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Martin Gerbert Frasch, CHU Ste-Justine Research
Centre, Dept. of Obstetrics-Gynecology, Université
de Montréal
Fields Institute, Stewart Library
Mathematical properties
of fetal heart rate variability and electroencephalogram:
a journey from complex signal bioinformatics to bedside
fetal health monitoring
Antenatal brain injury remains
a major cause of long-term neurodevelopmental sequelae
in children and adults. Fetal inflammation and acidemia
play a major role in the etiology of antenatal brain
injury. These pathologic conditions are difficult to
diagnose and new early and non-invasive indicators are
urgently needed. Recent studies have identified fetal
heart rate (FHR) variability (fHRV) and electroencephalogram
(EEG) measures that reflect changes in inflammation
and acidemia. Hence, fHRV monitoring and fetal EEG hold
promise as continuous, sensitive and specific modalities
that may identify fetuses at risk of adverse outcomes
and requiring intervention. The fHRV measures of interest
include time and complexity/entropy/information flow
domain measures reflecting vagal modulation of fHRV.
Fetal EEG frequency and amplitude characteristics change
predictably in relation to changes in FHR with worsening
fetal acidemia as it is observed during labour when
EEG can be used as an ancillary monitoring tool in addition
to fHRV. We need to identify the best subset of fHRV
and EEG measures able to reliably detect fetal inflammation
or acidemia. Platforms such as the continuous individualized
multiorgan variability analysis can then be used to
test clinically whether certain mathematical fHRV and
EEG properties may better predict fetal compromise in
human pregnancy than current FHR analysis techniques.
A paradigm shift is needed in electronic fetal monitoring
from low to high resolution FHR acquisition and addition
of EEG monitoring during labour. Eventually, for the
new fHRV and EEG monitoring to become accepted on bedside,
it needs to be implemented on the basis of the very
widely used ultrasound-based FHR monitors. Evidence
exists that such approach will succeed. References:
doi:10.1016/j.jcrc.2011.02.033 and 10.1371/journal.pone.0022100.
Ramin Abolfath, University of Texas at
Dallas and Ottawa University
Molecular
simulations of radio-biological effects: DNA damage
by ionizing radiation
In this talk I briefly review
mathematical and computational approaches in modeling
therapeutic ionizing radiation interaction with biological
systems. In particular, I present recent progress in
large scale molecular simulation on initial damage of
DNA-molecules interacting with randomly distributed
clusters of diatomic OH-radicals that are primary products
of megavoltage ionizing radiation. Chemical pathways
for carbonyl- and hydroxyl-hole formation in the sugar-moiety
rings are identified. We show that gradual grow up of
the holes lead to DNA-bases and DNA-backbone damage
that collectively propagate to DNA single and double
strand breaks. I conclude with remarks on possible mechanisms
in controlling radio resistivity and sensitivity and
developing dosimetry-based techniques for modeling radio-biological
effects.
Refs: J. Phys. Chem. A
115, 11045 (2011); J. Phys. Chem. B 113, 6938 (2009);
Journal of Computational Chemistry 31, 2601 (2010).
Animations:
http://qmsimulator.wordpress.com/
Tuesday, November 22,
2011 -- 3:30 p.m. Craig Simmons, University of Toronto Mechanics-based insights
into heart valve disease
In aortic heart valve disease,
fibrotic and calcific lesions form focally in predictable
locations in one layer of the valve leaflets, suggesting
that the cellular microenvironment in the disease-prone
regions is permissive to pathological development. The
cellular microenvironment is defined in part by biomechanical
factors, and our studies suggest that hemodynamics and
tissue elasticity are important regulators of layer-specific
valve cell phenotypes and focal pathological alterations.
In this talk, I will describe our progress in characterizing
heart valve cell and tissue micromechanical properties
and their link to cellular and molecular processes that
contribute to heart valve disease progression.
Friday, July 22, 2011 -- 3:30pm Professor Philip Maini, Oxford University Modelling aspects of tumour growth The dynamics of cancerous
tumour growth is a highly complex process involving
interactions at many different scales. We consider a
few simple models for tumour growth addressing, (i)
the acid-mediated invasion hypothesis, (ii) somatic
evolution, (iii) colorectal cancer, (iv) vascular tumour
growth. The modelling approaches range from coupled
systems of partial differential equations to hybrid
cellular automata, to individual-cell-based models.
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