A Search for Resonant Structures in the Zodiacal Cloud with COBE DIRBE: The Mars Wake and Jupiter's Trojan Clouds

We searched the COBE DIRBE Sky and Zodi Atlas for a wake of dust trailing Mars and for Trojan dust near Jupiter's L5 Lagrange point. We compare the DIRBE images to a model Mars wake based on the empirical model of the Earth's wake as seen by the DIRBE and place a 3-sigma upper limit on the fractional overdensity of particles in the Mars wake of 18% of the fractional overdensity trailing the Earth. We place a 3-sigma upper limit on the effective emitting area of large (10-100 micron diameter) particles trapped at Jupiter's L5 Lagrange point of 6 x 10^17 cm^2, assuming that these large dust grains are distributed in space like the Trojan asteroids. We would have detected the Mars wake if the surface area of dust in the wake scaled simply as the mass of the planet times the Poynting-Robertson time scale.Comment: Sixteen pages, and figures 1, 2, 3a, 3b, 4, 5, 6, and 7. Accepted for publication in Icaru

Developing CBM in the Powder River Basin

5 pages (includes some color illustrations and maps)

Developing CBM in the Powder River Basin

5 pages (includes some color illustrations and maps)

Deitsch, Däätsch, Düütsch and Dietsch: The Varieties of Kansas German Dialects after 150 Years of German Group Settlement in Kansas

This is the published version, made available with permission of the editor

Murine Cytomegalovirus Disrupts Splenic Dendritic Cell Subsets via Type I Interferon-Dependent and -Independent Mechanisms

Dendritic cells (DC) are well-known modulators of immunity. This heterogeneous population is composed of defined subsets that exhibit functional specialization and are critical in initiating responses to pathogens. As such, many infectious agents employ strategies to disrupt DC functioning in attempts to evade the immune system. In some instances, this manifests as an outright loss of these cells. Previous work has suggested that, in the absence of an efficient natural killer (NK) cell response, murine cytomegalovirus (MCMV) induces large amounts of interferon (IFN)-I. This heightened IFN-I response is thought to contribute to conventional DC (cDC) loss and delayed development of T cell immunity. However, the precise role of IFN-I in such cDC loss remains unclear. We investigated the effects of licensed NK cells and IFN-I signaling on splenic cDC subsets during MCMV infection and found that a licensed NK cell response partially protects cDC numbers, but does not prevent increases in serum IFN-I. This suggested that high residual IFN-I could contribute to cDC loss. Therefore, we used multiple strategies to modulate IFN-I signaling during MCMV infection including plasmacytoid DC depletion, IFN-I receptor (IFNAR) blockade, and genetic ablation of IFNAR expression. Interestingly, restriction of IFN-I signals did not substantially preserve either CD8+ or CD4+ DC total numbers, but resulted in significant retention and/or accumulation of the splenic CD8− CD4− [double negative (DN)] subset. However, the DN DC effect manifested in a DC-extrinsic manner since IFNAR-deficient cells were not preferentially retained over their IFNAR wild-type counterparts in a mixed-chimera setting. Our results show that IFN-I signaling is not responsible for overt cDC toxicity in the setting of acute MCMV infection and emphasize that additional mechanisms contribute to DC loss and require exploration