Anomalously localized states and multifractal correlations of critical wavefunctions in two-dimensional electron systems with spin-orbital interactions

Anomalously localized states (ALS) at the critical point of the Anderson transition are studied for the SU(2) model belonging to the two-dimensional symplectic class. Giving a quantitative definition of ALS to clarify statistical properties of them, the system-size dependence of a probability to find ALS at criticality is presented. It is found that the probability increases with the system size and ALS exist with a finite probability even in an infinite critical system, though the typical critical states are kept to be multifractal. This fact implies that ALS should be eliminated from an ensemble of critical states when studying critical properties from distributions of critical quantities. As a demonstration of the effect of ALS to critical properties, we show that the distribution function of the correlation dimension of critical wavefunctions becomes a delta function in the thermodynamic limit only if ALS are eliminated.Comment: 7 pages, 6 figure

Impact of clinical phenotypes on management and outcomes in European atrial fibrillation patients: a report from the ESC-EHRA EURObservational Research Programme in AF (EORP-AF) General Long-Term Registry

Background: Epidemiological studies in atrial fibrillation (AF) illustrate that clinical complexity increase the risk of major adverse outcomes. We aimed to describe European AF patients\u2019 clinical phenotypes and analyse the differential clinical course. Methods: We performed a hierarchical cluster analysis based on Ward\u2019s Method and Squared Euclidean Distance using 22 clinical binary variables, identifying the optimal number of clusters. We investigated differences in clinical management, use of healthcare resources and outcomes in a cohort of European AF patients from a Europe-wide observational registry. Results: A total of 9363 were available for this analysis. We identified three clusters: Cluster 1 (n = 3634; 38.8%) characterized by older patients and prevalent non-cardiac comorbidities; Cluster 2 (n = 2774; 29.6%) characterized by younger patients with low prevalence of comorbidities; Cluster 3 (n = 2955;31.6%) characterized by patients\u2019 prevalent cardiovascular risk factors/comorbidities. Over a mean follow-up of 22.5 months, Cluster 3 had the highest rate of cardiovascular events, all-cause death, and the composite outcome (combining the previous two) compared to Cluster 1 and Cluster 2 (all P <.001). An adjusted Cox regression showed that compared to Cluster 2, Cluster 3 (hazard ratio (HR) 2.87, 95% confidence interval (CI) 2.27\u20133.62; HR 3.42, 95%CI 2.72\u20134.31; HR 2.79, 95%CI 2.32\u20133.35), and Cluster 1 (HR 1.88, 95%CI 1.48\u20132.38; HR 2.50, 95%CI 1.98\u20133.15; HR 2.09, 95%CI 1.74\u20132.51) reported a higher risk for the three outcomes respectively. Conclusions: In European AF patients, three main clusters were identified, differentiated by differential presence of comorbidities. Both non-cardiac and cardiac comorbidities clusters were found to be associated with an increased risk of major adverse outcomes

Computational analysis of nonuniform expansion in polyurethane foams

This paper computationally investigates heterogeneity in the distribution of foam fraction in chemically expanding blown polyurethane foam. The experimentally observed disparity in the volumes of expanded foam when an equal mass of the foaming mixture was injected into tubes of different dimensions motivated this study. To understand this phenomenon, attributed to local variations in the thermal and rheological properties of the expanding system, we explore available data from free-rise foam-expansion experiments in different geometries. Inspired by the mathematical framework for the microstructure modelling of bubble growth in viscous liquids, we study the reacting mixture as a continuum and formulate appropriate mathematical models that account for spatial inhomogeneity in the foam-expansion process. The nonlinear coupled system of partial differential equations governing flow was numerically solved using finite-volume techniques, and the associated results are presented and discussed with graphical illustrations. The proximity of the foaming-mixture core to the external environment and the thickness of a thermal-diffusion layer formed near the bounding geometry was seen to influence the distribution of the foam fraction. Our simulations showed an average spatial variation of about 1.1% in the distribution of solid foam fraction from the walls to the core, as verified with data from μ CT scan analysis of the expanded foam. This also reflects the distribution of void fraction in the foam matrix. The models were validated with experimental data, and our results favourably compared with the experiment observations

Impaired autophagy induces chronic atrophic pancreatitis in mice via sex- and nutrition-dependent processes.

BACKGROUND & AIMS: Little is known about the mechanisms of the progressive tissue destruction, inflammation, and fibrosis that occur during development of chronic pancreatitis. Autophagy is involved in multiple degenerative and inflammatory diseases, including pancreatitis, and requires the protein autophagy related 5 (ATG5). We created mice with defects in autophagy to determine its role in pancreatitis. METHODS: We created mice with pancreas-specific disruption of Atg5 (Ptf1aCre(ex1);Atg5(F/F) mice), and compared them to control mice. Pancreata were collected and histology, immunohistochemistry, transcriptome, and metabolome analyses were performed. ATG5-deficient mice were placed on diets containing 25% palm oil and compared to those on a standard diet. Another set of mice received the antioxidant N-acetylcysteine. Pancreatic tissues were collected from 8 patients with chronic pancreatitis (CP) and compared to pancreata from ATG5-deficient mice. RESULTS: Mice with pancreas-specific disruption of Atg5 developed atrophic CP, independent of β-cell function; a greater proportion of male mice developed CP than females. Pancreata from ATG5-deficient mice had signs of inflammation, necrosis, acinar-to-ductal metaplasia, and acinar-cell hypertrophy; this led to tissue atrophy and degeneration. Based on transcriptome and metabolome analyses, ATG5-deficient mice produced higher levels of reactive oxygen species than control mice, and had insufficient activation of glutamate-dependent metabolism. Pancreata from these mice had reduced autophagy, increased levels of p62, and increases in endoplasmic reticulum stress and mitochondrial damage, compared with tissues from control mice; p62 signaling to Nqo1 and p53 was also activated. Dietary antioxidants, especially in combination with palm oil-derived fatty acids, blocked progression to CP and pancreatic acinar atrophy. Tissues from patients with CP had many histologic similarities to those from ATG5-deficient mice. CONCLUSIONS: Mice with pancreas-specific disruption of Atg5 develop a form of CP similar to that of humans. CP development appears to involve defects in autophagy, glutamate-dependent metabolism, and increased production of reactive oxygen species. These mice might be used to identify therapeutic targets for CP