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Tensor currents are the only quark bilinear operators lacking a non-perturbative determination of their renormalisation group (RG) running between hadronic and electroweak scales. We develop the setup to carry out the computation in lattice QCD via standard recursive finite-size scaling techniques, and provide results for the RG running of tensor currents in Nf=0 and Nf=2 QCD in the continuum for various Schrödinger Functional schemes. The matching factors between bare and renormalisation group invariant currents are also determined for a range of values of the lattice spacing relevant for large-volume simulations, thus enabling a fully non-perturbative renormalization of physical amplitudes mediated by tensor currents. [ABSTRACT FROM AUTHOR]

We discuss the renormalization properties of the full set of $$\Delta F=2$$ operators involved in BSM processes, including the definition of RGI versions of operators that exhibit mixing under RG transformations. As a first step for a fully non-perturbative determination of the scale-dependent renormalization factors and their runnings, we introduce a family of appropriate Schrödinger Functional schemes, and study them in perturbation theory. This allows, in particular, to determine the NLO anomalous dimensions of all $$\Delta F=1,2$$ operators in these schemes. Finally, we discuss the systematic uncertainties related to the use of NLO perturbation theory for the RG running of four-quark operators to scales in the GeV range, in both our SF schemes and standard $${\overline{\mathrm{MS}}}$$ and RI-MOM schemes. Large truncation effects are found for some of the operators considered. [ABSTRACT FROM AUTHOR]

We present a lattice QCD determination of light quark masses with three sea-quark flavours ( N f = 2 + 1 ). Bare quark masses are known from PCAC relations in the framework of CLS lattice computations with a non-perturbatively improved Wilson-Clover action and a tree-level Symanzik improved gauge action. They are fully non-perturbatively improved, including the recently computed Symanzik counter-term b A - b P . The mass renormalisation at hadronic scales and the renormalisation group running over a wide range of scales are known non-perturbatively in the Schrödinger functional scheme. In the present paper we perform detailed extrapolations to the physical point, obtaining (for the four-flavour theory) m u / d (2 GeV) = 3.54 (12) (9) MeV and m s (2 GeV) = 95.7 (2.5) (2.4) MeV in the MS ¯ scheme. For the mass ratio we have m s / m u / d = 27.0 (1.0) (0.4) . The RGI values in the three-flavour theory are M u / d = 4.70 (15) (12) MeV and M s = 127.0 (3.1) (3.2) MeV . [ABSTRACT FROM AUTHOR]

The California bay laurel or Umbellularia californica (Hook. & Arn.) Nutt., is known as the 'headache tree' because the inhalation of its vapours can cause severe headache crises. However, the underlying mechanism of the headache precipitating properties of Umbellularia californica is unknown. The monoterpene ketone umbellulone, the major volatile constituent of the leaves of Umbellularia californica, has irritating properties, and is a reactive molecule that rapidly binds thiols. Thus, we hypothesized that umbellulone stimulates the transient receptor potential ankyrin 1 channel in a subset of peptidergic, nocioceptive neurons, activating the trigeminovascular system via this mechanism. Umbellulone, from µM to sub-mM concentrations, selectively stimulated transient receptor potential ankyrin 1-expressing HEK293 cells and rat trigeminal ganglion neurons, but not untransfected cells or neurons in the presence of the selective transient receptor potential ankyrin 1 antagonist, HC-030031. Umbellulone evoked a calcium-dependent release of calcitonin gene-related peptide from rodent trigeminal nerve terminals in the dura mater. In wild-type mice, umbellulone elicited excitation of trigeminal neurons and released calcitonin gene-related peptide from sensory nerve terminals. These two responses were absent in transient receptor potential ankyrin 1 deficient mice. Umbellulone caused nocioceptive behaviour after stimulation of trigeminal nerve terminals in wild-type, but not transient receptor potential ankyrin 1 deficient mice. Intranasal application or intravenous injection of umbellulone increased rat meningeal blood flow in a dose-dependent manner; a response selectively inhibited by systemic administration of transient receptor potential ankyrin 1 or calcitonin gene-related peptide receptor antagonists. These data indicate that umbellulone activates, through a transient receptor potential ankyrin 1-dependent mechanism, the trigeminovascular system, thereby causing nocioceptive responses and calcitonin gene-related peptide release. Pharmacokinetics of umbellulone, given by either intravenous or intranasal administration, suggest that transient receptor potential ankyrin 1 stimulation, which eventually results in meningeal vasodilatation, may be produced via two different pathways, depending on the dose. Transient receptor potential ankyrin 1 activation may either be caused directly by umbellulone, which diffuses from the nasal mucosa to perivascular nerve terminals in meningeal vessels, or by stimulation of trigeminal endings within the nasal mucosa and activation of reflex pathways. Transient receptor potential ankyrin 1 activation represents a plausible mechanism for Umbellularia californica-induced headache. Present data also strengthen the hypothesis that a series of agents, including chlorine, cigarette smoke, formaldehyde and others that are known to be headache triggers and recently identified as transient receptor potential ankyrin 1 agonists, utilize the activation of this channel on trigeminal nerves to produce head pain. [ABSTRACT FROM AUTHOR]

Background and Purpose: The transient receptor potential ankyrin receptor 1 (TRPA1) is a cation channel, co-expressed with the pro-tussive transient receptor potential vanilloid type 1 (TRPV1) channel in primary sensory neurons. TRPA1 is activated by a series of irritant exogenous and endogenous alpha,beta-unsaturated aldehydes which seem to play a role in airway diseases. We investigated whether TRPA1 agonists provoke cough in guinea pigs and whether TRPA1 antagonists inhibit this response.Experimental Approach: Animals were placed in a Perspex box, and cough sounds were recorded and counted by observers unaware of the treatment used.Key Results: Inhalation of two selective TRPA1 agonists, allyl isothiocyanate and cinnamaldehyde, dose-dependently caused cough in control guinea pigs, but not in those with airway sensory nerves desensitized by capsaicin. Coughs elicited by TRPA1 agonists were reduced by non-selective (camphor and gentamicin) and selective (HC-030031) TRPA1 antagonists, whereas they were unaffected by the TRPV1 antagonist, capsazepine. Acrolein and crotonaldehyde, two alpha,beta-unsaturated aldehydes recently identified as TRPA1 stimulants and contained in cigarette smoke, air pollution or produced endogenously by oxidative stress, caused a remarkable tussive effect, a response that was selectively inhibited by HC-030031. Part of the cough response induced by cigarette smoke inhalation was inhibited by HC-030031, suggesting the involvement of TRPA1.Conclusions and Implications: A novel pro-tussive pathway involves the TRPA1 channel, expressed by capsaicin-sensitive airway sensory nerves and is activated by a series of exogenous (cigarette smoke) and endogenous irritants. These results suggest TRPA1 may be a novel target for anti-tussive medicines. [ABSTRACT FROM AUTHOR]

We perform a non-perturbative study of the scale-dependent renormalisation factors of a complete set of dimension-six four-fermion operators without power subtractions. The renormalisation-group (RG) running is determined in the continuum limit for a specific Schrödinger Functional (SF) renormalisation scheme in the framework of lattice QCD with two dynamical flavours (Nf=2). The theory is regularised on a lattice with a plaquette Wilson action and O(a)-improved Wilson fermions. For one of these operators, the computation had been performed in Dimopoulos et al. (JHEP 0805, 065 (2008). arXiv:0712.2429); the present work completes the study for the rest of the operator basis, on the same simulations (configuration ensembles). The related weak matrix elements arise in several operator product expansions; in ΔF=2 transitions they contain the QCD long-distance effects, including contributions from beyond-Standard Model (BSM) processes. Some of these operators mix under renormalisation and their RG-running is governed by anomalous dimension matrices. In Papinutto et al. (Eur Phys J C 77(6), 376 (2017). arXiv:1612.06461) the RG formalism for the operator basis has been worked out in full generality and the anomalous dimension matrix has been calculated in NLO perturbation theory. Here the discussion is extended to the matrix step-scaling functions, which are used in finite-size recursive techniques. We rely on these matrix-SSFs to obtain non-perturbative estimates of the operator anomalous dimensions for scales ranging from O(ΛQCD) to O(MW). [ABSTRACT FROM AUTHOR]

We determine from first principles the quark mass anomalous dimension in Nf=3 QCD between the electroweak and hadronic scales. This allows for a fully non-perturbative connection of the perturbative and non-perturbative regimes of the Standard Model in the hadronic sector. The computation is carried out to high accuracy, employing massless O(a)-improved Wilson quarks and finite-size scaling techniques. We also provide the matching factors required in the renormalisation of light quark masses from lattice computations with O(a)-improved Wilson fermions and a tree-level Symanzik improved gauge action. The total uncertainty due to renormalisation and running in the determination of light quark masses in the SM is thus reduced to about 1%. [ABSTRACT FROM AUTHOR]