5,668 research outputs found
Magnetic and pair correlations of the Hubbard model with next-nearest-neighbor hopping
A combination of analytical approaches and quantum Monte Carlo simulations is
used to study both magnetic and pairing correlations for a version of the
Hubbard model that includes second-neighbor hopping as a
model for high-temperature superconductors. Magnetic properties are analyzed
using the Two-Particle Self-Consistent approach. The maximum in magnetic
susceptibility as a function of doping appears both at finite
and at but for two totally different physical reasons. When
, it is induced by antiferromagnetic correlations while at
it is a band structure effect amplified by interactions.
Finally, pairing fluctuations are compared with -matrix results to
disentangle the effects of van Hove singularity and of nesting on
superconducting correlations. The addition of antiferromagnetic fluctuations
increases slightly the -wave superconducting correlations despite the
presence of a van Hove singularity which tends to decrease them in the
repulsive model. Some aspects of the phase diagram and some subtleties of
finite-size scaling in Monte Carlo simulations, such as inverted finite-size
dependence, are also discussed.Comment: Revtex, 8 pages + 15 uuencoded postcript figure
Magnetic properties of the three-dimensional Hubbard model at half filling
We study the magnetic properties of the 3d Hubbard model at half-filling in
the TPSC formalism, previously developed for the 2d model. We focus on the
N\'eel transition approached from the disordered side and on the paramagnetic
phase. We find a very good quantitative agreement with Dynamical Mean-Field
results for the isotropic 3d model. Calculations on finite size lattices also
provide satisfactory comparisons with Monte Carlo results up to the
intermediate coupling regime. We point out a qualitative difference between the
isotropic 3d case, and the 2d or anisotropic 3d cases for the double occupation
factor. Even for this local correlation function, 2d or anisotropic 3d cases
are out of reach of DMF: this comes from the inability of DMF to account for
antiferromagnetic fluctuations, which are crucial.Comment: RevTex, 9 pages +10 figure
Tailoring Anderson localization by disorder correlations in 1D speckle potentials
We study Anderson localization of single particles in continuous, correlated,
one-dimensional disordered potentials. We show that tailored correlations can
completely change the energy-dependence of the localization length. By
considering two suitable models of disorder, we explicitly show that disorder
correlations can lead to a nonmonotonic behavior of the localization length
versus energy. Numerical calculations performed within the transfer-matrix
approach and analytical calculations performed within the phase formalism up to
order three show excellent agreement and demonstrate the effect. We finally
show how the nonmonotonic behavior of the localization length with energy can
be observed using expanding ultracold-atom gases
Gynecologic Oncologist Views Influencing Referral to Outpatient Specialty Palliative Care
Early specialty palliative care is underutilized for patients with advanced gynecologic malignancies. We sought to understand how gynecologic oncologistsβ views influence outpatient specialty palliative care referral to help inform strategies for improvement
Erratum to βCirculating Levels of MicroRNA from Children with Newly Diagnosed Type 1 Diabetes and Healthy Controls: Evidence That miR-25 Associates to Residual Beta-Cell Function and Glycaemic Control during Disease Progressionβ
Pairing fluctuations and pseudogaps in the attractive Hubbard model
The two-dimensional attractive Hubbard model is studied in the weak to
intermediate coupling regime by employing a non-perturbative approach. It is
first shown that this approach is in quantitative agreement with Monte Carlo
calculations for both single-particle and two-particle quantities. Both the
density of states and the single-particle spectral weight show a pseudogap at
the Fermi energy below some characteristic temperature T*, also in good
agreement with quantum Monte Carlo calculations. The pseudogap is caused by
critical pairing fluctuations in the low-temperature renormalized classical
regime of the two-dimensional system. With increasing temperature
the spectral weight fills in the pseudogap instead of closing it and the
pseudogap appears earlier in the density of states than in the spectral
function. Small temperature changes around T* can modify the spectral weight
over frequency scales much larger than temperature. Several qualitative results
for the s-wave case should remain true for d-wave superconductors.Comment: 20 pages, 12 figure
Exciton Spin Dynamics in Semiconductor Quantum Wells
In this paper we will review Exciton Spin Dynamics in Semiconductor Quantum
Wells. The spin properties of excitons in nanostructures are determined by
their fine structure. We will mainly focus in this review on GaAs and InGaAs
quantum wells which are model systems.Comment: 55 pages, 27 figure
Bone Morphogenetic Protein 9 Protects against Neonatal Hyperoxia-Induced Impairment of Alveolarization and Pulmonary Inflammation.
Aim: Effective treatment of premature infants with bronchopulmonary dysplasia (BPD) is lacking. We hypothesize that bone morphogenetic protein 9 (BMP9), a ligand of the TGF-Ξ² family that binds to the activin receptor-like kinase 1 (ALK1)-BMP receptor type 2 (BMPR2) receptor complex, may be a novel therapeutic option for BPD. Therefore, we investigated the cardiopulmonary effects of BMP9 in neonatal Wistar rats with hyperoxia-induced BPD. Methods: Directly after birth Wistar rat pups were exposed to 100% oxygen for 10 days. From day 2 rat pups received BMP9 (2.5 ΞΌg/kg, twice a day) or 0.9% NaCl by subcutaneous injection. Beneficial effects of BMP9 on aberrant alveolar development, lung inflammation and fibrosis, and right ventricular hypertrophy (RVH) were investigated by morphometric analysis and cytokine production. In addition, differential mRNA expression of BMP9 and its receptor complex: ALK1, BMPR2, and Endoglin, and of the ALK1 downstream target transmembrane protein 100 (TMEM100) were studied during the development of experimental BPD. Expression of the BMP9 receptor complex and TMEM100 was studied in human endothelial and epithelial cell cultures and the effect of BMP9 on inflammatory cytokine production and TMEM100 expression was studied in endothelial cell cultures. Results:ALK1, ALK2, BMPRII, TMEM100, and Endoglin were differentially expressed in experimental BPD, suggesting a role for BMP9-dependent signaling in the development of (experimental) BPD. TMEM100 was expressed in the wall of blood vessels, showing an elastin-like expression pattern in arterioles. Expression of TMEM100 mRNA and protein was decreased after exposure to hyperoxia. BMP9 treatment of rat pups with hyperoxia-induced experimental BPD reduced alveolar enlargement, lung septal thickness and fibrosis, and prevented inflammation, but did not attenuate vascular remodeling and RVH. The anti-inflammatory effect of BMP9 was confirmed in vitro. Highest expression of ALK1, BMPR2, and TMEM100 was observed in human endothelial cell cultures. Stimulation of human endothelial cell cultures with BMP9 reduced their pro-inflammatory cytokine response and induced TMEM100 expression in pulmonary arterial endothelial cells. Conclusion: BMP9 protects against neonatal hyperoxia-induced BPD by improving aberrant alveolar development, inflammation and fibrosis, demonstrating its therapeutic potential for premature infants with severe BPD
Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline
The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable genetic elements, particularly retrotransposons. There are many different types of retrotransposon in mammalian genomes, and these target different points in germline development to amplify and integrate into new genomic locations. Germ cells, and their pluripotent developmental precursors, have evolved a variety of genome defence mechanisms that suppress retrotransposon activity and maintain genome stability across the generations. Here, we review recent advances in understanding how retrotransposon activity is suppressed in the mammalian germline, how genes involved in germline genome defence mechanisms are regulated, and the consequences of mutating these genome defence genes for the developing germline
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