Edge magnetoplasmons in periodically modulated structures

We present a microscopic treatment of edge magnetoplasmons (EMP's) within the random-phase approximation for strong magnetic fields, low temperatures, and filling factor $\nu =1(2)$, when a weak short-period superlattice potential is imposed along the Hall bar. The modulation potential modifies both the spatial structure and the dispersion relation of the fundamental EMP and leads to the appearance of a novel gapless mode of the fundamental EMP. For sufficiently weak modulation strengths the phase velocity of this novel mode is almost the same as the group velocity of the edge states but it should be quite smaller for stronger modulation. We discuss in detail the spatial structure of the charge density of the renormalized and the novel fundamental EMP's.Comment: 8 pages, 4 figure

On the Treewidth of Dynamic Graphs

Dynamic graph theory is a novel, growing area that deals with graphs that change over time and is of great utility in modelling modern wireless, mobile and dynamic environments. As a graph evolves, possibly arbitrarily, it is challenging to identify the graph properties that can be preserved over time and understand their respective computability. In this paper we are concerned with the treewidth of dynamic graphs. We focus on metatheorems, which allow the generation of a series of results based on general properties of classes of structures. In graph theory two major metatheorems on treewidth provide complexity classifications by employing structural graph measures and finite model theory. Courcelle's Theorem gives a general tractability result for problems expressible in monadic second order logic on graphs of bounded treewidth, and Frick & Grohe demonstrate a similar result for first order logic and graphs of bounded local treewidth. We extend these theorems by showing that dynamic graphs of bounded (local) treewidth where the length of time over which the graph evolves and is observed is finite and bounded can be modelled in such a way that the (local) treewidth of the underlying graph is maintained. We show the application of these results to problems in dynamic graph theory and dynamic extensions to static problems. In addition we demonstrate that certain widely used dynamic graph classes naturally have bounded local treewidth

Predicting outcomes in rheumatoid arthritis related interstitial lung disease

Aims: To compare radiology-based prediction models in rheumatoid arthritis-related interstitial lung disease (RA-ILD) to identify patients with a progressive fibrosis phenotype.Methods: RAILD patients had CTs scored visually and by CALIPER and forced vital capacity (FVC) measurements. Outcomes were evaluated using three techniques: 1.Scleroderma system evaluating visual ILD extent and FVC values; 2.Fleischer Society IPF diagnostic guidelines applied to RAILD; 3.CALIPER scores of vessel-related structures (VRS). Outcomes were compared to IPF patients.Results: On univariable Cox analysis, all three staging systems strongly predicted outcome: Scleroderma System:HR=3.78, p=9×10-5; Fleischner System:HR=1.98, p=2×10-3; 4.4% VRS threshold:HR=3.10, p=4×10-4 When the Scleroderma and Fleischner Systems were combined, termed the Progressive Fibrotic System (C-statistic=0.71), they identified a patient subset (n=36) with a progressive fibrotic phenotype and similar 4-year survival to IPF.On multivariable analysis, with adjustment for patient age, gender and smoking status, when analysed alongside the Progressive Fibrotic System, the VRS threshold of 4.4% independently predicted outcome (Model C-statistic=0.77).Conclusions: The combination of two visual CT-based staging systems identified 23% of an RAILD cohort with an IPF-like progressive fibrotic phenotype. The addition of a computer-derived VRS threshold further improved outcome prediction and model fit, beyond that encompassed by RAILD measures of disease severity and extent

Height Systems and Vertical Datums: a Review in the Australian Context

This paper reviews (without equations) the various definitions of height systems and vertical geodetic datum surfaces, together with their practical realisation for users in Australia. Excluding geopotential numbers, a height system is a one-dimensional coordinate system used to express the metric distance (height) of a point from some reference surface. Its definition varies according to the reference surface chosen and the path along which the height is measured. A vertical geodetic datum is the practical realisation of a height system and its reference surface for users, nominally tied to mean sea level. In Australia, the normal-orthometric height system is used, which is embedded in the Australian Height Datum (AHD). The AHD was realised by the adjustment of ~195,000 km of spirit-levelling observations fixed to limited-term observations of mean sea level at multiple tide-gauges. The paper ends by giving some explanation of the problems with the AHD and of the differences between the AHD and the national geoid model, pointing out that it is preferable to recompute the AHD

Increased central adiposity and decreased subcutaneous adipose tissue 11β-hydroxysteroid dehydrogenase type 1 are associated with deterioration in glucose tolerance-A longitudinal cohort study

Objective and Context. Increasing adiposity, ageing and tissue‐specific regeneration of cortisol through the activity of 11β‐hydroxysteroid dehydrogenase type 1 have been associated with deterioration in glucose tolerance. We undertook a longitudinal, prospective clinical study to determine if alterations in local glucocorticoid metabolism track with changes in glucose tolerance. Design, Patients, and Measurements. Sixty‐five overweight/obese individuals (mean age 50.3 ± 7.3 years) underwent oral glucose tolerance testing, body composition assessment, subcutaneous adipose tissue biopsy and urinary steroid metabolite analysis annually for up to 5 years. Participants were categorized into those in whom glucose tolerance deteriorated (“deteriorators”) or improved (“improvers”). Results. Deteriorating glucose tolerance was associated with increasing total and trunk fat mass and increased subcutaneous adipose tissue expression of lipogenic genes. Subcutaneous adipose tissue 11β‐HSD1 gene expression decreased in deteriorators, and at study completion, it was highest in the improvers. There was a significant negative correlation between change in area under the curve glucose and 11β‐HSD1 expression. Global 11β‐HSD1 activity did not change and was not different between deteriorators and improvers at baseline or follow‐up. Conclusion. Longitudinal deterioration in metabolic phenotype is not associated with increased 11β‐HSD1 activity, but decreased subcutaneous adipose tissue gene expression. These changes may represent a compensatory mechanism to decrease local glucocorticoid exposure in the face of an adverse metabolic phenotype

Models of <i>KPTN</i>-related disorder implicate mTOR signalling in cognitive and overgrowth phenotypes

KPTN-related disorder is an autosomal recessive disorder associated with germline variants in KPTN (previously known as kaptin), a component of the mTOR regulatory complex KICSTOR. To gain further insights into the pathogenesis of KPTN-related disorder, we analysed mouse knockout and human stem cell KPTN loss-of-function models. Kptn -/- mice display many of the key KPTN-related disorder phenotypes, including brain overgrowth, behavioural abnormalities, and cognitive deficits. By assessment of affected individuals, we have identified widespread cognitive deficits (n = 6) and postnatal onset of brain overgrowth (n = 19). By analysing head size data from their parents (n = 24), we have identified a previously unrecognized KPTN dosage-sensitivity, resulting in increased head circumference in heterozygous carriers of pathogenic KPTN variants. Molecular and structural analysis of Kptn-/- mice revealed pathological changes, including differences in brain size, shape and cell numbers primarily due to abnormal postnatal brain development. Both the mouse and differentiated induced pluripotent stem cell models of the disorder display transcriptional and biochemical evidence for altered mTOR pathway signalling, supporting the role of KPTN in regulating mTORC1. By treatment in our KPTN mouse model, we found that the increased mTOR signalling downstream of KPTN is rapamycin sensitive, highlighting possible therapeutic avenues with currently available mTOR inhibitors. These findings place KPTN-related disorder in the broader group of mTORC1-related disorders affecting brain structure, cognitive function and network integrity.</p