NNLO zero-jettiness beam and soft functions to higher orders in the dimensional-regularization parameter ε

We present the calculation of the next-to-next-to-leading order (NNLO) zero-jettiness beam and soft functions, up to the second order in the expansion in the dimensional regularization parameter ϵ. These higher order terms are needed for the computation of the next-to-next-to-next-to-leading order (N$^{3}$LO) zero-jettiness soft and beam functions. As a byproduct, we confirm the Ο(ϵ$^{0}$) results for NNLO beam and soft functions available in the literature by Gaunt et al. (JHEP 4:113, 2014), Gaunt et al. (JHEP 8:20, 2014), Boughezal et al. (Phys Rev D 96:34001, 2017), Monni et al. (JHEP 8:10, 2011) and Kelley et al. (Phys Rev D 84:45022, 2011)

Same-hemisphere three-gluon-emission contribution to the zero-jettiness soft function at N3LO QCD

We complete the calculation of the three-gluon-emission contribution to the same-hemisphere part of the zero-jettiness soft function at next-to-next-to-next-to-leading order in perturbative QCD.Comment: 9 pages, 1 appendi

Beam functions for N-jettiness at N3^3LO in perturbative QCD

We present a calculation of all matching coefficients for N-jettiness beam functions at next-to-next-to-next-to-leading order (N$^3$LO) in perturbative quantum chromodynamics (QCD). Our computation is performed starting from the respective collinear splitting kernels, which we integrate using the axial gauge. We use reverse unitarity to map the relevant phase-space integrals to loop integrals, which allows us to employ multi-loop techniques including integration-by-parts identities and differential equations. We find a canonical basis and use an algorithm to establish non-trivial partial fraction relations among the resulting master integrals, which allows us to reduce their number substantially. By use of regularity conditions, we express all necessary boundary constants in terms of an independent set, which we compute by direct integration of the corresponding integrals in the soft limit. In this way, we provide an entirely independent calculation of the matching coefficients which were previously computed in ref. [1]

Beam functions for N-jettiness at N3^3LO in perturbative QCD

We present a calculation of all matching coefficients for N-jettiness beam functions at next-to-next-to-next-to-leading order (N$^3$LO) in perturbative quantum chromodynamics (QCD). Our computation is performed starting from the respective collinear splitting kernels, which we integrate using the axial gauge. We use reverse unitarity to map the relevant phase-space integrals to loop integrals, which allows us to employ multi-loop techniques including integration-by-parts identities and differential equations. We find a canonical basis and use an algorithm to establish non-trivial partial fraction relations among the resulting master integrals, which allows us to reduce their number substantially. By use of regularity conditions, we express all necessary boundary constants in terms of an independent set, which we compute by direct integration of the corresponding integrals in the soft limit. In this way, we provide an entirely independent calculation of the matching coefficients which were previously computed in arXiv:2006.03056

Examination of BDNF Treatment on BACE1 Activity and Acute Exercise on Brain BDNF Signaling

Perturbations in metabolism results in the accumulation of beta-amyloid peptides, which is a pathological feature of Alzheimer’s disease. Beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) is the rate limiting enzyme responsible for beta-amyloid production. Obesogenic diets increase BACE1 while exercise reduces BACE1 activity, although the mechanisms are unknown. Brain-derived neurotropic factor (BDNF) is an exercise inducible neurotrophic factor, however, it is unknown if BDNF is related to the effects of exercise on BACE1. The purpose of this study was to determine the direct effect of BDNF on BACE1 activity and to examine neuronal pathways induced by exercise. C57BL/6J male mice were assigned to either a low (n = 36) or high fat diet (n = 36) for 10 weeks. To determine the direct effect of BDNF on BACE1, a subset of mice (low fat diet = 12 and high fat diet n = 12) were used for an explant experiment where the brain tissue was directly treated with BDNF (100 ng/ml) for 30 min. To examine neuronal pathways activated with exercise, mice remained sedentary (n = 12) or underwent an acute bout of treadmill running at 15 m/min with a 5% incline for 120 min (n = 12). The prefrontal cortex and hippocampus were collected 2-h post-exercise. Direct treatment with BDNF resulted in reductions in BACE1 activity in the prefrontal cortex (p < 0.05), but not the hippocampus. The high fat diet reduced BDNF content in the hippocampus; however, the acute bout of exercise increased BDNF in the prefrontal cortex (p < 0.05). These novel findings demonstrate the region specific differences in exercise induced BDNF in lean and obese mice and show that BDNF can reduce BACE1 activity, independent of other exercise-induced alterations. This work demonstrates a previously unknown link between BDNF and BACE1 regulation.Brock Library Open Access Publishing Fun

Versatile transporter apparatus for experiments with optically trapped Bose-Einstein condensates

We describe a versatile and simple scheme for producing magnetically and optically-trapped Rb-87 Bose-Einstein condensates, based on a moving-coil transporter apparatus. The apparatus features a TOP trap that incorporates the movable quadrupole coils used for magneto-optical trapping and long-distance magnetic transport of atomic clouds. As a stand-alone device, this trap allows for the stable production of condensates containing up to one million atoms. In combination with an optical dipole trap, the TOP trap acts as a funnel for efficient loading, after which the quadrupole coils can be retracted, thereby maximizing optical access. The robustness of this scheme is illustrated by realizing the superfluid-to-Mott insulator transition in a three-dimensional optical lattice

Fusion of the 1H NMR data of serum, urine and exhaled breath condensate in order to discriminate chronic obstructive pulmonary disease and obstructive sleep apnea syndrome

Chronic obstructive pulmonary disease, COPD, affects the condition of the entire human organism and causes multiple comorbidities. Pathological lung changes lead to quantitative changes in the composition of the metabolites in different body fluids. The obstructive sleep apnea syndrome, OSAS, occurs in conjunction with chronic obstructive pulmonary disease in about 10–20 % of individuals who have COPD. Both conditions share the same comorbidities and this makes differentiating them difficult. The aim of this study was to investigate whether it is possible to diagnose a patient with either COPD or the OSA syndrome using a set of selected metabolites and to determine whether the metabolites that are present in one type of biofluid (serum, exhaled breath condensate or urine) or whether a combination of metabolites that are present in two biofluids or whether a set of metabolites that are present in all three biofluids are necessary to correctly diagnose a patient. A quantitative analysis of the metabolites in all three biofluid samples was performed using 1H NMR spectroscopy. A multivariate bootstrap approach that combines partial least squares regression with the variable importance in projection score (VIP-score) and selectivity ratio (SR) was adopted in order to construct discriminant diagnostic models for the groups of individuals with COPD and OSAS. A comparison study of all of the discriminant models that were constructed and validated showed that the discriminant partial least squares model using only ten urine metabolites (selected with the SR approach) has a specificity of 100 % and a sensitivity of 86.67 %. This model (AUCtest = 0.95) presented the best prediction performance. The main conclusion of this study is that urine metabolites, among the others, present the highest probability for correctly identifying patents with COPD and the lowest probability for an incorrect identification of the OSA syndrome as developed COPD. Another important conclusion is that the changes in the metabolite levels of exhaled breath condensates do not appear to be specific enough to differentiate between patients with COPD and OSA