Alex Szatmary

Dynamic ray tracing for modeling optical cell manipulation

Current methods for predicting stress distribution on a cell surface due to optical trapping forces are based on a traditional ray optics scheme for fixed geometries. Cells are typically modeled as solid spheres as this facilitates optical force calculation. Under such applied forces however, real and non-rigid cells can deform, so assumptions inherent in traditional ray optics methods begin to break down. In this work, we implement a dynamic ray tracing technique to calculate the stress distribution on a deformable cell induced by optical trapping. Here, cells are modeled as three-dimensional elastic capsules with a discretized surface with associated hydrodynamic forces calculated using the Immersed Boundary Method. We use this approach to simulate the transient deformation of spherical, ellipsoidal and biconcave capsules due to external optical forces induced by a single diode bar optical trap for a range of optical powers.

Adhesive Interactions between the Load Surface and the Actin Filament Tips Control the Mechanical Response of Branched Actin Networks

The force-velocity relationships of branched actin network have been investigated intensively, which yields conflicting results both in theory and in experiments. We previously established an integrated model that unifies different aspects of the dynamics of branched actin network, including the growth, the branching, and the capping events. The stochastic simulations of our model showed that upon the resistance from the load, the branched actin network is capable of reinforcing itself, which underscores the basis of both the concave and the convex force-velocity relationships. In the current work, we extend our model by incorporating the adhesive interactions between the actin filament tips and the load surface. Our simulation results reveal that such adhesive interactions critically impact the force-velocity relationships and the geometry of branched actin network.

Elastic capsule deformation in general irrotational linear flows

Knowledge of the response of elastic capsules to imposed fluid flow is necessary for predicting deformation and motion of biological cells and synthetic capsules in microfluidic devices and in the microcirculation. Capsules have been studied in shear, planar extensional, and axisymmetric extensional flows. Here, the flow gradient matrix of a general irrotational linear flow is characterized by two parameters, its strain rate, defined as the maximum of the principal strain rates, and by a new term, q, the difference in the two lesser principal strain rates, scaled by the maximum principal strain rate; this characterization is valid for ellipsoids in irrotational linear flow, and it gives good results for spheres in general linear flows at low capillary numbers. We demonstrate that deformable non-spherical particles align with the principal axes of an imposed irrotational flow. Thus, it is most practical to model deformation of non-spherical particles already aligned with the flow, rather than considering each arbitrary orientation. Capsule deformation was modeled for a sphere, a prolate spheroid, and an oblate spheroid, subjected to combinations of uniaxial, biaxial, and planar extensional flows; modeling was performed using the immersed boundary method. The time response of each capsule to each flow was found, as were the steady-state deformation factor, mean strain energy, and surface area. For a given capillary number, planar flows led to more deformation than uniaxial or biaxial extensional flows. Capsule behavior in all cases was bounded by the response of capsules to uniaxial, biaxial, and planar extensional flow.

Deformation of White Blood Cells Firmly Adhered to Endothelium

Circulating white blood cells adhere to endothelium near an infection site; this occurs because infection causes ligands to be expressed on activated endothelium. Initially, a white blood cell rolls on the substrate, but eventually forms a firm adhesion, allowing it to crawl through the endothelial layer toward the infected tissue. A computational model of bond kinetics, cell deformability, and fluid dynamics was used to model the forces experienced by a cell during this process. The cell was modeled as a fluid-filled membrane; on its surface were hundreds of deformable microvilli—little fingers, ruffles in the white blood cell’s wrinkly membrane. These microvilli were deformable and their tips were decorated with PSGL-1 chemical receptors which bound to P-selectin ligands on the surface. Softer cells and cells subjected to higher fluid shear stress deformed more, and having more contact area, they formed more bonds and were able to resist more hydrodynamic load.Copyright