INT191586

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Context Info
Confidence 0.58
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 8
Disease Relevance 9.44
Pain Relevance 1.17

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

extracellular space (THBD) plasma membrane (THBD) embryo development (THBD)
Anatomy Link Frequency
endothelial cells 2
plasma 1
monocytes 1
brain 1
smooth muscle cells 1
THBD (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 100 97.48 Very High Very High Very High
Inflammatory marker 6 83.60 Quite High
Inflammatory response 12 75.04 Quite High
cytokine 58 71.76 Quite High
cva 26 64.44 Quite High
rheumatoid arthritis 6 55.52 Quite High
aspirin 7 19.92 Low Low
Central nervous system 2 19.04 Low Low
corticosteroid 20 5.00 Very Low Very Low Very Low
ischemia 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Injury 100 100.00 Very High Very High Very High
Pulmonary Hypertension 18 99.50 Very High Very High Very High
INFLAMMATION 144 98.72 Very High Very High Very High
Atherosclerosis 71 98.28 Very High Very High Very High
Brain Injury 144 97.32 Very High Very High Very High
Disease 64 96.96 Very High Very High Very High
Leptospirosis 40 96.92 Very High Very High Very High
Thrombocytopenia 26 93.92 High High
Infection 31 93.04 High High
Coronary Artery Disease 156 92.88 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In sera of patients with PAH, high concentrations of thrombomodulin (TM) and von Willebrand factor antigen (vWFAg) secreted from Weibel-Palade bodies imply an activated state of the endothelial cells.
Localization (secreted) of thrombomodulin in endothelial cells associated with pulmonary hypertension
1) Confidence 0.58 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2911856 Disease Relevance 1.53 Pain Relevance 0.16
In sera of patients with PAH, high concentrations of thrombomodulin (TM) and von Willebrand factor antigen (vWFAg) secreted from Weibel-Palade bodies imply an activated state of the endothelial cells.
Localization (secreted) of TM in endothelial cells associated with pulmonary hypertension
2) Confidence 0.58 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2911856 Disease Relevance 1.51 Pain Relevance 0.16
Any TF, TM and D-D present was sandwiched by the immobilized capture antibody and the enzyme-linked monoclonal antibody specific for these analytes.
Localization (present) of TM
3) Confidence 0.42 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819256 Disease Relevance 0 Pain Relevance 0
Although the biological relevance of changes in sTM in brain injury is not well characterized [35], emerging data from clinical and animal studies suggest that increases in endogenous sTM or exogenous administration of TM may have potent antithrombotic/antiinflammatory properties in inflammatory disease [107].
Localization (administration) of TM in brain associated with inflammation, disease and brain injury
4) Confidence 0.39 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819256 Disease Relevance 1.24 Pain Relevance 0.27
1 could enhance atherogenesis by mediating excessive extracellular matrix accumulation [21] and by down-regulating thrombomodulin, promoting thrombogenesis at the sites of vessel wall injury, where it is released from platelets, smooth muscle cells and monocytes [22].
Localization (released) of thrombomodulin in platelets associated with atherosclerosis and injury
5) Confidence 0.28 Published 2007 Journal Cardiovasc Diabetol Section Body Doc Link PMC1976604 Disease Relevance 1.33 Pain Relevance 0.19
Analysis of hematologic molecular markers showed that 11-DH-TXB2 and TM in the plasma were elevated significantly.
Localization (elevated) of TM in plasma
6) Confidence 0.15 Published 2006 Journal BMC Infect Dis Section Abstract Doc Link PMC1434752 Disease Relevance 1.03 Pain Relevance 0.03
1 could enhance atherogenesis by mediating excessive extracellular matrix accumulation [21] and by down-regulating thrombomodulin, promoting thrombogenesis at the sites of vessel wall injury, where it is released from platelets, smooth muscle cells and monocytes [22].
Localization (released) of thrombomodulin in monocytes associated with atherosclerosis and injury
7) Confidence 0.09 Published 2007 Journal Cardiovasc Diabetol Section Body Doc Link PMC1976604 Disease Relevance 1.33 Pain Relevance 0.19
1 could enhance atherogenesis by mediating excessive extracellular matrix accumulation [21] and by down-regulating thrombomodulin, promoting thrombogenesis at the sites of vessel wall injury, where it is released from platelets, smooth muscle cells and monocytes [22].
Localization (released) of thrombomodulin in smooth muscle cells associated with atherosclerosis and injury
8) Confidence 0.09 Published 2007 Journal Cardiovasc Diabetol Section Body Doc Link PMC1976604 Disease Relevance 1.33 Pain Relevance 0.19

General Comments

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