INT197102

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.65
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 5
Disease Relevance 2.89
Pain Relevance 0.17

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

extracellular region (FLT4) plasma membrane (FLT4) nucleus (FLT4)
cytoplasm (FLT4)
Anatomy Link Frequency
plasma 1
anterior 1
posterior 1
platelet 1
keratinocytes 1
FLT4 (Homo sapiens)
Pain Link Frequency Relevance Heat
iatrogenic 4 78.04 Quite High
cytokine 27 66.40 Quite High
Pain 18 22.24 Low Low
pain flank 1 15.36 Low Low
Osteoarthritis 12 5.00 Very Low Very Low Very Low
Paracetamol 4 5.00 Very Low Very Low Very Low
headache 4 5.00 Very Low Very Low Very Low
drug abuse 2 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
Inflammation 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 8 98.44 Very High Very High Very High
Lymphedema 154 98.16 Very High Very High Very High
Rupture 12 98.04 Very High Very High Very High
Cancer 19 94.72 High High
Dislocations 84 92.40 High High
Helminth Infection 120 91.56 High High
Peritonitis 3 91.52 High High
Disease Progression 6 88.48 High High
Renal Cancer 15 85.32 High High
Injury 6 78.32 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Given that the sVEGFR-3 are secreted into the plasma following overstimulation of the lymphangiogenesis system [59,60], these data indicate that the stimulation of lymphangiogenesis followed by lymphatic dilation may be reduced by doxycycline, and the VEGF-C/VEGFR-3 system may constitute a major mediator of pathological lymphatic dilation.
Localization (secreted) of sVEGFR-3 in plasma
1) Confidence 0.65 Published 2006 Journal PLoS Pathogens Section Body Doc Link PMC1564427 Disease Relevance 0.52 Pain Relevance 0
Contributing causes included exhaustive surgical release, poor posterior offset restitution, PCL incompetence, or component malpositioning.
Localization (release) of PCL in posterior
2) Confidence 0.60 Published 2010 Journal Indian Journal of Orthopaedics Section Body Doc Link PMC2947733 Disease Relevance 0.51 Pain Relevance 0.04
In this genetic model, sVEGFR-3 is secreted at high levels by basal epidermal keratinocytes and binds the lymphangiogenesis factors VEGF-C and VEGF-D, thereby preventing them from activating membrane-bound VEGFR-3 on lymphatic endothelium [36].
Localization (secreted) of sVEGFR-3 in keratinocytes
3) Confidence 0.57 Published 2006 Journal PLoS Pathogens Section Body Doc Link PMC1564427 Disease Relevance 0.77 Pain Relevance 0.06
Extensor mechanism incompetence, inadequate balancing of the PCL, excessive release of posterolateral structures, polyethylene post rupture, hyperextension, a broken polyethylene insert anterior to the post, or a direct traumatism may all contribute to anteroposterior TKA dislocation.18

C.

Localization (release) of PCL in anterior associated with rupture and dislocations
4) Confidence 0.57 Published 2010 Journal Indian Journal of Orthopaedics Section Body Doc Link PMC2947733 Disease Relevance 0.47 Pain Relevance 0.07
In addition, the targets of sunitinib involve vascular endothelial growth factor receptors (VEGFR1, VEGFR2 and VEGFR3), platelet-derived growth factor receptors (PDGFR?
Localization (receptors) of VEGFR3 in platelet
5) Confidence 0.05 Published 2010 Journal World J Surg Oncol Section Body Doc Link PMC2890518 Disease Relevance 0.64 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox