INT290923

From wiki-pain
Revision as of 20:24, 22 September 2012 by Daniel (Talk | contribs)

(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to: navigation, search
Context Info
Confidence 0.48
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 5
Disease Relevance 3.62
Pain Relevance 0.14

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

cell differentiation (Angpt1) signal transduction (Angpt1) extracellular space (Angpt1)
extracellular region (Angpt1) plasma membrane (Angpt1) molecular_function (Angpt1)
Anatomy Link Frequency
HGF 1
heart 1
Angpt1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
cytokine 12 100.00 Very High Very High Very High
ischemia 14 73.36 Quite High
fibrosis 47 55.08 Quite High
Inflammation 5 5.00 Very Low Very Low Very Low
Angina 3 5.00 Very Low Very Low Very Low
Percutaneous transluminal coronary angioplasty 3 5.00 Very Low Very Low Very Low
Central nervous system 2 5.00 Very Low Very Low Very Low
Neuronal nitric oxide synthase 2 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
Inflammatory response 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Diabetes Mellitus 279 99.48 Very High Very High Very High
Myocardial Infarction 219 99.30 Very High Very High Very High
Fibrosis 50 98.32 Very High Very High Very High
Ventricular Remodeling 30 96.92 Very High Very High Very High
Stress 8 89.36 High High
Injury 4 79.84 Quite High
Cancer 2 75.16 Quite High
Cv Unclassified Under Development 11 73.36 Quite High
Heart Rate Under Development 6 67.40 Quite High
Apoptosis 11 63.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Upon treatment with a combination of adenoviral vectors encoding VEGF and Ang-1 in the nondiabetic MI (CVAMI) animals, we documented an increase in the levels of Ang-1 (1.3-fold) and Tie-2 (1.3-fold) 4 days after the gene transfer compared with the Ad.LacZ-treated nondiabetic MI (CLZMI) group (Fig. 4C and D).
Positive_regulation (increase) of Ang-1 associated with myocardial infarction
1) Confidence 0.48 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 1.11 Pain Relevance 0
The therapy significantly reduced the ventricular remodeling as evidenced by the significant reduction in the collagenous fibrotic tissue and improvement in the myocardial functions in conjunction with significant increase in the levels of VEGF and its receptor Flk-1, Ang-1 and its receptor Tie-2, p-MK2, and antiapoptotic survivin.
Positive_regulation (increase) of Ang-1 associated with fibrosis and ventricular remodeling
2) Confidence 0.48 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 1.15 Pain Relevance 0.03
The increase in the expression of the receptors Flk-1 and Tie-2 that we observed upon gene therapy can be correlated to the increased expression of their ligands: VEGF and Ang-1, respectively.
Positive_regulation (increase) of Ang-1
3) Confidence 0.35 Published 2010 Journal Diabetes Section Body Doc Link PMC2797944 Disease Relevance 1.06 Pain Relevance 0.03
In conclusion ShhMSCs showed upregulation of several angiogenic cytokines and signaling molecules including Ang-1, VEGF, IGF, HGF, iNOS and netrin-1.
Positive_regulation (upregulation) of Ang-1 in HGF associated with cytokine
4) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0 Pain Relevance 0.05
Interestingly, activation of Shh signaling caused upregulation of pro-angiogenic growth factors including vascular endothelial growth factor (VEGF) and angiopoietin-1 which resulted in an increased angiogenic response and globally improved the heart function.
Positive_regulation (upregulation) of angiopoietin-1 in heart
5) Confidence 0.13 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2797399 Disease Relevance 0.29 Pain Relevance 0.04

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox