Strong-coupling branching of FQHL edges

We have developed a theory of quasiparticle backscattering in a system of point contacts formed between single-mode edges of several Fractional Quantum Hall Liquids (FQHLs) with in general different filling factors $\nu_j$ and one common single-mode edge $\nu_0$ of another FQHL. In the strong-tunneling limit, the model of quasiparticle backscattering is obtained by the duality transformation of the electron tunneling model. The new physics introduced by the multi-point-contact geometry of the system is coherent splitting of backscattered quasiparticles at the point contacts in the course of propagation along the common edge $\nu_0$. The ``branching ratios'' characterizing the splitting determine the charge and exchange statistics of the edge quasiparticles that can be different from those of Laughlin's quasiparticles in the bulk of FQHLs. Accounting for the edge statistics is essential for the system of more than one point contact and requires the proper description of the flux attachement to tunneling electrons.Comment: 12 pages, 2 figure

Proposal for reading out anyon qubits in non-abelian ν=12/5\nu = 12/5 quantum Hall state

To detect non-abelian statistics in the $\nu = 12/5$ quantum Hall state through interferometry, we apply an analysis similar to the ones proposed for the non-abelian $\nu = 5/2$ quantum Hall state. The result is that the amplitude of the Aharonov-Bohm oscillation of this interference is dependent on the internal states of quasiholes, but, in contrast to the $\nu = 5/2$ quantum Hall state, independent of the number of quasiholes. However, if the quasiholes are in a superposition state, it is necessary for the interferometer to have certain additional features to obtain the coefficients.Comment: 16 pages, 2 figures, Latex. Reference added, some errors corrected, some content changed, some changes in the abstrac

Effects of Intravenous Aspirin on Prostaglandin Synthesis and Kidney Function in Intensive Care Patients

The effects of intravenous acetylsalicylic acid (1.0 g bolus) on renal function and prostaglandin synthesis were evaluated in a prospective, controlled study in eight patients in an intensive care unit. Four of these patients had congestive heart failure. Administration of acetylsalicylic acid caused significant antidiuresis (−56%), antinatriuresis (−82%), renin suppression (−26%) and decreased GFR (−41%). All of these changes were completely reversible within 1-2 hours and tended to be more pronounced in the patients with congestive heart failure. Urinary excretion of prostaglandin E was depressed profoundly (−93%) and did not return to more than 45% of control 6 h after the administration of acetylsalicylic acid. We conclude that intravenous acetylsalicylic acid affects kidney function in a manner similar to other prostaglandin synthesis inhibitors. Its effects are, however, short-lived. The inhibition of urinary PGE2 excretion outlasts GFR depression, antidiuresis, antinatriuresis and renin suppression by several hour

A Gauge-Independent Mechanism for Confinement and Mass Gap: Part II -- G=SU(2) and D=3

We apply to the case of gauge group G = SU(2) in three dimensions a recently proposed gauge-independent mechanism for confinement that is based on a particular form of the dual spin foam framework for lattice gauge theory. Explicit formulae for interaction factors and their asymptotics are introduced and their behavior in different sectors of the theory are identified and analyzed. We arrive at several elementary properties of the dual theory that represent one scenario by which confinement may be realized at weak coupling. We conclude with an outlook for further development of this approach.Comment: 18 pages, 3 figure

genomepy: genes and genomes at your fingertips

Analyzing a functional genomics experiment, such as ATAC-, ChIP- or RNA-sequencing, requires reference data including a genome assembly and gene annotation. These resources can generally be retrieved from different organizations and in different versions. Most bioinformatic workflows require the user to supply this genomic data manually, which can be a tedious and error-prone process. Here we present genomepy, which can search, download, and preprocess the right genomic data for your analysis. Genomepy can search genomic data on NCBI, Ensembl, UCSC and GENCODE, and compare available gene annotations to enable an informed decision. The selected genome and gene annotation can be downloaded and preprocessed with sensible, yet controllable, defaults. Additional supporting data can be automatically generated or downloaded, such as aligner indexes, genome metadata and blacklists. Genomepy is freely available at https://github.com/vanheeringen-lab/genomepy under the MIT license and can be installed through pip or bioconda

Whole body and hepatic insulin action in normal, starved, and diabetic rats

In normal (N), 3-days starved (S), and streptozotocin-treated (65 mg/kg) 3-days diabetic (D) rats we examined the in vivo dose-response relationship between plasma insulin levels vs. whole body glucose uptake (BGU) and inhibition of hepatic glucose production (HGP) in conscious rats, as determined with the four-step sequential hyperinsulinemic euglycemic clamp technique, combined with [3-3H]glucose infusion. Twelve-hour fasting (basal) HGP was 3.0 +/- 0.2, 2.1 +/- 0.2, and 5.4 +/- 0.5 mg/min in N, S, and D rats, respectively. Next, all rats were clamped at matched glycemia (6 mM). Lowering plasma glucose in D rats from +/- 20 to 6.0 mM did not increase plasma norepinephrine, epinephrine, glucagon, and corticosterone levels. For BGU, insulin sensitivity was increased (70 +/- 11 microU/ml) in S and unchanged (113 +/- 21 microU/ml) in D compared with N rats (105 +/- 10 microU/ml). Insulin responsiveness was unchanged (12.4 +/- 0.8 mg/min) in S and decreased (8.5 +/- 0.8 mg/min) in D compared with N rats (12.3 +/- 0.7 mg/min). For HGP, insulin sensitivity was unchanged (68 +/- 10 microU/ml) in S and decreased (157 +/- 21 microU/ml) in D compared with N rats (71 +/- 5 microU/ml). Insulin responsiveness was identical among N, S, and D rats (complete suppression of HGP). In summary, 1) insulin resistance in D rats is caused by hepatic insensitivity and by a reduction in BGU responsiveness. 2) S rats show normal hepatic insulin action, but insulin sensitivity for BGU is increased. Therefore, S and D rats both suffering from a comparable catabolic state (10-15% body wt loss in 3 days) show opposite effects on in vivo insulin action. This indicates that in vivo insulin resistance in D rats is not caused by the catabolic state per se