106 results match your criteria: "Center for Biomedical Computing[Affiliation]"
Bioinformatics
November 2009
Center for Biomedical Computing, University of Verona, Strada le Grazie, 15 -37134 Verona, Italy.
Summary: The increasing availability of large network datasets along with the progresses in experimental high-throughput technologies have prompted the need for tools allowing easy integration of experimental data with data derived form network computational analysis. In order to enrich experimental data with network topological parameters, we have developed the Cytoscape plug-in CentiScaPe. The plug-in computes several network centrality parameters and allows the user to analyze existing relationships between experimental data provided by the users and node centrality values computed by the plug-in.
View Article and Find Full Text PDFHum Mol Genet
October 2009
i2b2 National Center for Biomedical Computing, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Analysis of recently available microarray expression data sets obtained from immortalized cell lines of the individuals represented in the HapMap project have led to inconclusive comparisons across cohorts with different ancestral continent of origin (ACOO). To address this apparent inconsistency, we applied a novel approach to accentuate population-specific gene expression signatures for the CEU [homogeneous US residents with northern and western European ancestry (HapMap samples)] and YRI [homogenous Yoruba people of Ibadan, Nigeria (HapMap samples)] trios. In this report, we describe how four independent data sets point to the differential expression across ACOO of gene networks implicated in transforming the normal lymphoblast into immortalized lymphoblastoid cells.
View Article and Find Full Text PDFWiley Interdiscip Rev Syst Biol Med
December 2010
Department of Pathology, The Center for Biomedical Computing (CBMC), University of Verona, Verona, Italy.
Modulation of leukocyte adhesiveness is critical to leukocyte function during the immune response. A central paradigm in this phenomenon is represented by integrin activation, which is controlled by inside-out signal transduction mechanisms triggered by selectins, chemoattractants and TcR-bound Ag and facilitated by mechanochemical forces. Integrins are heterodimeric adhesive receptors differently expressed on all leukocyte subtypes.
View Article and Find Full Text PDFMath Biosci
August 2009
Center for Biomedical Computing at Simula Research Laboratory, P.O. Box 134, 1325 Lysaker, Norway.
We investigate the possibility of using body surface potential maps to image the extracellular potassium concentration during regional ischemia. The problem is formulated as an inverse problem based on a linear approximation of the bidomain model, where we minimize the difference between the results of the model and observations of body surface potentials. The minimization problem is solved by a one-shot technique, where the original PDE system, an adjoint problem, and the relation describing the minimum, are solved simultaneously.
View Article and Find Full Text PDFAnn Biomed Eng
July 2009
Center for Biomedical Computing, Simula Research Laboratory, P.O. Box 134, 1325, Lysaker, Norway.
Atrial flutter is a common supraventricular tachycardia that can be treated using radiofrequency catheter ablation, a procedure that is guided by electroanatomical mapping systems. In this paper, we propose an algorithm for incorporating mapping data into computer simulations of atrial electrical activity with the purpose of creating a more accurate map of electrical activation. The algorithm takes as input the extracellular potential values recorded at a number of sites throughout the atria and estimates the activation time for the entire atrial domain.
View Article and Find Full Text PDFMath Biosci
June 2008
Center for Biomedical Computing, Simula Research Laboratory, P.O. Box 134, 1325 Lysaker, Norway.
The purpose of this paper is to study the stability of steady state solutions of the Monodomain model equipped with Luo-Rudy I kinetics. It is well established that re-entrant arrhythmias can be created in computational models of excitable cells. Such arrhythmias can be initiated by applying an external stimulus that interacts with a partially refractory region, and spawn breaking waves that can eventually generate extremely complex wave patterns commonly referred to as fibrillation.
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