Universal transport near a quantum critical Mott transition in two dimensions

We discuss the universal transport signatures near a zero-temperature continuous Mott transition between a Fermi liquid (FL) and a quantum spin liquid in two spatial dimensions. The correlation-driven transition occurs at fixed filling and involves fractionalization of the electron: upon entering the spin liquid, a Fermi surface of neutral spinons coupled to an internal gauge field emerges. We present a controlled calculation of the value of the zero temperature universal resistivity jump predicted to occur at the transition. More generally, the behavior of the universal scaling function that collapses the temperature and pressure dependent resistivity is derived, and is shown to bear a strong imprint of the emergent gauge fluctuations. We further predict a universal jump of the thermal conductivity across the Mott transition, which derives from the breaking of conformal invariance by the damped gauge field, and leads to a violation of the Wiedemann-Franz law in the quantum critical region. A connection to organic salts is made, where such a transition might occur. Finally, we present some transport results for the pure rotor O(N) CFT.Comment: 27 pages, 16 figure

Nonequilibrium quantum criticality in bilayer itinerant ferromagnets

We present a theory of nonequilibrium quantum criticality in a coupled bilayer system of itinerant electron magnets. The model studied consists of the first layer subjected to an inplane current and open to an external substrate. The second layer is closed and subject to no direct external drive, but couples to the first layer via short-ranged spin exchange interaction. No particle exchange is assumed between the layers. Starting from a microscopic fermionic model, we derive an effective action in terms of two coupled bosonic fields which are related to the magnetization fluctuations of the two layers. When there is no interlayer coupling, the two bosonic modes possess different dynamical critical exponents z with z=2 (z=3) for the first (second) layer. This results in multi-scale quantum criticality in the coupled system. It is shown that the linear coupling between the two fields leads to a low energy fixed point characterized by the larger dynamical critical exponent z=3. The perturbative renormalization group is used to compute the correlation length in the quantum disordered and quantum critical regimes. We also derive the stochastic dynamics obeyed by the critical fluctuations in the quantum critical regime. Comparing the nonequilibrium situation to the thermal equilibrium scenario, where the whole system is at a temperature T, we find that the nonequilibrium drive does not always play the role of temperature.Comment: 20+ pages, 3 figures; Revised version as accepted by PRB, added figure of mean field phase diagra

The Dynamics of Quantum Criticality Revealed by Quantum Monte Carlo and Holography

Understanding the dynamics of quantum systems without long-lived excitations (quasiparticles) constitutes an important yet challenging problem. Although numerical techniques can yield results for the dynamics in imaginary time, their reliable continuation to real time has proved difficult. We tackle this issue using the superfluid–insulator quantum critical point of bosons on a two-dimensional lattice, where quantum fluctuations destroy quasiparticles. We present quantum Monte Carlo simulations for two separate lattice realizations. Their low-frequency conductivities turn out to have the same universal dependence on imaginary frequency and temperature. Using the structure of the real-time dynamics of conformal field theories described by the holographic gauge/gravity duality, we then make progress on the problem of analytically continuing the numerical data to real time. Our method yields quantitative and experimentally testable results on the frequency-dependent conductivity near the quantum critical point. Extensions to other observables and universality classes are discussed.Physic

Conformal field theories at nonzero temperature: Operator product expansions, Monte Carlo, and holography

We compute the nonzero temperature conductivity of conserved flavor currents in conformal field theories (CFTs) in 2+1 space-time dimensions. At frequencies much greater than the temperature, ℏω≫kBT, the ω dependence can be computed from the operator product expansion (OPE) between the currents and operators, which acquire a nonzero expectation value at T>0. Such results are found to be in excellent agreement with quantum Monte Carlo studies of the O(2) Wilson-Fisher CFT. Results for the conductivity and other observables are also obtained in vector 1/N expansions. We match these large ω results to the corresponding correlators of holographic representations of the CFT: the holographic approach then allows us to extrapolate to small ℏω/(kBT). Other holographic studies implicitly only used the OPE between the currents and the energy-momentum tensor, and this yields the correct leading large ω behavior for a large class of CFTs. However, for the Wilson-Fisher CFT, a relevant “thermal” operator must also be considered, and then consistency with the Monte Carlo results is obtained without a previously needed ad hoc rescaling of the T value. We also establish sum rules obeyed by the conductivity of a wide class of CFTs.Physic

Short-term, high-fat diet accelerates disuse atrophy and protein degradation in a muscle-specific manner in mice

Background: A short-term high-fat diet impairs mitochondrial function and the ability of skeletal muscle to respond to growth stimuli, but it is unknown whether such a diet alters the ability to respond to atrophy signals. The purpose of this study was to determine whether rapid weigh gain induced by a high-fat (HF) diet accelerates denervation-induced muscle atrophy. Methods: Adult, male mice (C57BL/6) were fed a control or HF (60 % calories as fat) diet for 3 weeks (3wHF). Sciatic nerve was sectioned unilaterally for the final 5 or 14 days of the diet. Soleus and extensor digitorum longus (EDL) muscles were removed and incubated in vitro to determine rates of protein degradation and subsequently homogenized for determination of protein levels of LC3, ubiquitination, myosin heavy chain (MHC) distribution, and mitochondrial subunits. Results: When mice were fed the 3wHF diet, whole-body fat mass more than doubled, but basal (innervated) muscle weights, rates of protein degradation, LC3 content, mitochondrial protein content, and myosin isoform distribution were not significantly different than with the control diet in either soleus or EDL. However in the 14 day denervated soleus, the 3wHF diet significantly augmented loss of mass, proteolysis rate, amount of the autophagosome marker LC3 II, and the amount of overall ubiquitination as compared to the control fed mice. On the contrary, the 3wHF diet had no significant effect in the EDL on amount of mass loss, proteolysis rate, LC3 levels, or ubiquitination. Fourteen days denervation also induced a loss of mitochondrial proteins in the soleus but not the EDL, regardless of the diet. Conclusions: Taken together, a short-term, high-fat diet augments denervation muscle atrophy by induction of protein degradation in the mitochondria-rich soleus but not in the glycolytic EDL. These findings suggest that the denervation-induced loss of mitochondria and HF diet-induced impairment of mitochondrial function may combine to promote skeletal muscle atrophy

Charge separation technique for metal–oxide–silicon capacitors in the presence of hydrogen deactivated dopants

An improved charge separation technique for metal-oxide-silicon (MOS) capacitors is presented which accounts for the deactivation of substrate dopants by hydrogen at elevated irradiation temperatures or small irradiation biases. Using high-frequency capacitance-voltage (C-V) measurements, radiation-induced inversion voltage shifts are separated into components due to oxide trapped charge, interface traps and deactivated dopants, where the latter is computed from a reduction in Si capacitance. In the limit of no radiation-induced dopant deactivation, this approach reduces to the standard midgap charge separation technique used widely for the analysis of room-temperature irradiations. The technique is demonstrated on a p-type MOS capacitor irradiated with {sup 60}Co {gamma}-rays at 100 C and zero bias, where the dopant deactivation is significant

Spin-orbit density wave induced hidden topological order in URu2Si2

The conventional order parameters in quantum matters are often characterized by 'spontaneous' broken symmetries. However, sometimes the broken symmetries may blend with the invariant symmetries to lead to mysterious emergent phases. The heavy fermion metal URu2Si2 is one such example, where the order parameter responsible for a second-order phase transition at Th = 17.5 K has remained a long-standing mystery. Here we propose via ab-initio calculation and effective model that a novel spin-orbit density wave in the f-states is responsible for the hidden-order phase in URu2Si2. The staggered spin-orbit order 'spontaneous' breaks rotational, and translational symmetries while time-reversal symmetry remains intact. Thus it is immune to pressure, but can be destroyed by magnetic field even at T = 0 K, that means at a quantum critical point. We compute topological index of the order parameter to show that the hidden order is topologically invariant. Finally, some verifiable predictions are presented.Comment: (v2) Substantially modified from v1, more calculation and comparison with experiments are include

Constitutively Active CaMKKα Stimulates Skeletal Muscle Glucose Uptake in Insulin-Resistant Mice In Vivo

In insulin-sensitive skeletal muscle, the expression of constitutively active Ca(2+)/calmodulin-dependent protein kinase kinase α (caCaMKKα) stimulates glucose uptake independent of insulin signaling (i.e., Akt and Akt-dependent TBC1D1/TBC1D4 phosphorylation). Our objectives were to determine whether caCaMKKα could stimulate glucose uptake additively with insulin in insulin-sensitive muscle, in the basal state in insulin-resistant muscle, and if so, to determine whether the effects were associated with altered TBC1D1/TBC1D4 phosphorylation. Mice were fed a control or high-fat diet (60% kcal) for 12 weeks to induce insulin resistance. Muscles were transfected with empty vector or caCaMKKα plasmids using in vivo electroporation. After 2 weeks, caCaMKKα protein was robustly expressed. In insulin-sensitive muscle, caCaMKKα increased basal in vivo [(3)H]-2-deoxyglucose uptake approximately twofold, insulin increased glucose uptake approximately twofold, and caCaMKKα plus insulin increased glucose uptake approximately fourfold. caCaMKKα did not increase basal TBC1D1 (Ser(237), Thr(590), Ser(660), pan-Thr/Ser) or TBC1D4 (Ser(588), Thr(642), pan-Thr/Ser) phosphorylation. In insulin-resistant muscle, caCaMKKα increased basal glucose uptake approximately twofold, and attenuated high-fat diet–induced basal TBC1D1 (Thr(590), pan-Thr/Ser) and TBC1D4 (Ser(588), Thr(642), pan-Thr/Ser) phosphorylation. In cell-free assays, CaMKKα increased TBC1D1 (Thr(590), pan-Thr/Ser) and TBC1D4 (Ser(588), pan-Thr/Ser) phosphorylation. Collectively, these results demonstrate that caCaMKKα stimulates glucose uptake additively with insulin, and in insulin-resistant muscle, and alters the phosphorylation of TBC1D1/TBC1D4