The structural change of a phospholipid bilayer in water under the action of a shock wave is numerically studied with unsteady nonequilibrium molecular dynamics simulations. The action of shock waves is modeled by the momentum change of water molecules, and thereby we demonstrate that the resulting collapse and rebound of the bilayer are followed by the penetration of water molecules into the hydrophobic region of the bilayer. The high-speed phenomenon that occurs during the collapse and rebound of the bilayer is analyzed in detail, particularly focusing on the change of bilayer thickness, the acyl chain bend angles, the lateral fluidity of lipid molecules, and the penetration rate of water molecules. The result shows that the high-speed phenomenon can be divided into two stages: in the first stage the thickness of bilayer and the order parameter are rapidly reduced, and then in the second stage they are recovered relatively slowly. It is in the second stage that water molecules are steadily introduced into the hydrophobic region. The penetration of water molecules is enhanced by the shock wave impulse and this qualitatively agrees with a recent experimental result.

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Rupture of biological cell membrane under mechanical stresses is critical for cell viability. It is triggered by local rearrangements of membrane molecules. We investigated the effects of stretching speed on mechanical rupture of phospholipid/cholesterol bilayers using unsteady molecular dynamics simulations. We focused on pore formation, the trigger of rupture, in a 40 mol% cholesterol-including bilayer. The unsteady stretching was modeled by proportional and temporal scaling of atom positions at stretching speeds from 0.025 to 30 m/s. The effects of the stretching speed on the critical areal strain, where the pore forms, is composed of two regimes. At low speeds (<1.0 m/s), the critical areal strain is insensitive to speed, whereas it significantly increases at higher speeds. Also, the strain is larger than that of a pure bilayer, regardless of the stretching speeds, which qualitatively agrees with available experimental data. Transient recovery of the cholesterol and phospholipid molecular orientations was evident at lower speeds, suggesting the formation of a stretch-induced interdigitated gel-like phase. However, this recovery was not confirmed at higher speeds or for the pure bilayer. The different responses of the molecular orientations may help explain the two regimes for the effect of stretching speed on pore formation.

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Unsteady and nonequilibrium molecular dynamics simulations of the response of dipalmitoylphosphatidylcholine (DPPC) bilayers to the shock waves of various incident angles are presented. The action of an incident shock wave is modeled by adding a momentum in an oblique direction to water molecules adjacent to a bilayer. We thereby elucidate the effects of incident shock angles on (i) collapse and rebound of the bilayer, (ii) lateral displacement of headgroups, (iii) tilts of lipid molecules, (iv) water penetration into the hydrophobic region of the bilayer, and (v) momentum transfer across the bilayer. The number of water molecules delivered into the hydrophobic region is found to be insensitive to incident shock angles. The most important structural changes are the lateral displacement of headgroups and tilts of lipid molecules, which are observed only in the half of the bilayer directly exposed to a shock wave for all incident shock angles studied here. As a result, only the normal component of the added oblique momentum is substantially transferred across the bilayer. This also suggests that the irradiation by shock waves may induce a jet-like streaming of the cytoplasm toward the nucleus.

We demonstrate the self-organization process of a stable pore structure in a phospholipid bilayer by unsteady and nonequilibrium molecular dynamics simulations. The simulation is started from an initial state including some amount of water molecules in its hydrophobic region, which is a model of a cell membrane stimulated by ultrasound radiation for the membrane permeabilization (sonoporation). We show that, in several nanoseconds, the bilayer-water system can spontaneously develop into a water-filled pore structure without any mechanical and electrical forcing from outside, when the initial number of water molecules in the hydrophobic region exceeds a critical value. The increase in the initial number of water molecules enhances the probability of pore formation, and sometimes induces the formation of transient micellelike structures of phospholipid molecules.

We investigate the collapse of a lipid-coated nanobubble and subsequent formation of a lipid vesicle by coarse grained molecular dynamics simulations. A spherical nanobubble coated with a phospholipid monolayer in water is a model of an aqueous dispersion of phospholipids under negative pressure during sonication. When subjected to a positive pressure, the bubble shape deforms into an irregular spherical shape and the monolayer starts to buckle and fold locally. The local folds grow rapidly in multiple directions and forming a discoidal membrane with folds of various amplitudes. Folds of small amplitude disappear in due course and the membrane develops into a unilamellar vesicle via a bowl shape. Folds with large amplitude develop into a bowl shape and a multivesicular shape forms. The membrane shape due to bubble collapse can be an important factor governing the vesicular shape during sonication.

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