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World Biotechnology 2016
August 15-17, 2016
Volume 6 Issue 5(Suppl)
J Biotechnol Biomater 2016
ISSN: 2155-952X JBTBM, an open access journal
conferenceseries
.com
August 15-17, 2016 Sao Paulo, Brazil
Biotechnology World Convention
Glaucia C Pereira et al., J Biotechnol Biomater 2016, 6:5(Suppl)
http://dx.doi.org/10.4172/2155-952X.C1.058A multi-layer non-Newtonian model of cardiovascular inflammation
Glaucia C Pereira
1
and
Kis Zoltan
2
1
Icelandic Institute for Intelligent Machines, Iceland
2
Imperial College London, UK
C
ellular functions related to the maintenance of homoeostasis are regulated by shear forces sensed by endothelial cells. The
endothelial cells sense local changes in shear stress. The resulting signals are either transduced into chemical responses
or transmitted to the surroundings to regulate the cellular activity. In the current literature, models of blood flow applied to
the characterization of atherosclerotic plaques consider blood as a Newtonian fluid because of the characteristic length of the
domain. At predilection sites for plaque deposition, the diameter of the blood particles is much smaller than the normal arterial
diameter. However, under disease condition, the proportions can dramatically change due to a reduction greater than 80% in
the arterial cross-section, in cases of severe stenosis. Here we show that in diseased arteries, the local particle concentration
can peak at locations associated to high inflammation. We found that such locations are correlated to the vulnerable plaque
phenotype, which is prone to rupture. Our results demonstrate that at locations of high particle concentration, blood particles
change the shear stress distribution and magnitude. Therefore, the non-Newtonian blood flow assumption provides new
insights in the characterization of plaque built up. These results are combined to
in vitro
experiments that suggest the influence
of blood particles in the activity of cytokines. An unbalance in pro and anti-inflammatory cytokines has been associated to an
increase in inflammation and, consequently, in the volume of plaques forming. We anticipate our work to be a starting point for
a more sophisticated multi-scale model, which combines experimental findings and computational modeling to characterize
arterial segments affected by atherosclerosis. Such model includes a coupling between the distending arterial wall and the non-
Newtonian blood flow.
Biography
Glaucia C Pereira is a Principal Investigator in Machine Learning and Bioinformatics at the Icelandic Institute for Intelligent Machines. She is a former Member of
Imperial College London and a past Researcher Visitor at the University of Cambridge, where she worked with microfluidics and computational bio-fluid mechanics
applied to cardiovascular inflammation. She has also worked for both the Spanish and the Brazilian government, as a Researcher. She is currently applying
knowledge from biomedical engineering, mathematics and computational systems engineering, while leading projects in the field of biotechnology, aiming at
advancing knowledge in basic sciences and translational biomedicine.
gd109@imperial.ac.uk