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

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Arrest of mammalian fibroblasts in G1 in response to actin inhibition is dependent on retinoblastoma pocket proteins but not on p53

p53 and the retinoblastoma (RB) pocket proteins are central to the control of progression through the G1 phase of the cell cycle. The RB pocket protein family is downstream of p53 and controls S-phase entry. Disruption of actin assembly arrests nontransformed mammalian fibroblasts in G1. We show that this arrest requires intact RB pocket protein function, but surprisingly does not require p53. Thus, mammalian fibroblasts with normal pocket protein function reversibly arrest in G1 on exposure to actin inhibitors regardless of their p53 status. By contrast, pocket protein triple knockout mouse embryo fibroblasts and T antigen–transformed rat embryo fibroblasts lacking both p53 and RB pocket protein function do not arrest in G1. Fibroblasts are very sensitive to actin inhibition in G1 and arrest at drug concentrations that do not affect cell adhesion or cell cleavage. Interestingly, G1 arrest is accompanied by inhibition of surface ruffling and by induction of NF2/merlin. The combination of failure of G1 control and of tetraploid checkpoint control can cause RB pocket protein–suppressed cells to rapidly become aneuploid and die after exposure to actin inhibitors, whereas pocket protein–competent cells are spared. Our results thus establish that RB pocket proteins can be uniquely targeted for tumor chemotherapy

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

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

Structure électronique des surfaces (110) des semiconducteurs de type zinc-blende par une méthode de liaisons fortes

The electronic structure of the (110) surface of zinc-blende crystals is studied in a simple tight-binding model. By comparison with the results obtained by the Green's function method it is shown that a good approximation to the bound states energy levels can be obtained by diagonalizing the hamiltonian in a few planes near the surface. This process, owing to its simplicity, can easily be extended to more realistic models including further interactions and self-consistency effects. Finally it is shown that, in this model, the results can be interpreted in terms of Phillips' ionicity.On étudie dans un modèle simple de liaisons fortes la structure électronique des surfaces (110) des cristaux du type de la blende. Comparant avec les résultats obtenus par la méthode des fonctions de Green, on montre qu'il est possible de déterminer de façon satisfaisante les énergies des états liés en diagonalisant l'hamiltonien dans les plans les plus voisins de la surface. Ce procédé, par sa simplicité, semble susceptible d'extension à des modèles plus élaborés, incluant des interactions plus lointaines ainsi que les effets de self-consistence. On montre enfin que dans le modèle utilisé, les résultats peuvent s'interpréter simplement en fonction de l'ionicité de Phillips

Tetraploid State Induces p53-dependent Arrest of Nontransformed Mammalian Cells in G1

A “spindle assembly” checkpoint has been described that arrests cells in G1 following inappropriate exit from mitosis in the presence of microtubule inhibitors. We have here addressed the question of whether the resulting tetraploid state itself, rather than failure of spindle function or induction of spindle damage, acts as a checkpoint to arrest cells in G1. Dihydrocytochalasin B induces cleavage failure in cells where spindle function and chromatid segregation are both normal. Notably, we show here that nontransformed REF-52 cells arrest indefinitely in tetraploid G1 following cleavage failure. The spindle assembly checkpoint and the tetraploidization checkpoint that we describe here are likely to be equivalent. Both involve arrest in G1 with inactive cdk2 kinase, hypophosphorylated retinoblastoma protein, and elevated levels of p21WAF1 and cyclin E. Furthermore, both require p53. We show that failure to arrest in G1 following tetraploidization rapidly results in aneuploidy. Similar tetraploid G1 arrest results have been obtained with mouse NIH3T3 and human IMR-90 cells. Thus, we propose that a general checkpoint control acts in G1 to recognize tetraploid cells and induce their arrest and thereby prevents the propagation of errors of late mitosis and the generation of aneuploidy. As such, the tetraploidy checkpoint may be a critical activity of p53 in its role of ensuring genomic integrity. </jats:p