Superconducting circuits have emerged as a competitive platform for quantum computation, satisfying the challenges of controllability, long coherence and strong interactions between individual systems. Here we apply this toolbox to the exploration of strongly correlated quantum matter, building a Bose-Hubbard lattice for photons in the strongly interacting regime. We develop a versatile recipe for dissipative preparation of incompressible many-body phases through reservoir engineering and apply it in our system to realize the first Mott insulator of photons. Site-and time-resolved readout of the lattice allows us to investigate the microscopic details of the thermalization process through the dynamics of defect propagation and removal in the Mott phase. These experiments demonstrate the power of superconducting circuits for studying strongly correlated matter in both coherent and engineered dissipative settings. In conjunction with recently demonstrated superconducting microwave Chern insulators, the approach demonstrated in this work will enable exploration of elusive topologically ordered phases of matter. arXiv:1807.11342v1 [cond-mat.quant-gas] 30 Jul 2018

Ribonucleotide reductase (RNR) catalyzes the rate-limiting step in nucleotide biosynthesis and plays a central role in genome maintenance. Although a number of regulatory mechanisms govern RNR activity, the physiologic effect of RNR deregulation had not previously been examined in an animal model. We show here that overexpression of the small RNR subunit potently and selectively induces lung neoplasms in transgenic mice and is mutagenic in cultured cells. Combining RNR deregulation with defects in DNA mismatch repair, the cellular mutation correction system, synergistically increased RNR-induced mutagenesis and carcinogenesis. Moreover, the proto-oncogene K-ras was identified as a frequent mutational target in RNR-induced lung neoplasms. Together, these results show that RNR deregulation promotes lung carcinogenesis through a mutagenic mechanism and establish a new oncogenic activity for a key regulator of nucleotide metabolism. Importantly, RNR-induced lung neoplasms histopathologically resemble human papillary adenocarcinomas and arise stochastically via a mutagenic mechanism, making RNR transgenic mice a valuable model for lung cancer.

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We realize a Λ system in a superconducting circuit, with metastable states exhibiting lifetimes up to 8 ms. We exponentially suppress the tunneling matrix elements involved in spontaneous energy relaxation by creating a "heavy" fluxonium, realized by adding a capacitive shunt to the original circuit design. The device allows for both cavity-assisted and direct fluorescent readouts, as well as state preparation schemes akin to optical pumping. Since direct transitions between the metastable states are strongly suppressed, we utilize Raman transitions for coherent manipulation of the states.

We autonomously stabilize arbitrary states of a qubit through parametric modulation of the coupling between a fixed frequency qubit and resonator. The coupling modulation is achieved with a tunable coupling design, in which the qubit and the resonator are connected in parallel to a superconducting quantum interference device. This allows for quasistatic tuning of the qubit-cavity coupling strength from 12 MHz to more than 300 MHz. Additionally, the coupling can be dynamically modulated, allowing for single-photon exchange in 6 ns. Qubit coherence times exceeding 20  μs are maintained over the majority of the range of tuning, limited primarily by the Purcell effect. The parametric stabilization technique realized using the tunable coupler involves engineering the qubit bath through a combination of photon nonconserving sideband interactions realized by flux modulation, and direct qubit Rabi driving. We demonstrate that the qubit can be stabilized to arbitrary states on the Bloch sphere with a worst-case fidelity exceeding 80%.

Qubit connectivity is an important property of a quantum processor, with an ideal processor having random access—the ability of arbitrary qubit pairs to interact directly. This a challenge with superconducting circuits, as state-of-the-art architectures rely on only nearest-neighbor coupling. Here, we implement a random access superconducting quantum information processor, demonstrating universal operations on a nine-qubit memory, with a Josephson junction transmon circuit serving as the central processor. The quantum memory uses the eigenmodes of a linear array of coupled superconducting resonators. We selectively stimulate vacuum Rabi oscillations between the transmon and individual eigenmodes through parametric flux modulation of the transmon frequency. Utilizing these oscillations, we perform a universal set of quantum gates on 38 arbitrary pairs of modes and prepare multimode entangled states, all using only two control lines. We thus achieve hardware-efficient random access multi-qubit control in an architecture compatible with long-lived microwave cavity-based quantum memories.

Introduction: Hip fractures represent an important health-care dilemma, costing the US$ billions annually. Hip fractures can diminish quality of life and significantly increase morbidity and mortality if not properly treated. Recent research has brought forth new information regarding treatment as well as information on emerging complications seen within the fixation constructs themselves. Significance: Understanding the pathoanatomy of hip fractures and the biomechanics of surgical fixation constructs is critical for successful treatment. In this article, we review the relevant anatomy and classification of femoral neck and intertrochanteric fractures. Furthermore, the biomechanics of hip fracture fixation strategies as well as implant-related complications are addressed. Results: Even though laboratory testing demonstrated that intramedullary nails have greater biomechanical stability, the clinical results between fixation constructs have been similar when the chosen implant (ie, sliding hip screw vs cephalomedullary nail) has been correctly applied to the specific fracture pattern. Recently, data have shown that when using cephalomedullary nails, there is potential for increased failure with cutout when using the helical blade versus the lag screw, with majority being the atypical “medial cutout.” Conclusion: The goal of surgical treatment of hip fractures is surgical treatment that allows for early mobilization and weight bearing. A full understanding of the anatomy and fracture characteristics will allow the surgeon to correctly apply the right implant to allow for uneventful healing. Surgeons need to be aware, however, of complications that can arise when using specific implants. Further research is ongoing to further determine the treatments that will allow optimal cost-effective care for the geriatric patient with hip fracture.

Intervertebral disc (IVD) degeneration and pathological spinal changes are major causes of back pain, which is the top cause of global disability. Obese and diabetic individuals are at increased risk for back pain and musculoskeletal complications. Modern diets contain high levels of advanced glycation end products (AGEs), cyto-toxic components which are known contributors to obesity, diabetes and accelerated aging pathologies. There is little information about potential effects of AGE rich diet on spinal pathology, which may be a contributing cause for back pain which is common in obese and diabetic individuals. This study investigated the role of specific AGE precursors (e.g. methylglyoxal-derivatives (MG)) on IVD and vertebral pathologies in aging C57BL6 mice that were fed isocaloric diets with standard (dMG+) or reduced amounts of MG derivatives (dMG-; containing 60-70% less dMG). dMG+ mice exhibited a pre-diabetic phenotype, as they were insulin resistant but not hyperglycemic. Vertebrae of dMG+ mice displayed increased cortical-thickness and cortical-area, greater MG-AGE accumulation and ectopic calcification in vertebral endplates. IVD morphology of dMG+ mice exhibited ectopic calcification, hypertrophic differentiation and glycosaminoglycan loss relative to dMG- mice. Overall, chronic exposure to dietary AGEs promoted age-accelerated IVD degeneration and vertebral alterations involving ectopic calcification which occurred in parallel with insulin resistance, and which were prevented with dMG- diet. This study described a new mouse model for diet-induced spinal degeneration, and results were in support of the hypothesis that chronic AGE ingestion could be a factor contributing to a pre-diabetic state, ectopic calcifications in spinal tissues, and musculoskeletal complications that are more generally known to occur with chronic diabetic conditions.