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Context Info
Confidence 0.21
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 3
Disease Relevance 3.48
Pain Relevance 0.28

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

extracellular space (LPL) small molecule metabolic process (LPL) extracellular region (LPL)
plasma membrane (LPL) lipid metabolic process (LPL)
Anatomy Link Frequency
liver 1
LPL (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 30 88.80 High High
Inflammatory marker 1 88.16 High High
Inflammation 16 80.56 Quite High
Bile 9 5.00 Very Low Very Low Very Low
tolerance 4 5.00 Very Low Very Low Very Low
Angina 3 5.00 Very Low Very Low Very Low
Inflammatory response 2 5.00 Very Low Very Low Very Low
Endocannabinoid 2 5.00 Very Low Very Low Very Low
COX2 1 5.00 Very Low Very Low Very Low
cINOD 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disorder Of Lipid Metabolism 282 98.76 Very High Very High Very High
Polycystic Ovary Syndrome 83 98.12 Very High Very High Very High
Obesity 57 96.08 Very High Very High Very High
Insulin Resistance 16 92.12 High High
INFLAMMATION 19 88.16 High High
Atherosclerosis 6 83.36 Quite High
Hypertension 12 78.52 Quite High
Diabetes Mellitus 20 71.84 Quite High
Coronary Heart Disease 7 70.24 Quite High
Syndrome 8 62.60 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
TNF-alpha also suppresses lipoprotein lipase and its release is inhibited by the thiazolidinediones and in PCOS, serum TNF-alpha is increased irrespective of obesity (Gonzalez et al 1999).
Localization (release) of lipoprotein lipase associated with obesity and polycystic ovary syndrome
1) Confidence 0.21 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC1994046 Disease Relevance 1.88 Pain Relevance 0.08
LPL activity is mostly regulated posttranslationally via altered secretion from liver of LPL-modulating factors, including apolipoprotein C-III (Apoc3), apolipoprotein A-V (Apoa5), Angiopoietin-like protein 3 (Angptl3), and Angiopoietin-like protein 4 (Angptl4).
Localization (secretion) of LPL in liver associated with disorder of lipid metabolism
2) Confidence 0.17 Published 2010 Journal PPAR Research Section Body Doc Link PMC2948931 Disease Relevance 0.36 Pain Relevance 0.19
LPL is principally responsible for the hydrolysis of TGs in TG-rich lipoprotein (TRL) and the release of free fatty acids, transforming large TRL particles into smaller TG-depleted remnant lipoproteins.
Localization (release) of LPL
3) Confidence 0.12 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2920871 Disease Relevance 1.23 Pain Relevance 0

General Comments

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