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A scaling law to predict the conformability of flexible sheets on spherical surfaces is derived and used to enhance the wrap. 

Magnetic actuation has emerged as a powerful and versatile mechanism for diverse applications, ranging from soft robotics, biomedical devices to functional metamaterials. This highly interdisciplinary research calls for an easy to use and efficient modeling/simulation platform that can be leveraged by researchers with different backgrounds. Here we present a lattice model for hard-magnetic soft materials by partitioning the elastic deformation energy into lattice stretching and volumetric change, so-called ‘magttice’. Magnetic actuation is realized through prescribed nodal forces in magttice. We further implement the model into the framework of a large-scale atomic/molecular massively parallel simulator (LAMMPS) for highly efficient parallel simulations. The magttice is first validated by examining the deformation of ferromagnetic beam structures, and then applied to various smart structures, such as origami plates and magnetic robots. After investigating the static deformation and dynamic motion of a soft robot, the swimming of the magnetic robot in water, like jellyfish's locomotion, is further studied by coupling the magttice and lattice Boltzmann method (LBM). These examples indicate that the proposed magttice model can enable more efficient mechanical modeling and simulation for the rational design of magnetically driven smart structures. 

We investigate the circulation of nano- and micro-particles, including spherical particles and filamentous nanoworms, with red blood cells (RBCs) suspension in a constricted channel that mimics a stenosed microvessel. Through three-dimensional simulations using the immersed boundary-based Lattice Boltzmann method, the influence of channel geometries, such as the length and ratio of the constriction, on the accumulation of particles is systematically studied. Firstly, we find that the accumulation of spherical particles with 1 μm diameter in the constriction increases with the increases of both the length and ratio of the constriction. This is attributed to the interaction between spheres and RBCs. The RBCs “carry” the spheres and they accumulate inside the constriction together, due to the altered local hydrodynamics induced by the existence of the constriction. Secondly, nanoworms demonstrate higher accumulation than that of spheres inside the constriction, which is associated with the escape of nanoworms from RBC clusters and their accumulation near the wall of main channel. The accumulated near-wall nanoworms will eventually enter the constriction, thus enhancing their concentration inside the constriction. However, an exceptional case occurs in the case of constrictions with large ratio and long length. In such circumstances, the RBCs aggregate together tightly and concentrate at the center of the channel, which makes the nanoworms hardly able to escape from RBC clusters, leading to a similar accumulation of nanoworms and spheres inside the constriction. This study may provide theoretical guidance for the design of nano- and micro-particles for biomedical engineering applications, such as drug delivery systems for patients with stenosed microvessels. 

Building upon our previous studies on interactions of amphiphilic Janus nanoparticles with glass-supported lipid bilayers, we study here how these Janus nanoparticles perturb the structural integrity and induce shape instabilities of membranes of giant unilamellar vesicles (GUVs). We show that 100 nm amphiphilic Janus nanoparticles disrupt GUV membranes at a threshold particle concentration similar to that in supported lipid bilayers, but cause drastically different membrane deformations, including membrane wrinkling, protrusion, poration, and even collapse of entire vesicles. By combining experiments with molecular simulations, we reveal how Janus nanoparticles alter local membrane curvature and collectively compress the membrane to induce shape transformation of vesicles. Our study demonstrates that amphiphilic Janus nanoparticles disrupt vesicle membranes differently and more effectively than uniform amphiphilic particles. 

The margination and adhesion of micro-particles (MPs) have been extensively investigated separately, due to their important applications in the biomedical field. However, the cascade process from margination to adhesion should play an important role in the transport of MPs in blood flow. To the best of our knowledge, this has not been explored in the past. Here we numerically study the margination behaviour of elastic MPs to blood vessel walls under the interplay of their deformability and adhesion to the vessel wall. We use the lattice Boltzmann method and molecular dynamics to solve the fluid dynamics and particle dynamics (including red blood cells (RBCs) and elastic MPs) in blood flow, respectively. Additionally, a stochastic ligand–receptor binding model is employed to capture the adhesion behaviours of elastic MPs on the vessel wall. Margination probability is used to quantify the localization of elastic MPs at the wall. Two dimensionless numbers are considered to govern the whole process: the capillary number $Ca$ , denoting the ratio of viscous force of fluid flow to elastic interfacial force of MP, and the adhesion number $Ad$ , representing the ratio of adhesion strength to viscous force of fluid flow. We systematically vary them numerically and a margination probability contour is obtained. We find that there exist two optimal regimes favouring high margination probability on the plane $Ca{-}Ad$ . The first regime, namely region I, is that with high adhesion strength and moderate particle stiffness; the other one, region II, has moderate adhesion strength and large particle stiffness. We conclude that the existence of optimal regimes is governed by the interplay of particle deformability and adhesion strength. The corresponding underlying mechanism is also discussed in detail. There are three major factors that contribute to the localization of MPs: (i) near-wall hydrodynamic collision between RBCs and MPs; (ii) deformation-induced migration due to the presence of the wall; and (iii) adhesive interaction between MPs and the wall. Mechanisms (i) and (iii) promote margination, while (ii) hampers margination. These three factors perform different roles and compete against each other when MPs are located in different regions of the flow channel, i.e. near-wall region. In optimal region I, adhesion outperforms deformation-induced migration; and in region II, the deformation-induced migration is small compared to the coupling of near-wall hydrodynamic collision and adhesion. The finding of optimal regimes can help the understanding of localization of elastic MPs at the wall under the adhesion effect in blood flow. More importantly, our results suggest that softer MP or stronger adhesion is not always the best choice for the localization of MPs.