An organ-on-electronic chip (organ-on-e-chip)—a three-dimensional (3D) biosensor array to decipher tissue electrical activity.

Significance: Small unilamellar vesicles formed via self-assembly of phospholipids or block copolymers have been investigated in the context of human physiology and biomedical research. Here, we present both energetics and thermodynamics analyses that incorporate nonlinear elasticity to predict, in a unique manner, the limiting size and size distribution of vesicles as well as to identify the conditions for the formation of stable open vesicles, disks, and closed spherical vesicles. In addition to providing a comprehensive understanding of vesicle formation, the framework presented here may be adapted to develop tools for in vivo liquid biopsies and to elucidate the biophysical features of extracellular vesicles, thus suggesting new approaches to diagnostics and therapeutics for cancer and other diseases.

Biological membranes are involved in numerous intriguing biophysical and biological cellular phenomena of different length scales, ranging from nanoscale raft formation, vesiculation, to microscale shape transformations. With extended length and time scales as compared to atomistic simulations, solvent-free coarse-grained membrane models have been exploited in mesoscopic membrane simulations. In this study, we present a one-particle-thick fluid membrane model, where each particle represents a cluster of lipid molecules. The model features an anisotropic interparticle pair potential with the interaction strength weighed by the relative particle orientations. With the anisotropic pair potential, particles can robustly self-assemble into fluid membranes with experimentally relevant bending rigidity. Despite its simple mathematical form, the model is highly tunable. Three potential parameters separately and effectively control diffusivity, bending rigidity, and spontaneous curvature of the model membrane. As demonstrated by selected examples, our model can naturally simulate dynamics of phase separation in multicomponent membranes and the topological change of fluid vesicles.

Significance: Our coarse-grained molecular dynamics (CGMD) simulations show that the deposition of nanoscale knobs, rather than spectrin network remodeling, is the primary cause of the dramatically increased stiffness of thePlasmodium falciparum(Pf)-infected red blood cell (RBC) membranes. Our analyses further reveal that the knobs stiffen the RBC membrane in a unique manner by simultaneously harnessing composite strengthening, strain hardening, and knob density-dependent vertical coupling effects. In addition to providing a fundamental understanding of the stiffening mechanism ofPf-infected RBCs, our simulation results suggest potential targets for antimalarial therapies.