Numerical computation of an Evans function for travelling waves

We demonstrate a geometrically inspired technique for computing Evans functions for the linearised operators about travelling waves. Using the examples of the F-KPP equation and a Keller-Segel model of bacterial chemotaxis, we produce an Evans function which is computable through several orders of magnitude in the spectral parameter and show how such a function can naturally be extended into the continuous spectrum. In both examples, we use this function to numerically verify the absence of eigenvalues in a large region of the right half of the spectral plane. We also include a new proof of spectral stability in the appropriate weighted space of travelling waves of speed $c \geq 2 \sqrt{\delta}$ in the F-KPP equation.Comment: 37 pages, 11 figure

Intelligent Integration of a Wind Farm to an Utility Power Network with Improved Voltage Stability

The increasing effect of wind energy generation will influence the dynamic behavior of power systems by interacting with conventional generation and loads. Due to the inherent characteristics of wind turbines, non-uniform power production causes variations in system voltage and frequency. Therefore, a wind farm requires high reactive power compensation. Flexible AC transmission systems (FACTS) devices such as SVCs inject reactive power into the system which helps in maintaining a better voltage profile. This paper presents the design of a linear and a nonlinear coordinating controller between a SVC and the wind farm inverter at the point of interconnection. The performances of the coordinating controllers are evaluated on the IEEE 12 bus FACTS benchmark power system where one of the generators is replaced by a wind farm supplying 300 MW. Results are presented to show that the voltage stability of the entire power system during small and large disturbances is improved

Coral Disease and Health Workshop: Coral Histopathology II

The health and continued existence of coral reef ecosystems are threatened by an increasing array of environmental and anthropogenic impacts. Coral disease is one of the prominent causes of increased mortality among reefs globally, particularly in the Caribbean. Although over 40 different coral diseases and syndromes have been reported worldwide, only a few etiological agents have been confirmed; most pathogens remain unknown and the dynamics of disease transmission, pathogenicity and mortality are not understood. Causal relationships have been documented for only a few of the coral diseases, while new syndromes continue to emerge. Extensive field observations by coral biologists have provided substantial documentation of a plethora of new pathologies, but our understanding, however, has been limited to descriptions of gross lesions with names reflecting these observations (e.g., black band, white band, dark spot). To determine etiology, we must equip coral diseases scientists with basic biomedical knowledge and specialized training in areas such as histology, cell biology and pathology. Only through combining descriptive science with mechanistic science and employing the synthesis epizootiology provides will we be able to gain insight into causation and become equipped to handle the pending crisis. One of the critical challenges faced by coral disease researchers is to establish a framework to systematically study coral pathologies drawing from the field of diagnostic medicine and pathology and using generally accepted nomenclature. This process began in April 2004, with a workshop titled Coral Disease and Health Workshop: Developing Diagnostic Criteria co-convened by the Coral Disease and Health Consortium (CDHC), a working group organized under the auspices of the U.S. Coral Reef Task Force, and the International Registry for Coral Pathology (IRCP). The workshop was hosted by the U.S. Geological Survey, National Wildlife Health Center (NWHC) in Madison, Wisconsin and was focused on gross morphology and disease signs observed in the field. A resounding recommendation from the histopathologists participating in the workshop was the urgent need to develop diagnostic criteria that are suitable to move from gross observations to morphological diagnoses based on evaluation of microscopic anatomy. (PDF contains 92 pages

Demonstration of integrated microscale optics in surface-electrode ion traps

In ion trap quantum information processing, efficient fluorescence collection is critical for fast, high-fidelity qubit detection and ion-photon entanglement. The expected size of future many-ion processors require scalable light collection systems. We report on the development and testing of a microfabricated surface-electrode ion trap with an integrated high numerical aperture (NA) micromirror for fluorescence collection. When coupled to a low NA lens, the optical system is inherently scalable to large arrays of mirrors in a single device. We demonstrate stable trapping and transport of 40Ca+ ions over a 0.63 NA micromirror and observe a factor of 1.9 enhancement in photon collection compared to the planar region of the trap.Comment: 15 pages, 8 figure

Constraints on Three-Neutrino Mixing from Atmospheric and Reactor Data

Observations of atmospheric neutrinos are usually analyzed using the simplifying approximation that either $\nu_\mu \leftrightarrow \nu_\tau$ or $\nu_e \leftrightarrow \nu_\mu$ two-flavor mixing is relevant. Here we instead consider the data using the simplifying approximation that only one neutrino mass scale is relevant. This approximation is the minimal three-flavor notation that includes the two relevant two-flavor approximations. The constraints in the parameter space orthogonal to the usual, two-flavor analyses are studied.Comment: 15 pages, preprint IUHET-26

Solar and atmospheric neutrino oscillations with three flavours

We analyze the solar and the atmospheric neutrino problems in the context of three flavour neutrino oscillations. We assume a mass hierarchy in the vacuum mass eigenvalues $\mu_3^2 \gg \mu_2^2 \geq \mu_1^2$, but make no approximation regarding the magnitudes of the mixing angles. We find that there are small but continuous bands in the parameter space where the constraints imposed by the current measurements of $\ {}^{71} Ga$, ${}^{37} Cl$ and Kamiokande experiments are satisfied at $1 \sigma$ level. The allowed parameter space increases dramatically if the error bars are enlarged to $1.6 \sigma$. The electron neutrino survival probability has different energy dependence in different regions of the parameter space. Measurement of the recoil electron energy spectrum in detectors that use $\nu - e$ scattering may distinguish between some of the allowed regions of parameter space. Finally we use the results for the parameter space admitted by the solar neutrinos as an input for the atmospheric neutrino problem and show that there exists a substantial region of parameter space in which both problems can be solved.Comment: 25 pages plus eight figures. Uses Revtex. Postcript files for figures sent separately as a uuencoded fil

Common Origin for the Solar and Atmospheric Neutrino Deficits

Some typos corrected, slightly different abstract, same plots, results and conclusions.Comment: 14 Latex pages, 3 figures attached as postscript files, IFP-472-UNC, PRL-TH-93/1

Dense mapping of IL18 shows no association in SLE

Systemic lupus erythematosus (SLE) is an autoimmune disease which behaves as a complex genetic trait. At least 20 SLE risk susceptibility loci have been mapped using both candidate gene and genome-wide association strategies. The gene encoding the pro-inflammatory cytokine, IL18, has been reported as a candidate gene showing an association with SLE. This pleiotropic cytokine is expressed in a range of immune cells and has been shown to induce interferon-γ and tumour necrosis factor-α. Serum interleukin-18 has been reported to be elevated in patients with SLE. Here we aimed to densely map single nucleotide polymorphisms (SNPs) across IL18 to investigate the association across this locus. We genotyped 36 across IL18 by Illumina bead express in 372 UK SLE trios. We also genotyped these SNPs in a further 508 non-trio UK cases and were able to accurately impute a dense marker set across IL18 in WTCCC2 controls with a total of 258 SNPs. To improve the study's power, we also imputed a total of 158 SNPs across the IL18 locus using data from an SLE genome-wide association study and performed association testing. In total, we analysed 1818 cases and 10 770 controls in this study. Our large well-powered study (98% to detect odds ratio = 1.5, with respect to rs360719) showed that no individual SNP or haplotype was associated with SLE in any of the cohorts studied. We conclude that we were unable to replicate the SLE association with rs360719 located upstream of IL18. No evidence for association with any other common variant at IL18 with SLE was found