Microstrip superconducting quantum interference device amplifiers with submicron Josephson junctions: enhanced gain at gigahertz frequencies

We present measurements of an amplifier based on a dc superconducting quantum interference device (SQUID) with submicron Al-AlOx-Al Josephson junctions. The small junction size reduces their self-capacitance and allows for the use of relatively large resistive shunts while maintaining nonhysteretic operation. This leads to an enhancement of the SQUID transfer function compared to SQUIDs with micron-scale junctions. The device layout is modified from that of a conventional SQUID to allow for coupling signals into the amplifier with a substantial mutual inductance for a relatively short microstrip coil. Measurements at 310 mK exhibit gain of 32 dB at 1.55 GHz.Comment: Version with high resolution figures at: http://physics.syr.edu/~bplourde/bltp-publications.ht

A novel RhoA/ROCK-CPI-17-MEF2C signaling pathway regulates vascular smooth muscle cell gene expression

Differentiation of vascular smooth muscle cells (VSMC) is a fundamental aspect of normal development and vascular disease. During contraction, VSMCs modulate calcium sensitivity through RhoA/ROCK-mediated inhibition of the myosin light chain phosphatase complex (MLCP). Previous studies have demonstrated that this signaling pathway functions in parallel to increase the expression of smooth muscle genes through the myocardin-family of co-activators. MEF2C fulfills a critical role in VSMC differentiation and regulates myocardin expression, leading us to investigate whether the RhoA/ROCK signaling cascade might regulate MEF2 activity. Depolarization-induced calcium signaling increased the expression of myocardin, which was sensitive to ROCK and p38 MAPK inhibition. We previously identified protein phosphatase 1α (PP1α), a known catalytic subunit of the MLCP in VSMCs, as a potent repressor of MEF2 activity. PP1α inhibition resulted in increased expression of myocardin, while ectopic expression of PP1α inhibited the induction of myocardin by MEF2C. Consistent with these data, shRNA-mediated suppression of a PP1α inhibitor, CPI-17, reduced myocardin expression and inhibited VSMC differentiation, suggesting a pivotal role for CPI-17 in regulating MEF2 activity. These data constitute evidence of a novel signaling cascade that links RhoA-mediated calcium sensitivity to MEF2-dependent myocardin expression in VSMCs through a mechanism involving p38 MAPK, PP1α, and CPI-17

Secretome Analysis of Skeletal Myogenesis Using SILAC and Shotgun Proteomics

Myogenesis, the formation of skeletal muscle, is a multistep event that commences with myoblast proliferation, followed by cell-cycle arrest, and finally the formation of multinucleated myotubes via fusion of mononucleated myoblasts. Each step is orchestrated by well-documented intracellular factors, such as cytoplasmic signalling molecules and nuclear transcription factors. Regardless, the key step in getting a more comprehensive understanding of the regulation of myogenesis is to explore the extracellular factors that are capable of eliciting the downstream intracellular factors. This could further provide valuable insight into the acute cellular response to extrinsic cues in maintaining normal muscle development. In this paper, we survey the intracellular factors that respond to extracellular cues that are responsible for the cascades of events during myogenesis: myoblast proliferation, cell-cycle arrest of myoblasts, and differentiation of myoblasts into myotubes. This focus on extracellular perspective of muscle development illustrates our mass spectrometry-based proteomic approaches to identify differentially expressed secreted factors during skeletal myogenesis

An objective functional characterisation of head movement impairment in individuals with neck muscle weakness due to Amyotrophic lateral sclerosis

Background: Neck muscle weakness and head drop are well recognised in patients with Amyotrophic lateral sclerosis (ALS), but an objective characterisation of the consequent head movement impairment is lacking. The aim of this study was to quantitatively characterise head movements in ALS compared to aged matched controls. Methods: We evaluated two groups, one of thirteen patients with ALS and one of thirteen age-matched controls, during the execution of a series of controlled head movements, performed while wearing two inertial sensors attached on the forehead and sternum, respectively. We quantified the differences between the two groups from the sensor data using indices of velocity, smoothness and movement coupling (intended as a measure of undesired out of plane movements). Findings: Results confirmed a general limitation in the ability of the ALS patients to perform and control head movements. High inter-patient variability was observed due to a wide range of observed functional impairment levels. The ability to extend the head backward and flex it laterally were the most compromised, with significantly lower angular velocity (P 0.8), reduced smoothness and greater presence of coupled movements with respect to the controls. A significant reduction of angular velocity (P 0.8) in extension, axial rotation and lateral flexion was observed when patients were asked to perform the movements as fast as possible. Interpretation: This pilot study is the first study providing a functional objective quantification of head movements in ALS. Further work involving different body areas and correlation with existing methods of evaluating neuromuscular function, such as dynamometry and EMG, is needed to explore the use of this approach as a marker of disease progression in ALS

Global gyrokinetic simulations of intrinsic rotation in ASDEX Upgrade Ohmic L-mode plasmas

Non-linear, radially global, turbulence simulations of ASDEX Upgrade (AUG) plasmas are performed and the nonlinear generated intrinsic flow shows agreement with the intrinsic flow gradients measured in the core of Ohmic L-mode plasmas at nominal parameters. Simulations utilising the kinetic electron model show hollow intrinsic flow profiles as seen in a predominant number of experiments performed at similar plasma parameters. In addition, significantly larger flow gradients are seen than in a previous flux-tube analysis (Hornsby et al {\it Nucl. Fusion} (2017)). Adiabatic electron model simulations can show a flow profile with opposing sign in the gradient with respect to a kinetic electron simulation, implying a reversal in the sign of the residual stress due to kinetic electrons. The shaping of the intrinsic flow is strongly determined by the density gradient profile. The sensitivity of the residual stress to variations in density profile curvature is calculated and seen to be significantly stronger than to neoclassical flows (Hornsby et al {\it Nucl. Fusion} (2017)). This variation is strong enough on its own to explain the large variations in the intrinsic flow gradients seen in some AUG experiments. Analysis of the symmetry breaking properties of the turbulence shows that profile shearing is the dominant mechanism in producing a finite parallel wave-number, with turbulence gradient effects contributing a smaller portion of the parallel wave-vector

Observation of quantum oscillations between a Josephson phase qubit and a microscopic resonator using fast readout

We have detected coherent quantum oscillations between Josephson phase qubits and microscopic critical-current fluctuators by implementing a new state readout technique that is an order of magnitude faster than previous methods. The period of the oscillations is consistent with the spectroscopic splittings observed in the qubit's resonant frequency. The results point to a possible mechanism for decoherence and reduced measurement fidelity in superconducting qubits and demonstrate the means to measure two-qubit interactions in the time domain

Experimental conditions to suppress edge localised modes by magnetic perturbations in the ASDEX Upgrade tokamak

Access conditions for full suppression of Edge Localised Modes (ELMs) by Magnetic Perturbations (MP) in low density high confinement mode (H-mode) plasmas are studied in the ASDEX Upgrade tokamak. The main empirical requirements for full ELM suppression in our experiments are: 1. The poloidal spectrum of the MP must be aligned for best plasma response from weakly stable kink-modes, which amplify the perturbation, 2. The plasma edge density must be below a critical value, $3.3 \times 10^{19}$~m$^{-3}$. The edge collisionality is in the range $\nu^*_i = 0.15-0.42$ (ions) and $\nu^*_e = 0.15-0.25$ (electrons). However, our data does not show that the edge collisionality is the critical parameter that governs access to ELM suppression. 3. The pedestal pressure must be kept sufficiently low to avoid destabilisation of small ELMs. This requirement implies a systematic reduction of pedestal pressure of typically 30\% compared to unmitigated ELMy H-mode in otherwise similar plasmas. 4. The edge safety factor $q_{95}$ lies within a certain window. Within the range probed so far, $q_{95}=3.5-4.2$, one such window, $q_{95}=3.57-3.95$ has been identified. Within the range of plasma rotation encountered so far, no apparent threshold of plasma rotation for ELM suppression is found. This includes cases with large cross field electron flow in the entire pedestal region, for which two-fluid MHD models predict that the resistive plasma response to the applied MP is shielded