Dynamics of a deformable self-propelled domain

We investigate the dynamical coupling between the motion and the deformation of a single self-propelled domain based on two different model systems in two dimensions. One is represented by the set of ordinary differential equations for the center of gravity and two tensor variables characterizing deformations. The other is an active cell model which has an internal mechanism of motility and is represented by the partial differential equation for deformations. Numerical simulations show a rich variety of dynamics, some of which are common to the two model systems. The origin of the similarity and the difference is discussed.Comment: 6 pages, 6 figure

Complex Contact-Based Dynamics of Microsphere Monolayers Revealed by Resonant Attenuation of Surface Acoustic Waves

Contact-based vibrations play an essential role in the dynamics of granular materials. Significant insights into vibrational granular dynamics have previously been obtained with reduced-dimensional systems containing macroscale particles. We study contact-based vibrations of a two-dimensional monolayer of micron-sized spheres on a solid substrate that forms a microscale granular crystal. Measurements of the resonant attenuation of laser-generated surface acoustic waves reveal three collective vibrational modes that involve displacements and rotations of the microspheres, as well as interparticle and particle-substrate interactions. To identify the modes, we tune the interparticle stiffness, which shifts the frequency of the horizontal-rotational resonances while leaving the vertical resonance unaffected. From the measured contact resonance frequencies we determine both particle-substrate and interparticle contact stiffnesses and find that the former is an order of magnitude larger than the latter. This study paves the way for investigating complex contact-based dynamics of microscale granular crystals and yields a new approach to studying micro- to nanoscale contact mechanics in multiparticle networks.National Science Foundation (U.S.) (Grant CMMI-1333858)United States. Army Research Office (Grant W911NF-15-1-0030)University of Washington. Royalty Research FoundationNational Science Foundation (U.S.) (Grant CHE-1111557

Dynamics of a deformable self-propelled particle under external forcing

We investigate dynamics of a self-propelled deformable particle under external field in two dimensions based on the model equations for the center of mass and a tensor variable characterizing deformations. We consider two kinds of external force. One is a gravitational-like force which enters additively in the time-evolution equation for the center of mass. The other is an electric-like force supposing that a dipole moment is induced in the particle. This force is added to the equation for the deformation tensor. It is shown that a rich variety of dynamics appears by changing the strength of the forces and the migration velocity of self-propelled particle

Modulation of MUC1 mucin as an escape mechanism of breast cancer cells from autologous cytotoxic T-lymphocytes

MUC1 mucin is known to serve as a target molecule in the killing of breast cancer cells by cytotoxic T-lymphocytes (CTLs). We searched for a possible mechanism allowing tumour cells to escape from autologous CTLs. When the killing of breast cancer cells by autologous lymphocytes was examined in 26 patients with breast cancer, significant tumour cell lysis was observed in 8 patients, whereas virtually no autologous tumour cell lysis was detected in as many as 18 patients. In the patients who showed negligible tumour cell lysis, the autologous tumour cells expressed MUC1-related antigenic epitopes much more weakly than the tumour cells in the patients who exhibited strong cytotoxicity (significant statistically at P< 0.0005–0.0045), suggesting that the unresponsiveness of cancer cells to CTLs observed in these patients was mainly due to loss of MUC1 expression or modulation of its antigenicity. A breast cancer cell line, NZK-1, established from one of the cytotoxicity-negative patients, did not express MUC1 and was resistant to killing by CTLs, while control breast cancer cell lines expressing MUC-1 were readily killed by CTLs. Transfection of NZK-1 cells with MUC1 cDNA induced significant lysis by autologous T-lymphocytes. These results supported the importance of MUC1 mucin in autologous anti-tumour immunity, but suggested that the major escape mechanism of tumour cells from autologous T-lymphocytes is the loss and/or modulation of MUC1 antigenicity on tumour cells, which would limit the effectiveness of possible immunotherapy designed to target the MUC1 mucin. © 2001 Cancer Research Campaign http://www.bjcancer.co

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