Comments on 1/16 BPS Quantum States and Classical Configurations

We formulate the problem of counting 1/16 BPS states of N = 4 Yang Mills theory as the enumeration of the local cohomology of an operator acting on holomorphic fields on C^2. We study aspects of the enumeration of this cohomology at finite N, especially for operators constructed only out of products of covariant derivatives of scalar fields, and compare our results to the states obtained from the quantization of giant gravitons and dual giants. We physically interpret the holomorphic fields that enter our conditions for supersymmetry semi-classically by deriving a set of Bogomolnyi equations for 1/16-BPS bosonic field configurations in N = 4 Yang Mills theory on R^4 with reality properties and boundary conditions appropriate to radial quantization. An arbitrary solution to these equations in the free theory is parameterized by holomorphic data on C^2 and lifts to a nearby solution of the interacting Bogomolnyi equations only when the constraints equivalent to Q cohomology are obeyed.Comment: 61 page

Integrating protein structural dynamics and evolutionary analysis with Bio3D

Abstract Background Popular bioinformatics approaches for studying protein functional dynamics include comparisons of crystallographic structures, molecular dynamics simulations and normal mode analysis. However, determining how observed displacements and predicted motions from these traditionally separate analyses relate to each other, as well as to the evolution of sequence, structure and function within large protein families, remains a considerable challenge. This is in part due to the general lack of tools that integrate information of molecular structure, dynamics and evolution. Results Here, we describe the integration of new methodologies for evolutionary sequence, structure and simulation analysis into the Bio3D package. This major update includes unique high-throughput normal mode analysis for examining and contrasting the dynamics of related proteins with non-identical sequences and structures, as well as new methods for quantifying dynamical couplings and their residue-wise dissection from correlation network analysis. These new methodologies are integrated with major biomolecular databases as well as established methods for evolutionary sequence and comparative structural analysis. New functionality for directly comparing results derived from normal modes, molecular dynamics and principal component analysis of heterogeneous experimental structure distributions is also included. We demonstrate these integrated capabilities with example applications to dihydrofolate reductase and heterotrimeric G-protein families along with a discussion of the mechanistic insight provided in each case. Conclusions The integration of structural dynamics and evolutionary analysis in Bio3D enables researchers to go beyond a prediction of single protein dynamics to investigate dynamical features across large protein families. The Bio3D package is distributed with full source code and extensive documentation as a platform independent R package under a GPL2 license from http://thegrantlab.org/bio3d/ .http://deepblue.lib.umich.edu/bitstream/2027.42/109747/1/12859_2014_Article_399.pd

Experimental and theoretical lifetimes and transition probabilities in Sb I

We present experimental atomic lifetimes for 12 levels in Sb I, out of which seven are reported for the first time. The levels belong to the 5p$^2$($^3$P)6s $^{2}$P, $^{4}$P and 5p$^2$($^3$P)5d $^{4}$P, $^{4}$F and $^{2}$F terms. The lifetimes were measured using time-resolved laser-induced fluorescence. In addition, we report new calculations of transition probabilities in Sb I using a Multiconfigurational Dirac-Hartree-Fock method. The physical model being tested through comparisons between theoretical and experimental lifetimes for 5d and 6s levels. The lifetimes of the 5d $^4$F$_{3/2, 5/2, 7/2}$ levels (19.5, 7.8 and 54 ns, respectively) depend strongly on the $J$-value. This is explained by different degrees of level mixing for the different levels in the $^4$F term.Comment: 10 page

High Quality Audio Coding with MDCTNet

We propose a neural audio generative model, MDCTNet, operating in the perceptually weighted domain of an adaptive modified discrete cosine transform (MDCT). The architecture of the model captures correlations in both time and frequency directions with recurrent layers (RNNs). An audio coding system is obtained by training MDCTNet on a diverse set of fullband monophonic audio signals at 48 kHz sampling, conditioned by a perceptual audio encoder. In a subjective listening test with ten excerpts chosen to be balanced across content types, yet stressful for both codecs, the mean performance of the proposed system for 24 kb/s variable bitrate (VBR) is similar to that of Opus at twice the bitrate.Comment: Five pages, five figure

Development of NASH in Obese Mice is Confounded by Adipose Tissue Increase in Inflammatory NOV and Oxidative Stress

Aim. Nonalcoholic steatohepatitis (NASH) is the consequence of insulin resistance, fatty acid accumulation, oxidative stress, and lipotoxicity.We hypothesize that an increase in the inflammatory adipokine NOV decreases antioxidant Heme Oxygenase 1 (HO- 1) levels in adipose and hepatic tissue, resulting in the development of NASH in obese mice. Methods. Mice were fed a high fat diet (HFD) and obese animals were administered an HO-1 inducer with or without an inhibitor of HO activity to examine levels of adipose-derived NOV and possible links between increased synthesis of inflammatory adipokines and hepatic pathology. Results. NASH mice displayed decreased HO-1 levels and HO activity, increased levels of hepatic heme, NOV, MMP2, hepcidin, and increased NAS scores and hepatic fibrosis. IncreasedHO-1 levels are associated with a decrease in NOV, improved hepatic NAS score, ameliorated fibrosis, and increases in mitochondrial integrity and insulin receptor phosphorylation. Adipose tissue function is disrupted in obesity as evidenced by an increase in proinflammatory molecules such as NOV and a decrease in adiponectin. Importantly, increased HO-1 levels are associated with a decrease of NOV, increased adiponectin levels, and increased levels of thermogenic and mitochondrial signaling associated genes in adipose tissue. Conclusions.These results suggest that the metabolic abnormalities in NASH are driven by decreased levels of hepatic HO-1 that is associated with an increase in the adipose-derived proinflammatory adipokine NOV in our obese mouse model of NASH. Concurrently, induction of HO-1 provides protection against insulin resistance as seen by increased insulin receptor phosphorylation. Pharmacological increases in HO-1 associated with decreases in NOV may offer a potential therapeutic approach in preventing fibrosis, mitochondrial dysfunction, and the development of NASH

The Spectrum of Yang Mills on a Sphere

In this note, we determine the representation content of the free, large N, SU(N) Yang Mills theory on a sphere by decomposing its thermal partition function into characters of the irreducible representations of the conformal group SO(4,2). We also discuss the generalization of this procedure to finding the representation content of N=4 Super Yang Mills.Comment: 18 pages v2. references added. typos fixe

Molecular Dynamics Simulations

figurasGroEL is an ATP dependent molecular chaperone that promotes the folding of a large number of substrate proteins in E. coli. Large-scale conformational transitions occurring during the reaction cycle have been characterized from extensive crystallographic studies. However, the link between the observed conformations and the mechanisms involved in the allosteric response to ATP and the nucleotide-driven reaction cycle are not completely established. Here we describe extensive (in total long) unbiased molecular dynamics (MD) simulations that probe the response of GroEL subunits to ATP binding. We observe nucleotide dependent conformational transitions, and show with multiple 100 ns long simulations that the ligand-induced shift in the conformational populations are intrinsically coded in the structure-dynamics relationship of the protein subunit. Thus, these simulations reveal a stabilization of the equatorial domain upon nucleotide binding and a concomitant “opening” of the subunit, which reaches a conformation close to that observed in the crystal structure of the subunits within the ADP-bound oligomer. Moreover, we identify changes in a set of unique intrasubunit interactions potentially important for the conformational transition.The Norwegian Research Council is acknowledged for CPU resources granted through the NOTUR supercomputing program (http://www.notur.no/) and Bergen Center for Computational Science for providing powerful computer facilities (http://www.bccs.uni.no/). Work at CSIC/UPV/EHU was financed by MICINN (Grant BUF2007-64452). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewe

Development of NASH in Obese Mice is Confounded by adipose Tissue Increase in Inflammatory NOV and Oxidative Stress

Aim: Nonalcoholic steatohepatitis (NASH) is the consequence of insulin resistance, fatty acid accumulation, oxidative stress, and lipotoxicity. We hypothesize that an increase in the inflammatory adipokine NOV decreases antioxidant Heme Oxygenase 1 (HO-1) levels in adipose and hepatic tissue, resulting in the development of NASH in obese mice. Methods: Mice were fed a high fat diet (HFD) and obese animals were administered an HO-1 inducer with or without an inhibitor of HO activity to examine levels of adipose-derived NOV and possible links between increased synthesis of inflammatory adipokines and hepatic pathology. Results: NASH mice displayed decreased HO-1 levels and HO activity, increased levels of hepatic heme, NOV, MMP2, hepcidin, and increased NAS scores and hepatic fibrosis. Increased HO-1 levels are associated with a decrease in NOV, improved hepatic NAS score, ameliorated fibrosis, and increases in mitochondrial integrity and insulin receptor phosphorylation. Adipose tissue function is disrupted in obesity as evidenced by an increase in proinflammatory molecules such as NOV and a decrease in adiponectin. Importantly, increased HO-1 levels are associated with a decrease of NOV, increased adiponectin levels, and increased levels of thermogenic and mitochondrial signaling associated genes in adipose tissue. Conclusions: These results suggest that the metabolic abnormalities in NASH are driven by decreased levels of hepatic HO-1 that is associated with an increase in the adipose-derived proinflammatory adipokine NOV in our obese mouse model of NASH. Concurrently, induction of HO-1 provides protection against insulin resistance as seen by increased insulin receptor phosphorylation. Pharmacological increases in HO-1 associated with decreases in NOV may offer a potential therapeutic approach in preventing fibrosis, mitochondrial dysfunction, and the development of NASH