188 research outputs found
Ferromagnetism of He Films in the Low Field Limit
We provide evidence for a finite temperature ferromagnetic transition in
2-dimensions as in thin films of He on graphite, a model system
for the study of two-dimensional magnetism. We perform pulsed and CW NMR
experiments at fields of 0.03 - 0.48 mT on He at areal densities of 20.5 -
24.2 atoms/nm. At these densities, the second layer of He has a
strongly ferromagnetic tendency. With decreasing temperature, we find a rapid
onset of magnetization that becomes independent of the applied field at
temperatures in the vicinity of 1 mK. Both the dipolar field and the NMR
linewidth grow rapidly as well, which is consistent with a large (order unity)
polarization of the He spins.Comment: 4 figure
Atomic micromotion and geometric forces in a triaxial magnetic trap
Non-adiabatic motion of Bose-Einstein condensates of rubidium atoms arising
from the dynamical nature of a time-orbiting-potential (TOP) trap was observed
experimentally. The orbital micromotion of the condensate in velocity space at
the frequency of the rotating bias field of the TOP was detected by a
time-of-flight method. A dependence of the equilibrium position of the atoms on
the sense of rotation of the bias field was observed. We have compared our
experimental findings with numerical simulations. The nonadiabatic following of
the atomic spin in the trap rotating magnetic field produces geometric forces
acting on the trapped atoms.Comment: 4 pages, 4 figure
Fluctuations in active membranes
Active contributions to fluctuations are a direct consequence of metabolic
energy consumption in living cells. Such metabolic processes continuously
create active forces, which deform the membrane to control motility,
proliferation as well as homeostasis. Membrane fluctuations contain therefore
valuable information on the nature of active forces, but classical analysis of
membrane fluctuations has been primarily centered on purely thermal driving.
This chapter provides an overview of relevant experimental and theoretical
approaches to measure, analyze and model active membrane fluctuations. In the
focus of the discussion remains the intrinsic problem that the sole fluctuation
analysis may not be sufficient to separate active from thermal contributions,
since the presence of activity may modify membrane mechanical properties
themselves. By combining independent measurements of spontaneous fluctuations
and mechanical response, it is possible to directly quantify time and
energy-scales of the active contributions, allowing for a refinement of current
theoretical descriptions of active membranes.Comment: 38 pages, 9 figures, book chapte
Performance of kevlar fibre-reinforced rubber composite armour against shaped-charge jet penetration
Curvature-coupling dependence of membrane protein diffusion coefficients
We consider the lateral diffusion of a protein interacting with the curvature
of the membrane. The interaction energy is minimized if the particle is at a
membrane position with a certain curvature that agrees with the spontaneous
curvature of the particle. We employ stochastic simulations that take into
account both the thermal fluctuations of the membrane and the diffusive
behavior of the particle. In this study we neglect the influence of the
particle on the membrane dynamics, thus the membrane dynamics agrees with that
of a freely fluctuating membrane. Overall, we find that this curvature-coupling
substantially enhances the diffusion coefficient. We compare the ratio of the
projected or measured diffusion coefficient and the free intramembrane
diffusion coefficient, which is a parameter of the simulations, with analytical
results that rely on several approximations. We find that the simulations
always lead to a somewhat smaller diffusion coefficient than our analytical
approach. A detailed study of the correlations of the forces acting on the
particle indicates that the diffusing inclusion tries to follow favorable
positions on the membrane, such that forces along the trajectory are on average
smaller than they would be for random particle positions.Comment: 16 pages, 8 figure
Sarcomeric Pattern Formation by Actin Cluster Coalescence
Contractile function of striated muscle cells depends crucially on the almost crystalline order of actin and myosin filaments in myofibrils, but the physical mechanisms that lead to myofibril assembly remains ill-defined. Passive diffusive sorting of actin filaments into sarcomeric order is kinetically impossible, suggesting a pivotal role of active processes in sarcomeric pattern formation. Using a one-dimensional computational model of an initially unstriated actin bundle, we show that actin filament treadmilling in the presence of processive plus-end crosslinking provides a simple and robust mechanism for the polarity sorting of actin filaments as well as for the correct localization of myosin filaments. We propose that the coalescence of crosslinked actin clusters could be key for sarcomeric pattern formation. In our simulations, sarcomere spacing is set by filament length prompting tight length control already at early stages of pattern formation. The proposed mechanism could be generic and apply both to premyofibrils and nascent myofibrils in developing muscle cells as well as possibly to striated stress-fibers in non-muscle cells
Reelin Is Involved in Transforming Growth Factor-Ξ²1-Induced Cell Migration in Esophageal Carcinoma Cells
Reelin (RELN), which is a glycoprotein secreted by Cajal-Retzius cells of the developing cerebral cortex, plays an important role in neuronal migration, but its role in cell migration and cancer metastasis is largely unclear. Here, we showed that cell motility was significantly increased in KYSE-510 cells by TGF-Ξ²1 treatment. Moreover, TGF-Ξ²1 decreased RELN mRNA expression and overexpression of Reelin at least partly reversed TGF-Ξ²1-induced cell migration in KYSE-30 cells. Furthermore, this negative regulation of Reelin expression by TGF-Ξ²1 was through Snail, one transcription factor which was induced by TGF-Ξ²1 in KYSE-510 cells. RELN promoter activity was reduced in parallel with the induction of Snail after TGF-Ξ²1 treatment and Snail suppressed both RELN promoter activity and expression through binding to E-box sequences in the RELN promoter region in ESCC cells. Knockdown of RELN induced cell migration in KYSE-510 cells, together with the increase of mesenchymal markers expression. Taken together, Reelin is an essential negative regulator in the TGF-Ξ²1-induced cell migration process, and is suppressed by TGF-Ξ² pathway at the transcriptional level through Snail regulation. Therefore, the correlation of Reelin and TGF-Ξ² pathway was critical in cancer metastasis, and Reelin could be one potential anti-metastasis target in future clinical practice
The Eps8/IRSp53/VASP Network Differentially Controls Actin Capping and Bundling in Filopodia Formation
There is a body of literature that describes the geometry and the physics of filopodia using either stochastic models or partial differential equations and elasticity and coarse-grained theory. Comparatively, there is a paucity of models focusing on the regulation of the network of proteins that control the formation of different actin structures. Using a combination of in-vivo and in-vitro experiments together with a system of ordinary differential equations, we focused on a small number of well-characterized, interacting molecules involved in actin-dependent filopodia formation: the actin remodeler Eps8, whose capping and bundling activities are a function of its ligands, Abi-1 and IRSp53, respectively; VASP and Capping Protein (CP), which exert antagonistic functions in controlling filament elongation. The model emphasizes the essential role of complexes that contain the membrane deforming protein IRSp53, in the process of filopodia initiation. This model accurately accounted for all observations, including a seemingly paradoxical result whereby genetic removal of Eps8 reduced filopodia in HeLa, but increased them in hippocampal neurons, and generated quantitative predictions, which were experimentally verified. The model further permitted us to explain how filopodia are generated in different cellular contexts, depending on the dynamic interaction established by Eps8, IRSp53 and VASP with actin filaments, thus revealing an unexpected plasticity of the signaling network that governs the multifunctional activities of its components in the formation of filopodia
Theoretical Model for Cellular Shapes Driven by Protrusive and Adhesive Forces
The forces that arise from the actin cytoskeleton play a crucial role in determining the cell shape. These include protrusive forces due to actin polymerization and adhesion to the external matrix. We present here a theoretical model for the cellular shapes resulting from the feedback between the membrane shape and the forces acting on the membrane, mediated by curvature-sensitive membrane complexes of a convex shape. In previous theoretical studies we have investigated the regimes of linear instability where spontaneous formation of cellular protrusions is initiated. Here we calculate the evolution of a two dimensional cell contour beyond the linear regime and determine the final steady-state shapes arising within the model. We find that shapes driven by adhesion or by actin polymerization (lamellipodia) have very different morphologies, as observed in cells. Furthermore, we find that as the strength of the protrusive forces diminish, the system approaches a stabilization of a periodic pattern of protrusions. This result can provide an explanation for a number of puzzling experimental observations regarding cellular shape dependence on the properties of the extra-cellular matrix
Multiscale Modeling of Red Blood Cell Mechanics and Blood Flow in Malaria
Red blood cells (RBCs) infected by a Plasmodium parasite in malaria may lose their membrane deformability with a relative membrane stiffening more than ten-fold in comparison with healthy RBCs leading to potential capillary occlusions. Moreover, infected RBCs are able to adhere to other healthy and parasitized cells and to the vascular endothelium resulting in a substantial disruption of normal blood circulation. In the present work, we simulate infected RBCs in malaria using a multiscale RBC model based on the dissipative particle dynamics method, coupling scales at the sub-cellular level with scales at the vessel size. Our objective is to conduct a full validation of the RBC model with a diverse set of experimental data, including temperature dependence, and to identify the limitations of this purely mechanistic model. The simulated elastic deformations of parasitized RBCs match those obtained in optical-tweezers experiments for different stages of intra-erythrocytic parasite development. The rheological properties of RBCs in malaria are compared with those obtained by optical magnetic twisting cytometry and by monitoring membrane fluctuations at room, physiological, and febrile temperatures. We also study the dynamics of infected RBCs in Poiseuille flow in comparison with healthy cells and present validated bulk viscosity predictions of malaria-infected blood for a wide range of parasitemia levels (percentage of infected RBCs with respect to the total number of cells in a unit volume).United States. National Institutes of Health (Grant R01HL094270)National Science Foundation (U.S.). (Grant CBET-0852948)Singapore-MIT Alliance for Research and Technology Cente
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