We study the dynamics of torque driven spherical spinners settled on a surface, and demonstrate that hydrodynamic interactions at finite Reynolds numbers can lead to a concentration dependent and non-uniform crystallisation. At semi-dilute concentrat
ions, we observe a rapid formation of a uniform hexagonal structure in the spinner monolayer. We attribute this to repulsive hydrodynamic interactions created by the secondary flow of the spinning particles. Increasing the surface coverage leads to a state with two co-existing spinner densities. The uniform hexagonal structure deviates into a high density crystalline structure surrounded by a continuous lower density hexatically ordered state. We show that this phase separation occurs due to a non-monotonic hydrodynamic repulsion, arising from a concentration dependent spinning frequency.
Flux of rigid or soft particles (such as drops, vesicles, red blood cells, etc.) in a channel is a complex function of particle concentration, which depends on the details of induced dissipation and suspension structure due to hydrodynamic interactio
ns with walls or between neighboring particles. Through two-dimensional and three-dimensional simulations and a simple model that reveals the contribution of the main characteristics of the flowing suspension, we discuss the existence of an optimal volume fraction for cell transport and its dependence on the cell mechanical properties. The example of blood is explored in detail, by adopting the commonly used modeling of red blood cells dynamics. We highlight the complexity of optimization at the level of a network, due to the antagonist evolution of local volume fraction and optimal volume fraction with the channels diameter. In the case of the blood network, the most recent results on the size evolution of vessels along the circulatory network of healthy organs suggest that the red blood cell volume fraction (hematocrit) of healthy subjects is close to optimality, as far as transport only is concerned. However, the hematocrit value of patients suffering from diverse red blood cel pathologies may strongly deviate from optimality.
Optimal hematocrit $H_o$ maximizes oxygen transport. In healthy humans, the average hematocrit $H$ is in the range of 40-45$%$, but it can significantly change in blood pathologies such as severe anemia (low $H$) and polycythemia (high $H$). Whether
the hematocrit level in humans corresponds to the optimal one is a long standing physiological question. Here, using numerical simulations with the Lattice Boltzmann method and two mechanical models of the red blood cell (RBC) we predict the optimal hematocrit, and explore how altering the mechanical properties of RBCs affects $H_o$. We develop a simplified analytical theory that accounts for results obtained from numerical simulations and provides insight into the physical mechanisms determining $H_o$. Our numerical and analytical models can easily be modified to incorporate a wide range of mechanical properties of RBCs as well as other soft particles thereby providing means for the rational design of blood substitutes. Our work lays the foundations for systematic theoretical study of the optimal hematocrit and its link with pathological RBCs associated with various diseases (e.g. sickle cell anemia, diabetes mellitus, malaria, elliptocytosis).
Driven or active suspensions can display fascinating collective behavior, where coherent motions or structures arise on a scale much larger than that of the constituent particles. Here, we report experiments and numerical simulations revealing that r
ed blood cells (RBCs) assemble into regular patterns in a confined shear flow. The order is of pure hydrodynamic and inertialess origin, and emerges from a subtle interplay between (i) hydrodynamic repulsion by the bounding walls which drives deformable cells towards the channel mid-plane and (ii) intercellular hydrodynamic interactions which can be attractive or repulsive depending on cell-cell separation. Various crystal-like structures arise depending on RBC concentration and confinement. Hardened RBCs in experiments and rigid particles in simulations remain disordered under the same conditions where deformable RBCs form regular patterns, highlighting the intimate link between particle deformability and the emergence of order. The difference in structuring ability of healthy (deformable) and diseased (stiff) RBCs creates a flow signature potentially exploitable for diagnosis of blood pathologies.
