Applying matrix product operators to model systems with long-range interactions

An algorithm is presented which computes a translationally invariant matrix product state approximation of the ground state of an infinite 1D system; it does this by embedding sites into an approximation of the infinite ``environment'' of the chain, allowing the sites to relax, and then merging them with the environment in order to refine the approximation. By making use of matrix product operators, our approach is able to directly model any long-range interaction that can be systematically approximated by a series of decaying exponentials. We apply our techniques to compute the ground state of the Haldane-Shastry model and present results.Comment: 7 pages, 3 figures; manuscript has been expanded and restructured in order to improve presentation of the algorith

Finite automata for caching in matrix product algorithms

A diagram is introduced for visualizing matrix product states which makes transparent a connection between matrix product factorizations of states and operators, and complex weighted finite state automata. It is then shown how one can proceed in the opposite direction: writing an automaton that ``generates'' an operator gives one an immediate matrix product factorization of it. Matrix product factorizations have the advantage of reducing the cost of computing expectation values by facilitating caching of intermediate calculations. Thus our connection to complex weighted finite state automata yields insight into what allows for efficient caching in matrix product algorithms. Finally, these techniques are generalized to the case of multiple dimensions.Comment: 18 pages, 19 figures, LaTeX; numerous improvements have been made to the manuscript in response to referee feedbac

Sparse Quantum Codes from Quantum Circuits

Sparse quantum codes are analogous to LDPC codes in that their check operators require examining only a constant number of qubits. In contrast to LDPC codes, good sparse quantum codes are not known, and even to encode a single qubit, the best known distance is O(√n log(n)), due to Freedman, Meyer and Luo. We construct a new family of sparse quantum subsystem codes with minimum distance n[superscript 1 - ε] for ε = O(1/√log n). A variant of these codes exists in D spatial dimensions and has d = n[superscript 1 - ε - 1/D], nearly saturating a bound due to Bravyi and Terhal. Our construction is based on a new general method for turning quantum circuits into sparse quantum subsystem codes. Using this prescription, we can map an arbitrary stabilizer code into a new subsystem code with the same distance and number of encoded qubits but where all the generators have constant weight, at the cost of adding some ancilla qubits. With an additional overhead of ancilla qubits, the new code can also be made spatially local.National Science Foundation (U.S.) (Grant CCF-1111382)United States. Army Research Office (Contract W911NF-12-1-0486

Entanglement Perturbation Theory for Antiferromagnetic Heisenberg Spin Chains

A recently developed numerical method, entanglement perturbation theory (EPT), is used to study the antiferromagnetic Heisenberg spin chains with z-axis anisotropy $\lambda$ and magnetic field B. To demonstrate the accuracy, we first apply EPT to the isotropic spin-1/2 antiferromagnetic Heisenberg model, and find that EPT successfully reproduces the exact Bethe Ansatz results for the ground state energy, the local magnetization, and the spin correlation functions (Bethe ansatz result is available for the first 7 lattice separations). In particular, EPT confirms for the first time the asymptotic behavior of the spin correlation functions predicted by the conformal field theory, which realizes only for lattice separations larger than 1000. Next, turning on the z-axis anisotropy and the magnetic field, the 2-spin and 4-spin correlation functions are calculated, and the results are compared with those obtained by Bosonization and density matrix renormalization group methods. Finally, for the spin-1 antiferromagnetic Heisenberg model, the ground state phase diagram in $\lambda$ space is determined with help of the Roomany-Wyld RG finite-size-scaling. The results are in good agreement with those obtained by the level-spectroscopy method.Comment: 12 pages, 14 figure

Protective effects of hydrogen-rich saline on monocrotaline-induced pulmonary hypertension in a rat model

<p>Abstract</p> <p>Background</p> <p>Hydrogen-rich saline has been reported to have antioxidant and anti-inflammatory effects and effectively protect against organ damage. Oxidative stress and inflammation contribute to the pathogenesis and/or development of pulmonary hypertension. In this study, we investigated the effects of hydrogen-rich saline on the prevention of pulmonary hypertension induced by monocrotaline in a rat model.</p> <p>Methods</p> <p>In male Sprague-Dawley rats, pulmonary hypertension was induced by subcutaneous administration of monocrotaline at a concentration of 6 mg/100 g body weight. Hydrogen-rich saline (5 ml/kg) or saline was administred intraperitoneally once daily for 2 or 3 weeks. Severity of pulmonary hypertension was assessed by hemodynamic index and histologic analysis. Malondialdehyde and 8-hydroxy-desoxyguanosine level, and superoxide dismutase activity were measured in the lung tissue and serum. Levels of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6) in serum were determined with enzyme-linked immunosorbent assay.</p> <p>Results</p> <p>Hydrogen-rich saline treatment improved hemodynamics and reversed right ventricular hypertrophy. It also decreased malondialdehyde and 8-hydroxy-desoxyguanosine levels, and increased superoxide dismutase activity in the lung tissue and serum, accompanied by a decrease in pro-inflammatory cytokines.</p> <p>Conclusions</p> <p>These results suggest that hydrogen-rich saline ameliorates the progression of pulmonary hypertension induced by monocrotaline in rats, which may be associated with its antioxidant and anti-inflammatory effects.</p

Cold and Ultracold Rydberg Atoms in Strong Magnetic Fields

Cold Rydberg atoms exposed to strong magnetic fields possess unique properties which open the pathway for an intriguing many-body dynamics taking place in Rydberg gases consisting of either matter or anti-matter systems. We review both the foundations and recent developments of the field in the cold and ultracold regime where trapping and cooling of Rydberg atoms have become possible. Exotic states of moving Rydberg atoms such as giant dipole states are discussed in detail, including their formation mechanisms in a strongly magnetized cold plasma. Inhomogeneous field configurations influence the electronic structure of Rydberg atoms, and we describe the utility of corresponding effects for achieving tightly trapped ultracold Rydberg atoms. We review recent work on large, extended cold Rydberg gases in magnetic fields and their formation in strongly magnetized ultracold plasmas through collisional recombination. Implications of these results for current antihydrogen production experiments are pointed out, and techniques for trapping and cooling of such atoms are investigated.Comment: 46 pages, 38 figures, to appear in Physics Report

Involvement of mast cells in monocrotaline-induced pulmonary hypertension in rats

Background: Mast cells (MCs) are implicated in inflammation and tissue remodeling. Accumulation of lung MCs is described in pulmonary hypertension (PH); however, whether MC degranulation and c-kit, a tyrosine kinase receptor critically involved in MC biology, contribute to the pathogenesis and progression of PH has not been fully explored.Methods: Pulmonary MCs of idiopathic pulmonary arterial hypertension (IPAH) patients and monocrotaline-injected rats (MCT-rats) were examined by histochemistry and morphometry. Effects of the specific c-kit inhibitor PLX and MC stabilizer cromolyn sodium salt (CSS) were investigated in MCT-rats both by the preventive and therapeutic approaches. Hemodynamic and right ventricular hypertrophy measurements, pulmonary vascular morphometry and analysis of pulmonary MC localization/counts/activation were performed in animal model studies.Results: There was a prevalence of pulmonary MCs in IPAH patients and MCT-rats as compared to the donors and healthy rats, respectively. Notably, the perivascular MCs were increased and a majority of them were degranulated in lungs of IPAH patients and MCT-rats (p < 0.05 versus donor and control, respectively). In MCT-rats, the pharmacological inhibitions of MC degranulation and c-kit with CSS and PLX, respectively by a preventive approach (treatment from day 1 to 21 of MCT-injection) significantly attenuated right ventricular systolic pressure (RVSP) and right ventricular hypertrophy (RVH). Moreover, vascular remodeling, as evident from the significantly decreased muscularization and medial wall thickness of distal pulmonary vessels, was improved. However, treatments with CSS and PLX by a therapeutic approach (from day 21 to 35 of MCT-injection) neither improved hemodynamics and RVH nor vascular remodeling.Conclusions: The accumulation and activation of perivascular MCs in the lungs are the histopathological features present in clinical (IPAH patients) and experimental (MCT-rats) PH. Moreover, the accumulation and activation of MCs in the lungs contribute to the development of PH in MCT-rats. Our findings reveal an important pathophysiological insight into the role of MCs in the pathogenesis of PH in MCT- rats

Chronic Allergic Inflammation Causes Vascular Remodeling and Pulmonary Hypertension in Bmpr2 Hypomorph and Wild-Type Mice

Loss-of-function mutations in the bone morphogenetic protein receptor type 2 (BMPR2) gene have been identified in patients with heritable pulmonary arterial hypertension (PAH); however, disease penetrance is low, suggesting additional factors play a role. Inflammation is associated with PAH and vascular remodeling, but whether allergic inflammation triggers vascular remodeling in individuals with BMPR2 mutations is unknown. Our goal was to determine if chronic allergic inflammation would induce more severe vascular remodeling and PAH in mice with reduced BMPR-II signaling. Groups of Bmpr2 hypomorph and wild-type (WT) Balb/c/Byj mice were exposed to house dust mite (HDM) allergen, intranasally for 7 or 20 weeks to generate a model of chronic inflammation. HDM exposure induced similar inflammatory cell counts in all groups compared to controls. Muscularization of pulmonary arterioles and arterial wall thickness were increased after 7 weeks HDM, more severe at 20 weeks, but similar in both groups. Right ventricular systolic pressure (RVSP) was measured by direct cardiac catheterization to assess PAH. RVSP was similarly increased in both HDM exposed groups after 20 weeks compared to controls, but not after 7 weeks. Airway hyperreactivity (AHR) to methacholine was also assessed and interestingly, at 20 weeks, was more severe in HDM exposed Bmpr2 hypomorph mice versus WT. We conclude that chronic allergic inflammation caused PAH and while the severity was mild and similar between WT and Bmpr2 hypomorph mice, AHR was enhanced with reduced BMPR-II signaling. These data suggest that vascular remodeling and PAH resulting from chronic allergic inflammation occurs independently of BMPR-II pathway alterations