Phase diagrams of the 2D t-t'-U Hubbard model from an extended mean field method

It is well-known from unrestricted Hartree-Fock computations that the 2D Hubbard model does not have homogeneous mean field states in significant regions of parameter space away from half filling. This is incompatible with standard mean field theory. We present a simple extension of the mean field method that avoids this problem. As in standard mean field theory, we restrict Hartree-Fock theory to simple translation invariant states describing antiferromagnetism (AF), ferromagnetism (F) and paramagnetism (P), but we use an improved method to implement the doping constraint allowing us to detect when a phase separated state is energetically preferred, e.g. AF and F coexisting at the same time. We find that such mixed phases occur in significant parts of the phase diagrams, making them much richer than the ones from standard mean field theory. Our results for the 2D t-t'-U Hubbard model demonstrate the importance of band structure effects.Comment: 6 pages, 5 figure

The interplay between double exchange, super-exchange, and Lifshitz localization in doped manganites

Considering the disorder caused in manganites by the substitution of Mn by Fe or Ga, we accomplish a systematic study of doped manganites begun in previous papers. To this end, a disordered model is formulated and solved using the Variational Mean Field technique. The subtle interplay between double exchange, super-exchange, and disorder causes similar effects on the dependence of T_C on the percentage of Mn substitution in the cases considered. Yet, in La$_{2/3}$Ca$_{1/3}$Mn$_{1-y}$Ga$_y$O$_3$ our results suggest a quantum critical point (QCP) for $y\approx 0.1-0.2$, associated to the localization of the electronic states of the conduction band. In the case of La$_x$Ca$_x$Mn$_{1-y}$Fe$_y$O$_3$ (with $x=1/3,3/8$) no such QCP is expected.Comment: 6 pages + 3 postscript figures. Largely extended discussio

Localization length in a random magnetic field

Kubo formula is used to get the d.c conductance of a statistical ensemble of two dimensional clusters of the square lattice in the presence of random magnetic fluxes. Fluxes traversing lattice plaquettes are distributed uniformly between minus one half and plus one half of the flux quantum. The localization length is obtained from the exponential decay of the averaged conductance as a function of the cluster side. Standard results are recovered when this numerical approach is applied to Anderson model of diagonal disorder. The localization length of the complex non-diagonal model of disorder remains well below 10 000 (in units of the lattice constant) in the main part of the band in spite of its exponential increase near the band edges.Comment: 12 two-column pages including 10 figures (epsfig), revtex, to appear in PR

Superconductivity of a Metallic Stripe Embedded in an Antiferromagnet

We study a simple model for the metallic stripes found in $La_{1.6-x}Nd_{0.4}Sr_xCuO_4$: two chain Hubbard ladder embedded in a static antiferromagnetic environments. We consider two cases: a ``topological stripe'', for which the phase of the Neel order parameter shifts by $\pi$ across the ladder, and a ``non-topological stripe'', for which there is no phase shift across the ladder. We perform one-loop renormalization group calculations to determine the low energy properties. We compare the results with those of the isolated ladder and show that for small doping superconductivity is enhanced in the topological stripe, and suppressed in the non-topological one. In the topological stripe, the superconducting order parameter is a mixture of a spin singlet component with zero momentum and a spin triplet component with momentum $\pi$. We argue that this mixture is generic, and is due to the presence of a new term in the quantum Ginzburg-Landau action. Some consequences of this mixing are discussed.Comment: 6 pages, 3 eps figure

Constrained-path quantum Monte Carlo simulations of the zero-temperature disordered two-dimensional Hubbard model

We study the effects of disorder on long-range antiferromagnetic correlations in the half-filled, two dimensional, repulsive Hubbard model at T=0. A mean field approach is first employed to gain a qualitative picture of the physics and to guide our choice for a trial wave function in a constrained path quantum Monte Carlo (CPQMC) method that allows for a more accurate treatment of correlations. Within the mean field calculation, we observe both Anderson and Mott insulating antiferromagnetic phases. There are transitions to a paramagnet only for relatively weak coupling, U < 2t in the case of bond disorder, and U < 4t in the case of on-site disorder. Using ground-state CPQMC we demonstrate that this mean field approach significantly overestimates magnetic order. For U=4t, we find a critical bond disorder of Vc = (1.6 +- 0.4)t even though within mean field theory no paramagnetic phase is found for this value of the interaction. In the site disordered case, we find a critical disorder of Vc = (5.0 +- 0.5)t at U=4t.Comment: Revtex, 13 pages, 15 figures. Minor changes to title and abstract, discussion and references added, figures 5, 6, 8, 9 replaced with easier to read version

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 $\omega < T$ 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

Levodopa-Induced Dyskinesia Is Associated with Increased Thyrotropin Releasing Hormone in the Dorsal Striatum of Hemi-Parkinsonian Rats

Background Dyskinesias associated with involuntary movements and painful muscle contractions are a common and severe complication of standard levodopa (L-DOPA, L-3,4-dihydroxyphenylalanine) therapy for Parkinson's disease. Pathologic neuroplasticity leading to hyper-responsive dopamine receptor signaling in the sensorimotor striatum is thought to underlie this currently untreatable condition. Methodology/Principal Findings Quantitative real-time polymerase chain reaction (PCR) was employed to evaluate the molecular changes associated with L-DOPA-induced dyskinesias in Parkinson's disease. With this technique, we determined that thyrotropin releasing hormone (TRH) was greatly increased in the dopamine-depleted striatum of hemi-parkinsonian rats that developed abnormal movements in response to L-DOPA therapy, relative to the levels measured in the contralateral non-dopamine-depleted striatum, and in the striatum of non-dyskinetic control rats. ProTRH immunostaining suggested that TRH peptide levels were almost absent in the dopamine-depleted striatum of control rats that did not develop dyskinesias, but in the dyskinetic rats, proTRH immunostaining was dramatically up-regulated in the striatum, particularly in the sensorimotor striatum. This up-regulation of TRH peptide affected striatal medium spiny neurons of both the direct and indirect pathways, as well as neurons in striosomes. Conclusions/Significance TRH is not known to be a key striatal neuromodulator, but intrastriatal injection of TRH in experimental animals can induce abnormal movements, apparently through increasing dopamine release. Our finding of a dramatic and selective up-regulation of TRH expression in the sensorimotor striatum of dyskinetic rat models suggests a TRH-mediated regulatory mechanism that may underlie the pathologic neuroplasticity driving dopamine hyper-responsivity in Parkinson's disease.Morris K. Udall Center for Excellence in Parkinson’s Research at MGH/MITNational Institutes of Health (U.S.) (NIH NS38372)American Parkinson Disease Association, Inc.University of Alabama at BirminghamMassachusetts General HospitalNational Institute of Diabetes and Digestive and Kidney Diseases (U.S.) (NIDDK/NIH grant R01 DK58148)National Institute of Neurological Disorders and Stroke (U.S.) (R01 NINDS/NIH grant NS045231)Stanley H. and Sheila G. Sydney FundMichael J. Fox Foundation for Parkinson's Researc

Advances in the treatment of prolactinomas

Prolactinomas account for approximately 40% of all pituitary adenomas and are an important cause of hypogonadism and infertility. The ultimate goal of therapy for prolactinomas is restoration or achievement of eugonadism through the normalization of hyperprolactinemia and control of tumor mass. Medical therapy with dopamine agonists is highly effective in the majority of cases and represents the mainstay of therapy. Recent data indicating successful withdrawal of these agents in a subset of patients challenge the previously held concept that medical therapy is a lifelong requirement. Complicated situations, such as those encountered in resistance to dopamine agonists, pregnancy, and giant or malignant prolactinomas, may require multimodal therapy involving surgery, radiotherapy, or both. Progress in elucidating the mechanisms underlying the pathogenesis of prolactinomas may enable future development of novel molecular therapies for treatment-resistant cases. This review provides a critical analysis of the efficacy and safety of the various modes of therapy available for the treatment of patients with prolactinomas with an emphasis on challenging situations, a discussion of the data regarding withdrawal of medical therapy, and a foreshadowing of novel approaches to therapy that may become available in the future

Genome-wide association meta-analysis identifies risk loci for abdominal aortic aneurysm and highlights PCSK9 as a therapeutic target

Abdominal aortic aneurysm (AAA) is a common disease with substantial heritability. In this study, we performed a genome-wide association meta-analysis from 14 discovery cohorts and uncovered 141 independent associations, including 97 previously unreported loci. A polygenic risk score derived from meta-analysis explained AAA risk beyond clinical risk factors. Genes at AAA risk loci indicate involvement of lipid metabolism, vascular development and remodeling, extracellular matrix dysregulation and inflammation as key mechanisms in AAA pathogenesis. These genes also indicate overlap between the development of AAA and other monogenic aortopathies, particularly via transforming growth factor β signaling. Motivated by the strong evidence for the role of lipid metabolism in AAA, we used Mendelian randomization to establish the central role of nonhigh-density lipoprotein cholesterol in AAA and identified the opportunity for repurposing of proprotein convertase, subtilisin/kexin-type 9 (PCSK9) inhibitors. This was supported by a study demonstrating that PCSK9 loss of function prevented the development of AAA in a preclinical mouse model.</p

Inter-Allelic Prion Propagation Reveals Conformational Relationships among a Multitude of [PSI] Strains

Immense diversity of prion strains is observed, but its underlying mechanism is less clear. Three [PSI] prion strains—named VH, VK, and VL—were previously isolated in the wild-type yeast genetic background. Here we report the generation and characterization of eight new [PSI] isolates, obtained by propagating the wild-type strains with Sup35 proteins containing single amino-acid alterations. The VH strain splits into two distinct strains when propagated in each of the three genetic backgrounds, harboring respectively single mutations of N21L, R28P, and Gi47 (i.e. insertion of a glycine residue at position 47) on the Sup35 N-terminal prion-forming segment. The six new strains exhibit complex inter-conversion patterns, and one of them continuously mutates into another. However, when they are introduced back into the wild-type background, all 6 strains revert to the VH strain. We obtain two more [PSI] isolates by propagating VK and VL with the Gi47 and N21L backgrounds, respectively. The two isolates do not transmit to other mutant backgrounds but revert to their parental strains in the wild-type background. Our data indicate that a large number of [PSI] strains can be built on three basic Sup35 amyloid structures. It is proposed that the three basic structures differ by chain folding topologies, and sub-strains with the same topology differ in distinct ways by local structural adjustments. This “large number of variations on a small number of basic themes” may also be operative in generating strain diversities in other prion elements. It thus suggests a possible general scheme to classify a multitude of prion strains