SOCS-1 (Fig. 5A, bottom).
Protein_catabolism (degradation) of TLR4
5) Confidence 0.55 Published 2010 Journal mBio Section Body Doc Link PMC2962435 Disease Relevance 0 Pain Relevance 0.06
SOCS3 is a negative modulator of inflammatory cytokine signaling [58] and can be induced by inflammatory stimuli such as LPS, TNF-?
Protein_catabolism (as) of LPS associated with inflammation, inflammatory stimuli and cytokine
6) Confidence 0.55 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2409311 Disease Relevance 0.58 Pain Relevance 0.45
Kinase phosphorylation downstream of ceramide/TLR4
Protein_catabolism (ceramide) of TLR4
7) Confidence 0.54 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2944801 Disease Relevance 0.13 Pain Relevance 0
Nasal delivery of rPorB improved the protective capacity of LPS against F. tularensis challenge
Protein_catabolism (capacity) of LPS in Nasal
8) Confidence 0.34 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2886834 Disease Relevance 0.32 Pain Relevance 0
LPS administration
Protein_catabolism (administration) of LPS
9) Confidence 0.28 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 0.41 Pain Relevance 0.36
Triad3A acts as an E3 ubiquitin ligase promoting the degradation of TLR 4 and 9.
Protein_catabolism (degradation) of TLR 4
10) Confidence 0.13 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.18 Pain Relevance 0.18
LPS is known to rapidly activate transcriptional activity of NF-?
Protein_catabolism (known) of LPS
11) Confidence 0.07 Published 2008 Journal Journal of Neuroendocrinology Section Body Doc Link PMC2229370 Disease Relevance 0.26 Pain Relevance 0.30
Lipopolysaccharide (LPS)
Protein_catabolism (Lipopolysaccharide) of LPS
12) Confidence 0.05 Published 2010 Journal Exp Transl Stroke Med Section Body Doc Link PMC2830184 Disease Relevance 0.81 Pain Relevance 0.48
LPS: lipopolysaccharide
Protein_catabolism (lipopolysaccharide) of LPS
13) Confidence 0.05 Published 2004 Journal J Neuroinflammation Section Body Doc Link PMC483059 Disease Relevance 0.89 Pain Relevance 0.57
In addition, the interaction of repeated opening and closing of alveoli and LPS was found to increase iNOS expression, and an iNOS inhibitor attenuated accumulation of inflammatory cells in the lungs and restored blood gases.
Protein_catabolism (alveoli) of LPS in blood associated with inflammation and thoracotomy
14) Confidence 0.01 Published 2008 Journal Journal of Korean Medical Science Section Body Doc Link PMC2526521 Disease Relevance 1.46 Pain Relevance 0.22
This demonstrated that LPS could increase the expression of total and phospho-MKP-1, while curcumin or SB might amplify this result.

9 Curcumin inhibits LPS-induced degradation of I-?

Protein_catabolism (degradation) of LPS
15) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2945766 Disease Relevance 0.36 Pain Relevance 0.20

General Comments

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