Accelerated adiabatic quantum gates: optimizing speed versus robustness

We develop new protocols for high-fidelity single qubit gates that exploit and extend theoretical ideas for accelerated adiabatic evolution. Our protocols are compatible with qubit architectures with highly isolated logical states, where traditional approaches are problematic; a prime example are superconducting fluxonium qubits. By using an accelerated adiabatic protocol we can enforce the desired adiabatic evolution while having gate times that are comparable to the inverse adiabatic energy gap (a scale that is ultimately set by the amount of power used in the control pulses). By modelling the effects of decoherence, we explore the tradeoff between speed and robustness that is inherent to shortcuts-to-adiabaticity approaches

Engineering Fast High-Fidelity Quantum Operations With Constrained Interactions

Understanding how to tailor quantum dynamics to achieve a desired evolution is a crucial problemin almost all quantum technologies. We present a very general method for designing high-efficiencycontrol sequences that are always fully compatible with experimental constraints on available inter-actions and their tunability. Our approach reduces in the end to finding control fields by solvinga set of time-independent linear equations. We illustrate our method by applying it to a numberof physically-relevant problems: the strong-driving limit of a two-level system, fast squeezing in aparametrically driven cavity, the leakage problem in transmon qubit gates, and the acceleration ofSNAP gates in a qubit-cavity system

Differential regulation of Krüppel-like factor family transcription factor expression in neonatal rat cardiac myocytes: effects of endothelin-1, oxidative stress and cytokines

Krüppel-like transcription factors (Klfs) modulate fundamental cell processes. Cardiac myocytes are terminally-differentiated, but hypertrophy in response to stimuli such as endothelin-1. H2O2 or cytokines promote myocyte apoptosis. Microarray studies of neonatal rat myocytes identified several Klfs as endothelin-1-responsive genes. We used quantitative PCR for further analysis of Klf expression in neonatal rat myocytes. In response to endothelin-1, Klf2 mRNA expression was rapidly increased ( approximately 9-fold; 15-30 min) with later increases in expression of Klf4 and Klf6 ( approximately 5-fold; 30-60 min). All were regulated as immediate early genes (cycloheximide did not inhibit the increases in expression). Klf5 expression was increased at 1-2 h ( approximately 13-fold) as a second phase response (cycloheximide inhibited the increase). These increases were transient and attenuated by U0126. H2O2 increased expression of Klf2, Klf4 and Klf6, but interleukin-1beta or tumor necrosis factor alpha downregulated Klf2 expression with no effect on Klf4 or Klf6. Of the Klfs which repress transcription, endothelin-1 rapidly downregulated expression of Klf3, Klf11 and Klf15. The dynamic regulation of expression of multiple Klf family members in cardiac myocytes suggests that, as a family, they are actively involved in regulating phenotypic responses (hypertrophy and apoptosis) to extracellular stimuli

Introduction to Quantum Noise, Measurement and Amplification

The topic of quantum noise has become extremely timely due to the rise of quantum information physics and the resulting interchange of ideas between the condensed matter and AMO/quantum optics communities. This review gives a pedagogical introduction to the physics of quantum noise and its connections to quantum measurement and quantum amplification. After introducing quantum noise spectra and methods for their detection, we describe the basics of weak continuous measurements. Particular attention is given to treating the standard quantum limit on linear amplifiers and position detectors using a general linear-response framework. We show how this approach relates to the standard Haus-Caves quantum limit for a bosonic amplifier known in quantum optics, and illustrate its application for the case of electrical circuits, including mesoscopic detectors and resonant cavity detectors.Comment: Substantial improvements over initial version; include supplemental appendices

Dynamics of a nanomechanical resonator coupled to a superconducting single-electron transistor

We present an analysis of the dynamics of a nanomechanical resonator coupled to a superconducting single electron transistor (SSET) in the vicinity of the Josephson quasiparticle (JQP) and double Josephson quasiparticle (DJQP) resonances. For weak coupling and wide separation of dynamical timescales, we find that for either superconducting resonance the dynamics of the resonator is given by a Fokker-Planck equation, i.e., the SSET behaves effectively as an equilibrium heat bath, characterised by an effective temperature, which also damps the resonator and renormalizes its frequency. Depending on the gate and drain-source voltage bias points with respect to the superconducting resonance, the SSET can also give rise to an instability in the mechanical resonator marked by negative damping and temperature within the appropriate Fokker-Planck equation. Furthermore, sufficiently close to a resonance, we find that the Fokker-Planck description breaks down. We also point out that there is a close analogy between coupling a nanomechanical resonator to a SSET in the vicinity of the JQP resonance and Doppler cooling of atoms by means of lasers

Simultaneous readout of two charge qubits

We consider a system of two solid state charge qubits, coupled to a single read-out device, consisting of a single-electron transistor (SET). The conductance of each tunnel junction is influenced by its neighboring qubit, and thus the current through the transistor is determined by the qubits' state. The full counting statistics of the electrons passing the transistor is calculated, and we discuss qubit dephasing, as well as the quantum efficiency of the readout. The current measurement is then compared to readout using real-time detection of the SET island's charge state. For the latter method we show that the quantum efficiency is always unity. Comparing the two methods a simple geometrical interpretation of the quantum efficiency of the current measurement appears. Finally, we note that full quantum efficiency in some cases can be achieved measuring the average charge of the SET island, in addition to the average current.Comment: 11 pages with 5 figure

Regulation of the cardiomyocyte transcriptome vs translatome by endothelin-1 and insulin: translational regulation of 5' terminal oligopyrimidine tract (TOP) mRNAs by insulin

Background: Changes in cellular phenotype result from underlying changes in mRNA transcription and translation. Endothelin-1 stimulates cardiomyocyte hypertrophy with associated changes in mRNA/protein expression and an increase in the rate of protein synthesis. Insulin also increases the rate of translation but does not promote overt cardiomyocyte hypertrophy. One mechanism of translational regulation is through 5' terminal oligopyrimidine tracts (TOPs) that, in response to growth stimuli, promote mRNA recruitment to polysomes for increased translation. TOP mRNAs include those encoding ribosomal proteins, but the full panoply remains to be established. Here, we used microarrays to compare the effects of endothelin-1 and insulin on the global transcriptome of neonatal rat cardiomyocytes, and on mRNA recruitment to polysomes (i.e. the translatome). Results: Globally, endothelin-1 and insulin (1 h) promoted >1.5-fold significant (false discovery rate 1.25-fold significant changes in expression in total and/or polysomal RNA induced by endothelin-1 or insulin, respectively, of which ~35% of endothelin-1-responsive and ~56% of insulin-responsive transcripts were translationally regulated. Of mRNAs for established proteins recruited to polysomes in response to insulin, 49 were known TOP mRNAs with a further 15 probable/possible TOP mRNAs, but 49 had no identifiable TOP sequences or other consistent features in the 5' untranslated region. Conclusions: Endothelin-1, rather than insulin, substantially affects global transcript expression to promote cardiomyocyte hypertrophy. Effects on RNA recruitment to polysomes are subtle, with differential effects of endothelin-1 and insulin on specific transcripts. Furthermore, although insulin promotes recruitment of TOP mRNAs to cardiomyocyte polysomes, not all recruited mRNAs are TOP mRNAs

Optomechanical circuits for nanomechanical continuous variable quantum state processing

We propose and analyze a nanomechanical architecture where light is used to perform linear quantum operations on a set of many vibrational modes. Suitable amplitude modulation of a single laser beam is shown to generate squeezing, entanglement, and state-transfer between modes that are selected according to their mechanical oscillation frequency. Current optomechanical devices based on photonic crystals may provide a platform for realizing this scheme.Comment: 11 pages, 5 figure

p90 ribosomal S6 kinases play a significant role in early gene regulation in the cardiomyocyte response to Gq protein-coupled receptor stimuli, endothelin-1 and α1-adrenergic receptor agonists

Extracellular signal-regulated kinases 1/2 (ERK1/2) and their substrates, p90 ribosomal S6 kinases (RSKs), phosphorylate different transcription factors, contributing differentially to transcriptomic profiles. In cardiomyocytes, ERK1/2 are required for >70% of the transcriptomic response to endothelin-1. Here, we investigated the role of RSKs in the transcriptomic responses to Gq protein-coupled receptor agonists, endothelin-1, phenylephrine (generic α1-adrenergic receptor agonist) and A61603 (α1A-adrenergic receptor selective). Phospho-ERK1/2 and phospho-RSKs appeared in cardiomyocyte nuclei within 2-3 min of stimulation (endothelin-1>a61603≈phenylephrine). All agonists increased nuclear RSK2, but only endothelin-1 increased nuclear RSK1 content. PD184352 (inhibits ERK1/2 activation) and BI-D1870 (inhibits RSKs) were used to dissect the contribution of RSKs to the endothelin-1-responsive transcriptome. Of 213 RNAs upregulated at 1 h, 51% required RSKs for upregulation whereas 29% required ERK1/2 but not RSKs. The transcriptomic response to phenylephrine overlapped with, but was not identical to, endothelin-1. As with endothelin-1, PD184352 inhibited upregulation of most phenylephrine-responsive transcripts, but the greater variation in effects of BI-D1870 suggests that differential RSK signalling influences global gene expression. A61603 induced similar changes in RNA expression in cardiomyocytes as phenylephrine, indicating that the signal was mediated largely through α1A-adrenergic receptors. A61603 also increased expression of immediate early genes in perfused adult rat hearts and, as in cardiomyocytes, upregulation of the majority of genes was inhibited by PD184352. PD184352 or BI-D1870 prevented the increased surface area induced by endothelin-1 in cardiomyocytes. Thus, RSKs play a significant role in regulating cardiomyocyte gene expression and hypertrophy in response to Gq protein-coupled receptor stimulation