INT166878

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Context Info
Confidence 0.44
First Reported 2005
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 9
Total Number 10
Disease Relevance 8.21
Pain Relevance 4.81

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

cytosol (Ccl3) extracellular space (Ccl3) extracellular region (Ccl3)
intracellular (Ccl3) cytoskeleton organization (Ccl3) kinase activity (Ccl3)
Anatomy Link Frequency
SCN 1
plaques 1
Ccl3 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 327 99.68 Very High Very High Very High
Inflammatory mediators 3 99.62 Very High Very High Very High
chemokine 353 99.48 Very High Very High Very High
cINOD 30 99.44 Very High Very High Very High
Sciatic nerve 5 99.00 Very High Very High Very High
corticosteroid 8 97.88 Very High Very High Very High
Neuropathic pain 5 97.72 Very High Very High Very High
antagonist 117 96.56 Very High Very High Very High
Multiple sclerosis 254 94.96 High High
Brush evoked pain 3 89.20 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 328 99.68 Very High Very High Very High
Multiple Sclerosis 403 98.88 Very High Very High Very High
Lymphedema 45 98.68 Very High Very High Very High
Recurrence 66 98.60 Very High Very High Very High
Diabetes Mellitus 154 98.12 Very High Very High Very High
Neuropathic Pain 8 97.72 Very High Very High Very High
Hematological Disease 4 97.12 Very High Very High Very High
Disease 108 96.40 Very High Very High Very High
Demyelinating Disease 313 94.96 High High
Inflammatory Bowel Disease 1 91.00 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
MIP-1alpha mRNA and its protein were dramatically up-regulated after PSL, and MIP-1alpha was localized on macrophages and Schwann cells in the injured sciatic nerve (SCN).
Regulation (regulated) of MIP-1alpha in SCN associated with sciatic nerve
1) Confidence 0.44 Published 2010 Journal Pain Section Abstract Doc Link 20223588 Disease Relevance 0.79 Pain Relevance 0.85
The up-regulation of CCL3 and CCL4 vs. down-regulation of CCL2 suggests opposed functions of these chemokines in the disease process in T1D.
Regulation (regulation) of CCL3 associated with chemokine, diabetes mellitus and disease
2) Confidence 0.41 Published 2008 Journal Current Genomics Section Body Doc Link PMC2685644 Disease Relevance 1.11 Pain Relevance 0.16
From a range of chemokines measured, corrected for total protein levels, only CCL3, CCL5 and CCL11 were modulated significantly by H4R antagonism or ani-IL-13 treatment.
Regulation (modulated) of CCL3 associated with chemokine
3) Confidence 0.31 Published 2010 Journal Respir Res Section Body Doc Link PMC2914735 Disease Relevance 0.17 Pain Relevance 0.32
while other inflammatory mediators such as MCP-3 and MIP1a were inhibited by NSAID treatment in lymphedema mice.
Regulation (were) of MIP1a associated with inflammatory mediators, cinod and lymphedema
4) Confidence 0.30 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2791214 Disease Relevance 1.14 Pain Relevance 1.23
Second, previous studies suggested the involvement of CCL2, CCL7, CCL8, CCL5 and CCL3 molecules in the development of plaques [39,46].
Regulation (involvement) of CCL3 in plaques
5) Confidence 0.27 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC554759 Disease Relevance 0.46 Pain Relevance 0.30
The concentrations of CCL2, CCL3, CCL5, TNF?
Regulation (concentrations) of CCL3
6) Confidence 0.20 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2596102 Disease Relevance 0.13 Pain Relevance 0.11
Conversely, anti-IL-13 treatment significantly inhibited CCL11 production, with no effect on CCL3 or CCL5.
Neg (no) Regulation (effect) of CCL3
7) Confidence 0.19 Published 2010 Journal Respir Res Section Body Doc Link PMC2914735 Disease Relevance 0.15 Pain Relevance 0.32
CCL2, CCL3, CCL5, CCL7, CCL8, etc...) are transcriptionally regulated during inflammation and mediate the recruitment of inflammatory cells to target tissues.
Regulation (regulated) of CCL3 associated with inflammation
8) Confidence 0.16 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC554759 Disease Relevance 0.55 Pain Relevance 0.62
With the exception of well defined changes in the CCL2, CCL3 and CCL5 levels in the CSF during relapses, most investigators observed no differences in various clinical forms of the disease [56,61,64,66].
Neg (exception) Regulation (changes) of CCL3 associated with disease and recurrence
9) Confidence 0.16 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC554759 Disease Relevance 2.32 Pain Relevance 0.75
This study emphasizes the importance of CCL2 and CCL3 in the development of active EAE in rats.
Regulation (importance) of CCL3 associated with multiple sclerosis
10) Confidence 0.07 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC554759 Disease Relevance 1.39 Pain Relevance 0.15

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