Habitat Characteristics and Nesting Ecology of Golden Eagles in Arizona

Golden Eagles (Aquila chrysaetos) have a broad range globally and in general are well-studied. However, Arizona’s Golden Eagle population remained essentially unstudied until 2011, when Arizona Game and Fish Department (AZGFD) began nest surveys for cliff nesting Golden Eagles throughout the state. As a result of this data collection, the natural history of Arizona’s Golden Eagles is finally revealing itself. This dissertation outlined a reliable description of their nesting phenology that provides a framework for timing surveys and a baseline to monitor the effects of climate change on Golden Eagles. The mean date for egg-laying was February 14 and pairs nesting in the high desert initiate nesting about ten days later than their southern counterparts. A brief study collecting prey remains determined that Black-tailed Jack Rabbit (Lepus californicus) was the central prey species for Golden Eagles in northern Arizona. The results of a multiscale habitat suitability model (HSM) determined that slope between 18º-28º was the most important habitat characteristics for Golden Eagles and the sagebrush landcover was the least important. The multiscale productivity prediction model did not predict with high accuracy; however, the results did reveal some data gaps and provided guidance for adjustments in the future. The results of this entire dissertation can guide future research priorities for Golden Eagles in Arizona. For example, more research on Golden Eagle prey dynamics is needed to determine the impact prey have on their nesting success. Additional research should focus on adding human impact factors such as recreational activity or elemental mining as possible factors that negatively influence nesting productivity. Finally, quantifying climate features on a finer temporal scale should be considered and continued nest site data collection will increase the sample size for more informative results

Controlling chaos in spatially extended beam-plasma system by the continuous delayed feedback

In present paper we discuss the control of complex spatio-temporal dynamics in a {spatially extended} non-linear system (fluid model of Pierce diode) based on the concepts of controlling chaos in the systems with few degrees of freedom. A presented method is connected with stabilization of unstable homogeneous equilibrium state and the unstable spatio-temporal periodical states analogous to unstable periodic orbits of chaotic dynamics of the systems with few degrees of freedom. We show that this method is effective and allows to achieve desired regular dynamics chosen from a number of possible in the considered system.Comment: 12 pages, 12 figure

Structural and Magnetic Properties of [(CH₃)₃NH] CuCl₃2H₂O

The crystal structure at room temperature and the low-temperature heat capacity and magnetic susceptibilities of single crystals of [(CH3)3 NH]CuCl3 2H2O are reported. The monoclinic crystals belong to the space group P21c with a=7.479(10), b=7.864(11), c=16.730(23), =91.98(3)°, and Z=4. The structure consists of chains of edge-sharing [CuCl4(OH2)2] octahedra running along the a axis. Each copper atom is coordinated in a square plane by two water molecules and two chlorine atoms, with two more chlorine atoms at a longer distance. The susceptibility data can be fitted adequately between 1.5 and 20°K by a CurieWeiss law [ga=2.080.01, gb=2.020.01; gc=2.110.01; a=(0.380.03)°K, b=(0.360.03)°K, c=(0.410.03)°K], but the susceptibility parallel to the chain can be better fitted as an Ising linear chain. Measurements perpendicular to the chain are not as well fitted by the Ising model. The heat capacity, which consists primarily of a lattice contribution above 3°K, begins to rise as the temperature falls below 3°K, but long-range order does not set in above 1°K, the lowest temperature attained in this work. Both Ising and Heisenberg linear-chain models fit the low-temperature data with |Jk| \u3c1°K. The results are compared with those reported for the compounds CuCl2 2H2O and CuCl2 2NC5H5. © 1972 The American Physical Society

Nonequilibrium Transport through a Kondo Dot in a Magnetic Field: Perturbation Theory

Using nonequilibrium perturbation theory, we investigate the nonlinear transport through a quantum dot in the Kondo regime in the presence of a magnetic field. We calculate the leading logarithmic corrections to the local magnetization and the differential conductance, which are characteristic of the Kondo effect out of equilibrium. By solving a quantum Boltzmann equation, we determine the nonequilibrium magnetization on the dot and show that the application of both a finite bias voltage and a magnetic field induces a novel structure of logarithmic corrections not present in equilibrium. These corrections lead to more pronounced features in the conductance, and their form calls for a modification of the perturbative renormalization group.Comment: 16 pages, 7 figure

A fractal set from the binary reflected Gray code

The permutation associated with the decimal expression of the binary reflected Gray code with N bits is considered. Its cycle structure is studied. Considered as a set of points, its self-similarity is pointed out. As a fractal, it is shown to be the attractor of an IFS. For large values of N the set is examined from the point of view of time series analysis

Kondo effect in quantum dots

We review mechanisms of low-temperature electronic transport through a quantum dot weakly coupled to two conducting leads. Transport in this case is dominated by electron-electron interaction. At temperatures moderately lower than the charging energy of the dot, the linear conductance is suppressed by the Coulomb blockade. Upon further lowering of the temperature, however, the conductance may start to increase again due to the Kondo effect. We concentrate on lateral quantum dot systems and discuss the conductance in a broad temperature range, which includes the Kondo regime

An antibiotic from an uncultured bacterium binds to an immutable target

Antimicrobial resistance is a leading mortality factor worldwide. Here, we report the discovery of clovibactin, an antibiotic isolated from uncultured soil bacteria. Clovibactin efficiently kills drug-resistant Gram-positive bacterial pathogens without detectable resistance. Using biochemical assays, solid-state nuclear magnetic resonance, and atomic force microscopy, we dissect its mode of action. Clovibactin blocks cell wall synthesis by targeting pyrophosphate of multiple essential peptidoglycan precursors (C 55PP, lipid II, and lipid III WTA). Clovibactin uses an unusual hydrophobic interface to tightly wrap around pyrophosphate but bypasses the variable structural elements of precursors, accounting for the lack of resistance. Selective and efficient target binding is achieved by the sequestration of precursors into supramolecular fibrils that only form on bacterial membranes that contain lipid-anchored pyrophosphate groups. This potent antibiotic holds the promise of enabling the design of improved therapeutics that kill bacterial pathogens without resistance development. </p

Comparison between clinical grading and navigation data of knee laxity in ACL-deficient knees

<p>Abstract</p> <p>Background</p> <p>The latest version of the navigation system for anterior cruciate ligament (ACL) reconstruction has the supplementary ability to assess knee stability before and after ACL reconstruction. In this study, we compared navigation data between clinical grades in ACL-deficient knees and also analyzed correlation between clinical grading and navigation data.</p> <p>Methods</p> <p>150 ACL deficient knees that received primary ACL reconstruction using an image-free navigation system were included. For clinical evaluation, the Lachman, anterior drawer, and pivot shift tests were performed under general anesthesia and were graded by an examiner. For the assessment of knee stability using the navigation system, manual tests were performed again before ACL reconstruction. Navigation data were recorded as anteroposterior (AP) displacement of the tibia for the Lachman and anterior drawer tests, and both AP displacement and tibial rotation for the pivot shift test.</p> <p>Results</p> <p>Navigation data of each clinical grade were as follows; Lachman test grade 1+: 10.0 mm, grade 2+: 13.2 ± 3.1 mm, grade 3+: 14.5 ± 3.3 mm, anterior drawer test grade 1+: 6.8 ± 1.4 mm, grade 2+: 7.4 ± 1.8 mm, grade 3+: 9.1 ± 2.3 mm, pivot shift test grade 1+: 3.9 ± 1.8 mm/21.5° ± 7.8°, grade 2+: 4.8 ± 2.1 mm/21.8° ± 7.1°, and grade 3+: 6.0 ± 3.2 mm/21.1° ± 7.1°. There were positive correlations between clinical grading and AP displacement in the Lachman, and anterior drawer tests. Although positive correlations between clinical grading and AP displacement in pivot shift test were found, there were no correlations between clinical grading and tibial rotation in pivot shift test.</p> <p>Conclusions</p> <p>In response to AP force, the navigation system can provide the surgeon with correct objective data for knee laxity in ACL deficient knees. During the pivot shift test, physicians may grade according to the displacement of the tibia, rather than rotation.</p

Teixobactin kills bacteria by a two-pronged attack on the cell envelope

Antibiotics that use novel mechanisms are needed to combat antimicrobial resistance1–3. Teixobactin4 represents a new class of antibiotics with a unique chemical scaffold and lack of detectable resistance. Teixobactin targets lipid II, a precursor of peptidoglycan5. Here we unravel the mechanism of teixobactin at the atomic level using a combination of solid-state NMR, microscopy, in vivo assays and molecular dynamics simulations. The unique enduracididine C-terminal headgroup of teixobactin specifically binds to the pyrophosphate-sugar moiety of lipid II, whereas the N terminus coordinates the pyrophosphate of another lipid II molecule. This configuration favours the formation of a β-sheet of teixobactins bound to the target, creating a supramolecular fibrillar structure. Specific binding to the conserved pyrophosphate-sugar moiety accounts for the lack of resistance to teixobactin4. The supramolecular structure compromises membrane integrity. Atomic force microscopy and molecular dynamics simulations show that the supramolecular structure displaces phospholipids, thinning the membrane. The long hydrophobic tails of lipid II concentrated within the supramolecular structure apparently contribute to membrane disruption. Teixobactin hijacks lipid II to help destroy the membrane. Known membrane-acting antibiotics also damage human cells, producing undesirable side effects. Teixobactin damages only membranes that contain lipid II, which is absent in eukaryotes, elegantly resolving the toxicity problem. The two-pronged action against cell wall synthesis and cytoplasmic membrane produces a highly effective compound targeting the bacterial cell envelope. Structural knowledge of the mechanism of teixobactin will enable the rational design of improved drug candidates