We analyse a generic motility model, with the motility mechanism arising by contractile stress due to the interaction of myosin and actin. A hydrodynamic active polar gel theory is used to model the cytoplasm of a cell and is combined with a Helfrich-type model to account for membrane properties. The overall model allows consideration of the motility without the necessity for local adhesion. Besides a detailed numerical approach together with convergence studies for the highly nonlinear free boundary problem, we also compare the induced flow field of the motile cell with that of classical squirmer models and identify the motile cell as a puller or pusher, depending on the strength of the myosin -actin interactions.

The processes of protrusion and retraction during cell movement are driven by the turnover and reorganization of the actin cytoskeleton. Within a reaction-diffusion model which combines processes along the cell membrane with processes within the cytoplasm a Turing type instability is used to form the necessary polarity to distinguish between cell front and rear and to initiate the formation of different organizational arrays within the cytoplasm leading to protrusion and retraction. A simplified biochemical network model for the activation of GTPase which accounts for the different dimensionality of the cell membrane and the cytoplasm is used for this purpose and combined with a classical Helfrich type model to account for bending and stiffness effects of the cell membrane. In addition streaming within the cytoplasm and the extracellular matrix is taken into account. Combining these phenomena allows to simulate the dynamics of cells and to reproduce the primary phenomenology of cell motility. The coupled model is formulated within a phase field approach and solved using adaptive finite elements.

We consider a generic model for cell motility. Even if a comprehensive understanding of cell motility remains elusive, progress has been achieved in its modelling using a whole-cell physical model. The model takes into account the main mechanisms of cell motility, actin polymerization, actin-myosin dynamics and substrate mediated adhesion (if applicable), and combines them with steric cell-cell and hydrodynamic interactions. The model predicts the onset of collective cell migration, which emerges spontaneously as a result of inelastic collisions of neighbouring cells. Each cell here modelled as an active polar gel is accomplished with two vortices if it moves. Upon collision of two cells, the two vortices which come close to each other annihilate. This leads to a rotation of the cells and together with the deformation and the reorientation of the actin filaments in each cell induces alignment of these cells and leads to persistent translational collective migration. The effect for low Reynolds numbers is as strong as in the non-hydrodynamic model, but it decreases with increasing Reynolds number.

We numerically investigate margination of white blood cells and demonstrate the dependency on a number of conditions including hematocrit, the deformability of the cells and the Reynolds number. A detailed mesoscopic hydrodynamic Helfrich-type model is derived, validated and used for the simulations to provides a quantitative description of the margination of white blood cells. Previous simulation results, obtained with less detailed models, could be confirmed, e.g. the largest probability of margination of white blood cells at an intermediate range of hematocrit values and a decreasing tendency with increasing deformability. The consideration of inertia effects, which become of relevance in small vessels, also shows a dependency and leads to less pronounced margination of white blood cells with increasing Reynolds number. Author SummaryWhite blood cells can only properly function if they adhere to the vessel walls. To facilitate the adhesion, white blood cells migrate toward the vessel walls in blood flow through a process called margination. We model and simulate the process and analyse dependencies on a number of conditions including hematocrit, deformability and Reynolds number. A detailed mesoscopic hydrodynamic Helfrich-type model is derived, validated, and used for the simulations. Besideds the confirmation of previous results, obtained with less detailed models, we show a less pronounced margination of white blood cells with increasing Reynolds number. Inertia effects, previously neglected, become of relevance in small vessels, where the cells may experience Reynolds numbers of order unity or higher. These results are also of relevence for the margination of other cell types.

The complex [Cu(en) 2 (H 2 O)](sy) 2 (en)(H 2 O) 2 has been synthesized and characterized by its electronic and vibrational spectra. The molecular structure of the complex has been determined by X-ray diffraction methods. The complex crystallizes in the orthorhombic space group Pnma with unit-cell parameters a = 10.7236 (5), b = 20.4660(10), c = 14.4523(11)Å and Z = 4. In the cation, the Cu(II) ion has a distorted square pyramidal coordination with two bidendate (en) ligands forming the basal plane and a H 2 O molecule in the apical position. The complex cations and syringate anions constitute chains along the b axis in -A-B-A-fashion. The members of the chains are linked by through N-H···O hydrogen bonds. The (en) molecules are responsible for connecting adjacent layers.