K_{l 3} and \pi_{e 3} transition form factors

$K_{\ell 3}$ and $\pi_{e 3}$ transition form factors are calculated as an application of Dyson-Schwinger equations. The role of nonanalytic contributions to the quark--W-boson vertex is elucidated. A one-parameter model for this vertex provides a uniformly good description of these transitions, including the value of the scalar form factor of the kaon at the Callan-Treiman point. The $K_{\ell 3}$ form factors, $f_\pm^K$, are approximately linear on $t\in [m_e^2,m_\mu^2]$ and have approximately the same slope. $f_-^K(0)$ is a measure of the Euclidean constituent-quark mass ratio: $M^E_s/M^E_u$. In the isospin symmetric limit: $-f_+^\pi(0)= F_\pi(t)$, the electromagnetic pion form factor, and $f_-^\pi(t)\equiv 0$.Comment: 11 pages (incl. 3 figures), elsart.sty, epsf.st

Dissimilatory nitrate reduction to ammonium coupled to Fe(II) oxidation in sediments of a periodically hypoxic estuary

Estuarine sediments are critical for the remediation of large amounts of anthropogenic nitrogen (N) loading via production of N₂ from nitrate by denitrification. However, nitrate is also recycled within sediments by dissimilatory nitrate reduction to ammonium (DNRA). Understanding the factors that influence the balance between denitrification and DNRA is thus crucial to constraining coastal N budgets. A potentially important factor is the availability of different electron donors (organic carbon, reduced iron and sulfur). Both denitrification and DNRA may be linked to ferrous iron oxidation, however the contribution of Fe(II)-fueled nitrate reduction in natural environments is practically unknown. This study investigated how nitrate-dependent Fe²⁺ oxidation affects the partitioning between nitrate reduction pathways using ¹⁵N-tracing methods in sediments along the salinity gradient of the periodically hypoxic Yarra River estuary, Australia. Increased dissolved Fe²⁺ availability resulted in significant enhancement of DNRA rates from around 10–20% total nitrate reduction in control incubations to over 40% in those with additional Fe²⁺, at several sites. Increases in DNRA at some locations were accompanied by reductions in denitrification. Significant correlations were observed between Fe²⁺ oxidation and DNRA rates, with reaction ratios corresponding to the stoichiometry of Fe²⁺-dependent DNRA. Our results provide experimental evidence for a direct coupling of DNRA to Fe²⁺ oxidation across an estuarine gradient, suggesting that Fe²⁺ availability may exert substantial control on the balance between retention and removal of bioavailable N. Thus, DNRA linked to Fe²⁺ oxidation may be of general importance to environments with Fe-rich sediments

Secure Electromagnetic Buildings Using Slow Phase Switching Frequency Selective Surfaces

The concept of a secure electromagnetic building which can successfully prohibit wireless communications is presented. Wireless security is achieved using a slow phase switching technique and can be realized by time varying the transmission properties of a frequency selective surface to increase the bit error rate of the unwanted signal. Results are presented which demonstrate that a technique of phase switching at rates much lower than the baseband data rate can be used successfully. The system has been implemented using a reconfigurable dual polarized dual layer frequency selective surface incorporating varactor diodes where over 100° of phase change can be achieved for voltage changes of ±0–3V. A vector signal analyzer was used to evaluate the bit error rate performance of the system for a GSM signal operating at 2GHz. Bit error rates are shown to be as high as 36% which are sufficient to successfully prohibit wireless communication. The solution is also shown to be robust over a wide range of incidence angles which is important for real world applications where the location of the prohibited wireless source may be unknown or mobile. Furthermore, as the system is reconfigurable the building can be switched between a secure and non-secure mode

Charge symmetry breaking via rho-omega mixing from model quark-gluon dynamics

The quark-loop contribution to the $\rho^0-\omega$ mixing self-energy function is calculated using a phenomenologically successful QCD-based model field theory in which the $\rho^0$ and $\omega$ mesons are composite $\bar{q}q$ bound states. In this calculation the dressed quark propagator, obtained from a model Dyson-Schwinger equation, is confining. In contrast to previous studies, the meson-$\bar{q}q$ vertex functions are characterised by a strength and range determined by the dynamics of the model; and the calculated off-mass-shell behaviour of the mixing amplitude includes the contribution from the calculated diagonal meson self-energies. The mixing amplitude is shown to be very sensitive to the small isovector component of dynamical chiral symmetry breaking. The spacelike quark-loop mixing-amplitude generates an insignificant charge symmetry breaking nuclear force.Comment: 11 Pages, 3 figures uuencoded and appended to this file, REVTEX 3.0. ANL-PHY-7718-TH-94, KSUCNR-004-94. [!! PostScript file format corrected. Retrieve by anonymous ftp from theory.phy.anl.gov (130.202.20.190), directory pub: mget wpfig*.ps Three files.

Retraction Notice of the Article: The DYRK-family kinase Pom1 phosphorylates the F-BAR protein Cdc15 to prevent division at cell poles

Division site positioning is critical for both symmetric and asymmetric cell divisions. In many organisms, positive and negative signals cooperate to position the contractile actin ring for cytokinesis. In rod-shaped fission yeast Schizosaccharomyces pombe cells, division at midcell is achieved through positive Mid1/anillin-dependent signaling emanating from the central nucleus and negative signals from the dual-specificity tyrosine phosphorylation-regulated kinase family kinase Pom1 at the cell poles. In this study, we show that Pom1 directly phosphorylates the F-BAR protein Cdc15, a central component of the cytokinetic ring. Pom1-dependent phosphorylation blocks Cdc15 binding to paxillin Pxl1 and C2 domain protein Fic1 and enhances Cdc15 dynamics. This promotes ring sliding from cell poles, which prevents septum assembly at the ends of cells with a displaced nucleus or lacking Mid1. Pom1 also slows down ring constriction. These results indicate that a strong negative signal from the Pom1 kinase at cell poles converts Cdc15 to its closed state, destabilizes the actomyosin ring, and thus promotes medial septation

K -> pi pi and a light scalar meson

We explore the Delta-I= 1/2 rule and epsilon'/epsilon in K -> pi pi transitions using a Dyson-Schwinger equation model. Exploiting the feature that QCD penguin operators direct K^0_S transitions through 0^{++} intermediate states, we find an explanation of the enhancement of I=0 K -> pi pi transitions in the contribution of a light sigma-meson. This mechanism also affects epsilon'/epsilon.Comment: 7 pages, REVTE

Off-Shell Axial Anomaly via the \gamma^* \pi^0 -> \gamma Transition

The $\gamma^* \pi^0 \rightarrow \gamma$ form factor, including the extension off the pion mass-shell, is obtained from a generalized impulse approximation within a QCD-based model field theory known to provide an excellent description of the pion charge form factor. This approach implements dressing of the vertex functions and propagators consistent with dynamical chiral symmetry breaking, gauge invariance, quark confinement and perturbative QCD. Soft nonperturbative behavior, dictated by the axial anomaly, is found to evolve to the perturbative QCD limit only for \mbox{$Q^2 \geq 20~{\rm GeV}^2$}.Comment: 10 Pages, 3 figures (uuencoded and appended), REVTE

Selected nucleon form factors and a composite scalar diquark

A covariant, composite scalar diquark, Fadde'ev amplitude model for the nucleon is used to calculate pseudoscalar, isoscalar- and isovector-vector, axial-vector and scalar nucleon form factors. The last yields the nucleon sigma-term and on-shell sigma-nucleon coupling. The calculated form factors are soft, and the couplings are generally in good agreement with experiment and other determinations. Elements in the dressed-quark-axial-vector vertex that are not constrained by the Ward-Takahashi identity contribute ~20% to the magnitude of g_A. The calculation of the nucleon sigma-term elucidates the only unambiguous means of extrapolating meson-nucleon couplings off the meson mass-shell.Comment: 12 pages, REVTEX, 5 figures, epsfi

Low-energy QCD: Chiral coefficients and the quark-quark interaction

A detailed investigation of the low-energy chiral expansion is presented within a model truncation of QCD. The truncation allows for a phenomenological description of the quark-quark interaction in a framework which maintains the global symmetries of QCD and permits a $1/N_c$ expansion. The model dependence of the chiral coefficients is tested for several forms of the quark-quark interaction by varying the form of the running coupling, $\alpha (q^2)$, in the infrared region. The pattern in the coefficients that arises at tree level is consistent with large $N_c$ QCD, and is related to the model truncation.Comment: 28 pages, Latex, 6 postscript figures available on request to [email protected]

A meta-analysis of protein binding of flucloxacillin in healthy volunteers and hospitalized patients

Objectives: The aim of this study was to develop a mechanistic protein-binding model to predict the unbound flucloxacillin concentrations in different patient populations. Methods: A mechanistic protein-binding model was fitted to the data using non-linear mixed-effects modelling. Data were obtained from four datasets, containing 710 paired total and unbound flucloxacillin concentrations from healthy volunteers, non-critically ill and critically ill patients. A fifth dataset with data from hospitalized patients was used for evaluation of our model. The predictive performance of the mechanistic model was evaluated and compared with the calculation of the unbound concentration with a fixed unbound fraction of 5%. Finally, we performed a fit-for-use evaluation, verifying whether the model-predicted unbound flucloxacillin concentrations would lead to clinically incorrect dose adjustments. Results: The mechanistic protein-binding model predicted the unbound flucloxacillin concentrations more accurately than assuming an unbound fraction of 5%. The mean prediction error varied between -26.2% to 27.8% for the mechanistic model and between -30.8% to 83% for calculation with a fixed factor of 5%. The normalized root mean squared error varied between 36.8% and 69% respectively between 57.1% and 134%. Predicting the unbound concentration with the use of the mechanistic model resulted in 6.1% incorrect dose adjustments versus 19.4% if calculated with a fixed unbound fraction of 5%. Conclusions: Estimating the unbound concentration with a mechanistic protein-binding model outperforms the calculation with the use of a fixed protein binding factor of 5%, but neither demonstrates acceptable performance. When performing dose individualization of flucloxacillin, this should be done based on measured unbound concentrations rather than on estimated unbound concentrations from the measured total concentrations. In the absence of an assay for unbound concentrations, the mechanistic binding model should be preferred over assuming a fixed unbound fraction of 5%