Nonperturbative functional renormalization-group approach to transport in the vicinity of a (2+1)(2+1)-dimensional O(NN)-symmetric quantum critical point

Using a nonperturbative functional renormalization-group approach to the two-dimensional quantum O($N$) model, we compute the low-frequency limit $\omega\to 0$ of the zero-temperature conductivity in the vicinity of the quantum critical point. Our results are obtained from a derivative expansion to second order of a scale-dependent effective action in the presence of an external (i.e., non-dynamical) non-Abelian gauge field. While in the disordered phase the conductivity tensor $\sigma(\omega)$ is diagonal, in the ordered phase it is defined, when $N\geq 3$, by two independent elements, $\sigma_{\rm A}(\omega)$ and $\sigma_{\rm B}(\omega)$, respectively associated to SO($N$) rotations which do and do not change the direction of the order parameter. For $N=2$, the conductivity in the ordered phase reduces to a single component $\sigma_{\rm A}(\omega)$. We show that $\lim_{\omega\to 0}\sigma(\omega,\delta)\sigma_{\rm A}(\omega,-\delta)/\sigma_q^2$ is a universal number which we compute as a function of $N$ ($\delta$ measures the distance to the quantum critical point, $q$ is the charge and $\sigma_q=q^2/h$ the quantum of conductance). On the other hand we argue that the ratio $\sigma_{\rm B}(\omega\to 0)/\sigma_q$ is universal in the whole ordered phase, independent of $N$ and, when $N\to\infty$, equal to the universal conductivity $\sigma^*/\sigma_q$ at the quantum critical point.Comment: 25 pages, 4 figure

Superuniversal transport near a (2+1)(2 + 1)-dimensional quantum critical point

We compute the zero-temperature conductivity in the two-dimensional quantum $\mathrm{O}(N)$ model using a nonperturbative functional renormalization-group approach. At the quantum critical point we find a universal conductivity $\sigma^*/\sigma_Q$ (with $\sigma_Q=q^2/h$ the quantum of conductance and $q$ the charge) in reasonable quantitative agreement with quantum Monte Carlo simulations and conformal bootstrap results. In the ordered phase the conductivity tensor is defined, when $N\geq 3$, by two independent elements, $\sigma_{\mathrm{A}}(\omega)$ and $\sigma_{\mathrm{B}}(\omega)$, respectively associated to $\mathrm{O}(N)$ rotations which do and do not change the direction of the order parameter. Whereas $\sigma_{\mathrm{A}}(\omega\to 0)$ corresponds to the response of a superfluid (or perfect inductance), the numerical solution of the flow equations shows that $\lim_{\omega\to 0}\sigma_{\mathrm{B}}(\omega)/\sigma_Q=\sigma_{\mathrm{B}}^*/\sigma_Q$ is a superuniversal (i.e. $N$-independent) constant. These numerical results, as well as the known exact value $\sigma_{\mathrm{B}}^*/\sigma_Q=\pi/8$ in the large-$N$ limit, allow us to conjecture that $\sigma_{\mathrm{B}}^*/\sigma_Q=\pi/8$ holds for all values of $N$, a result that can be understood as a consequence of gauge invariance and asymptotic freedom of the Goldstone bosons in the low-energy limit.Comment: 6 pages, 4 figures, published versio

Ammonia : this is not the end but rather the end of the beginning

Hepatic encephalopathy (HE) represents a wide spectrum of neurological or neuropsychological symptoms caused by liver disease and/or portosystemic shunts. The major role of hyperammonemia in association with systemic inflammation and oxidative stress in the pathogenesis of HE has progressively emerged. However, the cascading downstream effects caused by these pathogenic factors remain unresolved. The underlying abnormalities which are thought to cause HE include modification of glutamatergic and GABAergic neurotransmission, mitochondrial dysfunction, energy impairment, lactate dyshomeostasis, increased blood-brain barrier permeability, brain edema/astrocyte swelling, as well as accumulation of toxic compounds (manganese, bile acids, indols)

Sympatric Dreissena species in the Meuse River : towards a dominance shift from zebra to quagga mussels

The rapid spread of the quagga mussel, Dreissena rostriformis, in Western Europe is of particular concern since the species is known to have serious ecological and economic impacts, similar to those of the well-established zebra mussel, Dreissena polymorpha. This study aimed (1) to provide an update on the quagga mussel distribution in several Belgian inland waterways, and (2) to check if a shift in dominance between Dreissena species is occurring. Using density measurements and artificial substrate samplers, we compared population dynamics for both species at different time-points based on size-frequency distribution. Our results show that quagga mussels are spreading rapidly throughout Belgium via a number of possible invasion fronts based around large rivers and canals. The quagga mussel became the dominant dreissenid species in both the Meuse River and a number of Belgian canals. In just three years, quagga mussel’s relative abundance increased from 2.9% (±2.9) to 52.6% (±43.1) of the total dreissenid population in the Meuse River. The most rapid increase in abundance has occurred in the Albert Canal, where quagga mussels achieved a mean relative abundance of 80% two years after the first observation. In the Meuse River, the quagga mussel displays a faster growth rate and/or earlier reproduction than the zebra mussel. We discuss different mechanisms that could explain the quagga mussel’s apparent competitive advantage over the zebra mussel

Mild hypothermia in the prevention of brain edema in acute liver failure: mechanisms and clinical prospects

Mild hypothermia (32 degrees C-35 degrees C) reduces intracranial pressure in patients with acute liver failure and may offer an effective adjunct therapy in the management of these patients. Studies in experimental animals suggest that this beneficial effect of hypothermia is the result of a decrease in blood-brain ammonia transfer resulting in improvement in brain energy metabolism and normalization of glutamatergic synaptic regulation. Improvement in brain energy metabolism by hypothermia may result from a reduction in ammonia-induced decrease of brain glucose (pyruvate) oxidation. Restoration of normal glutamatergic synaptic regulation by hypothermia may be the consequence of the removal of ammonia-induced decreases in expression of astrocytic glutamate transporters resulting in normal glutamate neurotransmitter inactivation in brain. Randomized controlled clinical trials of hypothermia are required to further evaluate its clinical impact

La3TaO7 derivatives with Weberite structure type: Possible electrolytes for solid oxide fuel cells and high temperature electrolysers

In this study, with the aim to enhance the ionic conduction of known structures by defect chemistry, the La2O3-Ta2O5 system was considered with a focus on the La3TaO7 phase whose structure is of Weberite type. In order to predict possible preferential substitution sites and substitution elements, atomistic simulation was used as a first approach. A solid solution La3−xSrxTaO7−x/2 was confirmed by X-ray diffraction and Raman spectroscopy; it extends for a substitution ratio up to x = 0.15. Whereas La3TaO7 is a poor oxide ion conductor (σ700 °C = 2 × 10−5S.cm−1), at 700 °C, its ionic conductivity is increased by more than one order of magnitude when 3.3% molar strontium is introduced in the structure (σ700 °C = 2 × 10−4S.cm−1)

The 2HA line of Medicago truncatula has characteristics of an epigenetic mutant that is weakly ethylene insensitive

BACKGROUND The Medicago truncatula 2HA seed line is highly embryogenic while the parental line Jemalong rarely produces embryos. The 2HA line was developed from one of the rare Jemalong regenerates and this method for obtaining a highly regenerable genotype in M. truncatula is readily reproducible suggesting an epigenetic mechanism. Microarray transcriptomic analysis showed down regulation of an ETHYLENE INSENSITIVE 3-like gene in 2HA callus which provided an approach to investigating epigenetic regulation of genes related to ethylene signalling and the 2HA phenotype. Ethylene is involved in many developmental processes including somatic embryogenesis (SE) and is associated with stress responses. RESULTS Microarray transcriptomic analysis showed a significant number of up-regulated transcripts in 2HA tissue culture, including nodule and embryo specific genes and transposon-like genes, while only a few genes were down-regulated, including an EIN3-like gene we called MtEIL1. This reduced expression was associated with ethylene insensitivity of 2HA plants that was further investigated. The weak ethylene insensitivity affected root and nodule development. Sequencing of MtEIL1 found no difference between 2HA and wild-type plants. DNA methylation analysis of MtEIL1 revealed significant difference between 2HA and wild-type plants. Tiling arrays demonstrated an elevated level of miRNA in 2HA plants that hybridised to the antisense strand of the MtEIL1 gene. AFLP-like methylation profiling revealed more differences in DNA methylation between 2HA and wild-type. Segregation analysis demonstrated the recessive nature of the eil1 phenotype and the dominant nature of the SE trait. CONCLUSIONS We have demonstrated that EIL1 of Medicago truncatula (MtEIL1) is epigenetically silenced in the 2HA seed line. The possible cause is an elevated level of miRNA that targets its 3'UTR and is also associated with DNA methylation of MtEIL1. Down regulation of MtEIL1 makes it possible to form nodules in the presence of ethylene and affects root growth under normal conditions. Segregation analysis showed no association between MtEIL1 expression and SE in culture but the role and mechanism of ethylene signalling in the process of plant regeneration through SE requires further investigation. The work also suggests that epigenetic changes to a particular gene induced in culture can be fixed in regenerated plants.This work was funded by the Australian Research Council (CEO348212) through the ARC Centre of Excellence for Integrative Legume Research (CILR)

Effects of hypothermia on brain glucose metabolism in acute liver failure: a H/C-nuclear magnetic resonance study

Mild hypothermia has a protective effect on brain edema and encephalopathy in both experimental and human acute liver failure. The goals of the present study were to examine the effects of mild hypothermia (35°C) on brain metabolic pathways using combined 1H and 13C-Nuclear Magnetic Resonance (NMR) spectroscopy, a technique which allows the study not only of metabolite concentrations but also their de novo synthesis via cell-specific pathways in the brain. :1H and 13C NMR spectroscopy using [1-13C] glucose was performed on extracts of frontal cortex obtained from groups of rats with acute liver failure induced by hepatic devascularization whose body temperature was maintained either at 37°C (normothermic) or 35°C (hypothermic), and appropriate sham-operated controls. At coma stages of encephalopathy in the normothermic acute liver failure animals, glutamine concentrations in frontal cortex increased 3.5-fold compared to sham-operated controls (P < 0.001). Comparable increases of brain glutamine were observed in hypothermic animals despite the absence of severe encephalopathy (coma). Brain glutamate and aspartate concentrations were respectively decreased to 60.9% ± 7.7% and 42.2% ± 5.9% (P < 0.01) in normothermic animals with acute liver failure compared to control and were restored to normal values by mild hypothermia. Concentrations of lactate and alanine in frontal cortex were increased to 169.2% ± 15.6% and 267.3% ± 34.0% (P < 0.01) respectively in normothermic rats compared to controls. Furthermore, de novo synthesis of lactate and alanine increased to 446.5% ± 48.7% and 707.9% ± 65.7% (P < 0.001), of control respectively, resulting in increased fractional 13C-enrichments in these cytosolic metabolites. Again, these changes of lactate and alanine concentrations were prevented by mild hypothermia. Mild hypothermia (35°C) prevents the encephalopathy and brain edema resulting from hepatic devascularization, selectively normalizes lactate and alanine synthesis from glucose, and prevents the impairment of oxidative metabolism associated with this model of ALF, but has no significant effect on brain glutamine. These findings suggest that a deficit in brain glucose metabolism rather than glutamine accumulation is the major cause of the cerebral complications of acute liver failure