Identification of Boundary Conditions Using Natural Frequencies

The present investigation concerns a disc of varying thickness of whose flexural stiffness $D$ varies with the radius $r$ according to the law $D=D_0 r^m$, where $D_0$ and $m$ are constants. The problem of finding boundary conditions for fastening this disc, which are inaccessible to direct observation, from the natural frequencies of its axisymmetric flexural oscillations is considered. The problem in question belongs to the class of inverse problems and is a completely natural problem of identification of boundary conditions. The search for the unknown conditions for fastening the disc is equivalent to finding the span of the vectors of unknown conditions coefficients. It is shown that this inverse problem is well posed. Two theorems on the uniqueness and a theorem on stability of the solution of this problem are proved, and a method for establishing the unknown conditions for fastening the disc to the walls is indicated. An approximate formula for determining the unknown conditions is obtained using first three natural frequencies. The method of approximate calculation of unknown boundary conditions is explained with the help of three examples of different cases for the fastening the disc (rigid clamping, free support, elastic fixing). Keywords: Boundary conditions, a disc of varying thickness,inverse problem, Plucker condition.Comment: 19 page

Topological Entanglement Entropy of a Bose-Hubbard Spin Liquid

The Landau paradigm of classifying phases by broken symmetries was demonstrated to be incomplete when it was realized that different quantum Hall states could only be distinguished by more subtle, topological properties. Today, the role of topology as an underlying description of order has branched out to include topological band insulators, and certain featureless gapped Mott insulators with a topological degeneracy in the groundstate wavefunction. Despite intense focus, very few candidates for these topologically ordered "spin liquids" exist. The main difficulty in finding systems that harbour spin liquid states is the very fact that they violate the Landau paradigm, making conventional order parameters non-existent. Here, we uncover a spin liquid phase in a Bose-Hubbard model on the kagome lattice, and measure its topological order directly via the topological entanglement entropy. This is the first smoking-gun demonstration of a non-trivial spin liquid, identified through its entanglement entropy as a gapped groundstate with emergent Z2 gauge symmetry.Comment: 4+ pages, 3 figure

A Rydberg Quantum Simulator

Following Feynman and as elaborated on by Lloyd, a universal quantum simulator (QS) is a controlled quantum device which reproduces the dynamics of any other many particle quantum system with short range interactions. This dynamics can refer to both coherent Hamiltonian and dissipative open system evolution. We investigate how laser excited Rydberg atoms in large spacing optical or magnetic lattices can provide an efficient implementation of a universal QS for spin models involving (high order) n-body interactions. This includes the simulation of Hamiltonians of exotic spin models involving n-particle constraints such as the Kitaev toric code, color code, and lattice gauge theories with spin liquid phases. In addition, it provides the ingredients for dissipative preparation of entangled states based on engineering n-particle reservoir couplings. The key basic building blocks of our architecture are efficient and high-fidelity n-qubit entangling gates via auxiliary Rydberg atoms, including a possible dissipative time step via optical pumping. This allows to mimic the time evolution of the system by a sequence of fast, parallel and high-fidelity n-particle coherent and dissipative Rydberg gates.Comment: 8 pages, 4 figure

Endothelin receptor B antagonists decrease glioma cell viability independently of their cognate receptor

Background: Endothelin receptor antagonists inhibit the progression of many cancers, but research into their influence on glioma has been limited. Methods: We treated glioma cell lines, LN-229 and SW1088, and melanoma cell lines, A375 and WM35, with two endothelin receptor type B (ETRB)-specific antagonists, A-192621 and BQ788, and quantified viable cells by the capacity of their intracellular esterases to convert non-fluorescent calcein AM into green-fluorescent calcein. We assessed cell proliferation by labeling cells with carboxyfluorescein diacetate succinimidyl ester and quantifying the fluorescence by FACS analysis. We also examined the cell cycle status using BrdU/propidium iodide double staining and FACS analysis. We evaluated changes in gene expression by microarray analysis following treatment with A-192621 in glioma cells. We examined the role of ETRB by reducing its expression level using small interfering RNA (siRNA). Results: We report that two ETRB-specific antagonists, A-192621 and BQ788, reduce the number of viable cells in two glioma cell lines in a dose- and time-dependent manner. We describe similar results for two melanoma cell lines. The more potent of the two antagonists, A-192621, decreases the mean number of cell divisions at least in part by inducing a G2/M arrest and apoptosis. Microarray analysis of the effects of A-192621 treatment reveals up-regulation of several DNA damage-inducible genes. These results were confirmed by real-time RT-PCR. Importantly, reducing expression of ETRB with siRNAs does not abrogate the effects of either A-192621 or BQ788 in glioma or melanoma cells. Furthermore, BQ123, an endothelin receptor type A (ETRA)-specific antagonist, has no effect on cell viability in any of these cell lines, indicating that the ETRB-independent effects on cell viability exhibited by A-192621 and BQ788 are not a result of ETRA inhibition. Conclusion: While ETRB antagonists reduce the viability of glioma cells in vitro, it appears unlikely that this effect is mediated by ETRB inhibition or cross-reaction with ETRA. Instead, we present evidence that A-192621 affects glioma and melanoma viability by activating stress/DNA damage response pathways, which leads to cell cycle arrest and apoptosis. This is the first evidence linking ETRB antagonist treatment to enhanced expression of DNA damage-inducible genes

Virtual Compton Scattering off a Spinless Target in AdS/QCD

We study the doubly virtual Compton scattering off a spinless target $\gamma^*P\to\gamma^*P'$ within the Anti-de Sitter(AdS)/QCD formalism. We find that the general structure allowed by the Lorentz invariance and gauge invariance of the Compton amplitude is not easily reproduced with the standard recipes of the AdS/QCD correspondence. In the soft-photon regime, where the semi-classical approximation is supposed to apply best, we show that the measurements of the electric and magnetic polarizabilities of a target like the charged pion in real Compton scattering, can already serve as stringent tests.Comment: 21 pages, version to be published in JHEP

Heavy Flavour Production at Tevatron and Parton Shower Effects

We present hadron-level predictions from the Monte Carlo generator Cascade and numerical calculations of charm and beauty production at the Fermilab Tevatron within the framework of the $k_T$-factorization QCD approach. Our consideration is based on the CCFM-evolved unintegrated gluon densities in a proton. The performed analysis covers the total and differential cross sections of open charm and beauty quarks, $B$ and $D$ mesons (or rather muons from their semileptonic decays) and the total and differential cross sections of $b \bar b$ di-jet hadroproduction. We study the theoretical uncertainties of our calculations and investigate the effects coming from parton showers in initial and final states. Our predictions are compared with the recent experimental data taken by the D0 and CDF collaborations. Special attention is put on the specific angular correlations between the final-state particles. We demonstrate that the final state parton shower plays a crucial role in the description of such observables. The decorrelated part of angular separations can be fully described, if the process $gg^*\rightarrow gg$ is included.Comment: Fig 8,9 10 replaced, small corrections in text A discussion of the delta phi results is adde

Central Exclusive Production in QCD

We investigate the theoretical description of the central exclusive production process, h1+h2 -> h1+X+h2. Taking Higgs production as an example, we sum logarithmically enhanced corrections appearing in the perturbation series to all orders in the strong coupling. Our results agree with those originally presented by Khoze, Martin and Ryskin except that the scale appearing in the Sudakov factor, mu=0.62 \sqrt{\hat{s}}, should be replaced with mu=\sqrt{\hat{s}}, where \sqrt{\hat{s}} is the invariant mass of the centrally produced system. We confirm this result using a fixed-order calculation and show that the replacement leads to approximately a factor 2 suppression in the cross-section for central system masses in the range 100-500 GeV.Comment: 41 pages, 19 figures; minor typos fixed; version published in JHE

A Fokker-Planck formalism for diffusion with finite increments and absorbing boundaries

Gaussian white noise is frequently used to model fluctuations in physical systems. In Fokker-Planck theory, this leads to a vanishing probability density near the absorbing boundary of threshold models. Here we derive the boundary condition for the stationary density of a first-order stochastic differential equation for additive finite-grained Poisson noise and show that the response properties of threshold units are qualitatively altered. Applied to the integrate-and-fire neuron model, the response turns out to be instantaneous rather than exhibiting low-pass characteristics, highly non-linear, and asymmetric for excitation and inhibition. The novel mechanism is exhibited on the network level and is a generic property of pulse-coupled systems of threshold units.Comment: Consists of two parts: main article (3 figures) plus supplementary text (3 extra figures

Kinome rewiring reveals AURKA limits PI3K-pathway inhibitor efficacy in breast cancer.

Dysregulation of the PI3K-AKT-mTOR signaling network is a prominent feature of breast cancers. However, clinical responses to drugs targeting this pathway have been modest, possibly because of dynamic changes in cellular signaling that drive resistance and limit drug efficacy. Using a quantitative chemoproteomics approach, we mapped kinome dynamics in response to inhibitors of this pathway and identified signaling changes that correlate with drug sensitivity. Maintenance of AURKA after drug treatment was associated with resistance in breast cancer models. Incomplete inhibition of AURKA was a common source of therapy failure, and combinations of PI3K, AKT or mTOR inhibitors with the AURKA inhibitor MLN8237 were highly synergistic and durably suppressed mTOR signaling, resulting in apoptosis and tumor regression in vivo. This signaling map identifies survival factors whose presence limits the efficacy of targeted therapies and reveals new drug combinations that may unlock the full potential of PI3K-AKT-mTOR pathway inhibitors in breast cancer