Interference, Coulomb blockade, and the identification of non-abelian quantum Hall states

We examine the relation between different electronic transport phenomena in a Fabry-Perot interferometer in the fractional quantum Hall regime. In particular, we study the way these phenomena reflect the statistics of quantum Hall quasi-particles. For two series of states we examine, one abelian and one non-abelian, we show that the information that may be obtained from measurements of the lowest order interference pattern in an open Fabry-Perot interferometer is identical to the one that may be obtained from the temperature dependence of Coulomb blockade peaks in a closed interferometer. We argue that despite the similarity between the experimental signatures of the two series of states, interference and Coulomb blockade measurements are likely to be able to distinguish between abelian and non-abelian states, due to the sensitivity of the abelian states to local perturbations, to which the non-abelian states are insensitive.Comment: 10 pages. Published versio

Partition Functions of Non-Abelian Quantum Hall States

Partition functions of edge excitations are obtained for non-Abelian Hall states in the second Landau level, such as the anti-Read-Rezayi state, the Bonderson-Slingerland hierarchy and the Wen non-Abelian fluid, as well as for the non-Abelian spin-singlet state. The derivation is straightforward and unique starting from the non-Abelian conformal field theory data and solving the modular invariance conditions. The partition functions provide a complete account of the excitation spectrum and are used to describe experiments of Coulomb blockade and thermopower.Comment: 42 pages, 3 figures; published version; minor corrections to sect. 4.

Oral History of Ilan C. Halperin

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Minimum urine flow rate during water deprivation: Importance of the permeability of urea in the inner medulla

Minimum urine flow rate during water deprivation: Importance of the permeability of urea in the inner medulla. We evaluated whether altering the rate of excretion of sodium (Na) and chloride (Cl) when antidiuretic hormone (ADH) acts would cause urea to behave as an ‘effective’ or ‘ineffective’ urinary solute. Urine composition was compared to that in the excised papillary tip in rats treated with DDAVP while on a normal or a low electrolyte diet; half the rats were given a urea load. Studies were also carried out in humans who were water restricted for 12 to 16 hours and given DDAVP. One group had a high rate of NaCl excretion induced by a thiazide diuretic, while the other group consumed a low salt diet to decrease the rate of excretion of electrolytes. Urea (3 mmol/kg) was ingested after the control urine samples were collected. On the high salt protocols, the urine flow rate was directly proportional to the rate of excretion of electrolytes (‘non-urea’ osmoles) and there was no change in the ‘non-urea’ osmolality despite large changes in Na and Cl excretion rates. After urea was administered, there was no change in urine flow rate, ‘non-urea’ osmolality, or ‘non-urea’ osmole excretion rate, whereas the urinary urea concentration, urine osmolality and the rate of excretion of urea were higher. The papilla of the salt-loaded rats had a similar urea concentration to that in the urine. In contrast, in the low electrolyte excretion protocols, the sum of the concentrations of ‘non-urea’ osmoles in the urine was much lower than that in the excised papilla, and the converse applied to urea. Similar changes were observed in the composition of the urine in human subjects with high and low rates of excretion of electrolytes. We conclude that urea appears to be an ‘ineffective’ urine osmole when there is a high rate of salt excretion, whereas urea is an ‘effective’ osmole when there is a low rate of excretion of electrolytes

Alteration of Actin Organization by Jaspamide Inhibits Ruffling, but not Phagocytosis or Oxidative Burst, in HL-60 Cells and Human Monocytes

Jaspamide, a naturally occurring cyclic peptide isolated from the marine sponge Hemiastrella minor, has fungicidal and growth-inhibiting activities. Exposure of promyelocytic HL-60 cells and human monocytes to jaspamide induces a dramatic reorganization of actin from a typical fibrous network to focal aggregates. HL-60 cells exposed to 5 × 10−8 mol/L or 10−7 mol/L jaspamide exhibited a reduced proliferation rate. In addition, 10−7mol/L jaspamide induced maturation of HL-60 cells as indicated by the appearance of a lobulated nucleus in 55% ± 5% of the cells and immunophenotypic maturation of the leukemia cells (upregulation of CD16 and CD14 B antigens). Further characterization has shown that F-actin is aggregated both in HL-60 cells and in human monocytes exposed to 10−7 mol/L jaspamide. Well-spread cultured human monocytes contracted and adopted round shapes after treatment with jaspamide. Moreover, a dose-dependent increase in both total actin and de novo synthesized portions of the soluble actin was observed in jaspamide-treated HL-60 cells. Jaspamide treatment inhibits ruffling and intracellular movement in HL-60 cells and monocytes, but does not affect phagocytic activity or respiratory burst activity. The consequential effects of jaspamide-induced actin reorganization on ruffling, versus its negligible effect on phagocytosis and oxidative burst, may shed light on molecular mechanisms of actin involvement in these processes. Jaspamide disrupts the actin cytoskeleton of normal and malignant mammalian cells with no significant effect on phagocytic activity and may, therefore, be considered as a novel therapeutic agent.</jats:p