The Determination of alpha_s from Tau Decays Revisited

We revisit the determination of alpha_s(m_tau) using a fit to inclusive tau hadronic spectral moments in light of (1) the recent calculation of the fourth-order perturbative coefficient K_4 in the expansion of the Adler function, (2) new precision measurements from BABAR of e+e- annihilation cross sections, which decrease the uncertainty in the separation of vector and axial-vector spectral functions, and (3) improved results from BABAR and Belle on tau branching fractions involving kaons. We estimate that the fourth-order perturbative prediction reduces the theoretical uncertainty, introduced by the truncation of the series, by 20% with respect to earlier determinations. We discuss to some detail the perturbative prediction and show that the effect of the incomplete knowledge of the series is reduced by using the so-called contour-improved calculation, as opposed to fixed-order perturbation theory which manifests convergence problems. The corresponding theoretical uncertainties are studied at the tau and Z mass scales. Nonperturbative contributions extracted from the most inclusive fit are small, in agreement with earlier determinations. Systematic effects from quark-hadron duality violation are estimated with simple models and found to be within the quoted systematic errors. The fit gives alpha_s(m_tau) = 0.344 +- 0.005 +- 0.007, where the first error is experimental and the second theoretical. After evolution to M_Z we obtain alpha_s(M_Z) = 0.1212 +- 0.0005 +- 0.0008 +- 0.0005, where the errors are respectively experimental, theoretical and due to the evolution. The result is in agreement with the corresponding NNNLO value derived from essentially the Z width in the global electroweak fit. The alpha_s(M_Z) determination from tau decays is the most precise one to date.Comment: 22 pages, 7 figure

Active tuberculosis, sequelae and COVID-19 co-infection: first cohort of 49 cases.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) pandemic has attracted interest because of its global rapid spread, clinical severity, high mortality rate, and capacity to overwhelm healthcare systems [1, 2]. SARS-CoV-2 transmission occurs mainly through droplets, although surface contamination contributes and debate continues on aerosol transmission [3\u20135]

Mutation in LBX1/Lbx1 precludes transcription factor cooperativity and causes congenital hypoventilation in humans and mice

The respiratory rhythm is generated by the preBötzinger complex in the medulla oblongata, and is modulated by neurons in the retrotrapezoid nucleus (RTN), which are essential for accelerating respiration in response to high CO2. Here we identify a LBX1 frameshift (LBX1FS) mutation in patients with congenital central hypoventilation. The mutation alters the C-terminal but not the DNA-binding domain of LBX1. Mice with the analogous mutation recapitulate the breathing deficits found in humans. Furthermore, the mutation only interferes with a small subset of Lbx1 functions, and in particular with development of RTN neurons that coexpress Lbx1 and Phox2b. Genome-wide analyses in a cell culture model show that Lbx1FS and wild-type Lbx1 proteins are mostly bound to similar sites, but that Lbx1FS is unable to cooperate with Phox2b. Thus, our analyses on Lbx1FS (dys)function reveals an unusual pathomechanism; that is, a mutation that selectively interferes with the ability of Lbx1 to cooperate with Phox2b, and thus impairs the development of a small subpopulation of neurons essential for respiratory control