First Observation of Coherent π0\pi^0 Production in Neutrino Nucleus Interactions with Eν<E_{\nu}< 2 GeV

The MiniBooNE experiment at Fermilab has amassed the largest sample to date of $\pi^0$s produced in neutral current (NC) neutrino-nucleus interactions at low energy. This paper reports a measurement of the momentum distribution of $\pi^0$s produced in mineral oil (CH$_2$) and the first observation of coherent $\pi^0$ production below 2 GeV. In the forward direction, the yield of events observed above the expectation for resonant production is attributed primarily to coherent production off carbon, but may also include a small contribution from diffractive production on hydrogen. Integrated over the MiniBooNE neutrino flux, the sum of the NC coherent and diffractive modes is found to be (19.5 $\pm$1.1 (stat) $\pm$2.5 (sys))% of all exclusive NC $\pi^0$ production at MiniBooNE. These measurements are of immediate utility because they quantify an important background to MiniBooNE's search for $\nu_{\mu} \to \nu_e$ oscillations.Comment: Submitted to Phys. Lett.

Test of Lorentz and CPT violation with Short Baseline Neutrino Oscillation Excesses

The sidereal time dependence of MiniBooNE electron neutrino and anti-electron neutrino appearance data are analyzed to search for evidence of Lorentz and CPT violation. An unbinned Kolmogorov-Smirnov test shows both the electron neutrino and anti-electron neutrino appearance data are compatible with the null sidereal variation hypothesis to more than 5%. Using an unbinned likelihood fit with a Lorentz-violating oscillation model derived from the Standard Model Extension (SME) to describe any excess events over background, we find that the electron neutrino appearance data prefer a sidereal time-independent solution, and the anti-electron neutrino appearance data slightly prefer a sidereal time-dependent solution. Limits of order 10E-20 GeV are placed on combinations of SME coefficients. These limits give the best limits on certain SME coefficients for muon neutrino to electron neutrino and anti-muon neutrino to anti-electron neutrino oscillations. The fit values and limits of combinations of SME coefficients are provided.Comment: 14 pages, 3 figures, and 2 tables, submitted to Physics Letters

Highly-parallelized simulation of a pixelated LArTPC on a GPU

The rapid development of general-purpose computing on graphics processing units (GPGPU) is allowing the implementation of highly-parallelized Monte Carlo simulation chains for particle physics experiments. This technique is particularly suitable for the simulation of a pixelated charge readout for time projection chambers, given the large number of channels that this technology employs. Here we present the first implementation of a full microphysical simulator of a liquid argon time projection chamber (LArTPC) equipped with light readout and pixelated charge readout, developed for the DUNE Near Detector. The software is implemented with an end-to-end set of GPU-optimized algorithms. The algorithms have been written in Python and translated into CUDA kernels using Numba, a just-in-time compiler for a subset of Python and NumPy instructions. The GPU implementation achieves a speed up of four orders of magnitude compared with the equivalent CPU version. The simulation of the current induced on 10^3 pixels takes around 1 ms on the GPU, compared with approximately 10 s on the CPU. The results of the simulation are compared against data from a pixel-readout LArTPC prototype

AXR4 Is Required for Localization of the Auxin Influx Facilitator AUX1

The AUX1 and PIN auxin influx and efflux facilitators are key regulators of root growth and development. For root gravitropism to occur, AUX1 and PIN2 must transport auxin via the lateral root cap to elongating epidermal cells. Genetic studies suggest that AXR4 functions in the same pathway as AUX1. Here we show that AXR4 is a previously unidentified accessory protein of the endoplasmic reticulum (ER) that regulates localization of AUX1 but not of PIN proteins. Loss of AXR4 resulted in abnormal accumulation of AUX1 in the ER of epidermal cells, indicating that the axr4 agravitropic phenotype is caused by defective AUX1 trafficking in the root epidermis