Observation of a many-body dynamical phase transition with a 53-qubit quantum simulator.

A quantum simulator is a type of quantum computer that controls the interactions between quantum bits (or qubits) in a way that can be mapped to certain quantum many-body problems. As it becomes possible to exert more control over larger numbers of qubits, such simulators will be able to tackle a wider range of problems, such as materials design and molecular modelling, with the ultimate limit being a universal quantum computer that can solve general classes of hard problems. Here we use a quantum simulator composed of up to 53 qubits to study non-equilibrium dynamics in the transverse-field Ising model with long-range interactions. We observe a dynamical phase transition after a sudden change of the Hamiltonian, in a regime in which conventional statistical mechanics does not apply. The qubits are represented by the spins of trapped ions, which can be prepared in various initial pure states. We apply a global long-range Ising interaction with controllable strength and range, and measure each individual qubit with an efficiency of nearly 99 per cent. Such high efficiency means that arbitrary many-body correlations between qubits can be measured in a single shot, enabling the dynamical phase transition to be probed directly and revealing computationally intractable features that rely on the long-range interactions and high connectivity between qubits.

Kaleidoscope of quantum phases in a long-range interacting spin-1 chain.

Motivated directly by recent trapped-ion quantum simulation experiments, we carry out a comprehensive study of the phase diagram of a spin-1 chain with XXZ-type interactions that decay as 1/rα , using a combination of finite and infinite-size DMRG calculations, spin-wave analysis, and field theory. In the absence of long-range interactions, varying the spin-coupling anisotropy leads to four distinct and well-studied phases: a ferromagnetic Ising phase, a disordered XY phase, a topological Haldane phase, and an antiferromagnetic Ising phase. If long-range interactions are antiferromagnetic and thus frustrated, we find primarily a quantitative change of the phase boundaries. On the other hand, ferromagnetic (nonfrustrated) long-range interactions qualitatively impact the entire phase diagram. Importantly, for α ≲ 3 long-range interactions destroy the Haldane phase, break the conformal symmetry of the XY phase, give rise to a new phase that spontaneously breaks a U(1) continuous symmetry, and introduce a possibly exotic tricritical point with no direct parallel in short-range interacting spin chains. Importantly, we show that the main signatures of all five phases found could be observed experimentally in the near future.

Topological phases with long-range interactions.

Topological phases of matter are primarily studied in systems with short-range interactions. In nature, however, nonrelativistic quantum systems often exhibit long-range interactions. Under what conditions topological phases survive such interactions, and how they are modified when they do, is largely unknown. By studying the symmetry-protected topological phase of an antiferromagnetic spin-1 chain with 1/r α interactions, we show that two very different outcomes are possible, depending on whether or not the interactions are frustrated. While unfrustrated long-range interactions can destroy the topological phase for α ≲ 3, the topological phase survives frustrated interactions for all α > 0. Our conclusions are based on strikingly consistent results from large-scale matrix-product-state simulations and effective-field-theory calculations, and we expect them to hold for more general interacting spin systems. The models we study can be naturally realized in trapped-ion quantum simulators, opening the prospect for experimental investigation of the issues confronted here.

Effect of morphine preconditioning in the delayed phase on the expression of p38 mitogen-activated protein kinase in a rabbit model of myocardial ischemia-reperfusion injury.

This study aimed to investigate the protective effects of delayed morphine preconditioning on myocardial ischemia-reperfusion injury. We randomly divided 30 rabbits into three groups with 10 rab-bits in each group as follows: sham operation group (C group), isch-emia-reperfusion group (I/R group), and morphine pretreatment group (M group). Rabbits in C Group received left coronary without blocking for 160 min. The left descending artery of rabbits in the I/R group was blocked for 40 min and reperfused for 120 min. Rabbits in the M group received intravenous administration of 1.0 mg/kg morphine; after 24 h, rabbits in this group received the same treatment as that administered to the I/R group. We determined tumor necrosis factor alpha (TNF-α) levels in blood samples from the internal carotid artery of rabbits in each group 20 min before occlusion of the left descending coronary artery, 20 and 40 min after occlusion of the left descending coronary artery, and 1 and 2 h after myocardial reperfusion. After 120 min of reperfusion, immunoblotting was used to measure the activity levels of myocardial p38 mitogen-activated protein kinase (MAPK); in addition, the infarct size was measured. Compared to the I/R group, the M group showed a significant decrease in TNF-α levels, p38 MAPK activity, and the myocardial infarct size (I/R group 37.8% ± 1.7% vs 21.5% ± 2.4%; P < 0.05). Thus, morphine preconditioning in the delayed phase may exert protective effects on myocardial I/R injury by inhibiting myocar-dial p38 MAPK activity and decreasing TNF-α production.

Optimal quantum control of multimode couplings between trapped ion qubits for scalable entanglement.

We demonstrate entangling quantum gates within a chain of five trapped ion qubits by optimally shaping optical fields that couple to multiple collective modes of motion. We individually address qubits with segmented optical pulses to construct multipartite entangled states in a programmable way. This approach enables high-fidelity gates that can be scaled to larger qubit registers for quantum computation and simulation.

Robust quantum state transfer in random unpolarized spin chains.

We propose and analyze a new approach for quantum state transfer between remote spin qubits. Specifically, we demonstrate that coherent quantum coupling between remote qubits can be achieved via certain classes of random, unpolarized (infinite temperature) spin chains. Our method is robust to coupling-strength disorder and does not require manipulation or control over individual spins. In principle, it can be used to attain perfect state transfer over an arbitrarily long range via purely Hamiltonian evolution and may be particularly applicable in a solid-state quantum information processor. As an example, we demonstrate that it can be used to attain strong coherent coupling between nitrogen-vacancy centers separated by micrometer distances at room temperature. Realistic imperfections and decoherence effects are analyzed.

Synthesis of CoOOH nanorods and application as coating materials of nickel hydroxide for high temperature Ni-MH cells.

Studies on nanoscale materials have received great interest in both fundamental and applied aspects in recent years. In this letter, we report the synthesis of CoOOH nanorods and their possible applications as coating materials on nickel hydroxide for high-temperature nickel-metal hydride (Ni-MH) cells. The morphology and structure of CoOOH nanorods and coated nickel hydroxide particles are investigated by transmission electron microscopy, X-ray diffraction, and scanning electron microscopy, respectively. The electrochemical properties in the cylindrical AA size Ni-MH cells are evaluated. Our results show that the Ni-MH cells, where the positive electrodes are composed of such nanometer sized CoOOH coatings, have a higher capacity available and good performance at elevated temperatures of >50 degrees C.

Frequent genetic heterogeneity in the clonal evolution of gynecological carcinosarcoma and its influence on phenotypic diversity.

Carcinosarcomas of the uterus, ovaries, and fallopian tubes are highly aggressive neoplasms with incompletely understood histogenesis. Although recent immunohistochemical, cell culture, and molecular genetic studies all favor these cancers to be monoclonal in origin, the extent of intratumoral genetic heterogeneity in these tumors with divergent histology has not been reported previously. For this study, we microdissected a total of 172 carcinomatous or sarcomatous foci from 17 gynecological carcinosarcomas and analyzed allelic status with 41 microsatellite markers on chromosomal arms 1p, 1q, 3p, 4q, 5q, 6q, 8p, 9p, 10q, 11p, 11q, 13q, 16q, 17p, 17q, 18q, and 22q. With the exception of a single case with microsatellite instability, we found shared allelic losses and retentions among multiple individually dissected foci of each case, strongly supportive of the concept of a monoclonal origin for these neoplasms. In eight of these cases, we also found heterogeneous patterns of allelic loss at limited numbers of chromosomal loci in either the carcinomatous or sarcomatous components of the neoplasms. These heterogeneous patterns of allelic losses were consistent with either genetic progression or genetic diversion occurring during the clonal evolution of these neoplasms. In two cases, we found the specific patterns of genetic progression to be consistent with sarcomatous components of the neoplasms arising from carcinomatous components. We conclude that most of the gynecological carcinosarcomas have a monoclonal origin, and that genetic progression and diversion parallel the development of divergent phenotypes in these tumors. Because phenotypically divergent areas of the tumors share numerous genetic alterations, this divergence most likely occurs relatively late in the evolution of these tumors.

A comparison of the anti-rhinoviral drug binding pocket in HRV14 and HRV1A.

The three-dimensional structures of two human rhinovirus serotypes (HRV14 and HRV1A) are compared when complexed with various antiviral agents. Although these agents all bind into the same hydrophobic pocket, the exact viral-drug interactions differ. In the absence of drugs, the pocket is occupied by a fatty acid in HRV1A, but is empty in HRV14 except for two water molecules. The conformation of each drug is dependent upon the shape of the hydrophobic pocket. In HRV14 the major residues determining the shape of the binding site are Y1128, P1174 and M1224, corresponding to I1125, M1169 and I1220 in HRV1A. When there is no cofactor or a drug in the pocket, the entrance to the pocket is open. However, the entrance is closed when the pocket is occupied by a cofactor or a drug. There are relatively small conformational changes when the agents displace the natural cofactor in HRV1A. In contrast, there are much larger conformational changes on binding a drug in HRV14. These differences cause an inhibition of viral attachment in HRV14 but not in HRV1A. Binding of the drugs results in three additional interprotomer hydrogen bonds in HRV14 and one in HRV1A. These hydrogen bonds and a potential loss of flexibility upon efficient packing of the pocket may contribute to the inhibition of uncoating in both serotypes.

Effect of dexamethasone on Coxsackievirus B2-infected rat beating heart cells in culture.

The effects of dexamethasone on cultured rat beating heart cells experimentally infected with coxsackievirus B2 were investigated at an early stage (1-3 days) post challenge. Changes in the release of the cardiac enzyme, aspartate amino-transferase (AST), beating %, cytopathic effect (CPE), virus titre, ultrastructure and alterations of the electrical activity were evaluated. The protective effects of dexamethasone on infected cells were abolished except the release of AST at 5 days post infection. These results suggest that steroids may benefit patients with severe myocarditis if conventional therapy for protection of the myocardium and modulation of immunologic function are concomitantly given.

Crystallization of cauliflower mosaic virus.

Cauliflower mosaic virus has been crystallized in hanging and sitting drops. The hexagonal and octahedrally shaped crystals are up to 0.5 mm in mean diameter. The octahedrally shaped crystals diffract to about 27 A resolution. The results are discussed in relation to the lability and aggregation of the virions.

Treatment of experimental Coxsackie B-3 viral myocarditis with Astragalus membranaceus in mice.

A murine model system for observing the effect of Astragalus Membranaceus (AM) on experimental myocarditis caused by Coxsackie B-3 virus (CB3V) was developed in 4-week-old male BALB/C mice. Gross, histopathologic and ultrastructural examinations of the infected-AM treated group showed that the severity and involved area of the myocardial lesions became milder and smaller than those in the infected-NS treated mice. The total lesion area, and the total lesion area/total myocardial area examined (%) and virus titer in the former group were also smaller and lower than those in the latter group. The results suggest that AM is effective in the inhibition of Coxsackie B virus propagation and protection of myocardium in mouse myocarditis.

[Effect of dexamethasone on Coxsackie B-2 virus-infected rat beating heart cells in culture].

The effects of dexamethasone (Dex) on cultured rat beating heart cells infected with 100 TCID-50 Coxsackie virus B-2 (CB2V) were observed. The beating % began to decrease in the infected group 2 or 3 d post-challenge. Meanwhile, the cytopathic effect (CPE) appeared rapidly from 1+ to 3+. In the infected and Dex-treated group 1 h after inoculation, the beating % and CPE in the whole flask were significantly higher and less, respectively, than that in the group infected (P less than 0.05) at the same intervals. At 5 d after challenge, the beating % in the whole flask was significantly higher than that in the infected group. The cardiac enzyme-aspartate aminotransferase (AST) in the infected group was higher than that in the infected and Dex-treated group (P less than 0.01) through 3-5 d post-challenge. Moreover, the AST levels in these 2 groups were also higher than that in the uninfected group, Dex control group at the same intervals (P less than 0.01). Ultrastructural findings were parallel to the results of CPE through 1-5 d post-challenge in these 4 groups. It is suggested that the protective effect of Dex on cultured beating heart cells infected with CB2V occurred in the early stages after infection. It is surmised that steroids can probably save the lives of patients with severe myocarditis if the conventional therapy for protecting the myocardium and improving immunity were administered together.

[Cytotoxic effects of changrolin, lidocaine and amiodarone on ultrastructure of cultured rat beating cardiac myocytes].

Ultrastructural and morphological alterations of cultured rat beating cardiac myocytes treated with changrolin (CRL), lidocaine (Lid), and amiodarone (Ami) were studied. After the cultures were treated with CRL 100 micrograms/ml for 24 h, the beating of the myocytes stopped, the configuration and fine structure were destroyed, while the nuclei showed pyknotic deformation and reduced in size. The membrane and structures of mitochondria were disrupted and myofibrils fragmented and disrupted. In addition, a lot of vacuoles with characteristic dense particles were found in the cytoplasm. Similar alterations were seen when Lid 1000 micrograms/ml and Ami 50 micrograms/ml were added to the cultures. Normal beating networks of myocytes were examined under inverted microscopy after the cultured cells were treated with CRL 25 micrograms/ml, Lid 250 micrograms/ml or Ami 6.25 micrograms/ml. The ultrastructure of some regions of the myocytes showed very slight damage. The results indicated that the dosage of CRL and Lid generally used in anti-arrhythmic therapy basically exerted no harm to myocytes. However, caution should be taken when Ami was given intravenously, since its effective serum concentration was close to the dosage which could cause slight damage to the ultrastructure of cultured cells.

Paramyosin and the catch mechanism.

We propose here the formation by molluscan and notochord muscles in the catch state of three-dimensional, entangled network structures composed of bent and sometimes entwined paramyosin thick filaments including myosin intermediate filaments and disordered actin thin filaments; in the relaxed state the three forms lie in parallel. The intact forms of bivalve (Andonta pacifica, Heude) muscle paramyosin are those of 120 and 95 kDa (beta-paramyosin). The 102 kDa form (alpha-paramyosin) is the proteinase cleavage product of 120 kDa paramyosin. Paramyosin could be phosphorylated in vitro by cyclic AMP-dependent protein kinase. The amino acid phosphorylated was at the serine residue. Paramyosin from muscles treated with acetylcholine (catch state) was phosphorylated to a greater extent than that of untreated muscles (normal state) and even more so in the case of serotonin-treated muscles (relaxed state). Actin markedly inhibited the phosphorylation of paramyosin in vitro.

In vitro studies on the nucleocapsid-associated RNA polymerase of wheat rosette stunt virus.

RNA-dependent RNA polymerase activity was detected in both virion and nucleocapsid preparations of wheat rosette stunt virus, a plant rhabdovirus. The presence of nonionic detergent such as Nonidet P40 was essential for activity in reaction mixtures containing virions. The polymerase product was proved to be single-stranded RNA. By two-step controlled dissociation of the nucleocapsids, four subviral fractions (L protein, NS-N-RNA complex, NS protein, and N-RNA complex) were prepared. None of these fractions showed RNA polymerase activity when assayed individually. In experiments combining the various fractions, RNA synthesis was observed only when the L and NS proteins and the N-RNA complex were present in reaction mixtures.