INT263327

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Context Info
Confidence 0.08
First Reported 2006
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 2.95
Pain Relevance 0.42

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

nucleoplasm (NFKB2) extracellular matrix organization (NFKB2) DNA binding (NFKB2)
cytoplasm (NFKB2) cytosol (NFKB2) signal transduction (NFKB2)
Anatomy Link Frequency
adipose tissue 2
NFKB2 (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 3 99.56 Very High Very High Very High
Inflammation 34 98.12 Very High Very High Very High
Inflammatory response 5 97.68 Very High Very High Very High
Etanercept 1 72.56 Quite High
antagonist 1 70.64 Quite High
alcohol 7 5.00 Very Low Very Low Very Low
Inflammatory marker 3 5.00 Very Low Very Low Very Low
cINOD 1 5.00 Very Low Very Low Very Low
anesthesia 1 5.00 Very Low Very Low Very Low
diabetic neuropathy 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Insulin Resistance 7 99.62 Very High Very High Very High
INFLAMMATION 43 98.12 Very High Very High Very High
Obesity 36 96.16 Very High Very High Very High
Apnoea 48 94.40 High High
Diabetes Mellitus 66 93.52 High High
Stress 5 88.40 High High
Nicotine Addiction 62 85.28 High High
Sleep Disorders 13 79.68 Quite High
Lung Cancer 1 78.00 Quite High
Disease 13 68.96 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
to its receptors results in the activation of major transcription factors such as AP-1 and NFkB which in turn induce genes involved in acute and chronic inflammatory responses (9).
Positive_regulation (results) of Positive_regulation (activation) of NFkB associated with inflammatory response
1) Confidence 0.08 Published 2006 Journal Journal of Korean Medical Science Section Body Doc Link PMC2721922 Disease Relevance 0.99 Pain Relevance 0.29
It has been suggested that insulin resistance, through both the activation of nuclear factor kappa B by increased levels of cytokines (i.e., IL-6 and TNF-alpha) and the releasing of free fatty acids by excess adipose tissue, is involved in the pathogenic mechanisms leading to SAHS in humans [17].
Positive_regulation (increased) of Positive_regulation (activation) of nuclear factor kappa B in adipose tissue associated with apnoea, obesity, insulin resistance and cytokine
2) Confidence 0.08 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2650786 Disease Relevance 1.96 Pain Relevance 0.12

General Comments

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