The Grow-Shrink strategy for learning Markov network structures constrained by context-specific independences

Markov networks are models for compactly representing complex probability distributions. They are composed by a structure and a set of numerical weights. The structure qualitatively describes independences in the distribution, which can be exploited to factorize the distribution into a set of compact functions. A key application for learning structures from data is to automatically discover knowledge. In practice, structure learning algorithms focused on "knowledge discovery" present a limitation: they use a coarse-grained representation of the structure. As a result, this representation cannot describe context-specific independences. Very recently, an algorithm called CSPC was designed to overcome this limitation, but it has a high computational complexity. This work tries to mitigate this downside presenting CSGS, an algorithm that uses the Grow-Shrink strategy for reducing unnecessary computations. On an empirical evaluation, the structures learned by CSGS achieve competitive accuracies and lower computational complexity with respect to those obtained by CSPC.Comment: 12 pages, and 8 figures. This works was presented in IBERAMIA 201

Beyond the Spin Model Approximation for Ramsey Spectroscopy

Ramsey spectroscopy has become a powerful technique for probing non-equilibrium dynamics of internal (pseudospin) degrees of freedom of interacting systems. In many theoretical treatments, the key to understanding the dynamics has been to assume the external (motional) degrees of freedom are decoupled from the pseudospin degrees of freedom. Determining the validity of this approximation -- known as the spin model approximation -- is complicated, and has not been addressed in detail. Here we shed light in this direction by calculating Ramsey dynamics exactly for two interacting spin-1/2 particles in a harmonic trap. We focus on $s$-wave-interacting fermions in quasi-one and two-dimensional geometries. We find that in 1D the spin model assumption works well over a wide range of experimentally-relevant conditions, but can fail at time scales longer than those set by the mean interaction energy. Surprisingly, in 2D a modified version of the spin model is exact to first order in the interaction strength. This analysis is important for a correct interpretation of Ramsey spectroscopy and has broad applications ranging from precision measurements to quantum information and to fundamental probes of many-body systems

Bald Eagles at the Savanna Army Depot

Eagle Valley Environmentalists Technical Report #SADE-81, Research Report conducted December 1980 - March 1981, under a contract with the United States Arm

First- and Second Order Phase Transitions in the Holstein-Hubbard Model

We investigate metal-insulator transitions in the Holstein-Hubbard model as a function of the on-site electron-electron interaction U and the electron-phonon coupling g. We use several different numerical methods to calculate the phase diagram, the results of which are in excellent agreement. When the electron-electron interaction U is dominant the transition is to a Mott-insulator; when the electron-phonon interaction dominates, the transition is to a localised bipolaronic state. In the former case, the transition is always found to be second order. This is in contrast to the transition to the bipolaronic state, which is clearly first order for larger values of U. We also present results for the quasiparticle weight and the double-occupancy as function of U and g.Comment: 6 pages, 5 figure

Dynamic response functions for the Holstein-Hubbard model

We present results on the dynamical correlation functions of the particle-hole symmetric Holstein-Hubbard model at zero temperature, calculated using the dynamical mean field theory which is solved by the numerical renormalization group method. We clarify the competing influences of the electron-electron and electron-phonon interactions particularity at the different metal to insulator transitions. The Coulomb repulsion is found to dominate the behaviour in large parts of the metallic regime. By suppressing charge fluctuations, it effectively decouples electrons from phonons. The phonon propagator shows a characteristic softening near the metal to bipolaronic transition but there is very little softening on the approach to the Mott transition.Comment: 13 pages, 19 figure

IMPAIRED NITRIC OXIDE-MEDIATED FLOW-INDUCED DILATION IN ARTERIOLES OF SPONTANEOUSLY HYPERTENSIVE RATS

We tested the hypothesis that impairment of flow-dependent dilator mechanisms of skeletal muscle arterioles is one of the underlying reasons for the increased peripheral resistance in hypertension. Isolated, cannulated arterioles (approximate to 55 mu m) of gracilis muscle of 12-week-old spontaneously hypertensive (SH) and normotensive Wistar (NW) rats were investigated. At a constant perfusion pressure (80 mm Hg), the active diameters of NW and SH arterioles were 57.7+/-1.9 and 51.5+/-3.2 mu m, whereas their passive diameters (Ca2+-free solution) were 113.6+/-2.9 and 101.7+/-2.9 mu m, respectively. Flow-induced dilation was elicited by increases in flow of the perfusion solution from 0 to 25 mu L/min in 5-mu L/min steps. This response was significantly less in arterioles of SH compared with NW rats. For example, at 25-mu L/min flow, the diameter of arterioles of SH rats was approximate to 56% less (P<.05) than those of NW rats. Indomethacin, an inhibitor of prostaglandin synthesis, significantly attenuated the flow-diameter curve in both strains of rats. In contrast, N-Omega-nitro-L-arginine, a nitric oxide synthase inhibitor, significantly shifted the flow-diameter curve to the right in NW rats, but it did not affect the flow-diameter curve in SH rats. Thus, the present findings demonstrate that in gracilis muscle arterioles of normotensive rats in response to increases in flow (shear stress), prostaglandins and nitric oxide are coreleased, resulting in a dilation. In early hypertension, however, there is a reduced arteriolar dilation to increases in flow that is due to the impairment of the nitric oxide-mediated portion of the flow-dependent arteriolar dilation. (Circ Res. 1994;74:416-421.