Ultrasoft Renormalization in Non-Relativistic QCD

For Non-Relativistic QCD the velocity renormalization group correlates the renormalization scales for ultrasoft, potential and soft degrees of freedom. Here we discuss the renormalization of operators by ultrasoft gluons. We show that renormalization of soft vertices can induce new operators, and also present a procedure for correctly subtracting divergences in mixed potential-ultrasoft graphs. Our results affect the running of the spin-independent potentials in QCD. The change for the NNLL t-tbar cross section near threshold is very small, being at the 1% level and essentially independent of the energy. We also discuss implications for analyzing situations where mv^2 ~ Lambda_QCD.Comment: 31 pages, 11 fig

The Evolution of Cloud Cores and the Formation of Stars

For a number of starless cores, self-absorbed molecular line and column density observations have implied the presence of large-amplitude oscillations. We examine the consequences of these oscillations on the evolution of the cores and the interpretation of their observations. We find that the pulsation energy helps support the cores and that the dissipation of this energy can lead toward instability and star formation. In this picture, the core lifetimes are limited by the pulsation decay timescales, dominated by non-linear mode-mode coupling, and on the order of ~few x 10^5--10^6 yr. Notably, this is similar to what is required to explain the relatively low rate of conversion of cores into stars. For cores with large-amplitude oscillations, dust continuum observations may appear asymmetric or irregular. As a consequence, some of the cores that would be classified as supercritical may be dynamically stable when oscillations are taken into account. Thus, our investigation motivates a simple hydrodynamic picture, capable of reproducing many of the features of the progenitors of stars without the inclusion of additional physical processes, such as large-scale magnetic fields.Comment: 12 pages, 7 figures, submitted to Ap

Synaptic vesicle binding of α-synuclein is modulated by β- and γ-synucleins

a-synuclein, b-synuclein, and g-synuclein are abundantly expressed proteins in the vertebrate nervous system. a-synuclein functions in neurotransmitter release by binding to and clustering synaptic vesicles and chaperoning SNARE-complex assembly. Pathologically, aggregates originating from soluble pools of a-synuclein are deposited into Lewy bodies in Parkinson’s disease and related synucleinopathie

Deep level transient spectroscopy (DLTS) study of defects introduced in antimony doped Ge by 2 MeV proton irradiation

Please read the abstract in the article.The South African National Research Foundation and Monash University, South Africa.http://www.elsevier.com/locate/physbnf201

B decay and the Upsilon mass

Theoretical predictions for inclusive semileptonic B decay rates are rewritten in terms of the Upsilon(1S) meson mass instead of the b quark mass, using a modified perturbation expansion. This method gives theoretically consistent and phenomenologically useful results. Perturbation theory is well behaved, and the largest theoretical error in the predictions coming from the uncertainty in the quark mass is eliminated. The results are applied to the determination of $|V_{cb}|$, $|V_{ub}|$, and $\lambda_1$.Comment: 8 pages revte

Exon junction complex shapes the transcriptome by repressing recursive splicing

Recursive splicing (RS) starts by defining an “RS-exon,” which is then spliced to the preceding exon, thus creating a recursive 5′ splice site (RS-5ss). Previous studies focused on cryptic RS-exons, and now we find that the exon junction complex (EJC) represses RS of hundreds of annotated, mainly constitutive RS-exons. The core EJC factors, and the peripheral factors PNN and RNPS1, maintain RS-exon inclusion by repressing spliceosomal assembly on RS-5ss. The EJC also blocks 5ss located near exon-exon junctions, thus repressing inclusion of cryptic microexons. The prevalence of annotated RS-exons is high in deuterostomes, while the cryptic RS-exons are more prevalent in Drosophila, where EJC appears less capable of repressing RS. Notably, incomplete repression of RS also contributes to physiological alternative splicing of several human RS-exons. Finally, haploinsufficiency of the EJC factor Magoh in mice is associated with skipping of RS-exons in the brain, with relevance to the microcephaly phenotype and human diseases

Dense Cores in Perseus: The Influence of Stellar Content and Cluster Environment

We present the chemistry, temperature, and dynamical state of a sample of 193 dense cores or core candidates in the Perseus Molecular cloud and compare the properties of cores associated with young stars and clusters with those which are not. The combination of our NH3 and CCS observations with previous millimeter, sub-millimeter, and Spitzer data available for this cloud enable us both to determine core properties precisely and to accurately classify cores as starless or protostellar. The properties of cores in different cluster environments and before-and-after star formation provide important constraints on simulations of star-formation, particularly under the paradigm that the essence of star formation is set by the turbulent formation of prestellar cores. We separate the influence of stellar content from that of cluster environment and find that cores within clusters have (1) higher kinetic temperatures and (2) lower fractional abundances of CCS and NH3. Cores associated with protostars have (1) slightly higher kinetic temperatures (2) higher NH3 excitation temperatures), (3) are at higher column density, have (4) slightly more non-thermal/turbulent NH3 linewidths, have (5) higher masses and have (6) lower fractional abundance of CCS. We find that neither cluster environment nor protostellar content makes a significant difference to the dynamical state of cores as estimated by the virial parameter -- most cores in each category are gravitationally bound. Overall, cluster environment and protostellar content have a smaller influence on the properties of the cores than is typically assumed, and the variation within categories is larger than the differences between categories.Comment: 28 pages, 17 figures. Accepted to Ap

Prodromal phase: Differences in prodromal symptoms, risk factors and markers of vulnerability in first episode mania versus first episode psychosis with onset in late adolescence or adulthood

Objective: This study was aimed at identifying differences in the prodromal symptoms and their duration, risk factors and markers of vulnerability in patients presenting a first episode mania (FEM) or psychosis (FEP) with onset in late adolescence or adulthood in order to guide tailored treatment strategies. Methods: Patients with a FEM or FEP underwent a clinical assessment. Prodromes were evaluated with the Bipolar Prodrome Symptom Scale-Retrospective (BPSS-R). Chi-squared tests were conducted to assess specific prodromal symptoms, risk factors or markers of vulnerability between groups. Significant prodromal symptoms were entered in a stepwise forward logistic regression model. The probabilities of a gradual versus rapid onset pattern of the prodromes were computed with logistic regression models. Results: The total sample included 108 patients (FEM = 72, FEP = 36). Social isolation was associated with the prodromal stage of a FEP whilst Increased energy or goal-directed activity with the prodrome to a FEM. Physically slowed down presented the most gradual onset whilst Increased energy presented the most rapid. The presence of obstetric complications and difficulties in writing and reading during childhood were risk factors for FEP. As for markers of vulnerability, impairment in premorbid adjustment was characteristic of FEP patients. No specific risk factor or marker of vulnerability was identified for FEM. Conclusion: Early characteristics differentiating FEP from FEM were identified. These findings might help shape early identification and preventive intervention programmes

Torture at Times: Waterboarding in the Media

The current debate over waterboarding has spawned hundreds of newspaper articles in the last two years alone. However, waterboarding has been the subject of press attention for over a century. Examining the four newspapers with the highest daily circulation in the country, we found a significant and sudden shift in how newspapers characterized waterboarding. From the early 1930s until the modern story broke in 2004, the newspapers that covered waterboarding almost uniformly called the practice torture or implied it was torture: The New York Times characterized it thus in 81.5% (44 of 54) of articles on the subject and The Los Angeles Times did so in 96.3% of articles (26 of 27). By contrast, from 2002-2008, the studied newspapers almost never referred to waterboarding as torture. The New York Times called waterboarding torture or implied it was torture in just 2 of 143 articles (1.4%). The Los Angeles Times did so in 4.8% of articles (3 of 63). The Wall Street journal characterized the practice as torture in just 1 of 63 articles (1.6%). USA Today never called waterboarding torture or implied it was torture. In addition, the newspapers are much more likely to call waterboarding torture if a country other than the United States is the perpetrator. In The New York Times, 85.8% of articles (28 of 33) that dealt with a country other than the United States using waterboarding called it torture or implied it was torture while only 7.69% (16 of 208) did so when the United States was responsible. The Los Angeles Times characterized the practice as torture in 91.3% of articles (21 of 23) when another country was the violator, but in only 11.4% of articles (9 of 79) when the United States was the perpetrator

Cognitive Dysfunction in Huntington's Disease: Mechanisms and Therapeutic Strategies Beyond BDNF

One of the main focuses in Huntington's disease (HD) research, as well as in most of the neurodegenerative diseases, is the development of new therapeutic strategies, as currently there is no treatment to delay or prevent the progression of the disease. Neuronal dysfunction and neuronal death in HD are caused by a combination of interrelated pathogenic processes that lead to motor, cognitive and psychiatric symptoms. Understanding how mutant huntingtin impacts on a plethora of cellular functions could help to identify new molecular targets. Although HD has been classically classified as a neurodegenerative disease affecting voluntary movement, lately cognitive dysfunction is receiving increased attention as it is very invalidating for patients. Thus, an ambitious goal in HD research is to find altered molecular mechanisms that contribute to cognitive decline. In this review we have focused on those findings related to corticostriatal and hippocampal cognitive dysfunction in HD, as well as on the underlying molecular mechanisms, which constitute potential therapeutic targets. These include alterations in synaptic plasticity, transcriptional machinery, and neurotrophic and neurotransmitter signaling. This article is protected by copyright. All rights reserved