1,938 research outputs found
A Unified Term for Directed and Undirected Motility in Collective Cell Invasion
In this paper we develop mathematical models for collective cell motility.
Initially we develop a model using a linear diffusion-advection type equation
and fit the parameters to data from cell motility assays. This approach is
helpful in classifying the results of cell motility assay experiments. In
particular, this model can determine degrees of directed versus undirected
collective cell motility. Next we develop a model using a nonlinear diffusion
term that is able capture in a unified way directed and undirected collective
cell motility. Finally we apply the nonlinear diffusion approach to a problem
in tumor cell invasion, noting that neither chemotaxis or haptotaxis are
present in the system under consideration in this article
The Role of Osteocytes in Targeted Bone Remodeling: A Mathematical Model
Until recently many studies of bone remodeling at the cellular level have
focused on the behavior of mature osteoblasts and osteoclasts, and their
respective precursor cells, with the role of osteocytes and bone lining cells
left largely unexplored. This is particularly true with respect to the
mathematical modeling of bone remodeling. However, there is increasing evidence
that osteocytes play important roles in the cycle of targeted bone remodeling,
in serving as a significant source of RANKL to support osteoclastogenesis, and
in secreting the bone formation inhibitor sclerostin. Moreover, there is also
increasing interest in sclerostin, an osteocyte-secreted bone formation
inhibitor, and its role in regulating local response to changes in the bone
microenvironment. Here we develop a cell population model of bone remodeling
that includes the role of osteocytes, sclerostin, and allows for the
possibility of RANKL expression by osteocyte cell populations. This model
extends and complements many of the existing mathematical models for bone
remodeling but can be used to explore aspects of the process of bone remodeling
that were previously beyond the scope of prior modeling work. Through numerical
simulations we demonstrate that our model can be used to theoretically explore
many of the most recent experimental results for bone remodeling, and can be
utilized to assess the effects of novel bone-targeting agents on the bone
remodeling process
Towards a New Spatial Representation of Bone Remodeling
Irregular bone remodeling is associated with a number of bone diseases such
as osteoporosis and multiple myeloma.
Computational and mathematical modeling can aid in therapy and treatment as
well as understanding fundamental biology. Different approaches to modeling
give insight into different aspects of a phenomena so it is useful to have an
arsenal of various computational and mathematical models.
Here we develop a mathematical representation of bone remodeling that can
effectively describe many aspects of the complicated geometries and spatial
behavior observed.
There is a sharp interface between bone and marrow regions. Also the surface
of bone moves in and out, i.e. in the normal direction, due to remodeling.
Based on these observations we employ the use of a level-set function to
represent the spatial behavior of remodeling. We elaborate on a temporal model
for osteoclast and osteoblast population dynamics to determine the change in
bone mass which influences how the interface between bone and marrow changes.
We exhibit simulations based on our computational model that show the motion
of the interface between bone and marrow as a consequence of bone remodeling.
The simulations show that it is possible to capture spatial behavior of bone
remodeling in complicated geometries as they occur \emph{in vitro} and \emph{in
vivo}.
By employing the level set approach it is possible to develop computational
and mathematical representations of the spatial behavior of bone remodeling. By
including in this formalism further details, such as more complex cytokine
interactions and accurate parameter values, it is possible to obtain
simulations of phenomena related to bone remodeling with spatial behavior much
as \emph{in vitro} and \emph{in vivo}. This makes it possible to perform
\emph{in silica} experiments more closely resembling experimental observations.Comment: Math. Biosci. Eng., 9(2), 201
Multiple small monthly doses of dicyandiamide (DCD) did not reduce denitrification in Waikato dairy pasture
The effectiveness of multiple small doses of the nitrification inhibitor dicyandiamide (DCD) to decrease denitrification under warm moist conditions was tested in a 1-year field trial on a grazed dairy pasture. DCD was applied approximately every 4 weeks as an aqueous spray onto ten replicate plots 3 days after rotational grazing by dairy cows. Each application was at the rate of 3 kg DCD haā»Ā¹, with a total annual application of 33 kg haā»Ā¹. Denitrification was assessed 5 days after each DCD application using the acetylene block method. At the end of the trial, the rate of degradation of DCD under summer conditions was measured. DCD significantly decreased the mean annual nitrate concentration by about 17%. Denitrification and denitrification enzyme activity were highly variable and no significant effect of DCD in decreasing denitrification was detected. In the summer month of December, DCD degraded rapidly with an estimated half-life of 5 Ā± 3 days (mean and standard deviation)
Interaction of inhibition and synaptic plasticity in a model of the hippocampal CA1 microcircuit
CNS*2011 : Twentieth Annual Computational Neuroscience Meeting, Stockholm, Sweden, 23-28 July 2011. Poster presentationInformatikos fakultetasTaikomosios informatikos katedraVytauto Didžiojo universiteta
Modeling and Simulation of the Effects of Cyclic Loading on Articular Cartilage Lesion Formation
We present a model of articular cartilage lesion formation to simulate the
effects of cyclic loading. This model extends and modifies the
reaction-diffusion-delay model by Graham et al. 2012 for the spread of a lesion
formed though a single traumatic event. Our model represents "implicitly" the
effects of loading, meaning through a cyclic sink term in the equations for
live cells.
Our model forms the basis for in silico studies of cartilage damage relevant
to questions in osteoarthritis, for example, that may not be easily answered
through in vivo or in vitro studies.
Computational results are presented that indicate the impact of differing
levels of EPO on articular cartilage lesion abatement
Intersubject Regularity in the Intrinsic Shape of Human V1
Previous studies have reported considerable intersubject variability in the three-dimensional geometry of the human primary visual cortex (V1). Here we demonstrate that much of this variability is due to extrinsic geometric features of the cortical folds, and that the intrinsic shape of V1 is similar across individuals. V1 was imaged in ten ex vivo human hemispheres using high-resolution (200 Ī¼m) structural magnetic resonance imaging at high field strength (7 T). Manual tracings of the stria of Gennari were used to construct a surface representation, which was computationally flattened into the plane with minimal metric distortion. The instrinsic shape of V1 was determined from the boundary of the planar representation of the stria. An ellipse provided a simple parametric shape model that was a good approximation to the boundary of flattened V1. The aspect ration of the best-fitting ellipse was found to be consistent across subject, with a mean of 1.85 and standard deviation of 0.12. Optimal rigid alignment of size-normalized V1 produced greater overlap than that achieved by previous studies using different registration methods. A shape analysis of published macaque data indicated that the intrinsic shape of macaque V1 is also stereotyped, and similar to the human V1 shape. Previoud measurements of the functional boundary of V1 in human and macaque are in close agreement with these results
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