K to pi pi Amplitudes at Unphysical Kinematics Using Domain Wall Fermions

The use of chiral perturbation theory in extracting physical K to pi pi matrix elements from matrix elements calculated at unphysical kinematics is outlined. In particular, the possibility of utilizing pions with non-zero momentum in the final state, and of using partial quenching is discussed. Preliminary (not physically normalized) Delta I=3/2 (27,1) K to pi pi matrix elements are calculated on the RBC/UKQCD $24^3 \times 64$, $L_s=16$ lattices, using 2+1 dynamical flavors and domain wall fermions, with an inverse lattice spacing of $a^{-1}=1.729(28) GeV$. Effective mass plots are presented for a light sea quark mass of $m_l^{sea}=0.005$, and various valence quark masses. The plateaux are fit and $E_{\pi\pi}-m_K$ is extracted.Comment: 7 pages, 4 figures, Talk presented at the XXV International Symposium on Lattice Field Theory, July 30 - August 4 2007, Regensburg, German

Automated Lensing Learner: Automated Strong Lensing Identification with a Computer Vision Technique

Forthcoming surveys such as the Large Synoptic Survey Telescope (LSST) and Euclid necessitate automatic and efficient identification methods of strong lensing systems. We present a strong lensing identification approach that utilizes a feature extraction method from computer vision, the Histogram of Oriented Gradients (HOG), to capture edge patterns of arcs. We train a supervised classifier model on the HOG of mock strong galaxy-galaxy lens images similar to observations from the Hubble Space Telescope (HST) and LSST. We assess model performance with the area under the curve (AUC) of a Receiver Operating Characteristic (ROC) curve. Models trained on 10,000 lens and non-lens containing images images exhibit an AUC of 0.975 for an HST-like sample, 0.625 for one exposure of LSST, and 0.809 for 10-year mock LSST observations. Performance appears to continually improve with the training set size. Models trained on fewer images perform better in absence of the lens galaxy light. However, with larger training data sets, information from the lens galaxy actually improves model performance, indicating that HOG captures much of the morphological complexity of the arc finding problem. We test our classifier on data from the Sloan Lens ACS Survey and find that small scale image features reduces the efficiency of our trained model. However, these preliminary tests indicate that some parameterizations of HOG can compensate for differences between observed mock data. One example best-case parameterization results in an AUC of 0.6 in the F814 filter image with other parameterization results equivalent to random performance.Comment: 18 pages, 14 figures, summarizing results in figure

Delta I Equals Three Halfs Kaon To Two Pion Decays Using Lattice Quantum Chromodynamics with Domain Wall Fermions

We calculate matrix elements for kaon to two pion decays in the Delta I = 3/2 channel using lattice gauge theory simulations. From these we can extract the decay amplitude A2, for which the real part is related to the decay rate and can be compared to the experimental result Re(A2) = 1.484 x 10^(-8) GeV, and for which the imaginary part is related to direct charge-parity violation in the neutral kaon system. We report the results of one simulation with nearly physical particle masses and kinematics, specifically mK = 509.0(9.1) MeV, mPi = 142.8(2.5) MeV, and EPiPi = 485.7(8.0) MeV. This simulation was performed on RBC/UKQCD 32^3 x 64, Ls = 32 lattices, using 2+1 dynamical flavors of domain wall fermions and a Dislocation Suppressing Determinant Ratio plus Iwasaki gauge action, and with an inverse lattice spacing a^(-1) = 1.373(24) GeV so that the spatial extent of the lattice is 4.60 fm and mPi*L = 3.3. We find that Re(A2) = 1.461(87)stat(200)sys x 10^(-8) GeV, in good agreement with the experimental value. We also find Im(A2) = -8.67(45)stat(1.95)sys x 10^(-13) GeV, and Im(A2)/Re(A2) = -5.93(27)stat(1.42)sys x 10^(-5), however the value of Im(A2) depends on a rough hypothesis for some of the renormalization constants which have not yet been calculated, and thus we quote a large systematic error. We also report the results of a simulation involving a variety of kaon and pion masses and momenta, which was conducted in order to study the dependence of the decay amplitude on particle masses and kinematics, and to study the effect of not having exactly physical masses and kinematics in the first simulation. The use of the quenched approximation and smaller spatial volume in this second simulation allowed for multiple masses to be simulated in a reasonable amount of time, but introduced an uncontrolled approximation and forced us to use pion masses a bit larger than the phys- ical mass. The study was conducted on 24^3 x 64, Ls = 16 lattices, with the quenched Doubly Blocked Wilson 2 gauge action, and an inverse lattice spacing of a^(-1) = 1.31(2) GeV. We find that an extrapolation to physical masses and kinematics yields values Re(A2) = 2.25(18)stat x 10^(-8) GeV and Im(A2) = -13.44(84)stat x 10^(-13) GeV. These results are significantly larger than those of the full dynamical simulation and of experiment. We attribute this mainly to the an inaccurate determination of the lattice spacing a using the rho mass, since it comes in as a^(-3) in the calculation of A2. Finally, a third simulation is performed with 2+1 dynamical flavors of domain wall fermions on a finer 32^3 x 64, Ls = 16 lattice, but only with pions that have nearly zero momentum. It, and the quenched simulation, are used mainly to estimate the systematic error in the first simulation, which is taken as the final result

Ultradian glucocorticoid exposure directs gene-dependent and tissue-specific mRNA expression patterns in vivo

In this paper we report differential decoding of the ultradian corticosterone signal by glucocorticoid target tissues. Pulsatile corticosterone replacement in adrenalectomised rats resulted in different dynamics of Sgk1 mRNA production, with a distinct pulsatile mRNA induction profile observed in the pituitary in contrast to a non-pulsatile induction in the prefrontal cortex (PFC). We further report the first evidence for pulsatile transcriptional repression of a glucocorticoid-target gene in vivo, with pulsatile regulation of Pomc transcription in pituitary. We have explored a potential mechanism for differences in the induction dynamics of the same transcript (Sgk1) between the PFC and pituitary. Glucocorticoid receptor (GR) activation profiles were strikingly different in pituitary and prefrontal cortex, with a significantly greater dynamic range and shorter duration of GR activity detected in the pituitary, consistent with the more pronounced gene pulsing effect observed. In the prefrontal cortex, expression of Gilz mRNA was also non-pulsatile and exhibited a significantly delayed timecourse of increase and decrease when compared to Sgk1, additionally highlighting gene-specific regulatory dynamics during ultradian glucocorticoid treatment

Corticosterone pattern-dependent glucocorticoid receptor binding and transcriptional regulation within the liver

Ultradian glucocorticoid rhythms are highly conserved across mammalian species, however, their functional significance is not yet fully understood. Here we demonstrate that pulsatile corticosterone replacement in adrenalectomised rats induces a dynamic pattern of glucocorticoid receptor (GR) binding at ~3,000 genomic sites in liver at the pulse peak, subsequently not found during the pulse nadir. In contrast, constant corticosterone replacement induced prolonged binding at the majority of these sites. Additionally, each pattern further induced markedly different transcriptional responses. During pulsatile treatment, intragenic occupancy by active RNA polymerase II exhibited pulsatile dynamics with transient changes in enrichment, either decreased or increased depending on the gene, which mostly returned to baseline during the inter-pulse interval. In contrast, constant corticosterone exposure induced prolonged effects on RNA polymerase II occupancy at the majority of gene targets, thus acting as a sustained regulatory signal for both transactivation and repression of glucocorticoid target genes. The nett effect of these differences were consequently seen in the liver transcriptome as RNA-seq analysis indicated that despite the same overall amount of corticosterone infused, twice the number of transcripts were regulated by constant corticosterone infusion, when compared to pulsatile. Target genes that were found to be differentially regulated in a pattern-dependent manner were enriched in functional pathways including carbohydrate, cholesterol, glucose and fat metabolism as well as inflammation, suggesting a functional role for dysregulated glucocorticoid rhythms in the development of metabolic dysfunction

Signals for Lorentz Violation in Electrodynamics

An investigation is performed of the Lorentz-violating electrodynamics extracted from the renormalizable sector of the general Lorentz- and CPT-violating standard-model extension. Among the unconventional properties of radiation arising from Lorentz violation is birefringence of the vacuum. Limits on the dispersion of light produced by galactic and extragalactic objects provide bounds of 3 x 10^{-16} on certain coefficients for Lorentz violation in the photon sector. The comparative spectral polarimetry of light from cosmologically distant sources yields stringent constraints of 2 x 10^{-32}. All remaining coefficients in the photon sector are measurable in high-sensitivity tests involving cavity-stabilized oscillators. Experimental configurations in Earth- and space-based laboratories are considered that involve optical or microwave cavities and that could be implemented using existing technology.Comment: 23 pages REVTe

Pharmacological and rAAV Gene Therapy Rescue of Visual Functions in a Blind Mouse Model of Leber Congenital Amaurosis

BACKGROUND: Leber congenital amaurosis (LCA), a heterogeneous early-onset retinal dystrophy, accounts for ~15% of inherited congenital blindness. One cause of LCA is loss of the enzyme lecithin:retinol acyl transferase (LRAT), which is required for regeneration of the visual photopigment in the retina. METHODS AND FINDINGS: An animal model of LCA, the Lrat (−/−) mouse, recapitulates clinical features of the human disease. Here, we report that two interventions—intraocular gene therapy and oral pharmacologic treatment with novel retinoid compounds—each restore retinal function to Lrat (−/−) mice. Gene therapy using intraocular injection of recombinant adeno-associated virus carrying the Lrat gene successfully restored electroretinographic responses to ~50% of wild-type levels (p < 0.05 versus wild-type and knockout controls), and pupillary light responses (PLRs) of Lrat (−/−) mice increased ~2.5 log units (p < 0.05). Pharmacological intervention with orally administered pro-drugs 9-cis-retinyl acetate and 9-cis-retinyl succinate (which chemically bypass the LRAT-catalyzed step in chromophore regeneration) also caused long-lasting restoration of retinal function in LRAT-deficient mice and increased ERG response from ~5% of wild-type levels in Lrat (−/−) mice to ~50% of wild-type levels in treated Lrat (−/−) mice (p < 0.05 versus wild-type and knockout controls). The interventions produced markedly increased levels of visual pigment from undetectable levels to 600 pmoles per eye in retinoid treated mice, and ~1,000-fold improvements in PLR and electroretinogram sensitivity. The techniques were complementary when combined. CONCLUSION: Intraocular gene therapy and pharmacologic bypass provide highly effective and complementary means for restoring retinal function in this animal model of human hereditary blindness. These complementary methods offer hope of developing treatment to restore vision in humans with certain forms of hereditary congenital blindness