The local dust foregrounds in the microwave sky: I. Thermal emission spectra

Analyses of the cosmic microwave background (CMB) radiation maps made by the Wilkinson Microwave Anisotropy Probe (WMAP) have revealed anomalies not predicted by the standard inflationary cosmology. In particular, the power of the quadrupole moment of the CMB fluctuations is remarkably low, and the quadrupole and octopole moments are aligned mutually and with the geometry of the Solar system. It has been suggested in the literature that microwave sky pollution by an unidentified dust cloud in the vicinity of the Solar system may be the cause for these anomalies. In this paper, we simulate the thermal emission by clouds of spherical homogeneous particles of several materials. Spectral constraints from the WMAP multi-wavelength data and earlier infrared observations on the hypothetical dust cloud are used to determine the dust cloud's physical characteristics. In order for its emissivity to demonstrate a flat, CMB-like wavelength dependence over the WMAP wavelengths (3 through 14 mm), and to be invisible in the infrared light, its particles must be macroscopic. Silicate spheres from several millimetres in size and carbonaceous particles an order of magnitude smaller will suffice. According to our estimates of the abundance of such particles in the Zodiacal cloud and trans-neptunian belt, yielding the optical depths of the order of 1E-7 for each cloud, the Solar-system dust can well contribute 10 microKelvin (within an order of magnitude) in the microwaves. This is not only intriguingly close to the magnitude of the anomalies (about 30 microKelvin), but also alarmingly above the presently believed magnitude of systematic biases of the WMAP results (below 5 microKelvin) and, to an even greater degree, of the future missions with higher sensitivities, e.g. PLANCK.Comment: 33 pages, 9 figures, 1 table. The Astrophysical Journal, 2009, accepte

Steady, oscillatory, and unsteady subsonic Aerodynamics, production version 1.1 (SOUSSA-P1.1). Volume 2: User/programmer manual

A user/programmer manual for the computer program SOUSSA P 1.1 is presented. The program was designed to provide accurate and efficient evaluation of steady and unsteady loads on aircraft having arbitrary shapes and motions, including structural deformations. These design goals were in part achieved through the incorporation of the data handling capabilities of the SPAR finite element Structural Analysis computer program. As a further result, SOUSSA P possesses an extensive checkpoint/ restart facility. The programmer's portion of this manual includes overlay/subroutine hierarchy, logical flow of control, definition of SOUSSA P 1.1 FORTRAN variables, and definition of SOUSSA P 1.1 subroutines. Purpose of the SOUSSA P 1.1 modules, input data to the program, output of the program, hardware/software requirements, error detection and reporting capabilities, job control statements, a summary of the procedure for running the program and two test cases including input and output and listings are described in the user oriented portion of the manual

Effects of in vitro potassium on ammoniagenesis in rat and canine kidney tissue

Effects of in vitro potassium on ammoniagenesis in rat and canine kidney tissue. Decreased ammonium (NH4+) excretion is associated with hyperkalemia. To determine if potassium could directly influence renal ammonia production, we investigated ammoniagenesis by rat and canine renal cortical tissues in vitro at different potassium concentrations. Renal tissue from normal and acidotic rats and normal dogs incubated in glutamine, lactate, and 7 to 10mEq/liters of potassium or 25mEq/liters of potassium produced significantly less ammonia than slices incubating in glutamine, lactate, and 4 to 5mEq of potassium. Glutamate accumulation, which follows glutamine deamidation, did not decrease and even increased at 25mEq/liters of potassium. With glutamine as the sole substrate, decreased ammoniagenesis was seen only at higher potassium concentrations (> 16mEq/liters) than when lactate was also present. The depression to glutamine ammoniagenesis by high concentrations of potassium was partially obliterated in an anaerobic environment. When glutamate replaced glutamine as the precursor, renal ammonia produced by slices in 7 and 25mEq/liters was again significantly lower than by slices incubating in 4mEq/liters. We blocked glutamine synthesis by rat kidney slices with dl-methionine dl-sulfoximine when glutamate was the renal ammonia precursor. This essentially allows glutamate deamination to produce ammonia. Potassium depressed glutamate deamination significantly at 7mEq/liters (↓ 13%) and at 25mEq/liters of potassium (↓ 35%) as compared to 4mEq/liters. The above findings are consistent with a major depressive effect of in vitro potassium on glutamate deamination in rat and canine kidneys. Other evidence, especially from rat tissue studies, suggests that potassium also may affect glutamine deamination directly. Rat kidney slices incubating in the high potassium medium of 7mEq/liter or greater also consumed less oxygen in the presence of glutamine (P < 0.01), oxidatively decarboxylated less glutamine (P < 0.02) and produced less glucose from glutamine (P < 0.01).Effet du potassium in vitro sur l'ammoniogenèse dans tissu rénal de rat et de chien. Une diminution de l'excrétion d'ammoniaque (NH4+) est associée à l'hyperkaliémie. Afin de déterminer si le potassium peut influencer directement la production rénale d'ammoniac, nous avons étudié l'ammoniogenèse dans le tissu rénal cortical de rat et de chien in vitro à différentes concentrations de potassium. Du tissu rénal provenant de rats normaux et en acidose et de chiens normaux incubés dans de la glutamine, du lactate, et 7 à 10mEq/litres de potassium ou 25mEq/litres de potassium produit significativement moins d'ammoniac que des tranches incubées dans de la glutamine, du lactate, et 4 à 5mEq/litres de potassium. L'accumulation de glutamate, consécutive à la deamination de la glutamine, n'a pas diminué et même a augmenté à 25mEq/litres de potassium. Avec la glutamine comme seul substrat, la diminution de l'ammoniogenèse n'a été observée qu'à des concentrations de potassium supérieures (> 16mEq/litres) à celle nécessaire quand le lactate est présent. La dépression de l'ammoniogenèse due à la glutamine au moyen de concentrations élevées de potassium est partiellement abolie par un environnement anaérobique. Quand la glutamine est remplacée par du glutamate, le rénale d'ammoniac produit par des tranches dans des milieux à 7mEq/litres et 25mEq/litres est là encore significativement inférieur à celui produit par des tranches incubées dans un milieu à 4mEq/litres. Nous avons bloqué la synthèse de glutamine dans les tranches de rein de rat au moyen de la dl-méthionine dl-sulfoximine quand le glutamate était le précurseur de rénale d'ammoniac. Ceci permet à la déamination du glutamate de produire de l'ammoniac. Potassium diminue significativement la déamination du glutamate à 7mEq/litres (diminution de 13%), et à 25mEq/litres (diminution de 35%) par comparaison avec les valeurs obtenues à 4mEq/litres. Ces constatations sont compatibles avec un effet dépresseur majeur du potassium in vitro sur la déamination du glutamate dans les reins de rat et de chien. D'autres arguments, tirés essentiellement des études sur le tissu de rat, suggèrent que le potassium peut aussi affecter la déamination du glutamate directement. Des tranches de rein de rat incubées dans un milieu riche en potassium (7mEq/litres ou plus) consomment moins d'oxygène en présence de glutamine (P < 0,01), décarboxylent moins de glutamine par oxydation (P < 0,02) et produisent moins de glucose à partir de la glutamine (P < 0,01)

Lessons from LIMK1 enzymology and their impact on inhibitor design

LIM domain kinase 1 (LIMK1) is a key regulator of actin dynamics. It is thereby a potential therapeutic target for the prevention of fragile X syndrome and amyotrophic lateral sclerosis. Herein, we use X-ray crystallography and activity assays to describe how LIMK1 accomplishes substrate specificity, to suggest a unique ‘rock-and-poke’ mechanism of catalysis and to explore the regulation of the kinase by activation loop phosphorylation. Based on these findings, a differential scanning fluorimetry assay and a RapidFire mass spectrometry activity assay were established, leading to the discovery and confirmation of a set of small-molecule LIMK1 inhibitors. Interestingly, several of the inhibitors were inactive towards the closely related isoform LIMK2. Finally, crystal structures of the LIMK1 kinase domain in complex with inhibitors (PF-477736 and staurosporine, respectively) are presented, providing insights into LIMK1 plasticity upon inhibitor binding

The spectral weight of the Hubbard model through cluster perturbation theory

We calculate the spectral weight of the one- and two-dimensional Hubbard models, by performing exact diagonalizations of finite clusters and treating inter-cluster hopping with perturbation theory. Even with relatively modest clusters (e.g. 12 sites), the spectra thus obtained give an accurate description of the exact results. Thus, spin-charge separation (i.e. an extended spectral weight bounded by singularities) is clearly recognized in the one-dimensional Hubbard model, and so is extended spectral weight in the two-dimensional Hubbard model.Comment: 4 pages, 5 figure

Quasiparticle Dispersion of the 2D Hubbard Model: From an Insulator to a Metal

On the basis of Quantum-Monte-Carlo results the evolution of the spectral weight $A(\vec k, \omega)$ of the two-dimensional Hubbard model is studied from insulating to metallic behavior. As observed in recent photoemission experiments for cuprates, the electronic excitations display essentially doping-independent features: a quasiparticle-like dispersive narrow band of width of the order of the exchange interaction $J$ and a broad valence- and conduction-band background. The continuous evolution is traced back to one and the same many-body origin: the doping-dependent antiferromagnetic spin-spin correlation.Comment: 11 pages, REVtex, 4 figures (in uuencoded postscript format