INT192858

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Context Info
Confidence 0.47
First Reported 2006
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 4
Disease Relevance 1.71
Pain Relevance 0.38

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

cell adhesion (Itgam) nucleus (Itgam)
Anatomy Link Frequency
Neutrophils 1
microglia 1
F4/80 1
Itgam (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 27 100.00 Very High Very High Very High
cytokine 40 95.92 Very High Very High Very High
Central nervous system 34 89.76 High High
chemokine 10 68.60 Quite High
Inflammatory response 10 43.44 Quite Low
Spinal cord 3 40.20 Quite Low
ischemia 8 5.00 Very Low Very Low Very Low
imagery 4 5.00 Very Low Very Low Very Low
cerebral cortex 2 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 40 100.00 Very High Very High Very High
Apoptosis 20 99.74 Very High Very High Very High
Infection 233 97.24 Very High Very High Very High
Bacteremia 13 95.44 Very High Very High Very High
Mycobacterial Infection 146 90.88 High High
Injury 11 87.32 High High
Disease 15 73.76 Quite High
Alzheimer's Dementia 5 51.72 Quite High
Stroke 19 50.00 Quite Low
Necrosis 9 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
+ microglia peaked with 2% of the CD11b+CD45high population at 12–24 hours after pMCAO, while the proportion of TNF-?
Phosphorylation (population) of CD11b in microglia
1) Confidence 0.47 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2585073 Disease Relevance 0.09 Pain Relevance 0
Neutrophils from CR3-siRNA–transfected and –infected animals revealed greater expression of TLR2 and Fc?
Phosphorylation (Neutrophils) of CR3-siRNA in Neutrophils
2) Confidence 0.42 Published 2010 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2882833 Disease Relevance 0.16 Pain Relevance 0.05
Importantly, the current findings showing a lack of gene expression changes in microglia in response to NV infection are consistent with our previous analyses that have failed to show evidence of biochemical (e.g., iNOS, esterases, apoptosis, proteases, phosphorylations) or inflammatory changes (e.g., altered expression of MHC, CD11b, CD80, CD86, IL-1, IL-6, TNF alpha, F4/80, etc.) in microglia in vivo as early components of the pathogenic process (cf [7]).
Phosphorylation (phosphorylations) of CD11b in F4/80 associated with inflammation, apoptosis and infection
3) Confidence 0.15 Published 2006 Journal Retrovirology Section Body Doc Link PMC1475625 Disease Relevance 0.44 Pain Relevance 0.15
For this reason, we experimentally determined the timing of accumulation of Gr1+ neutrophilic population (CD11b+ Gr1+) (Figure 5a) [68] and Gr1+ monocytic population (CD11b?
Phosphorylation (population) of CD11b
4) Confidence 0.15 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020951 Disease Relevance 1.01 Pain Relevance 0.18

General Comments

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