Half-integer Higher Spin Fields in (A)dS from Spinning Particle Models

We make use of O(2r+1) spinning particle models to construct linearized higher-spin curvatures in (A)dS spaces for fields of arbitrary half-integer spin propagating in a space of arbitrary (even) dimension: the field potentials, whose curvatures are computed with the present models, are spinor-tensors of mixed symmetry corresponding to Young tableaux with D/2 - 1 rows and r columns, thus reducing to totally symmetric spinor-tensors in four dimensions. The paper generalizes similar results obtained in the context of integer spins in (A)dS.Comment: 1+18 pages; minor changes in the notation, references updated. Published versio

Gauge fields in (A)dS within the unfolded approach: algebraic aspects

It has recently been shown that generalized connections of the (A)dS space symmetry algebra provide an effective geometric and algebraic framework for all types of gauge fields in (A)dS, both for massless and partially-massless. The equations of motion are equipped with a nilpotent operator called $\sigma_-$ whose cohomology groups correspond to the dynamically relevant quantities like differential gauge parameters, dynamical fields, gauge invariant field equations, Bianchi identities etc. In the paper the $\sigma_-$-cohomology is computed for all gauge theories of this type and the field-theoretical interpretation is discussed. In the simplest cases the $\sigma_-$-cohomology is equivalent to the ordinary Lie algebra cohomology.Comment: 59 pages, replaced with revised verio

The role of chronic muscle (in)activity on carnosine homeostasis: a study with spinal-cord injured athletes

To examine the role of chronic (in)activity on muscle carnosine (MCarn) and how chronic (in)activity affects MCarn responses to β-alanine supplementation in spinal-cord injured athletes, sixteen male athletes with paraplegia were randomized (2:1 ratio) to receive β-alanine (n=11) or placebo (PL, n=5). They consumed 6.4 g‧d-1 of β-alanine or PL for 28 days. Muscle biopsies of the active deltoid and the inactive vastus lateralis (VL) were taken before and after supplementation. MCarn in the VL was also compared with the VL of a group of individuals without paraplegia (n=15). MCarn was quantified in whole muscle and in pools of individual fibers by High-performance Liquid Chromatography. MCarn was higher in chronically inactive VL vs. well-trained deltoid (32.0±12.0 vs. 20.5±6.1 mmol‧kg-1 DM; p=0.018). MCarn was higher in inactive vs. active VL (32.0±12.0 vs. 21.2±7.5 mmol‧kg-1 DM; p=0.011). In type-I fibers, MCarn was significantly higher in the inactive VL than in the active deltoid (38.3±4.7 vs. 27.3±11.8 mmol‧kg-1 DM, p=0.014). MCarn increased similarly between inactive VL and active deltoid in the β-alanine group (VL: 68.9±55.1%, p=0.0002; deltoid: 90.5±51.4%, p<0.0001), with no changes in the PL group. MCarn content was higher in the inactive VL than in the active deltoid and the active VL, but this is probably a consequence of fiber type shift (type I to type II) that occurs with chronic inactivity. Chronically inactive muscle showed an increase in MCarn after BA supplementation equally to the active muscle, suggesting that carnosine accretion following β-alanine supplementation is not influenced by muscle inactivity

Supercurrent anomalies in 4d SCFTs

We use holographic renormalization of minimal \mathcalN=2 gauged supergravity in order to derive the general form of the quantum Ward identities for 3d \mathcalN=2 and 4d \mathcalN=1 superconformal theories on general curved backgrounds, including an arbitrary fermionic source for the supercurrent. The Ward identities for 4d \mathcalN=1 theories contain both bosonic and fermionic global anomalies, which we determine explicitly up to quadratic order in the supercurrent source. The Ward identities we derive apply to any superconformal theory, independently of whether it admits a holographic dual, except for the specific values of the $a$ and $c$ anomaly coefficients, which are equal due to our starting point of a two-derivative bulk supergravity theory. In the case of 4d \mathcalN=1 superconformal theories, we show that the fermionic anomalies lead to an anomalous transformation of the supercurrent under rigid supersymmetry on backgrounds admitting Killing spinors, even if all anomalies are numerically zero on such backgrounds. The anomalous transformation of the supercurrent under rigid supersymmetry leads to an obstruction to the $Q$-exactness of the stress tensor in supersymmetric vacua, and may have implications for the applicability of localization techniques. We use this obstruction to the $Q$-exactness of the stress tensor in order to resolve a number of apparent paradoxes relating to the supersymmetric Casimir energy, the BPS condition for supsersymmetric vacua, and the compatibility of holographic renormalization with supersymmetry, that were presented in the literature

The Role of Actin Turnover in Retrograde Actin Network Flow in Neuronal Growth Cones

The balance of actin filament polymerization and depolymerization maintains a steady state network treadmill in neuronal growth cones essential for motility and guidance. Here we have investigated the connection between depolymerization and treadmilling dynamics. We show that polymerization-competent barbed ends are concentrated at the leading edge and depolymerization is distributed throughout the peripheral domain. We found a high-to-low G-actin gradient between peripheral and central domains. Inhibiting turnover with jasplakinolide collapsed this gradient and lowered leading edge barbed end density. Ultrastructural analysis showed dramatic reduction of leading edge actin filament density and filament accumulation in central regions. Live cell imaging revealed that the leading edge retracted even as retrograde actin flow rate decreased exponentially. Inhibition of myosin II activity before jasplakinolide treatment lowered baseline retrograde flow rates and prevented leading edge retraction. Myosin II activity preferentially affected filopodial bundle disassembly distinct from the global effects of jasplakinolide on network turnover. We propose that growth cone retraction following turnover inhibition resulted from the persistence of myosin II contractility even as leading edge assembly rates decreased. The buildup of actin filaments in central regions combined with monomer depletion and reduced polymerization from barbed ends suggests a mechanism for the observed exponential decay in actin retrograde flow. Our results show that growth cone motility is critically dependent on continuous disassembly of the peripheral actin network