INT112695

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Context Info
Confidence 0.36
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 3
Total Number 3
Disease Relevance 1.72
Pain Relevance 1.30

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

mitochondrion (Bax) endoplasmic reticulum (Bax) intracellular (Bax)
cytoplasm (Bax) cytosol (Bax) cell proliferation (Bax)
Anatomy Link Frequency
eosinophil 2
Bax (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 16 93.84 High High
Inflammation 17 69.20 Quite High
chemokine 4 66.76 Quite High
cytokine 24 65.20 Quite High
corticosteroid 5 5.00 Very Low Very Low Very Low
lidocaine 3 5.00 Very Low Very Low Very Low
agonist 2 5.00 Very Low Very Low Very Low
Nerve growth factor 1 5.00 Very Low Very Low Very Low
fibrosis 1 5.00 Very Low Very Low Very Low
withdrawal 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 87 98.92 Very High Very High Very High
Injury 10 93.56 High High
Targeted Disruption 8 73.68 Quite High
INFLAMMATION 16 69.20 Quite High
Asthma 24 62.88 Quite High
Cancer 3 42.96 Quite Low
Necrosis 5 42.48 Quite Low
Death 22 34.16 Quite Low
Disease 20 5.00 Very Low Very Low Very Low
Hypereosinophilic Syndrome 17 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The caspase inhibitor failed to prevent both the redistribution of Bax to the mitochondria and the loss of cytochrome c.
Negative_regulation (loss) of Protein_catabolism (redistribution) of Bax
1) Confidence 0.36 Published 2003 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 12946648 Disease Relevance 0.64 Pain Relevance 0.57
The caspase inhibitor failed to prevent both the redistribution of Bax to the mitochondria and the loss of cytochrome c.
Negative_regulation (prevent) of Protein_catabolism (redistribution) of Bax
2) Confidence 0.36 Published 2003 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 12946648 Disease Relevance 0.63 Pain Relevance 0.57
Nasal explants from atopic patients were shown to survive ex vivo using similar mechanisms to promote extramedullary eosinophil maturation and survival.83 These, as well as lung explants of Brown-Norway rats, exhibited rapid (6 hours) accumulation of MBP-positive cells after allergen challenge of the explants in vitro.86 The major signaling pathway of these events is associated with IL-5 receptor ligation leading to phosphorylation of JAK-2 and Lyn kinases, decreased BAX translocation, and ultimately decreased apoptosis.87 Additionally, GM-CSF appears to have a strong role in inhibiting eosinophil apoptosis at the tissue level.
Negative_regulation (decreased) of Protein_catabolism (translocation) of BAX in eosinophil associated with apoptosis
3) Confidence 0.09 Published 2010 Journal Allergy, Asthma & Immunology Research Section Body Doc Link PMC2846745 Disease Relevance 0.45 Pain Relevance 0.16

General Comments

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