INT285605

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Context Info
Confidence 0.01
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 1.25
Pain Relevance 0.16

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

plasma membrane (ROS1, Tlr4) cell differentiation (ROS1) cell proliferation (ROS1)
signal transduction (Tlr4) intracellular (Tlr4) cytoplasm (Tlr4)
ROS1 (Homo sapiens)
Tlr4 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammatory response 4 89.08 High High
Inflammatory mediators 8 66.08 Quite High
cytokine 7 61.28 Quite High
Dopamine 20 5.00 Very Low Very Low Very Low
Inflammation 16 5.00 Very Low Very Low Very Low
ketamine 15 5.00 Very Low Very Low Very Low
nMDA receptor 5 5.00 Very Low Very Low Very Low
isoflurane 5 5.00 Very Low Very Low Very Low
antagonist 4 5.00 Very Low Very Low Very Low
Neurotransmitter 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Endotoxemia 1 99.96 Very High Very High Very High
Sepsis 17 97.80 Very High Very High Very High
INFLAMMATION 26 88.68 High High
Bacterial Infection 1 76.88 Quite High
Tumor Necrosis Factor Receptor-associated Periodic Syndrome 4 70.56 Quite High
Bacterial Respiratory Disease 1 65.12 Quite High
Necrosis 3 55.44 Quite High
Cancer 16 55.08 Quite High
Death 18 51.92 Quite High
Stress 50 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
During LPS-induced endotoxemia, ROS was found to be significantly increased and was shown to limit the availability of NO, resulting in LPS-induced endothelial dysfunction, with the primary source of ROS identified as cyclooxygenase-2 (Cox-2) (Virdis et al., 2005).
ROS Binding (resulting) of LPS associated with endotoxemia
1) Confidence 0.01 Published 2009 Journal Toxicological Sciences Section Body Doc Link PMC2769059 Disease Relevance 1.25 Pain Relevance 0.16

General Comments

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