Implementation of a Toffoli Gate with Superconducting Circuits

The quantum Toffoli gate allows universal reversible classical computation. It is also an important primitive in many quantum circuits and quantum error correction schemes. Here we demonstrate the realization of a Toffoli gate with three superconducting transmon qubits coupled to a microwave resonator. By exploiting the third energy level of the transmon qubit, the number of elementary gates needed for the implementation of the Toffoli gate, as well as the total gate time can be reduced significantly in comparison to theoretical proposals using two-level systems only. We characterize the performance of the gate by full process tomography and Monte Carlo process certification. The gate fidelity is found to be $68.5\pm0.5$%.Comment: 4 pages, 5figure

Energy Relaxation in Nonlinear One-Dimensional Lattices

We study energy relaxation in thermalized one-dimensional nonlinear arrays of the Fermi-Pasta-Ulam type. The ends of the thermalized systems are placed in contact with a zero-temperature reservoir via damping forces. Harmonic arrays relax by sequential phonon decay into the cold reservoir, the lower frequency modes relaxing first. The relaxation pathway for purely anharmonic arrays involves the degradation of higher-energy nonlinear modes into lower energy ones. The lowest energy modes are absorbed by the cold reservoir, but a small amount of energy is persistently left behind in the array in the form of almost stationary low-frequency localized modes. Arrays with interactions that contain both a harmonic and an anharmonic contribution exhibit behavior that involves the interplay of phonon modes and breather modes. At long times relaxation is extremely slow due to the spontaneous appearance and persistence of energetic high-frequency stationary breathers. Breather behavior is further ascertained by explicitly injecting a localized excitation into the thermalized array and observing the relaxation behavior

Slowing Out of Equilibrium Near the QCD Critical Point

The QCD phase diagram may feature a critical end point at a temperature T and baryon chemical potential $\mu$ which is accessible in heavy ion collisions. The universal long wavelength fluctuations which develop near this Ising critical point result in experimental signatures which can be used to find the critical point. The magnitude of the observed effects depends on how large the correlation length $\xi$ becomes. Because the matter created in a heavy ion collision cools through the critical region of the phase diagram in a finite time, critical slowing down limits the growth of $\xi$, preventing it from staying in equilibrium. This is the fundamental nonequilibrium effect which must be calculated in order to make quantitative predictions for experiment. We use universal nonequilibrium dynamics and phenomenologically motivated values for the necessary nonuniversal quantities to estimate how much the growth of $\xi$ is slowed.Comment: 21 pages, 5 figures, reference added, typo corrected, to appear in Phys. Rev.

Asymmetric gap soliton modes in diatomic lattices with cubic and quartic nonlinearity

Nonlinear localized excitations in one-dimensional diatomic lattices with cubic and quartic nonlinearity are considered analytically by a quasi-discreteness approach. The criteria for the occurence of asymmetric gap solitons (with vibrating frequency lying in the gap of phonon bands) and small-amplitude, asymmetric intrinsic localized modes (with the vibrating frequency being above all the phonon bands) are obtained explicitly based on the modulational instabilities of corresponding linear lattice plane waves. The expressions of particle displacement for all these nonlinear localized excitations are also given. The result is applied to standard two-body potentials of the Toda, Born-Mayer-Coulomb, Lennard-Jones, and Morse type. The comparison with previous numerical study of the anharmonic gap modes in diatomic lattices for the standard two-body potentials is made and good agreement is found.Comment: 24 pages in Revtex, 2 PS figure

Ultrastructural analysis of sequential Cyprinid herpesvirus 3 morphogenesis in vitro

Cyprinid herpesvirus 3 (CyHV-3) is an alloherpesvirus, and it is the aetiological agent of koi herpesvirus disease. Although the complex morphogenic stages of the replication cycle of CyHV-3 were shown to resemble that of other members of the Herpesvirales, detailed analysis of the sequence and timing of these events was not definitively determined. This study describes these features through a time course using cyprinid cell cultures (KF-1 and CCB) infected with CyHV-3 (KHV isolate, H361) and analysed by transmission electron microscopy. Rapid viral entry was noted, with high levels of intracellular virus within 1–4 h post-infection (hpi). Intranuclear capsid assembly, paracrystalline array formation and primary envelopment of capsids occurred within 4 hpi. Between 1 and 3 days post-infection (dpi), intracytoplasmic secondary envelopment occurred, as well as budding of infectious virions at the plasma membrane. At 5–7 dpi, the cytoplasm contained cytopathic vacuoles, enveloped virions within vesicles, and abundant non-enveloped capsids; also there was frequent nuclear deformation. Several morphological features are suggestive of inefficient viral assembly, with production of non-infectious particles, particularly in KF-1 cells. The timing of this alloherpesvirus morphogenesis is similar to other members of the Herpesvirales, but there may be possible implications of using different cell lines for CyHV-3 propagation

E-Cadherin–dependent Growth Suppression is Mediated by the Cyclin-dependent Kinase Inhibitor p27KIP1

Recent studies have demonstrated the importance of E-cadherin, a homophilic cell–cell adhesion molecule, in contact inhibition of growth of normal epithelial cells. Many tumor cells also maintain strong intercellular adhesion, and are growth-inhibited by cell– cell contact, especially when grown in three-dimensional culture. To determine if E-cadherin could mediate contact-dependent growth inhibition of nonadherent EMT/6 mouse mammary carcinoma cells that lack E-cadherin, we transfected these cells with an exogenous E-cadherin expression vector. E-cadherin expression in EMT/6 cells resulted in tighter adhesion of multicellular spheroids and a reduced proliferative fraction in three-dimensional culture. In addition to increased cell–cell adhesion, E-cadherin expression also resulted in dephosphorylation of the retinoblastoma protein, an increase in the level of the cyclin-dependent kinase inhibitor p27kip1 and a late reduction in cyclin D1 protein. Tightly adherent spheroids also showed increased levels of p27 bound to the cyclin E-cdk2 complex, and a reduction in cyclin E-cdk2 activity. Exposure to E-cadherin–neutralizing antibodies in three-dimensional culture simultaneously prevented adhesion and stimulated proliferation of E-cadherin transfectants as well as a panel of human colon, breast, and lung carcinoma cell lines that express functional E-cadherin. To test the importance of p27 in E-cadherin–dependent growth inhibition, we engineered E-cadherin–positive cells to express inducible p27. By forcing expression of p27 levels similar to those observed in aggregated cells, the stimulatory effect of E-cadherin–neutralizing antibodies on proliferation could be inhibited. This study demonstrates that E-cadherin, classically described as an invasion suppressor, is also a major growth suppressor, and its ability to inhibit proliferation involves upregulation of the cyclin-dependent kinase inhibitor p27

The response of the Antarctic Circumpolar Current to recent climate change

Observations show a significant intensification of the Southern Hemisphere westerlies, the prevailing winds between the latitudes of 30° and 60° S, over the past decades. A continuation of this intensification trend is projected by climate scenarios for the twenty-first century. The response of the Antarctic Circumpolar Current and the carbon sink in the Southern Ocean to changes in wind stress and surface buoyancy fluxes is under debate. Here we analyse the Argo network of profiling floats and historical oceanographic data to detect coherent hemispheric-scale warming and freshening trends that extend to depths of more than 1,000 m. The warming and freshening is partly related to changes in the properties of the water masses that make up the Antarctic Circumpolar Current, which are consistent with the anthropogenic changes in heat and freshwater fluxes suggested by climate models. However, we detect no increase in the tilt of the surfaces of equal density across the Antarctic Circumpolar Current, in contrast to coarse-resolution model studies. Our results imply that the transport in the Antarctic Circumpolar Current and meridional overturning in the Southern Ocean are insensitive to decadal changes in wind stress

Antisense PMO cocktails effectively skip dystrophin exons 45-55 in myotubes transdifferentiated from DMD patient fibroblasts

Antisense-mediated exon skipping has made significant progress as a therapeutic platform in recent years, especially in the case of Duchenne muscular dystrophy (DMD). Despite FDA approval of eteplirsen-the first-ever antisense drug clinically marketed for DMD-exon skipping therapy still faces the significant hurdles of limited applicability and unknown truncated protein function. In-frame exon skipping of dystrophin exons 45-55 represents a significant approach to treating DMD, as a large proportion of patients harbor mutations within this "hotspot" region. Additionally, patients harboring dystrophin exons 45-55 deletion mutations are reported to have exceptionally mild to asymptomatic phenotypes. Here, we demonstrate that a cocktail of phosphorodiamidate morpholino oligomers can effectively skip dystrophin exons 45-55 in vitro in myotubes transdifferentiated from DMD patient fibroblast cells. This is the first report of substantive exons 45-55 skipping in DMD patient cells. These findings help validate the use of transdifferentiated patient fibroblast cells as a suitable cell model for dystrophin exon skipping assays and further emphasize the feasibility of dystrophin exons 45-55 skipping in patients