Twisted Bethe equations from a twisted S-matrix

All-loop asymptotic Bethe equations for a 3-parameter deformation of AdS5/CFT4 have been proposed by Beisert and Roiban. We propose a Drinfeld twist of the AdS5/CFT4 S-matrix, together with c-number diagonal twists of the boundary conditions, from which we derive these Bethe equations. Although the undeformed S-matrix factorizes into a product of two su(2|2) factors, the deformed S-matrix cannot be so factored. Diagonalization of the corresponding transfer matrix requires a generalization of the conventional algebraic Bethe ansatz approach, which we first illustrate for the simpler case of the twisted su(2) principal chiral model. We also demonstrate that the same twisted Bethe equations can alternatively be derived using instead untwisted S-matrices and boundary conditions with operatorial twists.Comment: 42 pages; v2: a new appendix on sl(2) grading, 2 additional references, and some minor changes; v3: improved Appendix D, additional references, and further minor changes, to appear in JHE

Reaction rates and transport in neutron stars

Understanding signals from neutron stars requires knowledge about the transport inside the star. We review the transport properties and the underlying reaction rates of dense hadronic and quark matter in the crust and the core of neutron stars and point out open problems and future directions.Comment: 74 pages; commissioned for the book "Physics and Astrophysics of Neutron Stars", NewCompStar COST Action MP1304; version 3: minor changes, references updated, overview graphic added in the introduction, improvements in Sec IV.A.

Systematics of the cusp anomalous dimension

We study the velocity-dependent cusp anomalous dimension in supersymmetric Yang-Mills theory. In a paper by Correa, Maldacena, Sever, and one of the present authors, a scaling limit was identified in which the ladder diagrams are dominant and are mapped onto a Schrodinger problem. We show how to solve the latter in perturbation theory and provide an algorithm to compute the solution at any loop order. The answer is written in terms of harmonic polylogarithms. Moreover, we give evidence for two curious properties of the result. Firstly, we observe that the result can be written using a subset of harmonic polylogarithms only, at least up to six loops. Secondly, we show that in a light-like limit, only single zeta values appear in the asymptotic expansion, again up to six loops. We then extend the analysis of the scaling limit to systematically include subleading terms. This leads to a Schrodinger-type equation, but with an inhomogeneous term. We show how its solution can be computed in perturbation theory, in a way similar to the leading order case. Finally, we analyze the strong coupling limit of these subleading contributions and compare them to the string theory answer. We find agreement between the two calculations.Comment: 33 pages, 4 figures. Complete LO six-loop result added. Typos corrected. Version accepted for publicatio

APR-246/PRIMA-1MET inhibits thioredoxin reductase 1 and converts the enzyme to a dedicated NADPH oxidase

The low-molecular-weight compound APR-246 (PRIMA-1(MET)) restores wild-type conformation and function to mutant p53, and triggers apoptosis in tumor cells. We show here that APR-246 also targets the selenoprotein thioredoxin reductase 1 (TrxR1), a key regulator of cellular redox balance. APR-246 inhibited both recombinant TrxR1 in vitro and TrxR1 in cells. A Sec-to-Cys mutant of TrxR1 was not inhibited by APR-246, suggesting targeting of the selenocysteine residue in wild-type TrxR1. Preheated APR-246 and its conversion product methylene quinuclidinone (MQ) were much more efficient TrxR1 inhibitors than APR-246 itself, indicating that MQ is the active compound responsible for TrxR1 enzyme inhibition. TrxR1 inhibited by MQ was still functional as a pro-oxidant NADPH oxidase. Knockdown of TrxR1 caused a partial and reproducible attenuation of APR-246-induced tumor cell death independently of p53 status. Cellular TrxR1 activity was also inhibited by APR-246 irrespective of p53 status. We show that APR-246 can directly affect cellular redox status via targeting of TrxR1. Our findings provide an explanation for the previously observed effects of APR-246 on tumor cells lacking mutant p53

Preparation and characterization of NASICON type Li + ionic conductors

10.1007/s10008-012-1780-xJournal of Solid State Electrochemistry16103349-335