INT100376

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Context Info
Confidence 0.10
First Reported 2002
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 5
Disease Relevance 6.47
Pain Relevance 1.47

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

cytosol (Vhl) mitochondrion (Vhl) nucleus (Vhl)
extracellular matrix organization (Vhl) transcription factor binding (Vhl) cytoplasm (Vhl)
Anatomy Link Frequency
endothelial cells 4
central nervous system 2
Vhl (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Central nervous system 2 99.64 Very High Very High Very High
Sciatica 1 98.96 Very High Very High Very High
cINOD 16 97.86 Very High Very High Very High
dexamethasone 1 94.36 High High
Spinal cord 1 71.88 Quite High
imagery 2 66.88 Quite High
addiction 2 5.00 Very Low Very Low Very Low
Pain 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Renal Cancer 277 100.00 Very High Very High Very High
Cancer 129 99.92 Very High Very High Very High
Nerve Root Compression 1 98.96 Very High Very High Very High
Hypoxia 16 98.18 Very High Very High Very High
Syndrome 145 98.04 Very High Very High Very High
Hemangioblastoma 2 97.44 Very High Very High Very High
Disease 14 96.68 Very High Very High Very High
Von Hippel-lindau Syndrome 11 95.40 Very High Very High Very High
Pancreatic Cyst 2 93.24 High High
Hemangioma 2 93.20 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Taken together, these results indicate that NSAIDs inhibit hypoxia-induced angiogenesis in endothelial cells by inhibiting VEGF and Flt-1 expression through increased VHL expression and the resulting ubiquitination and degradation of HIF-1alpha.
Positive_regulation (increased) of Gene_expression (expression) of VHL in endothelial cells associated with hypoxia and cinod
1) Confidence 0.10 Published 2002 Journal FASEB J. Section Abstract Doc Link 11772947 Disease Relevance 0.89 Pain Relevance 0.61
Here we demonstrate that both nonselective (indomethacin) and COX-2-selective (NS-398) NSAIDs inhibit hypoxia-induced in vitro angiogenesis in gastric microvascular endothelial cells via coordinated sequential events: 1) increased expression of the von Hippel-Lindau (VHL) tumor suppressor, which targets proteins for ubiquitination leading to 2) reduced accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha) and, as a result, 3) reduced expression of vascular endothelial growth factor (VEGF) and its specific receptor Flt-1.
Positive_regulation (increased) of Gene_expression (expression) of VHL in endothelial cells associated with cancer, hypoxia and cinod
2) Confidence 0.09 Published 2002 Journal FASEB J. Section Abstract Doc Link 11772947 Disease Relevance 0.90 Pain Relevance 0.52
As renal tumors in VHL tend to be
Positive_regulation (tend) of Gene_expression (tumors) of VHL associated with renal cancer
3) Confidence 0.07 Published 2008 Journal Advances in Urology Section Body Doc Link PMC2495021 Disease Relevance 1.61 Pain Relevance 0.07
Extrarenal manifestations of VHL include central nervous system
Positive_regulation (manifestations) of Gene_expression (manifestations) of VHL in central nervous system associated with central nervous system
4) Confidence 0.07 Published 2008 Journal Advances in Urology Section Body Doc Link PMC2495021 Disease Relevance 1.96 Pain Relevance 0.08
As the main problem in VHL is uncontrolled angiogenesis by overexpressing VEGF and VEGF receptors, Thalidomide (400 mg, later 600 mg) was added.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of VHL
5) Confidence 0.07 Published 2007 Journal J Neurooncol Section Body Doc Link PMC1915654 Disease Relevance 1.11 Pain Relevance 0.18

General Comments

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