A fictitious domain method is used to perform fully resolved numerical simulations of particle-laden turbulent flow in a horizontal channel. The effects of large particles of diameter 0.05 and 0.1 times the channel height on the turbulence statistics and structures are investigated for different settling coefficients and volume fractions (0.79 %–7.08 %) for the channel Reynolds number being 5000. The results indicate the following. (a) When the particle sedimentation effect is negligible (i.e. neutrally buoyant), the presence of particles decreases the maximum r.m.s. of streamwise velocity fluctuation near the wall by weakening the intensity of the large-scale streamwise vortices, while increasing the r.m.s. of the streamwise fluctuating velocity in the region very close to the wall and in the centre region. On the other hand, the particles increase the r.m.s. of transverse and spanwise fluctuating velocities in the near-wall region by inducing the small-scale vortices. (b) When the particle settling effect is so substantial that most particles settle onto the bottom wall and form a particle sediment layer (SL), the SL plays the role of a rough wall and parts of the vortex structures shedding from the SL ascend into the core region and substantially increase the turbulence intensity there. (c) When the particle settling effect is moderate, the effects of particles on the turbulence are a combination of the former two situations, and the Shields number is a good parameter for measuring the particle settling effects (i.e. the particle concentration distribution in the transverse direction). The average velocities of the particle are smaller in the lower half-channel and larger in the upper half-channel compared to the local fluid velocities in the presence of gravity effects. The effects of the smaller particles on the turbulence are found to be stronger at the same particle volume fractions.

Malaria-infected red blood cells (iRBCs) become less deformable with the progression of infection and tend to occlude microcapillaries. This process has been investigated in vitro using microfluidic channels. The objective of this paper is to provide a quantitative basis for interpreting the experimental observations of iRBC occlusion of microfluidic channels. Using a particle-based model for the iRBC, we simulate the traverse of iRBCs through a converging microfluidic channel and explore the progressive loss of cell deformability due to three factors: the stiffening of the membrane, the reduction of the cell's surface-volume ratio, and the growing solid parasites inside the cell. When examined individually, each factor tends to hinder the passage of the iRBC and lengthen the transit time. Moreover, at sufficient magnitude, each may lead to obstruction of narrow microfluidic channels. We then integrate the three factors into a series of simulations that mimic the development of malaria infection through the ring, trophozoite, and schizont stages. These simulations successfully reproduce the experimental observation that with progression of infection, the iRBC transitions from passage to blockage in larger and larger channels. The numerical results suggest a scheme for quantifying iRBC rigidification through microfluidic measurements of the critical pressure required for passage.

The effects of large neutrally buoyant particles on the flow instability and turbulence transition in pipe flow are investigated with the fictitious domain method. The periodic boundary condition is introduced in the streamwise direction. The work comprises two parts. In the first part, the pressure gradient is kept constant, and the purpose is to study the particle-induced flow instability. In our previous study [X. Shao, Z. Yu, and B. Sun, Phys. Fluids 20, 103307 (2008)10.1063/1.3005427], it was observed that a particle of a/R = 0.1 (a and R being the radii of the particle and the tube, respectively) induced the flow structure characterized by two pairs of weak and stable streamwise vortices at the Reynolds number of 1000. In the present study, our results show that the flow structure loses stability at the Reynolds number of 1500. However, it is interesting that the system eventually reaches a stable state: the particle spirals forward along the tube wall, accompanied by a stable flow structure for the case of one single particle in the computational domain. In the second part of the present study, the flow flux is kept constant, and the purpose is to examine the effects of particles on the critical Reynolds number based on the mean velocity. Our results show that large particles trigger the turbulence transition at low particle volume fractions, but delay the transition as the particle volume fraction exceeds a critical value, in agreement with the previous experimental observation [J.-P. Matas, J. F. Morris, and É. Guazzelli, Phys. Rev. Lett. 90, 014501 (2003)10.1103/PhysRevLett.90.014501].

Recent experiments have investigated the response of smooth muscle cells to transient stretch-compress (SC) and compress-stretch (CS) maneuvers. The results indicate that the transient SC maneuver causes a sudden fluidization of the cell while the CS maneuver does not. To understand this asymmetric behavior, we have built a biomechanical model to probe the response of stress fibers to the two maneuvers. The model couples the cross-bridge cycle of myosin motors with a viscoelastic Kelvin-Voigt element that represents the stress fiber. Simulation results point to the sensitivity of the myosin detachment rate to tension as the cause for the asymmetric response of the stress fiber to the CS and SC maneuvers. For the SC maneuver, the initial stretch increases the tension in the stress fiber and suppresses myosin detachment. The subsequent compression then causes a large proportion of the myosin population to disengage rapidly from actin filaments. This leads to the disassembly of the stress fibers and the observed fluidization. In contrast, the CS maneuver only produces a mild loss of myosin motors and no fluidization.

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