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Blood, Vol. 111, Issue 7, 3872-3879, April 1, 2008
Genetic endothelial systems biology of sickle stroke risk
Blood Chang Milbauer et al.
111: 3872
Supplemental materials for: Milbauer et al
Files in this Data Supplement:
- Table S1. Patient data (PDF, 130 KB) -
TCD= Transcranial doppler. MRA=Magnetic resonance arteriogram. N=Not at risk. A= At risk.
- Table S2. Sources of systems lists (PDF, 18.3 KB) -
We wanted approximately 125 genes in each system. These genes were chosen from specific published articles on each of the 9 systems. Some of these articles showed pathways and/ or microarray lists or referenced Gene Ontology lists. In addition, pathway sources such as KEGG, BIOCARTA, STKE, CGAP and INGENUITY were utilized. Because we wanted limited numbers of genes, not all genes on the pathway were included. All genes used are known to be transcribed in endothelial cells. Some genes are important for several systems. We allowed some gene overlap between systems lists in order to maximize the chances of finding a system of importance.
- Table S3. Nine biological systems gene sets (PDF, 796 KB) -
Systems are: adhesion, angiogenesis, apoptosis, coagulation, hypoxia, inflammation, redox, shear stress, vasoregulation.
- Figure S1. BOEC expansion from buffy coat mononuclear cells of normal blood (JPG, 122 KB)
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On day 2 and for subsequent passages (indicated by arrow), the number of endothelial cells was confirmed by staining for P1H12 and vWF, and that number was consistent with the cell count by morphology. All data points plotted as mean +/− SD (n=5 for culture up to passage 6; n=4 for subsequent passages). Published in J Clin Invest 105(1): 71-77, 2000.
- Figure S2. Ingenuity map of top 59 inflammation list genes (JPG, 244 KB)
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Top 21 genes (yellow) and next 38 genes (magenta) that contributed to the Wald score are shown with biological relationships documented in the literature by Ingenuity.
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