1,792 research outputs found

    Casimir stresses in active nematic films

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    We calculate the Casimir stresses in a thin layer of active fluid with nematic order. By using a stochastic hydrodynamic approach for an active fluid layer of finite thickness L, we generalize the Casimir stress for nematic liquid crystals in thermal equilibrium to active systems. We show that the active Casimir stress differs significantly from its equilibrium counterpart. For contractile activity, the active Casimir stress, although attractive like its equilibrium counterpart, diverges logarithmically as L approaches a threshold of the spontaneous flow instability from below. In contrast, for small extensile activity, it is repulsive, has no divergence at any L and has a scaling with L different from its equilibrium counterpart

    Threshold logic implementation of a modular computer system design

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    Threshold logic implementation for LSI design of modular computer syste

    Independent regulation of P53 stabilisation and activation after Rb deletion in primary epithelial cells

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    We have previously reported that deletion of the retinoblastoma gene Rb leads to rapid but transient p53 stabilisation. We investigated here the pathways involved. We show that upon Rb-deletion dysregulated E2F activates p19(ARF) expression that localises in the nucleoli. There it interacts with MDM2, leading to P53 stabilisation. At the same time, ATR is activated, activating CHK1 that may phosphorylate P53 but also contribute to inhibition of MnSOD expression leading to accumulation of ROS (reactive oxygen species) and subsequent DNA injury, which in turn maintains ATR/CHK1 activated. However, from 72 h after Rb deletion, NPM interacts with P19ARF and concomitantly the interaction between p19(ARF) and MDM2 decreases leading to a return to P53 degradation. This occurs despite the persistence of the DNA damage response pathways. We therefore observe in primary cells not subjected to exogenous gene expression or exogenous DNA damaging treatment, activation of 2 concomitant pathways of activation of P53 that are dealt with in independent manner: an oncogenic pathway with rapid activation of ARF which is 'switched off' downstream of p19(ARF) activation after 72 h of induction and a DNA damage response pathway keeping a low level of transcriptionally active P53 sufficient to deal with a physiological elevation of oxidative DNA injury. A possible connection between the two pathways is discussed.Publisher PDFPeer reviewe

    Deficiency of G1 regulators P53, P21Cip1 and/or pRb decreases hepatocyte sensitivity to TGFbeta cell cycle arrest

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    TGFbeta is critical to control hepatocyte proliferation by inducing G1-growth arrest through multiple pathways leading to inhibition of E2F transcription activity. The retinoblastoma protein pRb is a key controller of E2F activity and G1/S transition which can be inhibited in viral hepatitis. It is not known whether the impairment of pRb would alter the growth inhibitory potential of TGFbeta in disease. We asked how Rb-deficiency would affect responses to TGFbeta-induced cell cycle arrest.Publisher PDFPeer reviewe

    Soft Listeria: actin-based propulsion of liquid drops

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    We study the motion of oil drops propelled by actin polymerization in cell extracts. Drops deform and acquire a pear-like shape under the action of the elastic stresses exerted by the actin comet. We solve this free boundary problem and calculate the drop shape taking into account the elasticity of the actin gel and the variation of the polymerization velocity with normal stress. The pressure balance on the liquid drop imposes a zero propulsive force if gradients in surface tension or internal pressure are not taken into account. Quantitative parameters of actin polymerization are obtained by fitting theory to experiment.Comment: 5 pages, 4 figure

    Nonequilibrium Fluctuations, Travelling Waves, and Instabilities in Active Membranes

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    The stability of a flexible fluid membrane containing a distribution of mobile, active proteins (e.g. proton pumps) is shown to depend on the structure and functional asymmetry of the proteins. A stable active membrane is in a nonequilibrium steady state with height fluctuations whose statistical properties are governed by the protein activity. Disturbances are predicted to travel as waves at sufficiently long wavelength, with speed set by the normal velocity of the pumps. The unstable case involves a spontaneous, pump-driven undulation of the membrane, with clumping of the proteins in regions of high activity.Comment: 4 two-column pages, two .eps figures included, revtex, uses eps
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