On the determination of anti-neutrino spectra from nuclear reactors

In this paper we study the effect of, well-known, higher order corrections to the allowed beta decay spectrum on the determination of anti-neutrino spectra resulting from the decays of fission fragments. In particular, we try to estimate the associated theory errors and find that induced currents like weak magnetism may ultimately limit our ability to improve the current accuracy and under certain circumstance could even largely increase the theoretical errors. We also perform a critical evaluation of the errors associated with our method to extract the anti-neutrino spectrum using synthetic beta spectra. It turns out, that a fit using only virtual beta branches with a judicious choice of the effective nuclear charge provides results with a minimal bias. We apply this method to actual data for U235, Pu239 and Pu241 and confirm, within errors, recent results, which indicate a net 3% upward shift in energy averaged anti-neutrino fluxes. However, we also find significant shape differences which can in principle be tested by high statistics anti-neutrino data samples.Comment: 20 pages, 5 figures, 9 tables, added references, version accepted for publication in Phys. Rev. C. Corrected errors in tab. 1 and eqs. 18 and 19. Results and conclusion unchange

A new analysis of 14O beta decay: branching ratios and CVC consistency

The ground-state Gamow-Teller transition in the decay of 14O is strongly hindered and the electron spectrum deviates markedly from the allowed shape. A reanalysis of the only available data on this spectrum changes the branching ratio assigned to this transition by seven standard deviations: our new result is (0.54 \pm 0.02)%. The Kurie plot data from two earlier publications are also examined and a revision to their published branching ratios is recommended. The required nuclear matrix elements are calculated with the shell model and, for the first time, consistency is obtained between the M1 matrix element deduced from the analog gamma transition in 14N and that deduced from the slope of the shape-correction function in the beta transition, a requirement of the conserved vector current hypothesis. This consistency is only obtained, however, if renormalized rather than free-nucleon operators are used in the shell-model calculations. In the mirror decay of 14C a similar situation occurs. Consistency between the 14C lifetime, the slope of the shape-correction function and the M1 matrix element from gamma decay can only be achieved with renormalized operators in the shell-model calculation.Comment: 9 pages; revtex4; one figur

Hormonal and uterine changes in pregnant and pseudopregnant gilts treated with hydrocortisone acetate

In the first experiment 11 gilts were injected with 5 mg of estradiol benzoate on d 11-15 of the estrous cycle to induce pseudopregnancy. Twice daily on d 21-30 gilts were administered either 5 mg per kg bodyweight (avg. wgt 120 kg) hydrocortisone acetate (HA) in sesame oil (5 ml) or sesame oil (control) subcutaneously (SQ). Blood samples (20 ml) were collected via jugular puncture on d 11, 21, and 31. Uterine flushings were obtained surgically the day following the last day of treatment (d 31). Twice daily injection of HA on d 21-30 significantly (p\u3c.001) elevated cortisol levels above that of control animals in plasma and uterine flushing on d 31. The percent distribution of cortisol in plasma [% unbound (UB-C), % corticosteroid binding globulin (CB6) bound (CBG—C), and % albumin bound (Alb-C)] was not different between treatments. Plasma CBG binding capacity (CBG-BC) was lower (p\u3c.001) following 10 d of treatment with HA compared to control gilts (7.4 versus 38.7 pmol/ml). Plasma progesterone (P4) levels were significantly (p\u3c.01) lower in HA treated gilts (8.9 ng/ml) compared to control gilts (17.8 ng/ml). Uterine Flush P4 levels were also decreased (p\u3c.001) compared to control gilts. Total plasma protein and albumin concentrations were similar (p\u3e.05) to control gilts. Total proteins in the uterine flush were lower (p\u3c.001) in HA treated gilts. Corpora lutea (CL) number and concentrations were not affected by treatment. Total CL weight was significantly (p\u3c.01) lower in HA treated gilts compared to control animals. In the second experiment 18 crossbred gilts exhibiting 2 normal estrous cycles (18-23 d) were naturally bred to a mature boar and randomly assigned to receive 5 mg/kg bodyweight (BW) HA (Trt 1), 2.5 mg/kg BW HA (Trt 2), or 5 ml sesame oil (control; Trt 3) twice daily on d 9-13 of pregnancy. Blood samples were collected on d 9, 11/ 13, and 20 of pregnancy. On d 46 ± 2 gilts slaughtered and reproductive tracts collected. CL number and CL weights were obtained. Number, weight, crown rump length, placental weight, allantoic and amniotic fluid volume of fetuses were measured and recorded. Plasma cortisol levels were increased (p\u3c.05) due to treatment on day 13. The distribution of cortisol (% UB-C, % CBG-C, and % Alb-C) was not different (p\u3e.05) between treatments. CBG-BC, plasma P4 levels, total proteins, CL number, CL weight, fetal number, fetal length, and placental weight were not affected by treatment. Fetal weights in Trt 2 (2.5 mg/kg HA) were significantly (p\u3c.05) lower compared to Trt 1 (5 mg/kg HA) and control gilts. Allantoic and amniotic fluid volumes were lower in Trt 2 (p\u3c.001 and p\u3c.05, respectively) compared to Trt 1 and control gilts. These results suggest that : a) HA affected P4 production in the ovary by retarding CL development, B) the HA treatment lowered total P4 output, as reflected by lowered P4 concentration in the plasma, and affected protein secretion in the uterus, C) uterine protein secretions were preferentially reduced in the component contributed by P4-induced, locally synthesized proteins but not by serum transudate, D) HA did not affect liver function as measured by total plasma protein concentration, E) HA affected CBG as evident by the decrease in CBG-BC concentrations and F) reduction in uterine secretory protein output may result in lowered fetal weight due to poor nutrition in utero

Characterization of spatio-temporal epidural event-related potentials for mouse models of psychiatric disorders.

Distinctive features in sensory event-related potentials (ERPs) are endophenotypic biomarkers of psychiatric disorders, widely studied using electroencephalographic (EEG) methods in humans and model animals. Despite the popularity and unique significance of the mouse as a model species in basic research, existing EEG methods applicable to mice are far less powerful than those available for humans and large animals. We developed a new method for multi-channel epidural ERP characterization in behaving mice with high precision, reliability and convenience and report an application to time-domain ERP feature characterization of the Sp4 hypomorphic mouse model for schizophrenia. Compared to previous methods, our spatio-temporal ERP measurement robustly improved the resolving power of key signatures characteristic of the disease model. The high performance and low cost of this technique makes it suitable for high-throughput behavioral and pharmacological studies

A structure-preserving split finite element discretization of the split wave equations

We introduce a new finite element (FE) discretization framework applicable for covariant split equations. The introduction of additional differential forms (DF) that form pairs with the original ones permits the splitting of the equations into topological momentum and continuity equations and metric-dependent closure equations that apply the Hodge-star operator. Our discretization framework conserves this geometrical structure and provides for all DFs proper FE spaces such that the differential operators hold in strong form. We introduce lowest possible order discretizations of the split 1D wave equations, in which the discrete momentum and continuity equations follow by trivial projections onto piecewise constant FE spaces, omitting partial integrations. Approximating the Hodge-star by nontrivial Galerkin projections (GP), the two discrete metric equations follow by projections onto either the piecewise constant (GP0) or piecewise linear (GP1) space. Our framework gives us three schemes with significantly different behavior. The split scheme using twice GP1 is unstable and shares the dispersion relation with the P1-P1 FE scheme that approximates both variables by piecewise linear spaces (P1). The split schemes that apply a mixture of GP1 and GP0 share the dispersion relation with the stable P1-P0 FE scheme that applies piecewise linear and piecewise constant (P0) spaces. However, the split schemes exhibit second order convergence for both quantities of interest. For the split scheme applying twice GP0, we are not aware of a corresponding standard formulation to compare with. Though it does not provide a satisfactory approximation of the dispersion relation as short waves are propagated much too fast, the discovery of the new scheme illustrates the potential of our discretization framework as a toolbox to study and find FE schemes by new combinations of FE spaces

E-cadherin and APC compete for the interaction with beta-catenin and the cytoskeleton

beta-Catenin is involved in the formation of adherens junctions of mammalian epithelia. It interacts with the cell adhesion molecule E-cadherin and also with the tumor suppressor gene product APC, and the Drosophila homologue of beta-catenin, armadillo, mediates morphogenetic signals. We demonstrate here that E-cadherin and APC directly compete for binding to the internal, armadillo-like repeats of beta-catenin; the NH2-terminal domain of beta-catenin mediates the interaction of the alternative E-cadherin and APC complexes to the cytoskeleton by binding to alpha-catenin. Plakoglobin (gamma-catenin), which is structurally related to beta-catenin, mediates identical interactions. We thus show that the APC tumor suppressor gene product forms strikingly similar associations as found in cell junctions and suggest that beta-catenin and plakoglobin are central regulators of cell adhesion, cytoskeletal interaction, and tumor suppression