ExoMars 2016 Schiaparelli Module Trajectory and Atmospheric Profiles Reconstruction: Analysis of the On-board Inertial and Radar Measurements

On 19th October 2016 Schiaparelli module of the ExoMars 2016 mission flew through the Mars atmosphere. After successful entry and descent under parachute, the module failed the last part of the descent and crashed on the Mars surface. Nevertheless the data transmitted in real time by Schiaparelli during the entry and descent, together with the entry state vector as initial condition, have been used to reconstruct both the trajectory and the profiles of atmospheric density, pressure and temperature along the traversed path. The available data-set is only a small sub-set of the whole data acquired by Schiaparelli, with a limited data rate (8 kbps) and a large gap during the entry because of the plasma blackout on the communications. This paper presents the work done by the AMELIA (Atmospheric Mars Entry and Landing Investigations and Analysis) team in the exploitation of the available inertial and radar data. First a reference trajectory is derived by direct integration of the inertial measurements and a strategy to overcome the entry data gap is proposed. First-order covariance analysis is used to estimate the uncertainties on all the derived parameters. Then a refined trajectory is computed incorporating the measurements provided by the on-board radar altimeter. The derived trajectory is consistent with the events reported in the telemetry and also with the impact point identified on the high-resolution images of the landing site. Finally, atmospheric profiles are computed tacking into account the aerodynamic properties of the module. Derived profiles result in good agreement with both atmospheric models and available remote sensing observations

Expression of Plet1 controls interstitial migration of murine small intestinal dendritic cells.

Under homeostatic conditions, dendritic cells (DCs) continuously patrol the intestinal lamina propria. Upon antigen encounter, DCs initiate C-C motif chemokine receptor 7 (CCR7) expression and migrate into lymph nodes to direct T cell activation and differentiation. The mechanistic underpinnings of DC migration from the tissues to lymph nodes have been largely elucidated, contributing greatly to our understanding of DC functionality and intestinal immunity. In contrast, the molecular mechanisms allowing DCs to efficiently migrate through the complex extracellular matrix of the intestinal lamina propria prior to antigen encounter are still incompletely understood. Here we show that small intestinal murine CD11b <sup>+</sup> CD103 <sup>+</sup> DCs express Placenta-expressed transcript 1 (Plet1), a glycophoshatidylinositol (GPI)-anchored surface protein involved in migration of keratinocytes during wound healing. In the absence of Plet1, CD11b <sup>+</sup> CD103 <sup>+</sup> DCs display aberrant migratory behavior, and accumulate in the small intestine, independent of CCR7 responsiveness. RNA-sequencing indicated involvement of Plet1 in extracellular matrix-interactiveness, and subsequent in-vitro migration assays revealed that Plet1 augments the ability of DCs to migrate through extracellular matrix containing environments. In conclusion, our findings reveal that expression of Plet1 facilitates homeostatic interstitial migration of small intestinal DCs

Expression of Plet1 controls interstitial migration of murine small intestinal dendritic cells

Under homeostatic conditions, dendritic cells (DCs) continuously patrol the intestinal lamina propria. Upon antigen encounter, DCs ini

IL-22 regulates lymphoid chemokine production and assembly of tertiary lymphoid organs.

The series of events leading to tertiary lymphoid organ (TLO) formation in mucosal organs following tissue damage remain unclear. Using a virus-induced model of autoantibody formation in the salivary glands of adult mice, we demonstrate that IL-22 provides a mechanistic link between mucosal infection, B-cell recruitment, and humoral autoimmunity. IL-22 receptor engagement is necessary and sufficient to promote differential expression of chemokine (C-X-C motif) ligand 12 and chemokine (C-X-C motif) ligand 13 in epithelial and fibroblastic stromal cells that, in turn, is pivotal for B-cell recruitment and organization of the TLOs. Accordingly, genetic and therapeutic blockade of IL-22 impairs and reverses TLO formation and autoantibody production. Our work highlights a critical role for IL-22 in TLO-induced pathology and provides a rationale for the use of IL-22-blocking agents in B-cell-mediated autoimmune conditions

A microeconometric study of theatre demand

We develop a model of theatre demand with learning by consuming, and test some of its implications on a large random sample of theatregoers and non-theatregoers. This seems to be the most comprehensive econometric study of demand for the theatre from individual data. We hypothesize that each time the consumer watches a play, he experiences a degree of pleasant or unpleasant surprise on the basis of which he will revise his future expectations of his own taste. The learning phase is likely to be unusually long for highly differentiated cultural goods. Our set of data contains unique information about the full price and the fixed cost of theatre, the objective quality of the outing, past experience of and taste for the theatre, and consumption of substitute leisure activities such as reading, television and cinema. Our methodology and data enable us to infer price elasticity on survey data from knowledge of theatregoing experience and taste. After controlling for many variables, we conclude that demand for the theatre is price-elastic, which contradicts previous estimates on aggregate time-series data. Moreover, we estimate demand conditional on past attendance after controlling for selectivity bias. Satisfaction reported by consumers after the last play is also estimated and interpreted as an ordinal conditional choice. Copyright Kluwer Academic Publishers 1996theatre demand, learning by consuming, individual data, conditional choice and satisfaction (JEL: Z1, L82),