Energy gap of the bimodal two-dimensional Ising spin glass

An exact algorithm is used to compute the degeneracies of the excited states of the bimodal Ising spin glass in two dimensions. It is found that the specific heat at arbitrary low temperature is not a self-averaging quantity and has a distribution that is neither normal or lognormal. Nevertheless, it is possible to estimate the most likely value and this is found to scale as L^3 T^(-2) exp(-4J/kT), for a L*L lattice. Our analysis also explains, for the first time, why a correlation length \xi ~ exp(2J/kT) is consistent with an energy gap of 2J. Our method allows us to obtain results for up to 10^5 disorder realizations with L <= 64. Distributions of second and third excitations are also shown.Comment: 4 pages, 4 figure

Finite-Size Scaling of the Domain Wall Entropy Distributions for the 2D ±J\pm J Ising Spin Glass

The statistics of domain walls for ground states of the 2D Ising spin glass with +1 and -1 bonds are studied for $L \times L$ square lattices with $L \le 48$, and $p$ = 0.5, where $p$ is the fraction of negative bonds, using periodic and/or antiperiodic boundary conditions. When $L$ is even, almost all domain walls have energy $E_{dw}$ = 0 or 4. When $L$ is odd, most domain walls have $E_{dw}$ = 2. The probability distribution of the entropy, $S_{dw}$, is found to depend strongly on $E_{dw}$. When $E_{dw} = 0$, the probability distribution of $|S_{dw}|$ is approximately exponential. The variance of this distribution is proportional to $L$, in agreement with the results of Saul and Kardar. For $E_{dw} = k > 0$ the distribution of $S_{dw}$ is not symmetric about zero. In these cases the variance still appears to be linear in $L$, but the average of $S_{dw}$ grows faster than $\sqrt{L}$. This suggests a one-parameter scaling form for the $L$-dependence of the distributions of $S_{dw}$ for $k > 0$.Comment: 13 page

Is it time to reappraise blood pressure thresholds and targets? Statement from the international society of hypertension - a global perspective

No abstract available

Finite-Size Scaling in the Energy-Entropy Plane for the 2D +- J Ising Spin Glass

For $L \times L$ square lattices with $L \le 20$ the 2D Ising spin glass with +1 and -1 bonds is found to have a strong correlation between the energy and the entropy of its ground states. A fit to the data gives the result that each additional broken bond in the ground state of a particular sample of random bonds increases the ground state degeneracy by approximately a factor of 10/3. For $x = 0.5$ (where $x$ is the fraction of negative bonds), over this range of $L$, the characteristic entropy defined by the energy-entropy correlation scales with size as $L^{1.78(2)}$. Anomalous scaling is not found for the characteristic energy, which essentially scales as $L^2$. When $x= 0.25$, a crossover to $L^2$ scaling of the entropy is seen near $L = 12$. The results found here suggest a natural mechanism for the unusual behavior of the low temperature specific heat of this model, and illustrate the dangers of extrapolating from small $L$.Comment: 9 pages, two-column format; to appear in J. Statistical Physic

Replica Cluster Variational Method: the Replica Symmetric solution for the 2D random bond Ising model

We present and solve the Replica Symmetric equations in the context of the Replica Cluster Variational Method for the 2D random bond Ising model (including the 2D Edwards-Anderson spin glass model). First we solve a linearized version of these equations to obtain the phase diagrams of the model on the square and triangular lattices. In both cases the spin-glass transition temperatures and the tricritical point estimations improve largely over the Bethe predictions. Moreover, we show that this phase diagram is consistent with the behavior of inference algorithms on single instances of the problem. Finally, we present a method to consistently find approximate solutions to the equations in the glassy phase. The method is applied to the triangular lattice down to T=0, also in the presence of an external field.Comment: 22 pages, 11 figure

Magneto infra-red absorption in high electronic density GaAs quantum wells

Magneto infra-red absorption measurements have been performed in a highly doped GaAs quantum well which has been lifted off and bonded to a silicon substrate, in order to study the resonant polaron interaction. It is found that the pinning of the cyclotron energy occurs at an energy close to that of the transverse optical phonon of GaAs. This unexpected result is explained by a model taking into account the full dielectric constant of the quantum well.Comment: 4 pages, 4 figures, to be published in Phys. Rev. Let

Legacy benefits of blood pressure treatment on cardiovascular events are primarily mediated by improved blood pressure variability: the ASCOT trial.

BACKGROUND AND AIMS: Visit-to-visit systolic blood pressure variability (BPV) is an important predictor of cardiovascular (CV) outcomes. The long-term effect of a period of blood pressure (BP) control, but with differential BPV, is uncertain. Morbidity and mortality follow-up of UK participants in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure-Lowering Arm has been extended for up to 21 years to determine the CV impact of mean systolic blood pressure (SBP) control and BPV during the trial, and amongst those allocated to amlodipine- and atenolol-based treatment. METHODS: Eight thousand five hundred and eighty hypertensive participants (4305 assigned to amlodipine ± perindopril-based and 4275 to atenolol ± diuretic-based treatment during the in-trial period (median 5.5 years) were followed for up to 21 years (median 17.4 years), using linked hospital and mortality records. A subgroup of participants (n = 2156) was followed up 6 years after the trial closure with a self-administered questionnaire and a clinic visit. In-trial mean SBP and standard deviation of visit-to-visit SBP as a measure of BPV, were measured using >100 000 BP measurements. Cox proportional hazard models were used to estimate the risk [hazard ratios (HRs)], associated with (i) mean with SBP and BPV during the in-trial period, for the CV endpoints occurring after the end of the trial and (ii) randomly assigned treatment to events following randomization, for the first occurrence of pre-specified CV outcomes. RESULTS: Using BP data from the in-trial period, in the post-trial period, although mean SBP was a predictor of CV outcomes {HR per 10 mmHg, 1.14 [95% confidence interval (CI) 1.10-1.17], P < .001}, systolic BPV independent of mean SBP was a strong predictor of CV events [HR per 5 mmHg 1.22 (95% CI 1.18-1.26), P < .001] and predicted events even in participants with well-controlled BP. During 21-year follow-up, those on amlodipine-based compared with atenolol-based in-trial treatment had significantly reduced risk of stroke [HR 0.82 (95% CI 0.72-0.93), P = .003], total CV events [HR 0.93 (95% CI 0.88-0.98), P = .008], total coronary events [HR 0.92 (95% CI 0.86-0.99), P = .024], and atrial fibrillation [HR 0.91 (95% CI 0.83-0.99), P = .030], with weaker evidence of a difference in CV mortality [HR 0.91 (95% CI 0.82-1.01), P = .073]. There was no significant difference in the incidence of non-fatal myocardial infarction and fatal coronary heart disease, heart failure, and all-cause mortality. CONCLUSIONS: Systolic BPV is a strong predictor of CV outcome, even in those with controlled SBP. The long-term benefits of amlodipine-based treatment compared with atenolol-based treatment in reducing CV events appear to be primarily mediated by an effect on systolic BPV during the trial period

Driving self-regulation and risky driving outcomes

Self-regulation has been associated with risky driving outcomes in the past but there are no available measures to assess driving-specific self-regulatory capacity. The present study assessed the association of a newly developed driving self-regulation measure with driving violations, errors, and lapses. Overall, 330 UK drivers completed measures of risky driving outcomes, driving anger, trait impulsivity, sensation seeking, normlessness, domain-general trait self-regulation plus a new unidimensional measure of Driving Self-Regulation Questionnaire (DSRQ-16). Bivariate correlation analysis indicated that the DSRQ-16 showed expected associations with both driving-related outcomes and factors, as well as with impulsivity traits and general self-regulation. Bootstrapped hierarchical linear regression models showed that the DSRQ-16 was significantly associated with driving violations, errors, and lapses after controlling for the effects of other relevant predictors. This is the first study to demonstrate the association of driving-specific self-regulation with risky driving behaviour, driving anger, impulsivity and related personality traits. Driving-specific self-regulation may present a novel target for road safety interventions, as well as a theoretically relevant component of models of risky driving behaviour

RhoJ interacts with the GIT-PIX complex and regulates focal adhesion disassembly

RhoJ is a Rho GTPase expressed in endothelial cells and tumour cells, which regulates cell motility, invasion, endothelial tube formation and focal adhesion numbers. This study aimed to further delineate the molecular function of RhoJ. Using timelapse microscopy RhoJ was found to regulate focal adhesion disassembly; small interfering RNA (siRNA)-mediated knockdown of RhoJ increased focal adhesion disassembly time, whereas expression of an active mutant (daRhoJ) decreased it. Furthermore, daRhoJ co-precipitated with the GIT–PIX complex, a regulator of focal adhesion disassembly. An interaction between daRhoJ and GIT1 was confirmed using yeast two-hybrid experiments, and this depended on the Spa homology domain of GIT1. GIT1, GIT2, β-PIX (also known as ARHGEF7) and RhoJ all colocalised in focal adhesions and depended on each other for their recruitment to focal adhesions. Functionally, the GIT–PIX complex regulated endothelial tube formation, with knockdown of both GIT1 and GIT2, or β-PIX phenocopying RhoJ knockdown. RhoJ-knockout mice showed reduced tumour growth and diminished tumour vessel density, identifying a role for RhoJ in mediating tumour angiogenesis. These studies give new insight into the molecular function of RhoJ in regulating cell motility and tumour vessel formation