/pdf/evidence-of-very-long-meandering-features-in-the-logarithmic-2m2f4f0daq.pdf

Evidence of very long meandering features in the logarithmic region of turbulent boundary layers

Coherent structures in wall turbulence transport momentum and provide a means of producing turbulent kinetic energy. Above the viscous wall layer, the hairpin vortex paradigm of Theodorsen coupled with the quasistreamwise vortex paradigm have gained considerable support from multidimensional visualization using particle image velocimetry and direct numerical simulation experiments. Hairpins can autogenerate to form packets that populate a significant fraction of the boundary layer, even at very high Reynolds numbers. The dynamics of packet formation and the ramifications of organization of coherent structures (hairpins or packets) into larger-scale structures are discussed. Evidence for a large-scale mechanism in the outer layer suggests that further organization of packets may occur on scales equal to and larger than the boundary layer thickness.

Hairpin vortex organization in wall turbulencea)

It has been thought that sheets of cells move by traction forces exerted by the cells at the leading edge of the sheet. Using traction microscopy to create a map of physical forces, it is now shown that in fact it is cells many rows from the front that do most of the work. Fundamental biological processes including morphogenesis, tissue repair and tumour metastasis require collective cell motions1,2,3, and to drive these motions cells exert traction forces on their surroundings4. Current understanding emphasizes that these traction forces arise mainly in ‘leader cells’ at the front edge of the advancing cell sheet5,6,7,8,9. Our data are contrary to that assumption and show for the first time by direct measurement that traction forces driving collective cell migration arise predominately many cell rows behind the leading front edge and extend across enormous distances. Traction fluctuations are anomalous, moreover, exhibiting broad non-Gaussian distributions characterized by exponential tails10,11,12. Taken together, these unexpected findings demonstrate that although the leader cell may have a pivotal role in local cell guidance, physical forces that it generates are but a small part of a global tug-of-war involving cells well back from the leading edge.

/pdf/physical-forces-during-collective-cell-migration-3s53rslx6s.pdf

Physical forces during collective cell migration

The Structure of Turbulent Shear Flow By Dr. A. A. Townsend. Pp. xii + 315. 8¾ in. × 5½ in. (Cambridge: At the University Press.) 40s.

/pdf/the-structure-of-turbulent-shear-flow-2yf3szhaqb.pdf

The Structure of Turbulent Shear Flow

A new numerical simulation of a turbulent channel in a large box at Reτ=2003 is described and briefly compared with simulations at lower Reynolds numbers and with experiments. Some of the fluctuation intensities, especially the streamwise velocity, do not scale well in wall units, both near and away from the wall. Spectral analysis traces the near-wall scaling failure to the interaction of the logarithmic layer with the wall. The present statistics can be downloaded from http://torroja.dmt.upm.es/ftp/channels. Further ones will be added to the site as they become available.

Scaling of the velocity fluctuations in turbulent channels up to Reτ=2003

During the subacute phase of acute myocardial infarction (AMI), the incidence of left ventricular thrombosis (LVT) can be as high as 15% to 20%. A method for assessing the risk of LVT would be of particular value in the setting of AMI, because prophylactic anticoagulation must be balanced against

Stasis Mapping Using Ultrasound: A Prospective Study in Acute Myocardial Infarction

Migrating cells exert traction forces when moving. Amoeboid cell migration is a common type of cell migration that appears in many physiological and pathological processes and is performed by a wide variety of cell types. Understanding the coupling of the biochemistry and mechanics underlying the process of migration has the potential to guide the development of pharmacological treatment or genetic manipulations to treat a wide range of diseases. The measurement of the spatiotemporal evolution of the traction forces that produce the movement is an important aspect for the characterization of the locomotion mechanics. There are several methods to calculate the traction forces exerted by the cells. Currently the most commonly used ones are traction force microscopy methods based on the measurement of the deformation induced by the cells on elastic substrate on which they are moving. Amoeboid cells migrate by implementing a motility cycle based on the sequential repetition of four phases. In this paper, we review the role that specific cytoskeletal components play in the regulation of the cell migration mechanics. We investigate the role of specific cytoskeletal components regarding the ability of the cells to perform the motility cycle effectively and the generation of traction forces. The actin nucleation in the leading edge of the cell, carried by the ARP2/3 complex activated through the SCAR/WAVE complex, has shown to be fundamental to the execution of the cyclic movement and to the generation of the traction forces. The protein PIR121, a member of the SCAR/WAVE complex, is essential to the proper regulation of the periodic movement and the protein SCAR, also included in the SCAR/WAVE complex, is necessary for the generation of the traction forces during migration. The protein Myosin II, an important F-actin cross-linker and motor protein, is essential to cytoskeletal contractility and to the generation and proper organization of the traction forces during migration.

Cytoskeletal Mechanics Regulating Amoeboid Cell Locomotion

Many biological and technological complex fluids exhibit tight microstructural alignment that confers them nematic mechanical properties. Among these we count liquid crystals and biopolymer networks, which are often available in microscopic amounts. However, current microrheological methods cannot measure the directional viscoelastic coefficients that appear in the constitutive relation of nematic complex fluids. This article presents directional two-point particle-tracking microrheology (D2PTM) – a novel microrheology technique to determine these coefficients. We establish the theoretical foundation for D2PTM by analyzing the motion of a probing microscopic particle embedded in a nematic complex fluid, and the mutual hydrodynamic interactions between pairs of distant particles. From this analysis, we generalize the formulation of two-point particle tracking microrheology for nematic complex fluids, and demonstrate that the new formulation provides sufficient information to fully characterize the anisotropic viscoelastic coefficients of such materials. We test D2PTM by simulating the Brownian motion of particles in nematic viscoelastic fluids with prescribed directional frequency-dependent shear moduli, showing that D2PTM accurately recovers the prescribed shear moduli. Furthermore, we experimentally validate D2PTM by applying it to a lyotropic nematic liquid crystal, and demonstrate that this new microrheology method provides results in agreement with dynamic light scattering measurements. Lastly, we illustrate the experimental application of the new technique to characterize nematic F-actin solutions. These experiments constitute the first microrheological measurement of the directional viscoelastic coefficients of an anisotropic soft material.

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Two-point particle tracking microrheology of nematic complex fluids

/pdf/two-point-particle-tracking-microrheology-of-nematic-complex-16v7ed6gcl.pdf

Two-Point Particle Tracking Microrheology of Nematic Complex Fluids

Streams of migratory cells are initiated by the formation of tandem pairs of cells connected head to tail to which other cells subsequently adhere. The mechanisms regulating the transition from single to streaming cell migration remain elusive, although several molecules have been suggested to be involved. In this work, we investigate the mechanics of the locomotion ofDictyosteliumtandem pairs by analyzing the spatiotemporal evolution of their traction adhesions (TAs). We find that in migrating wild-type tandem pairs, each cell exerts traction forces on stationary sites (∼80% of the time), and the trailing cell reuses the location of the TAs of the leading cell. Both leading and trailing cells form contractile dipoles and synchronize the formation of new frontal TAs with ∼54-s time delay. Cells not expressing the lectin discoidin I or moving on discoidin I-coated substrata form fewer tandems, but the trailing cell still reuses the locations of the TAs of the leading cell, suggesting that discoidin I is not responsible for a possible chemically driven synchronization process. The migration dynamics of the tandems indicate that their TAs' reuse results from the mechanical synchronization of the leading and trailing cells' protrusions and retractions (motility cycles) aided by the cell-cell adhesions.

/pdf/cooperative-cell-motility-during-tandem-locomotion-of-4g1pxtbqke.pdf

Juan C. del Álamo

Papers

Stasis Mapping Using Ultrasound: A Prospective Study in Acute Myocardial Infarction

Cytoskeletal Mechanics Regulating Amoeboid Cell Locomotion

Two-point particle tracking microrheology of nematic complex fluids

Two-Point Particle Tracking Microrheology of Nematic Complex Fluids

Cooperative cell motility during tandem locomotion of amoeboid cells