Comparing three basic models for seasonal influenza

In this paper we report the use of the open source Spatiotemporal Epidemiological Modeler (STEM, www.eclipse.org/stem) to compare three basic models for seasonal influenza transmission. The models are designed to test for possible differences between the seasonal transmission of influenza A and B. Model 1 assumes that the seasonality and magnitude of transmission do not vary between influenza A and B. Model 2 assumes that the magnitude of seasonal forcing (i.e., the maximum transmissibility), but not the background transmission or flu season length, differs between influenza A and B. Model 3 assumes that the magnitude of seasonal forcing, the background transmission, and flu season length all differ between strains. The models are all optimized using 10 years of surveillance data from 49 of 50 administrative divisions in Israel. Using a cross-validation technique, we compare the relative accuracy of the models and discuss the potential for prediction. We find that accounting for variation in transmission amplitude increases the predictive ability compared to the base. However, little improvement is obtained by allowing for further variation in the shape of the seasonal forcing function

Calfacilitin is a calcium channel modulator essential for initiation of neural plate development.

Calcium fluxes have been implicated in the specification of the vertebrate embryonic nervous system for some time, but how these fluxes are regulated and how they relate to the rest of the neural induction cascade is unknown. Here we describe Calfacilitin, a transmembrane calcium channel facilitator that increases calcium flux by generating a larger window current and slowing inactivation of the L-type CaV1.2 channel. Calfacilitin binds to this channel and is co-expressed with it in the embryo. Regulation of intracellular calcium by Calfacilitin is required for expression of the neural plate specifiers Geminin and Sox2 and for neural plate formation. Loss-of-function of Calfacilitin can be rescued by ionomycin, which increases intracellular calcium. Our results elucidate the role of calcium fluxes in early neural development and uncover a new factor in the modulation of calcium signalling