INT188674

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Context Info
Confidence 0.15
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 9
Total Number 9
Disease Relevance 7.54
Pain Relevance 2.34

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

Anatomy Link Frequency
brain 4
T cell 4
macrophage 3
effector T cells 2
granulocyte 1
Eae1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 161 100.00 Very High Very High Very High
imagery 30 99.60 Very High Very High Very High
Multiple sclerosis 90 98.84 Very High Very High Very High
Spinal cord 44 96.40 Very High Very High Very High
Central nervous system 211 95.96 Very High Very High Very High
chemokine 93 94.16 High High
Inflammatory response 10 92.88 High High
cytokine 91 89.52 High High
anesthesia 1 83.36 Quite High
Arthritis 6 83.04 Quite High
Disease Link Frequency Relevance Heat
Multiple Sclerosis 477 100.00 Very High Very High Very High
INFLAMMATION 168 100.00 Very High Very High Very High
Disease 126 99.96 Very High Very High Very High
Apoptosis 7 99.40 Very High Very High Very High
Paralysis 21 94.44 High High
Paraplegia 3 92.64 High High
Paraparesis 3 91.44 High High
Recurrence 3 91.04 High High
Central Nervous System Disease 100 88.72 High High
Targeted Disruption 17 87.92 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The latter findings were corroborated by histopathological examination of brain sections, which showed inhibition of mononuclear cell influx and inflammatory lesions on B2-/- mice after EAE induction.
Negative_regulation (inhibition) of Positive_regulation (induction) of EAE in brain associated with multiple sclerosis and inflammation
1) Confidence 0.15 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2596102 Disease Relevance 0.96 Pain Relevance 0.27
For example, both CCL2 and CCR2 are expressed in brains of patients with MS [52,53] and deletion of CCR2 leads to an almost complete inhibition of MOG35–55-induced EAE in mice [16].
Negative_regulation (inhibition) of Positive_regulation (induced) of EAE in brains associated with multiple sclerosis
2) Confidence 0.15 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2596102 Disease Relevance 1.10 Pain Relevance 0.37
After induction of EAE, mice underwent cerebral MRI between day 5 and 16 post T cell transfer on a 7 Tesla rodent scanner (Pharmascan 70/16AS, Bruker BioSpin, Ettlingen, Germany), applying a 20 mm RF-Quadrature-Volume head coil.
Negative_regulation (underwent) of Positive_regulation (induction) of EAE in T cell associated with multiple sclerosis and imagery
3) Confidence 0.08 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2978145 Disease Relevance 0.66 Pain Relevance 0.22
Data indicate that activated T cells are particularly susceptible to apoptosis [36], [37], which could have decreased the frequency of self-reactive effector T cells before EAE induction.
Negative_regulation (decreased) of Positive_regulation (induction) of EAE in effector T cells associated with multiple sclerosis and apoptosis
4) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3012729 Disease Relevance 1.08 Pain Relevance 0.16
Strikingly, EAE was prevented in a prophylactic treatment regimen of anti-CD40L, and, when EAE was induced in another cohort of animals, CD40L antibody treatment significantly reduced disease severity in an active treatment paradigm [54].
Negative_regulation (reduced) of Positive_regulation (induced) of EAE associated with multiple sclerosis and disease
5) Confidence 0.05 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC1298325 Disease Relevance 0.76 Pain Relevance 0.11
Treatment with anti–IL-17 or anti–granulocyte/macrophage-CSF inhibited EAE induced by transfer of IL-23–polarized, but not IL-12p70–polarized, cells.
Negative_regulation (inhibited) of Positive_regulation (induced) of EAE in macrophage associated with multiple sclerosis
6) Confidence 0.05 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2442630 Disease Relevance 0.43 Pain Relevance 0.33
Within our experimental paradigm, we found that GM-CSF neutralization is selectively effective for the suppression of EAE induced by IL-23–modulated cells (Fig. 5 B).
Negative_regulation (suppression) of Positive_regulation (induced) of EAE associated with multiple sclerosis
7) Confidence 0.05 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2442630 Disease Relevance 0.93 Pain Relevance 0.16
Most strikingly, the two forms of EAE respond differently to specific immunomodulatory interventions; neutralization of either GM-CSF or IL-17 suppressed EAE induced by IL-23–modulated, but not IL-12–modulated, myelin-specific T cells.
Negative_regulation (suppressed) of Positive_regulation (induced) of EAE in T cells associated with multiple sclerosis
8) Confidence 0.05 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2442630 Disease Relevance 1.19 Pain Relevance 0.38
Treatment with anti–IL-17 or anti–granulocyte/macrophage-CSF inhibited EAE induced by transfer of IL-23–polarized, but not IL-12p70–polarized, cells.
Negative_regulation (inhibited) of in granulocyte Positive_regulation (induced) of EAE in macrophage associated with multiple sclerosis
9) Confidence 0.02 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2442630 Disease Relevance 0.43 Pain Relevance 0.33

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