Killing spinors are Killing vector fields in Riemannian Supergeometry

A supermanifold M is canonically associated to any pseudo Riemannian spin manifold (M_0,g_0). Extending the metric g_0 to a field g of bilinear forms g(p) on T_p M, p\in M_0, the pseudo Riemannian supergeometry of (M,g) is formulated as G-structure on M, where G is a supergroup with even part G_0\cong Spin(k,l); (k,l) the signature of (M_0,g_0). Killing vector fields on (M,g) are, by definition, infinitesimal automorphisms of this G-structure. For every spinor field s there exists a corresponding odd vector field X_s on M. Our main result is that X_s is a Killing vector field on (M,g) if and only if s is a twistor spinor. In particular, any Killing spinor s defines a Killing vector field X_s.Comment: 14 pages, latex, one typo correcte

Superization of Homogeneous Spin Manifolds and Geometry of Homogeneous Supermanifolds

Let M_0=G_0/H be a (pseudo)-Riemannian homogeneous spin manifold, with reductive decomposition g_0=h+m and let S(M_0) be the spin bundle defined by the spin representation Ad:H->\GL_R(S) of the stabilizer H. This article studies the superizations of M_0, i.e. its extensions to a homogeneous supermanifold M=G/H whose sheaf of superfunctions is isomorphic to Lambda(S^*(M_0)). Here G is the Lie supergroup associated with a certain extension of the Lie algebra of symmetry g_0 to an algebra of supersymmetry g=g_0+g_1=g_0+S via the Kostant-Koszul construction. Each algebra of supersymmetry naturally determines a flat connection nabla^{S} in the spin bundle S(M_0). Killing vectors together with generalized Killing spinors (i.e. nabla^{S}-parallel spinors) are interpreted as the values of appropriate geometric symmetries of M, namely even and odd Killing fields. An explicit formula for the Killing representation of the algebra of supersymmetry is obtained, generalizing some results of Koszul. The generalized spin connection nabla^{S} defines a superconnection on M, via the super-version of a theorem of Wang.Comment: 50 page

Some Remarks on Avalanches Modelling: An Introduction to Shallow Flows Models

International audienceThe main goal of these notes is to present several depth-averaged models with application in granular avalanches. We begin by recalling the classical Saint-Venant or Shallow Water equations and present some extensions like the Saint-Venant-Exner model for bedload sediment transport. The first part is devoted to the derivation of several avalanche models of Savage-Hutter type, using a depth-averaging procedure of the 3D momentum and mass equations. First, the Savage-Hutter model for aerial avalanches is presented. Two other models for partially fluidized avalanches are then described: one in which the velocities of both the fluid and the solid phases are assumed to be equal, and another one in which both velocities are unknowns of the system. Finally, a Savage-Hutter model for submarine avalanches is derived. The second part is devoted to non-newtonian models, namely viscoplastic fluids. Indeed, a one-phase viscoplastic model can also be used to simulate fluidized avalanches. A brief introduction to Rheology and plasticity is presented in order to explain the Herschel-Bulkley constitutive law. We finally present the derivation of a shallow Herschel-Bulkley model

Revealing determinants of two‐phase dynamics of P53 network under gamma irradiation based on a reduced 2D relaxation oscillator model

This study proposes a two‐dimensional (2D) oscillator model of p53 network, which is derived via reducing the multidimensional two‐phase dynamics model into a model of ataxia telangiectasia mutated (ATM) and Wip1 variables, and studies the impact of p53‐regulators on cell fate decision. First, the authors identify a 6D core oscillator module, then reduce this module into a 2D oscillator model while preserving the qualitative behaviours. The introduced 2D model is shown to be an excitable relaxation oscillator. This oscillator provides a mechanism that leads diverse modes underpinning cell fate, each corresponding to a cell state. To investigate the effects of p53 inhibitors and the intrinsic time delay of Wip1 on the characteristics of oscillations, they introduce also a delay differential equation version of the 2D oscillator. They observe that the suppression of p53 inhibitors decreases the amplitudes of p53 oscillation, though the suppression increases the sustained level of p53. They identify Wip1 and P53DINP1 as possible targets for cancer therapies considering their impact on the oscillator, supported by biological findings. They model some mutations as critical changes of the phase space characteristics. Possible cancer therapeutic strategies are then proposed for preventing these mutations’ effects using the phase space approach