### Session EE: Biofluids III: General III - Flows and Diseases

Chair: James Brasseur, Pennsylvania State University
Room: 101E

 Sunday, November 22, 2009 4:15PM - 4:28PM EE.00001: Probing protein mechanical stability with controlled shear flows Jonathan Dusting , Lorna Ashton , Justin Leontini , Ewan Blanch , Stavroula Balabani Understanding and controlling protein aggregation or misfolding is of both fundamental and medical interest. The structural changes experienced by proteins in response to forces such as those generated within flows have not been well characterised, despite the importance of mechanics in many biological processes. By monitoring the structural conformation of proteins in different concentric cylinder flows using Raman Spectroscopy we have quantified the relative stability of $\beta$-sheet dominated proteins compared with those containing a greater proportion of $\alpha$-helix. To ensure that the fluid stresses are quantified accurately, a combined DNS and PIV approach has been undertaken for flow cell characterisation across the full range of operating Re. This is important for practical concentric cylinder geometries where the shear components are non-zero and spatially dependent, with the peak stresses located near the endwalls. Furthermore, recirculation regions appear well below the crtical Reynolds number for Taylor vortex formation. Sunday, November 22, 2009 4:28PM - 4:41PM EE.00002: A quasi-one-dimensional model for collapsible channel oscillations Draga Pihler-Puzovic , Timothy Pedley A fluid driven rapidly through a flexible tube exhibits self-excited oscillations. To model this phenomenon, we consider 2D high Re laminar flow of a Newtonian incompressible fluid through a collapsible channel. The channel has a section of an otherwise rigid wall replaced by a membrane with inertia, under longitudinal tension, with no bending stiffness and subject to the external pressure. Based on the analysis by Pedley and Stephanoff (\emph{JFM},85), membrane motion is coupled to the time-dependent behaviour of the core flow through a modified KdV equation. We focus on the importance of membrane inertia for the system. The stability of the problem is studied numerically. In the parameter regimes of interest the computations reveal transitional behaviour: initially small perturbation of the system decays in an oscillatory manner but beyond a certain time higher frequency oscillations start dominating and the system diverges. At the same time a switching between mode one in which the flexible wall has a single extremum, to higher modes with multiple extrema is observed. These results are discussed with respect to previous computations for 2D collapsible channels. Sunday, November 22, 2009 4:41PM - 4:54PM EE.00003: Phasic Relationships among Hemodynamic Properties of Pulsatile Flow in Microcirculations Jung Yeop Lee , Sang Joon Lee Pulsatile blood flows in \textit{omphalo-mesenteric} arteries of HH-stage 18 chicken embryos are measured using a time-resolved particle image velocimetry (PIV) technique to obtain hemodynamic information in microcirculations and compare hemodynamic properties of pulsatile blood flows. Due to the intrinsic features of pulsatile flow and complicated vessel network of microcirculation, an \textit{out}-\textit{of}-\textit{phase} motion of blood occurs in nearby vessel segments of bifurcations. This is mainly attributed to the morphological characteristics and peripheral resistance of vasculature. The \textit{out}-\textit{of}-\textit{phase} motion is quantitatively identified using the one-dimensional temporal cross-correlation function. This cross-correlation function is extended to establish the phasic relationships among hemodynamic properties such as velocity, shear rate, and acceleration. Velocity and shear rate are almost \textit{in phase}, as predicted theoretically. On the other hand, velocity (or shear rate) shows an almost 180$^{\circ}$ \textit{out}-\textit{of}-\textit{phase} against acceleration, which is quite larger than the theoretically predicted value. Sunday, November 22, 2009 4:54PM - 5:07PM EE.00004: Numerical Study on Flows of Red Blood Cells with Liposome-Encapsulated Hemoglobin at Microvascular Bifurcation Toru Hyakutake , Shigeki Tani , Yuki Akagi , Takeshi Matsumoto , Shinichiro Yanase Flow analysis at microvascular bifurcation after partial replacement of red blood cell (RBC) with liposome-encapsulated hemoglobin (LEH) was performed using the lattice Boltzmann method. A two-dimensional bifurcation model with a parent vessel and daughter branch was considered, and the distributions of the RBC, LEH, and oxygen fluxes were calculated. The immersed boundary method was employed to incorporate the fluid--membrane interaction between the flow field and deformable RBC When only RBCs flow into the daughter branches with unevenly distributed flows, plasma separation occurred and the RBC flow to the lower-flow branch was disproportionately decreased. On the other hand, when the half of RBC are replaced by LEH, the biasing of RBC flow was enhanced whereas LEH flowed favorably into the lower-flow branch, because many LEH within the parent vessel are suspended in the plasma layer, where no RBCs exist. Consequently, the branched oxygen fluxes became nearly proportional to flows. These results indicate that LEH facilitates oxygen supply to branches that are inaccessible to RBCs. Sunday, November 22, 2009 5:07PM - 5:20PM EE.00005: A Numerical Computation Model for Low-Density Lipoprotein (LDL) Aggregation and Deposition in the Human Artery Yongli Zhao , Shaobiao Cai , Albert Ratner Cholesterol caused cardiovascular events are commonly seen in human lives. These events are primarily believed to be caused by the built up of particles like low-density lipoprotein (LDL). When a large number of LDL circulates in the blood, it can gradually build up in the inner walls of the arteries. A thick, hard deposit plaque can be formed together with other substances. This type of plaque may clog those arteries and cause vascular problems. Clinical evidences suggest that LDL is related to cardiovascular events and the progression of coronary heart disease is due to its aggregation and deposition. This study presents an investigation of LDL aggregation and deposition based on particulate flow. A soft-sphere based particulate computational flow model is developed to represent LDL suspending in plasma. The transport, collision and adhesion phenomena of LDL particles are simulated to examine the physics involved in aggregation and deposition. A multiple-time step discrete-element approach is presented for efficiently simulating large number of LDL particles and their interactions. The roles the quality and quantity the LDL playing in the process of aggregation and deposition are determined. The study provides a new perspective for improving the understanding of the fundamentals as related to these particle-caused cardiovascular events. Sunday, November 22, 2009 5:20PM - 5:33PM EE.00006: A Comprehensive Fluid Dynamic-Diffusion Model of Blood Microcirculation with Focus on Sickle Cell Disease Francois Le Floch , Wesley L. Harris A novel methodology has been developed to address sickle cell disease, based on highly descriptive mathematical models for blood flow in the capillaries. Our investigations focus on the coupling between oxygen delivery and red blood cell dynamics, which is crucial to understanding sickle cell crises and is unique to this blood disease. The main part of our work is an extensive study of blood dynamics through simulations of red cells deforming within the capillary vessels, and relies on the use of a large mathematical system of equations describing oxygen transfer, blood plasma dynamics and red cell membrane mechanics. This model is expected to lead to the development of new research strategies for sickle cell disease. Our simulation model could be used not only to assess current researched remedies, but also to spur innovative research initiatives, based on our study of the physical properties coupled in sickle cell disease. Sunday, November 22, 2009 5:33PM - 5:46PM EE.00007: Investigating the fluid mechanics behind red blood cell-induced lateral platelet motion Lindsay Crowl Erickson , Aaron Fogelson Platelets play an essential role in blood clotting; they adhere to damaged tissue and release chemicals that activate other platelets. Yet in order to adhere, platelets must first come into contact with the injured vessel wall. Under arterial flow conditions, platelets have an enhanced concentration near blood vessel walls. This non-uniform cell distribution depends on the fluid dynamics of blood as a heterogeneous medium. We use a parallelized lattice Boltzmann-immersed boundary method to solve the flow dynamics of red cells and platelets in a periodic 2D vessel with no-slip boundary conditions. Red cells are treated as biconcave immersed boundary objects with isotropic Skalak membrane tension and an internal viscosity five times that of the surrounding plasma. Using this method we analyze the influence of shear rate, hematocrit, and red cell membrane properties on lateral platelet motion. We find that the effective diffusion of platelets is significantly lower near the vessel wall compared to the center of the vessel. Insight gained from this work could lead to significant improvements to current models for platelet adhesion where the presence of red blood cells is neglected due to computational intensity. Sunday, November 22, 2009 5:46PM - 5:59PM EE.00008: A Spatial-Temporal Model of Platelet Deposition and Blood Coagulation Under Flow Karin Leiderman Gregg , Aaron Fogelson In the event of a vascular injury, a blood clot will form to prevent bleeding. This response involves two intertwined processes: platelet aggregation and coagulation. Activated platelets are critical to coagulation in that they provide localized reactive surfaces on which many of the coagulation reactions occur. The final product from the coagulation cascade directly couples the coagulation system to platelet aggregation by acting as a strong activator of platelets and cleaving blood-borne fibrinogen into fibrin which then forms a mesh to help stabilize platelet aggregates. Together, the fibrin mesh and the platelet aggregates comprise a blood clot, which in some cases, can grow to occlusive diameters. Transport of coagulation proteins to and from the vicinity of the injury is controlled largely by the dynamics of the blood flow. It is crucial to learn how blood flow affects the growth of clots, and how the growing masses, in turn, feed back and affect the fluid motion. We have developed the first spatial-temporal model of platelet deposition and blood coagulation under flow that includes detailed decriptions of the coagulation biochemistry, chemical activation and deposition of blood platelets, as well as the two-way interaction between the fluid dynamics and the growing platelet mass. Sunday, November 22, 2009 5:59PM - 6:12PM EE.00009: Enhancement of Absorption by Micro-Mixing induced by Villi Motion Yanxing Wang , James Brasseur , Gino Banco Motions of surface villi create microscale flows that can couple with lumen-scale eddies to enhance absorption at the epithelium of the small intestine. Using a multigrid strategy within the lattice-Boltzmann framework, we model a macro-scale cavity flow with microscale villi'' in pendular motion on the lower surface and evaluate the couplings between macro and micro-scale fluid motions, scalar mixing, and uptake of passive scalar at the villi surface. We study the influences of pendular frequency, villous length, and villous groupings on absorption rate. The basic mechanism underlying the enhancement of absorption rate by a villous-induced micro-mixing layer'' (MML) is the microscale pumping'' of low concentration fluid from between groups of villi coupled with the return of high concentration fluid into the villi groups from the macroscale flow. The MML couples with the macrosacle eddies through a diffusion layer that separates micro and macro mixed layers. The absorption rate increases with frequency of villi oscillation due to enhanced vertical pumping. We discover a critical villus length above which absorption rate increases significantly. The absorption is influenced by villus groupings in a complex way due to the interference between vertical and horizontal geometry vs. MML scales. We conclude that optimized villi motility can enhance absorption and may underlie an explanation for the existence of villi in the gut. [Supported by NSF] Sunday, November 22, 2009 6:12PM - 6:25PM EE.00010: Multiscale modeling of blood flow in cerebral malaria Dmitry Fedosov , Bruce Caswell , George Karniadakis The main characteristics of the malaria disease are progressing changes in red blood cell (RBC) mechanical properties and geometry, and its cytoadhesion to the vascular endothelium. Malaria-infected RBCs become considerably stiff compared to healthy ones, and may bind to the vascular endothelium of arterioles and venules. This leads to a significant reduction of blood flow, and eventual vessel obstruction. Due to a non-trivial malaria-infected RBC adhesive dynamics and obstruction formations the blood flow in cerebral malaria is extremely complex. Here, we employ multiscale modeling to couple nanometer scales at the binding level, micrometer scales at the cell level and millimeter scales at the arteriole level. Blood flow in cerebral malaria is modeled using a coarse-grained RBC model developed in our group. The RBC adhesion is simulated based on the stochastic bond formation/breakage model, which is validated against recent experiments.