The reconfigurable Josephson circulator/directional amplifier

Circulators and directional amplifiers are crucial non-reciprocal signal routing and processing components involved in microwave readout chains for a variety of applications. They are particularly important in the field of superconducting quantum information, where the devices also need to have minimal photon losses to preserve the quantum coherence of signals. Conventional commercial implementations of each device suffer from losses and are built from very different physical principles, which has led to separate strategies for the construction of their quantum-limited versions. However, as recently proposed theoretically, by establishing simultaneous pairwise conversion and/or gain processes between three modes of a Josephson-junction based superconducting microwave circuit, it is possible to endow the circuit with the functions of either a phase-preserving directional amplifier or a circulator. Here, we experimentally demonstrate these two modes of operation of the same circuit. Furthermore, in the directional amplifier mode, we show that the noise performance is comparable to standard non-directional superconducting amplifiers, while in the circulator mode, we show that the sense of circulation is fully reversible. Our device is far simpler in both modes of operation than previous proposals and implementations, requiring only three microwave pumps. It offers the advantage of flexibility, as it can dynamically switch between modes of operation as its pump conditions are changed. Moreover, by demonstrating that a single three-wave process yields non-reciprocal devices with reconfigurable functions, our work breaks the ground for the development of future, more-complex directional circuits, and has excellent prospects for on-chip integration

Robust concurrent remote entanglement between two superconducting qubits

Entangling two remote quantum systems which never interact directly is an essential primitive in quantum information science and forms the basis for the modular architecture of quantum computing. When protocols to generate these remote entangled pairs rely on using traveling single photon states as carriers of quantum information, they can be made robust to photon losses, unlike schemes that rely on continuous variable states. However, efficiently detecting single photons is challenging in the domain of superconducting quantum circuits because of the low energy of microwave quanta. Here, we report the realization of a robust form of concurrent remote entanglement based on a novel microwave photon detector implemented in the superconducting circuit quantum electrodynamics (cQED) platform of quantum information. Remote entangled pairs with a fidelity of $0.57\pm0.01$ are generated at $200$ Hz. Our experiment opens the way for the implementation of the modular architecture of quantum computation with superconducting qubits.Comment: Main paper: 7 pages, 4 figures; Appendices: 14 pages, 9 figure

Suppression of piriform cortex activity in rat by corticotropin-releasing factor 1 and serotonin 2A/C receptors

The piriform cortex (PC) is richly innervated by Corticotropin-releasing factor (CRF) and Serotonin (5-HT) containing axons arising from central amygdala and Raphe nucleus. CRFR1 and 5-HT2A/2CRs have been shown to interact in manner where CRFR activation subsequently potentiates the activity of 5-HT2A/2CRs. The purpose of this study was to determine how the activation of CRFR1 and/or 5-HT2Rs modulates PC activity at both the circuit and cellular level. Voltage sensitive dye imaging showed that CRF acting through CRFR1 dampened activation of the layer II of PC and interneurons of endopiriform nucleus. Application of the selective 5-HT2A/CR agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) following CRFR1 activation potentiated this effect. Blocking the interaction between CRFR1 and 5-HT2R with a Tat-CRFR1-CT peptide abolished this potentiation. Application of forskolin did not mimic CRFR1 activity but instead blocked it, while a protein kinase A antagonist had no effect. However, activation and antagonism of protein kinase C (PKC) either mimicked or blocked CRF modulation respectively. DOI had no effect when applied alone indicating that the prior activation of CRFR1 receptors was critical for DOI to show significant effects similar to CRF. Patch clamp recordings showed that both CRF and DOI reduced the synaptic responsiveness of layer II pyramidal neurons. CRF had highly variable effects on interneurons within layer III, both increasing and decreasing their excitability, but DOI had no effect on the excitability of this group of neurons. These data show that CRF and serotonin, acting through both CRFR1 and 5-HT2A/CRs, reduce the activation of the PC. This modulation may be an important blunting mechanism of stressor behaviours mediated through the olfactory cortex

Altered Chromatin Occupancy of Master Regulators Underlies Evolutionary Divergence in the Transcriptional Landscape of Erythroid Differentiation

Erythropoiesis is one of the best understood examples of cellular differentiation. Morphologically, erythroid differentiation proceeds in a nearly identical fashion between humans and mice, but recent evidence has shown that networks of gene expression governing this process are divergent between species. We undertook a systematic comparative analysis of six histone modifications and four transcriptional master regulators in primary proerythroblasts and erythroid cell lines to better understand the underlying basis of these transcriptional differences. Our analyses suggest that while chromatin structure across orthologous promoters is strongly conserved, subtle differences are associated with transcriptional divergence between species. Many transcription factor (TF) occupancy sites were poorly conserved across species (∼25% for GATA1, TAL1, and NFE2) but were more conserved between proerythroblasts and cell lines derived from the same species. We found that certain cis-regulatory modules co-occupied by GATA1, TAL1, and KLF1 are under strict evolutionary constraint and localize to genes necessary for erythroid cell identity. More generally, we show that conserved TF occupancy sites are indicative of active regulatory regions and strong gene expression that is sustained during maturation. Our results suggest that evolutionary turnover of TF binding sites associates with changes in the underlying chromatin structure, driving transcriptional divergence. We provide examples of how this framework can be applied to understand epigenomic variation in specific regulatory regions, such as the β-globin gene locus. Our findings have important implications for understanding epigenomic changes that mediate variation in cellular differentiation across species, while also providing a valuable resource for studies of hematopoiesis

IKKα negatively regulates ASC-dependent inflammasome activation.

The inflammasomes are multiprotein complexes that activate caspase-1 in response to infections and stress, resulting in the secretion of pro-inflammatory cytokines. Here we report that IκB kinase α (IKKα) is a critical negative regulator of apoptosis-associated specklike protein containing a C-terminal caspase-activation-andrecruitment (CARD) domain (ASC)-dependent inflammasomes. IKKα controls the inflammasome at the level of the adaptor ASC, which interacts with IKKα in the nucleus of resting macrophages in an IKKα kinase-dependent manner. Loss of IKKα kinase activity results in inflammasome hyperactivation. Mechanistically, the downstream nuclear effector IKK-related kinase (IKKi) facilitates translocation of ASC from the nucleus to the perinuclear area during inflammasome activation. ASC remains under the control of IKKα in the perinuclear area following translocation of the ASC/IKKα complex. Signal 2 of NLRP3 activation leads to inhibition of IKKα kinase activity through the recruitment of PP2A, allowing ASC to participate in NLRP3 inflammasome assembly. Taken together, these findings reveal a IKKi-IKKα-ASC axis that serves as a common regulatory mechanism for ASC-dependent inflammasomes

Stabilizing entanglement autonomously between two superconducting qubits

Quantum error-correction codes would protect an arbitrary state of a multi-qubit register against decoherence-induced errors, but their implementation is an outstanding challenge for the development of large-scale quantum computers. A first step is to stabilize a non-equilibrium state of a simple quantum system such as a qubit or a cavity mode in the presence of decoherence. Several groups have recently accomplished this goal using measurement-based feedback schemes. A next step is to prepare and stabilize a state of a composite system. Here we demonstrate the stabilization of an entangled Bell state of a quantum register of two superconducting qubits for an arbitrary time. Our result is achieved by an autonomous feedback scheme which combines continuous drives along with a specifically engineered coupling between the two-qubit register and a dissipative reservoir. Similar autonomous feedback techniques have recently been used for qubit reset and the stabilization of a single qubit state, as well as for creating and stabilizing states of multipartite quantum systems. Unlike conventional, measurement-based schemes, an autonomous approach counter-intuitively uses engineered dissipation to fight decoherence, obviating the need for a complicated external feedback loop to correct errors, simplifying implementation. Instead the feedback loop is built into the Hamiltonian such that the steady state of the system in the presence of drives and dissipation is a Bell state, an essential building-block state for quantum information processing. Such autonomous schemes, broadly applicable to a variety of physical systems as demonstrated by a concurrent publication with trapped ion qubits, will be an essential tool for the implementation of quantum-error correction.Comment: 39 pages, 7 figure