Dissecting the Inner Galaxy with γ-Ray Pixel Count Statistics.

We combine adaptive template fitting and pixel count statistics in order to assess the nature of the Galactic Center excess in Fermi-LAT data. We reconstruct the flux distribution of point sources well below the Fermi-LAT detection threshold, and measure their radial and longitudinal profiles in the inner Galaxy. We find that all point sources and the bulge-correlated diffuse emission each contributes O(10%) of the total inner Galaxy emission, and disclose a potential subthreshold point-source contribution to the Galactic Center excess.

Simultaneous endo-epicardial-high density mapping of ventricular tachycardia with the use of multi-electrode mapping catheters.

We herein describe a case of VT in an ischemic cardiomyopathy patient utilizing a novel technique of simultaneous endo-epicardial high-density mapping. Epicardial access, in addition to retrograde aortic endocardial access, was performed. Following the creation of the respective endocardial and epicardial electrical substrate maps, activation mapping of the VT was then performed simultaneously with two overlapping HD Grid catheters. Full diastolic pathway mapping was achieved, with EGMs recorded in all segments of the diastolic interval, on the epicardial surface. This case highlights the feasibility of a technique that can reliably detect the presence of activation bridges in a 3D model of VT.

Endosome-mitochondria juxtaposition during apoptosis induced by H. pylori VacA.

The vacuolating cytotoxin (VacA) is an important virulence factor of Helicobacter pylori with pleiotropic effects on mammalian cells, including the ability to trigger mitochondria-dependent apoptosis. However, the mechanism by which VacA exerts its apoptotic function is unclear. Using a genetic approach, in this study we show that killing by VacA requires the proapoptotic Bcl-2 family members BAX and BAK at the mitochondrial level, but not adequate endoplasmic reticulum Ca²(+) levels, similarly controlled by BAX and BAK. A combination of subcellular fractionation and imaging shows that wild-type VacA, but not mutants in its channel-forming region, induces the accumulation of BAX on endosomes and endosome-mitochondria juxtaposition that precedes the retrieval of active BAX on mitochondria. It is noteworthy that in Bax- and Bak-deficient cells, VacA is unable to cause endosome-mitochondria juxtaposition and is not retrieved in mitochondria. Thus, VacA causes BAX/BAK-dependent juxtaposition of endosomes and mitochondria early in the process of cell death, revealing a new function for these proapoptotic proteins in the regulation of relative position of organelles.