Going beyond the Kaiser redshift-space distortion formula: a full general relativistic account of the effects and their detectability in galaxy clustering

Kaiser redshift-space distortion formula describes well the clustering of galaxies in redshift surveys on small scales, but there are numerous additional terms that arise on large scales. Some of these terms can be described using Newtonian dynamics and have been discussed in the literature, while the others require proper general relativistic description that was only recently developed. Accounting for these terms in galaxy clustering is the first step toward tests of general relativity on horizon scales. The effects can be classified as two terms that represent the velocity and the gravitational potential contributions. Their amplitude is determined by effects such as the volume and luminosity distance fluctuation effects and the time evolution of galaxy number density and Hubble parameter. We compare the Newtonian approximation often used in the redshift-space distortion literature to the fully general relativistic equation, and show that Newtonian approximation accounts for most of the terms contributing to velocity effect. We perform a Fisher matrix analysis of detectability of these terms and show that in a single tracer survey they are completely undetectable. To detect these terms one must resort to the recently developed methods to reduce sampling variance and shot noise. We show that in an all-sky galaxy redshift survey at low redshift the velocity term can be measured at a few sigma if one can utilize halos of mass M>10^12 Msun (this can increase to 10-sigma or more in some more optimistic scenarios), while the gravitational potential term itself can only be marginally detected. We also demonstrate that the general relativistic effect is not degenerate with the primordial non-Gaussian signature in galaxy bias, and the ability to detect primordial non-Gaussianity is little compromised.Comment: 13 pages, 5 figures, published in PR

Precision determination of absolute neutron flux

A technique for establishing the total neutron rate of a highly-collimated monochromatic cold neutron beam was demonstrated using a method of an alpha-gamma counter. The method involves only the counting of measured rates and is independent of neutron cross sections, decay chain branching ratios, and neutron beam energy. For the measurement, a target of 10B-enriched boron carbide totally absorbed the neutrons in a monochromatic beam, and the rate of absorbed neutrons was determined by counting 478keV gamma rays from neutron capture on 10B with calibrated high-purity germanium detectors. A second measurement based on Bragg diffraction from a perfect silicon crystal was performed to determine the mean de Broglie wavelength of the beam to a precision of 0.024 %. With these measurements, the detection efficiency of a neutron monitor based on neutron absorption on 6Li was determined to an overall uncertainty of 0.058 %. We discuss the principle of the alpha-gamma method and present details of how the measurement was performed including the systematic effects. We also describe how this method may be used for applications in neutron dosimetry and metrology, fundamental neutron physics, and neutron cross section measurements.Comment: 44 page

αV-Integrins Are Required for Mechanotransduction in MDCK Epithelial Cells

The properties of epithelial cells within tissues are regulated by their immediate microenvironment, which consists of neighboring cells and the extracellular matrix (ECM). Integrin heterodimers orchestrate dynamic assembly and disassembly of cell-ECM connections and thereby convey biochemical and mechanical information from the ECM into cells. However, the specific contributions and functional hierarchy between different integrin heterodimers in the regulation of focal adhesion dynamics in epithelial cells are incompletely understood. Here, we have studied the functions of RGD-binding αV-integrins in a Madin Darby Canine Kidney (MDCK) cell model and found that αV-integrins regulate the maturation of focal adhesions (FAs) and cell spreading. αV-integrin-deficient MDCK cells bound collagen I (Col I) substrate via α2β1-integrins but failed to efficiently recruit FA components such as talin, focal adhesion kinase (FAK), vinculin and integrin-linked kinase (ILK). The apparent inability to mature α2β1-integrin-mediated FAs and link them to cellular actin cytoskeleton led to disrupted mechanotransduction in αV-integrin deficient cells seeded onto Col I substrate