The Cepheid Phase Lag Revisited

We compute the phase lags between the radial velocity curves and the light curves $\Delta \Phi_1= \phi^{V_r}_1 - \phi^{mag}_1$ for classical Cepheid model sequences both in the linear and the nonlinear regimes. The nonlinear phase lags generally fall below the linear ones except for high period models where they lie above, and of course for low pulsation amplitudes where the two merge. The calculated phase lags show good agreement with the available observational data of normal amplitude Galactic Cepheids. The metallicity has but a moderate effect on the phase lag, while the mass-luminosity relation and the parameters of the turbulent convective model (time-dependent mixing length) mainly influence the modal selection and the period, which is then reflected in the period -- $\Delta \Phi_1$ diagram. We discuss the potential application of this observable as a discriminant for pulsation modes and as a test for ultra-low amplitudes (ULA) pulsation.Comment: 11 pages, 8 figures, accepted for publication in ApJ, minor revisions in the text and figures, (black and white version available from 2nd author's website

MARCH1 protects the lipid raft and tetraspanin web from MHCII proteotoxicity in dendritic cells

Dendritic cells (DCs) produce major histocompatibility complex II (MHCII) in large amounts to function as professional antigen presenting cells. Paradoxically, DCs also ubiquitinate and degrade MHCII in a constitutive manner. Mice deficient in the MHCII-ubiquitinating enzyme membrane-anchored RING-CH1, or the ubiquitin-acceptor lysine of MHCII, exhibit a substantial reduction in the number of regulatory T (Treg) cells, but the underlying mechanism was unclear. Here we report that ubiquitin-dependent MHCII turnover is critical to maintain homeostasis of lipid rafts and the tetraspanin web in DCs. Lack of MHCII ubiquitination results in the accumulation of excessive quantities of MHCII in the plasma membrane, and the resulting disruption to lipid rafts and the tetraspanin web leads to significant impairment in the ability of DCs to engage and activate thymocytes for Treg cell differentiation. Thus, ubiquitin-dependent MHCII turnover represents a novel quality-control mechanism by which DCs maintain homeostasis of membrane domains that support DC's Treg cell-selecting function