Non-axisymmetric oscillations of rapidly rotating relativistic stars by conformal flatness approximation

We present a new numerical code to compute non-axisymmetric eigenmodes of rapidly rotating relativistic stars by adopting spatially conformally flat approximation of general relativity. The approximation suppresses the radiative degree of freedom of relativistic gravity and the field equations are cast into a set of elliptic equations. The code is tested against the low-order f- and p-modes of slowly rotating stars for which a good agreement is observed in frequencies computed by our new code and those computed by the full theory. Entire sequences of the low order counter-rotating f-modes are computed, which are susceptible to an instability driven by gravitational radiation.Comment: 3 figures. To appear in Phys.Rev.

Beltrami-like fields created by baroclinic effect in two-fluid plasmas

A theory of two-dimensional plasma evolution with Beltrami-like flow and field due to baroclinic effect has been presented. Particular solution of the nonlinear two-fluid equations is obtained. This simple model can explain the generation of magnetic field without assuming the presence of a seed in the system. Coupled field and flow naturally grow together. The theory has been applied to estimate B-field in laser-induced plasmas and the result is in good agreement with experimental values.Comment: 3 page

Active regulator of SIRT1 is required for cancer cell survival but not for SIRT1 activity

The NAD+-dependent deacetylase SIRT1 is involved in diverse cellular processes, and has also been linked with multiple disease states. Among these, SIRT1 expression negatively correlates with cancer survival in both laboratory and clinical studies. Active regulator of SIRT1 (AROS) was the first reported post-transcriptional regulator of SIRT1 activity, enhancing SIRT1-mediated deacetylation and downregulation of the SIRT1 target p53. However, little is known regarding the role of AROS in regulation of SIRT1 during disease. Here, we report the cellular and molecular effects of RNAi-mediated AROS suppression, comparing this with the role of SIRT1 in a panel of human cell lines of both cancerous and non-cancerous origins. Unexpectedly, AROS is found to vary in its modulation of p53 acetylation according to cell context. AROS suppresses p53 acetylation only following the application of cell damaging stress, whereas SIRT1 suppresses p53 under all conditions analysed. This supplements the original characterization of AROS but indicates that SIRT1 activity can persist following suppression of AROS. We also demonstrate that knockdown of AROS induces apoptosis in three cancer cell lines, independent of p53 activation. Importantly, AROS is not required for the viability of three non-cancer cell lines indicating a putative role for AROS in specifically promoting cancer cell survival