Tame group actions on central simple algebras

We study actions of linear algebraic groups on finite-dimensional central simple algebras. We describe the fixed algebra for a broad class of such actions.Comment: 19 pages, LaTeX; slightly revised; final version will appear in Journal of Algebr

Functional complementation of UvsX and UvsY mutations in the mediation of T4 homologous recombination

Bacteriophage T4 homologous recombination events are promoted by presynaptic filaments of UvsX recombinase bound to single-stranded DNA (ssDNA). UvsY, the phage recombination mediator protein, promotes filament assembly in a concentration-dependent manner, stimulating UvsX at stoichiometric concentrations but inhibiting at higher concentrations. Recent work demonstrated that UvsX-H195Q/A mutants exhibit decreased ssDNA-binding affinity and altered enzymatic properties. Here, we show that unlike wild-type UvsX, the ssDNA-dependent ATPase activities of UvsX-H195Q/A are strongly inhibited by both low and high concentrations of UvsY protein. This inhibition is partially relieved by UvsY mutants with decreased ssDNA-binding affinity. The UvsX-H195Q mutant retains weak DNA strand exchange activity that is inhibited by wild-type UvsY, but stimulated by ssDNA-binding compromised UvsY mutants. These and other results support a mechanism in which the formation of competent presynaptic filaments requires a hand-off of ssDNA from UvsY to UvsX, with the efficiency of the hand-off controlled by the relative ssDNA-binding affinities of the two proteins. Other results suggest that UvsY acts as a nucleotide exchange factor for UvsX, enhancing filament stability by increasing the lifetime of the high-affinity, ATP-bound form of the enzyme. Our findings reveal new details of the UvsX/UvsY relationship in T4 recombination, which may have parallels in other recombinase/mediator systems

Interoception, Contemplative Practice, and Health

AcceptedArticleCopyright: © 2015 Farb, Daubenmier, Price, Gard, Kerr, Dunn, KLein, Paulus and Mehling.This Document is Protected by copyright and was first published by Frontiers. All rights reserved. it is reproduced with permission.Interoception can be broadly defined as the sense of signals originating within the body. As such, interoception is critical for our sense of embodiment, motivation and well-being. And yet, despite its importance, interoception remains poorly understood within modern science. This paper reviews interdisciplinary perspectives on interoception, with the goal of presenting a unified perspective from diverse fields such as neuroscience, clinical practice, and contemplative studies. It is hoped that this integrative effort will advance our understanding of how interoception determines well-being, and identify the central challenges to such understanding. To this end, we introduce an expanded taxonomy of interoceptive processes, arguing that many of these processes can be understood through an emerging predictive coding model for mind-body integration. The model, which describes the tension between expected and felt body sensation, parallels contemplative theories, and implicates interoception in a variety of affective and psychosomatic disorders. We conclude that maladaptive construal of bodily sensations may lie at the heart of many contemporary maladies, and that contemplative practices may attenuate these interpretative biases, restoring a person’s sense of presence and agency in the world

Generators for the hyperelliptic Torelli group and the kernel of the Burau representation at t = -1

We prove that the hyperelliptic Torelli group is generated by Dehn twists about separating curves that are preserved by the hyperelliptic involution. This verifies a conjecture of Hain. The hyperelliptic Torelli group can be identified with the kernel of the Burau representation evaluated at t = −1 and also the fundamental group of the branch locus of the period mapping, and so we obtain analogous generating sets for those. One application is that each component in Torelli space of the locus of hyperelliptic curves becomes simply connected when curves of compact type are added

Bounding Helly numbers via Betti numbers

We show that very weak topological assumptions are enough to ensure the existence of a Helly-type theorem. More precisely, we show that for any non-negative integers $b$ and $d$ there exists an integer $h(b,d)$ such that the following holds. If $\mathcal F$ is a finite family of subsets of $\mathbb R^d$ such that $\tilde\beta_i\left(\bigcap\mathcal G\right) \le b$ for any $\mathcal G \subsetneq \mathcal F$ and every $0 \le i \le \lceil d/2 \rceil-1$ then $\mathcal F$ has Helly number at most $h(b,d)$. Here $\tilde\beta_i$ denotes the reduced $\mathbb Z_2$-Betti numbers (with singular homology). These topological conditions are sharp: not controlling any of these $\lceil d/2 \rceil$ first Betti numbers allow for families with unbounded Helly number. Our proofs combine homological non-embeddability results with a Ramsey-based approach to build, given an arbitrary simplicial complex $K$, some well-behaved chain map $C_*(K) \to C_*(\mathbb R^d)$.Comment: 29 pages, 8 figure

Hyperbolic and semi-hyperbolic surface codes for quantum storage

We show how a hyperbolic surface code could be used for overhead-efficient quantum storage. We give numerical evidence for a noise threshold of 1.3% for the {4, 5}-hyperbolic surface code in a phenomenological noise model (as compared with 2.9% for the toric code). In this code family, parity checks are of weight 4 and 5, while each qubit participates in four different parity checks. We introduce a family of semi-hyperbolic codes that interpolate between the toric code and the {4, 5}-hyperbolic surface code in terms of encoding rate and threshold. We show how these hyperbolic codes outperform the toric code in terms of qubit overhead for a target logical error probability. We show how Dehn twists and lattice code surgery can be used to read and write individual qubits to this quantum storage medium

Peroxisome Proliferator-Activated Receptor-Gamma Agonists Suppress Tissue Factor Overexpression in Rat Balloon Injury Model with Paclitaxel Infusion

The role and underlying mechanisms of rosiglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonist, on myocardial infarction are poorly understood. We investigated the effects of this PPAR-γ agonist on the expression of tissue factor (TF), a primary molecule for thrombosis, and elucidated its underlying mechanisms. The PPAR-γ agonist inhibited TF expression in response to TNF-α in human umbilical vein endothelial cells, human monocytic leukemia cell line, and human umbilical arterial smooth muscle cells. The overexpression of TF was mediated by increased phosphorylation of mitogen-activated protein kinase (MAPK), which was blocked by the PPAR-γ agonist. The effective MAPK differed depending on each cell type. Luciferase and ChIP assays showed that transcription factor, activator protein-1 (AP-1), was a pivotal target of the PPAR-γ agonist to lower TF transcription. Intriguingly, two main drugs for drug-eluting stent, paclitaxel or rapamycin, significantly exaggerated thrombin-induced TF expression, which was also effectively blocked by the PPAR-γ agonist in all cell types. This PPAR-γ agonist did not impair TF pathway inhibitor (TFPI) in three cell types. In rat balloon injury model (Sprague-Dawley rats, n = 10/group) with continuous paclitaxel infusion, the PPAR-γ agonist attenuated TF expression by 70±5% (n = 4; P<0.0001) in injured vasculature. Taken together, rosiglitazone reduced TF expression in three critical cell types involved in vascular thrombus formation via MAPK and AP-1 inhibitions. Also, this PPAR-γ agonist reversed the paclitaxel-induced aggravation of TF expression, which suggests a possibility that the benefits might outweigh its risks in a group of patients with paclitaxel-eluting stent implanted

Synaptic Plasticity and NO-cGMP-PKG Signaling Regulate Pre- and Postsynaptic Alterations at Rat Lateral Amygdala Synapses Following Fear Conditioning

In vertebrate models of synaptic plasticity, signaling via the putative “retrograde messenger” nitric oxide (NO) has been hypothesized to serve as a critical link between functional and structural alterations at pre- and postsynaptic sites. In the present study, we show that auditory Pavlovian fear conditioning is associated with significant and long-lasting increases in the expression of the postsynaptically-localized protein GluR1 and the presynaptically-localized proteins synaptophysin and synapsin in the lateral amygdala (LA) within 24 hrs following training. Further, we show that rats given intra-LA infusion of either the NR2B-selective antagonist Ifenprodil, the NOS inhibitor 7-Ni, or the PKG inhibitor Rp-8-Br-PET-cGMPS exhibit significant decreases in training-induced expression of GluR1, synaptophysin, and synapsin immunoreactivity in the LA, while those rats infused with the PKG activator 8-Br-cGMP exhibit a significant increase in these proteins in the LA. In contrast, rats given intra-LA infusion of the NO scavenger c-PTIO exhibit a significant decrease in synapsin and synaptophysin expression in the LA, but no significant impairment in the expression of GluR1. Finally, we show that intra-LA infusions of the ROCK inhibitor Y-27632 or the CaMKII inhibitor KN-93 impair training-induced expression of GluR1, synapsin, and synaptophysin in the LA. These findings suggest that the NO-cGMP-PKG, Rho/ROCK, and CaMKII signaling pathways regulate fear memory consolidation, in part, by promoting both pre- and post-synaptic alterations at LA synapses. They further suggest that synaptic plasticity in the LA during auditory fear conditioning promotes alterations at presynaptic sites via NO-driven “retrograde signaling”