8 research outputs found

    Electronic transport through carbon nanotubes -- effects of structural deformation and tube chirality

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    Atomistic simulations using a combination of classical forcefield and Density-Functional-Theory (DFT) show that carbon atoms remain essentially sp2 coordinated in either bent tubes or tubes pushed by an atomically sharp AFM tip. Subsequent Green's-function-based transport calculations reveal that for armchair tubes there is no significant drop in conductance, while for zigzag tubes the conductance can drop by several orders of magnitude in AFM-pushed tubes. The effect can be attributed to simple stretching of the tube under tip deformation, which opens up an energy gap at the Fermi surface.Comment: To appear in Physical Review Letter

    Attachment of HeLa cells during early G1 phase

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    Both growth factor directed and integrin dependent signal transduction were shown to take place directly after completion of mitosis. The local activation of these signal transduction cascades was investigated in early G1 cells. Interestingly, various key signal transduction proteins were found in blebs at the cell membrane within 30 min after mitosis. These membrane blebs appeared in round, mitotic-like cells and disappeared rapidly during spreading of the cells in G1 phase. In addition to tyrosine-phosphorylated proteins, the blebs contained also phosphorylated FAK and phosphorylated MAP kinase. The formation of membrane blebs in round, mitotic cells before cell spreading is not specific for mitotic cells, because similar features were observed in trypsinized cells. Just before cell spreading also these cells exhibited membrane blebs containing active signal transduction proteins. Inhibition of signal transduction did not affect membrane bleb formation, suggesting that the membrane blebs were formed independent of signal transduction

    Unsteady Pressure and Velocity Measurements in 5x5 Rods Bundle Using Grids With and Without Mixing Vanes

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    International audienceThe vibration of rods is of prime importance to estimate their wearing due to the frictions with grids' elements. To predict this wearing, the forces exerted on the rods need to be identified and quantified. Pressure fluctuations are explored using an instrumented rod centred within a 5x5 rods bundle. Two configurations of spacer-grids are used: with and without mixing vanes respectively noted WMV and NMV. The position of the measurement point is rotated over 360° and its distance from the grids is varied from 0.5Dh_h to 20Dh_h. The results show the non-homogeneity of the azimuthal distribution of the pressure fluctuations in the near wake of the spacer-grids for both configurations. The return to a homogeneous azimuthal distribution of the pressure fluctuations is faster without mixing vanes than with mixing vanes. The intensities of the pressure fluctuations are (in average) higher for WMV than for NMV: higher by 13% and 136% respectively at distances 0.5Dh_h and 20Dh_h from the grids. Power law approximations show decreases of \langlePrmsP'_{rms}\rangleθ_\theta like (y/Dh)(y/D_h)0.46^{-0.46} and (y/Dh)(y/D_h)0.68^{-0.68}. respectively for the configurations WMV and NMV. The profiles of mean velocity and velocity fluctuations are explored around the instrumented rod using LDV. Results show oscillation of the profiles and a damping with the distance from the grids. Power law approximations show decreases of \langleVrmsV'_{rms}\ranglePsq/Vflow_{Psq}/V_{flow} ⁄ like (y/Dh)(y/D_h)0.38^{-0.38} and (y/Dh)(y/D_h)0.46^{-0.46}. respectively for WMV and NMV. Between 2Dh_h and 15Dh_h, the dimensionless ratio of "pressure fluctuations to velocity fluctuations" \langlePrmsP'_{rms}\rangleθ_\theta/121\over 2ρ\rho \langleVrmsV'_{rms}2^2\ranglePsq_{Psq} is found to increase by 70% and 100% respectively for the configurations NMV and WMV. This increase demonstrated by the combination of pressure and velocity measurements further reveals the complexity of the turbulent flow in the wake of spacer-grids

    Cytokinesis defects and cancer

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    Whole-genome and centrosome duplication as a consequence of cytokinesis failure can drive tumorigenesis in experimental model systems. However, whether cytokinesis failure is in fact an important cause of human cancers has remained unclear. In this Review, we summarize evidence that whole-genome-doubling events are frequently observed in human cancers and discuss the contribution that cytokinesis defects can make to tumorigenesis. We provide an overview of the potential causes of cytokinesis failure and discuss how tetraploid cells that are generated through cytokinesis defects are used in cancer as a transitory state on the route to aneuploidy. Finally, we discuss how cytokinesis defects can facilitate genetic diversification within the tumour to promote cancer development and could constitute the path of least resistance in tumour evolution
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