Whispering Gallery States of Antihydrogen

We study theoretically interference of the long-living quasistationary quantum states of antihydrogen atoms, localized near a concave material surface. Such states are an antimatter analog of the whispering gallery states of neutrons and matter atoms, and similar to the whispering gallery modes of sound and electro-magnetic waves. Quantum states of antihydrogen are formed by the combined effect of quantum reflection from van der Waals/Casimir-Polder (vdW/CP) potential of the surface and the centrifugal potential. We point out a method for precision studies of quantum reflection of antiatoms from vdW/CP potential; this method uses interference of the whispering gallery states of antihydrogen.Comment: 13 pages 7 figure

Fashion micro-enterprises in London, Berlin, Milan

This report provides an account of a series of interviews, observational visits and hosted events with 8-10 fashion designers in three cities: London, Berlin and Milan, carried out from 2012-2016. In some cases we interviewed the same designers two or three times over a period of nearly three years. The research project also entailed documented conversations and meetings with a range of fashion experts, consultants, legal advisors and policy makers in each city. Often these took place within the context of organised events undertaken as part of the research process. The aim was to investigate the kind of start-ups or micro-enterprises which have come into being in the last decade. We were interested in whether these were the outcome of pro-active urban creative economy policies or if they were self-organised initiatives, a reaction to the crisis of the euro-zone of 2008 and the consequent recession. Was it the case that long-term austerity policies and exceptionally high rates of youth and graduate unemployment across Europe had spawned these kinds of seemingly independent economic activities? We were also minded to consider the role of intellectual property (IP) and copyright in fashion as part of the wider UK government agenda for growth and wealth creation within the creative economy as a whole

Insulin-positive, Glut2-low cells present within mouse pancreas exhibit lineage plasticity and are enriched within extra-islet endocrine cell clusters

ABSTRACT: Regeneration of insulin-producing β-cells from resident pancreas progenitors requires an understanding of both progenitor identity and lineage plasticity. One model suggested that a rare β-cell sub-population within islets demonstrated multi-lineage plasticity. We hypothesized that β-cells from young mice (postnatal day 7, P7) exhibit such plasticity and used a model of islet dedifferentiation toward a ductal epithelial-cell phenotype to test this theory. RIPCre;Z/AP+/+ mice were used to lineage trace the fate of β-cells during dedifferentiation culture by a human placental alkaline phosphatase (HPAP) reporter. There was a significant loss of HPAP-expressing β-cells in culture, but remaining HPAP+ cells lost insulin expression while gaining expression of the epithelial duct cell marker cytokeratin-19 (Ck19). Flow cytometry and recovery of β-cell subpopulations from whole pancreas vs. islets suggest that the HPAP+Ck19+ cells had derived from insulin-positive, glucose-transporter-2-low (Ins+Glut2LO) cells, representing 3.5% of all insulin-expressing cells. The majority of these cells were found outside of islets within clusters of \u3c5 β-cells. These insulin+Glut2LO cells demonstrated a greater proliferation rate in vivo and in vitro as compared to insulin+Glut2+ cells at P7, were retained into adulthood, and a subset differentiated into endocrine, ductal, and neural lineages, illustrating substantial plasticity. Results were confirmed using RIPCre;ROSA- eYFP mice. Quantitative PCR data indicated these cells possess an immature β-cell phenotype. These Ins+Glut2LO cells may represent a resident population of cells capable of forming new, functional β-cells, and which may be potentially exploited for regenerative therapies in the future

Distinct mechanisms of planar polarization by the core and Fat-Dachsous planar polarity pathways in the Drosophila wing

Planar polarity describes the coordinated polarization of cells within a tissue plane, and in animals can be determined by the “core” or Fat-Dachsous pathways. Current models for planar polarity establishment involve two components: tissue-level “global” cues that determine the overall axis of polarity and cell-level feedback-mediated cellular polarity amplification. Here, we investigate the contributions of global cues versus cellular feedback amplification in the core and Fat-Dachsous pathways during Drosophila pupal wing development. We present evidence that these pathways generate planar polarity via distinct mechanisms. Core pathway function is consistent with strong feedback capable of self-organizing cell polarity, which can then be aligned with the tissue axis via weak or transient global cues. Conversely, generation of cell polarity by the Ft-Ds pathway depends on strong global cues in the form of graded patterns of gene expression, which can then be amplified by weak feedback mechanisms

Planar cell polarity: the Dachsous/Fat system contributes differently to the embryonic and larval stages of Drosophila.

The epidermal patterns of all three larval instars (L1-L3) ofDrosophilaare made by one unchanging set of cells. The seven rows of cuticular denticles of all larval stages are consistently planar polarised, some pointing forwards, others backwards. In L1 all the predenticles originate at the back of the cells but, in L2 and L3, they form at the front or the back of the cell depending on the polarity of the forthcoming denticles. We find that, to polarise all rows, the Dachsous/Fat system is differentially utilised; in L1 it is active in the placement of the actin-based predenticles but is not crucial for the final orientation of the cuticular denticles, in L2 and L3 it is needed for placement and polarity. We find Four-jointed to be strongly expressed in the tendon cells and show how this might explain the orientation of all seven rows. Unexpectedly, we find that L3 that lack Dachsous differ from larvae lacking Fat and we present evidence that this is due to differently mislocalised Dachs. We make some progress in understanding how Dachs contributes to phenotypes of wildtype and mutant larvae and adults.This work was generously supported by the Wellcome Trust: a Project Grant [086986] and, later, two successive Investigator Awards, [096645 and 107060] awarded to P.A.L., as well as [100986] to D.S. P.S. thanks Fundaçã o para a Ciência e a Tecnologia and the Cambridge Philosophical Society for research studentships.This is the final version of the article. It first appeared from The Company of Biologists via https://doi.org/10.1242/bio.01715

An increase in immature β-cells lacking Glut2 precedes the expansion of β-cell mass in the pregnant mouse

A compensatory increase in β-cell mass occurs during pregnancy to counter the associated insulin resistance, and a failure in adaptation is thought to contribute to gestational diabetes. Insulin-expressing but glucose-transporter-2-low (Ins+Glut2LO) progenitor cells are present in mouse and human pancreas, being predominantly located in extra-islet β-cell clusters, and contribute to the regeneration of the endocrine pancreas following induced ablation. We therefore sought to investigate the contribution of Ins+Glut2LO cells to β-cell mass expansion during pregnancy. Female C57Bl/6 mice were time mated and pancreata were collected at gestational days (GD) 6, 9, 12, 15, and 18, and postpartum D7 (n = 4/time-point) and compared to control (non-pregnant) animals. Beta cell mass, location, proliferation (Ki67+), and proportion of Ins+Glut2LO cells were measured using immunohistochemistry and bright field or confocal microscopy. Beta cell mass tripled by GD18 and β-cell proliferation peaked at GD12 in islets (6 β-cells) and small β-cell clusters (1–5 β-cells). The proportion and fraction of Ins+Glut2LO cells undergoing proliferation increased significantly at GD9 in both islets and clusters, preceding the increase in β-cell mass and proliferation, and their proliferation within clusters persisted until GD15. The overall number of clusters increased significantly at GD9. Quantitative PCR showed a significant increase in Pdx1 presence at GD9 vs. GD18 or control pancreas, and Pdx1 was visualized by immunohistochemistry within both Ins+Glut2LO and Ins+Glut2HI cells within clusters. These results indicate that Ins+Glut2LO cells are likely to contribute to β-cell mass expansion during pregnancy

Scattering of electromagnetic waves by many small perfectly conducting or impedance bodies

A theory of electromagnetic (EM) wave scattering by many small particles of an arbitrary shape is developed. The particles are perfectly conducting or impedance. For a small impedance particle of an arbitrary shape, an explicit analytical formula is derived for the scattering amplitude. The formula holds as a → 0, where a is a characteristic size of the small particle and the wavelength is arbitrary but fixed. The scattering amplitude for a small impedance particle is shown to be proportional to a2−κ, where κ ∈ [0,1) is a parameter which can be chosen by an experimenter as he/she wants. The boundary impedance of a small particle is assumed to be of the form ζ = ha−κ, where h = const, Reh ≥ 0. The scattering amplitude for a small perfectly conducting particle is proportional to a3, and it is much smaller than that for the small impedance particle. The many-body scattering problem is solved under the physical assumptions a ≪ d ≪ λ, where d is the minimal distance between neighboring particles and λ is the wavelength. The distribution law for the small impedance particles is N(∆) ∼ 1/a2−κ∆ N(x)dx as a → 0. Here, N(x) ≥ 0 is an arbitrary continuous function that can be chosen by the experimenter and N(∆) is the number of particles in an arbitrary sub-domain ∆. It is proved that the EM field in the medium where many small particles, impedance or perfectly conducting, are distributed, has a limit, as a → 0 and a differential equation is derived for the limiting field. On this basis, a recipe is given for creating materials with a desired refraction coefficient by embedding many small impedance particles into a given material. C 2015 AIP Publishing LLC. [http://dx.doi.org/10.1063/1.4929965

Decrease in Ins\u3csup\u3e+\u3c/sup\u3eGlut2\u3csup\u3eLO\u3c/sup\u3e β-cells with advancing age in mouse and human pancreas

The presence and location of resident pancreatic β-cell progenitors is controversial. A subpopulation of insulin-expressing but glucose transporter-2-low (Ins+Glut2LO) cells may represent multipotent pancreatic progenitors in adult mouse and in human islets, and they are enriched in small, extra-islet β-cell clusters (\u3e5 β cells) in mice. Here, we sought to identify and compare the ontogeny of these cells in mouse and human pancreata throughout life. Mouse pancreata were collected at postnatal days 7, 14, 21, 28, and at 3, 6, 12, and 18 months of age, and in the first 28 days after β-cell mass depletion following streptozotocin (STZ) administration. Samples of human pancreas were examined during fetal life (22-30 weeks gestation), infancy (0-1 year), childhood (2-9), adolescence (10-17), and adulthood (18-80). Tissues were analyzed by immunohistochemistry for the expression and location of insulin, GLUT2 and Ki67. The proportion of β cells within clusters relative to that in islets was higher in pancreas of human than of mouse at all ages examined, and decreased significantly at adolescence. In mice, the total number of Ins+Glut2LO cells decreased after 7 days concurrent with the proportion of clusters. These cells were more abundant in clusters than in islets in both species. A positive association existed between the appearance of new β cells after the STZ treatment of young mice, particularly in clusters and smaller islets, and an increased proportional presence of Ins+Glut2LO cells during early β-cell regeneration. These data suggest that Ins+Glut2LO cells are preferentially located within β-cell clusters throughout life in pancreas of mouse and human, and may represent a source of β-cell plasticity

The Mersey Estuary : sediment geochemistry

This report describes a study of the geochemistry of the Mersey estuary carried out between April 2000 and December 2002. The study was the first in a new programme of surveys of the geochemistry of major British estuaries aimed at enhancing our knowledge and understanding of the distribution of contaminants in estuarine sediments. The report first summarises the physical setting, historical development, geology, hydrography and bathymetry of the Mersey estuary and its catchment. Details of the sampling and analytical programmes are then given followed by a discussion of the sedimentology and geochemistry. The chemistry of the water column and suspended particulate matter have not been studied, the chief concern being with the geochemistry of the surface and near-surface sediments of the Mersey estuary and an examination of their likely sources and present state of contamination