A Formalism for the Systematic Treatment of Rapidity Logarithms in Quantum Field Theory

Many observables in QCD rely upon the resummation of perturbation theory to retain predictive power. Resummation follows after one factorizes the cross section into the rele- vant modes. The class of observables which are sensitive to soft recoil effects are particularly challenging to factorize and resum since they involve rapidity logarithms. In this paper we will present a formalism which allows one to factorize and resum the perturbative series for such observables in a systematic fashion through the notion of a "rapidity renormalization group". That is, a Collin-Soper like equation is realized as a renormalization group equation, but has a more universal applicability to observables beyond the traditional transverse momentum dependent parton distribution functions (TMDPDFs) and the Sudakov form factor. This formalism has the feature that it allows one to track the (non-standard) scheme dependence which is inherent in any scenario where one performs a resummation of rapidity divergences. We present a pedagogical introduction to the formalism by applying it to the well-known massive Sudakov form factor. The formalism is then used to study observables of current interest. A factorization theorem for the transverse momentum distribution of Higgs production is presented along with the result for the resummed cross section at NLL. Our formalism allows one to define gauge invariant TMDPDFs which are independent of both the hard scattering amplitude and the soft function, i.e. they are uni- versal. We present details of the factorization and resummation of the jet broadening cross section including a renormalization in pT space. We furthermore show how to regulate and renormalize exclusive processes which are plagued by endpoint singularities in such a way as to allow for a consistent resummation.Comment: Typos in Appendix C corrected, as well as a typo in eq. 5.6

Instabilities in extreme magnetoconvection

Thermal convection in an electrically conducting fluid (for example, a liquid metal) in the presence of a static magnetic field is considered in this chapter. The focus is on the extreme states of the flow, in which both buoyancy and Lorentz forces are very strong. It is argued that the instabilities occurring in such flows are often of unique and counter-intuitive nature due to the action of the magnetic field, which suppresses conventional turbulence and gives preference to two-dimensional instability modes not appearing in more conventional convection systems. Tools of numerical analysis suitable for such flows are discussed

The Evolution of Compact Binary Star Systems

We review the formation and evolution of compact binary stars consisting of white dwarfs (WDs), neutron stars (NSs), and black holes (BHs). Binary NSs and BHs are thought to be the primary astrophysical sources of gravitational waves (GWs) within the frequency band of ground-based detectors, while compact binaries of WDs are important sources of GWs at lower frequencies to be covered by space interferometers (LISA). Major uncertainties in the current understanding of properties of NSs and BHs most relevant to the GW studies are discussed, including the treatment of the natal kicks which compact stellar remnants acquire during the core collapse of massive stars and the common envelope phase of binary evolution. We discuss the coalescence rates of binary NSs and BHs and prospects for their detections, the formation and evolution of binary WDs and their observational manifestations. Special attention is given to AM CVn-stars -- compact binaries in which the Roche lobe is filled by another WD or a low-mass partially degenerate helium-star, as these stars are thought to be the best LISA verification binary GW sources.Comment: 105 pages, 18 figure

Identification of Host-Dependent Survival Factors for Intracellular Mycobacterium tuberculosis through an siRNA Screen

The stable infection of host macrophages by Mycobacterium tuberculosis (Mtb) involves, and depends on, the attenuation of the diverse microbicidal responses mounted by the host cell. This is primarily achieved through targeted perturbations of the host cellular signaling machinery. Therefore, in view of the dependency of the pathogen on host molecules for its intracellular survival, we wanted to test whether targeting such factors could provide an alternate route for the therapeutic management of tuberculosis. To first identify components of the host signaling machinery that regulate intracellular survival of Mtb, we performed an siRNA screen against all known kinases and phosphatases in murine macrophages infected with the virulent strain, H37Rv. Several validated targets could be identified by this method where silencing led either to a significant decrease, or enhancement in the intracellular mycobacterial load. To further resolve the functional relevance of these targets, we also screened against these identified targets in cells infected with different strains of multiple drug-resistant mycobacteria which differed in terms of their intracellular growth properties. The results obtained subsequently allowed us to filter the core set of host regulatory molecules that functioned independently of the phenotypic variations exhibited by the pathogen. Then, using a combination of both in vitro and in vivo experimentation, we could demonstrate that at least some of these host factors provide attractive targets for anti-TB drug development. These results provide a “proof-of-concept” demonstration that targeting host factors subverted by intracellular Mtb provides an attractive and feasible strategy for the development of anti-tuberculosis drugs. Importantly, our findings also emphasize the advantage of such an approach by establishing its equal applicability to infections with Mtb strains exhibiting a range of phenotypic diversifications, including multiple drug-resistance. Thus the host factors identified here may potentially be exploited for the development of anti-tuberculosis drugs

Continuous low- to moderate-intensity exercise training is as effective as moderate- to high-intensity exercise training at lowering blood HbA1c in obese type 2 diabetes patients

Aims/hypothesis: Exercise represents an effective interventional strategy to improve glycaemic control in type 2 diabetes patients. However, the impact of exercise intensity on the benefits of exercise training remains to be established. In the present study, we compared the clinical benefits of 6 months of continuous low- to moderate-intensity exercise training with those of continuous moderate- to high-intensity exercise training, matched for energy expenditure, in obese type 2 diabetes patients. Methods: Fifty male obese type 2 diabetes patients (age 59∈±∈8 years, BMI 32∈± ∈4 kg/m2) participated in a 6 month continuous endurance-type exercise training programme. All participants performed three supervised exercise sessions per week, either 55 min at 50% of whole body peak oxygen uptake left(VO2peak) (low to moderate intensity) or 40 min at 75% of VO2peak (moderate to high intensity). Oral glucose tolerance, blood glycated haemoglobin, lipid profile, body composition, maximal workload capacity, whole body and skeletal muscle oxidative capacity and skeletal muscle fibre type composition were assessed before and after 2 and 6 months of intervention. Results: The entire 6 month intervention programme was completed by 37 participants. Continuous endurance-type exercise training reduced blood glycated haemoglobin levels, LDL-cholesterol concentrations, body weight and leg fat mass, and increased VO2peak, lean muscle mass and skeletal muscle cytochrome c oxidase and citrate synthase activity (p∈<∈0. 05). No differences were observed between the groups training at low to moderate or moderate to high intensity. Conclusions/interpretation: When matched for energy cost, prolonged continuous low- to moderate-intensity endurance-type exercise training is equally effective as continuous moderate- to high-intensity training in lowering blood glycated haemoglobin and increasing whole body and skeletal muscle oxidative capacity in obese type 2 diabetes patients. © 2009 Springer-Verlag

Cholesterol Metabolism Is Required for Intracellular Hedgehog Signal Transduction In Vivo

We describe the rudolph mouse, a mutant with striking defects in both central nervous system and skeletal development. Rudolph is an allele of the cholesterol biosynthetic enzyme, hydroxysteroid (17-beta) dehydrogenase 7, which is an intriguing finding given the recent implication of oxysterols in mediating intracellular Hedgehog (Hh) signaling. We see an abnormal sterol profile and decreased Hh target gene induction in the rudolph mutant, both in vivo and in vitro. Reduced Hh signaling has been proposed to contribute to the phenotypes of congenital diseases of cholesterol metabolism. Recent in vitro and pharmacological data also indicate a requirement for intracellular cholesterol synthesis for proper regulation of Hh activity via Smoothened. The data presented here are the first in vivo genetic evidence supporting both of these hypotheses, revealing a role for embryonic cholesterol metabolism in both CNS development and normal Hh signaling

Improving the Alignment Quality of Consistency Based Aligners with an Evaluation Function Using Synonymous Protein Words

Most sequence alignment tools can successfully align protein sequences with higher levels of sequence identity. The accuracy of corresponding structure alignment, however, decreases rapidly when considering distantly related sequences (<20% identity). In this range of identity, alignments optimized so as to maximize sequence similarity are often inaccurate from a structural point of view. Over the last two decades, most multiple protein aligners have been optimized for their capacity to reproduce structure-based alignments while using sequence information. Methods currently available differ essentially in the similarity measurement between aligned residues using substitution matrices, Fourier transform, sophisticated profile-profile functions, or consistency-based approaches, more recently

A Component of Retinal Light Adaptation Mediated by the Thyroid Hormone Cascade

Analysis with DNA-microrrays and real time PCR show that several genes involved in the thyroid hormone cascade, such as deiodinase 2 and 3 (Dio2 and Dio3) are differentially regulated by the circadian clock and by changes of the ambient light. The expression level of Dio2 in adult rats (2–3 months of age) kept continuously in darkness is modulated by the circadian clock and is up-regulated by 2 fold at midday. When the diurnal ambient light was on, the expression level of Dio2 increased by 4–8 fold and a consequent increase of the related protein was detected around the nuclei of retinal photoreceptors and of neurons in inner and outer nuclear layers. The expression level of Dio3 had a different temporal pattern and was down-regulated by diurnal light. Our results suggest that DIO2 and DIO3 have a role not only in the developing retina but also in the adult retina and are powerfully regulated by light. As the thyroid hormone is a ligand-inducible transcription factor controlling the expression of several target genes, the transcriptional activation of Dio2 could be a novel genomic component of light adaptation