INT61039

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Context Info
Confidence 0.59
First Reported 1995
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 7
Total Number 11
Disease Relevance 9.51
Pain Relevance 2.44

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 (Ltb4r) plasma membrane (Ltb4r) signal transducer activity (Ltb4r)
Anatomy Link Frequency
bone marrow 3
joints 1
immune cells 1
lung 1
Ltb4r (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammatory mediators 25 100.00 Very High Very High Very High
Catecholamine 2 99.72 Very High Very High Very High
Inflammation 233 99.40 Very High Very High Very High
Endogenous opioid 2 99.00 Very High Very High Very High
Spinal cord 2 97.60 Very High Very High Very High
Arthritis 5 92.24 High High
Antinociceptive 4 90.48 High High
narcan 4 89.04 High High
Peripheral nerve injury 2 86.36 High High
Neuropathic pain 3 85.00 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 159 100.00 Very High Very High Very High
Hypersensitivity 433 99.88 Very High Very High Very High
Nervous System Injury 6 99.56 Very High Very High Very High
Pneumonia 105 99.40 Very High Very High Very High
Colitis 20 99.40 Very High Very High Very High
Adhesions 36 95.76 Very High Very High Very High
Increased Venous Pressure Under Development 5 92.48 High High
Arthritis 5 92.24 High High
Asthma 124 90.92 High High
Neuropathic Pain 4 85.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Semi-quantitative RT-PCR revealed that 5-LO, FLAP, LTC4s, BLT1, and CysLT1 mRNAs increased following SNI, but not CysLT2 mRNAs.
Localization (increased) of BLT1 associated with nervous system injury
1) Confidence 0.59 Published 2010 Journal Glia Section Abstract Doc Link 19908283 Disease Relevance 1.10 Pain Relevance 0.60
Risedronate, at 50 and 100 microg/kg, significantly inhibited LTB4 release into the joints compared with the NT group (2883.1 +/- 73.2, 1911.5 +/- 205.3 and 4709.9 +/- 237.2 pg/mL, respectively).
Localization (release) of LTB4 in joints
2) Confidence 0.11 Published 2006 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 16789926 Disease Relevance 0.71 Pain Relevance 0.47
This effect is associated with reduced cell infiltration and inhibition of TNF-alpha and LTB4 release and is not linked to an endogenous opioid-release mechanism.
Localization (release) of LTB4 associated with endogenous opioid
3) Confidence 0.09 Published 2006 Journal Clin. Exp. Pharmacol. Physiol. Section Abstract Doc Link 16789926 Disease Relevance 0.53 Pain Relevance 0.42
In parallel, LTB4 release by lung cells was prevented by estradiol and progesterone.
Localization (release) of LTB4 in lung
4) Confidence 0.05 Published 2010 Journal Respir Res Section Body Doc Link PMC2936382 Disease Relevance 1.00 Pain Relevance 0.27
Cultured-BAL cells of OVx allergic rats released elevated amounts of LTB4 and nitrites while bone marrow cells increased the release of TNF-?
Localization (released) of LTB4 in bone marrow associated with hypersensitivity
5) Confidence 0.05 Published 2010 Journal Respir Res Section Abstract Doc Link PMC2936382 Disease Relevance 0.94 Pain Relevance 0.13
Although OVx did not modify LTB4 release by bone marrow cells, estradiol treatment of rats decreased the LTB4 quantification whereas progesterone was ineffective (Fig. 8B).
Localization (release) of LTB4 in bone marrow
6) Confidence 0.05 Published 2010 Journal Respir Res Section Body Doc Link PMC2936382 Disease Relevance 0.67 Pain Relevance 0.04
Cells of OVx allergic rats released higher amounts of LTB4, an effect which was significantly prevented by estradiol or progesterone treatments before OVA- challenge (Fig. 8A).
Localization (released) of LTB4 associated with hypersensitivity
7) Confidence 0.05 Published 2010 Journal Respir Res Section Body Doc Link PMC2936382 Disease Relevance 0.65 Pain Relevance 0.07
We observed that cells collected of BAL and of bone marrow of OVx allergic rats significantly increased the release of inflammatory mediators such as LTB4, NO and TNF-?.
Localization (release) of LTB4 in bone marrow associated with inflammatory mediators and hypersensitivity
8) Confidence 0.05 Published 2010 Journal Respir Res Section Body Doc Link PMC2936382 Disease Relevance 1.13 Pain Relevance 0.18
Elastase and leukotriene B4 release were also significantly increased in active colitis compared with inactive colitis and controls.
Localization (release) of leukotriene B4 associated with colitis
9) Confidence 0.01 Published 1995 Journal Clin. Sci. Section Abstract Doc Link 8549067 Disease Relevance 1.29 Pain Relevance 0.06
Some of the paracrine mechanisms involve mediators emanating from the circulation (complement, catecholamines, GM-CSF) and released from other immune cells, (LTB4, PAF and TNF), or involve juxtacrine mechanisms such as regulation of expression and affinity of counter adhesion receptors, such as ICAM-1, on endothelial cells [21].
Localization (released) of LTB4 in immune cells associated with catecholamine and adhesions
10) Confidence 0.01 Published 2003 Journal BMC Immunol Section Body Doc Link PMC152650 Disease Relevance 0.26 Pain Relevance 0.13
Leukotriene B4 release was similar in inactive colitis and controls, whereas elastase release was higher in inactive colitis than in controls.
Localization (release) of Leukotriene B4 associated with colitis
11) Confidence 0.01 Published 1995 Journal Clin. Sci. Section Abstract Doc Link 8549067 Disease Relevance 1.24 Pain Relevance 0.06

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