Abelian Magnetic Monopole Dominance in Quark Confinement

We prove Abelian magnetic monopole dominance in the string tension of QCD. Abelian and monopole dominance in low energy physics of QCD has been confirmed for various quantities by recent Monte Carlo simulations of lattice gauge theory. In order to prove this dominance, we use the reformulation of continuum Yang-Mills theory in the maximal Abelian gauge as a deformation of a topological field theory of magnetic monopoles, which was proposed in the previous article by the author. This reformulation provides an efficient way for incorporating the magnetic monopole configuration as a topological non-trivial configuration in the functional integral. We derive a version of the non-Abelian Stokes theorem and use it to estimate the expectation value of the Wilson loop. This clearly exhibits the role played by the magnetic monopole as an origin of the Berry phase in the calculation of the Wilson loop in the manifestly gauge invariant manner. We show that the string tension derived from the diagonal (abelian) Wilson loop in the topological field theory (studied in the previous article) converges to that of the full non-Abelian Wilson loop in the limit of large Wilson loop. Therefore, within the above reformulation of QCD, this result (together with the previous result) completes the proof of quark confinement in QCD based on the criterion of the area law of the full non-Abelian Wilson loop.Comment: 33 pages, Latex, no figures, version accepted for publication in Phys. Rev. D (additions of sec. 4.5 and references, and minor changes

Autoantibodies against type I IFNs in patients with life-threatening COVID-19

Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-w (IFN-w) (13 patients), against the 13 types of IFN-a (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men

RcoA has pleiotropic effects on aspergillus nidulans cellular development

The definitive version is available at www.blackwell-synergy.comAspergillus nidulans rcoA encodes a member of the WD repeat family of proteins. The RcoA protein shares sequence similarity with other members of this protein family, including the Saccharomyces cerevisiae Tup1p and Neurospora crassa RCO1. Tup1p is involved in negative regulation of an array of functions including carbon catabolite repression. RCO1 functions in regulating pleiotropic developmental processes, but not carbon catabolite repression. In A. nidulans, deletion of rcoA (DrcoA), a recessive mutation, resulted in gross defects in vegetative growth, asexual spore production and sterigmatocystin (ST) biosynthesis. Expression of the asexual and ST pathway-specific regulatory genes, brlA and aflR, respectively, but not the signal transduction genes (i.e. flbA, fluG or fadA) regulating brlA and aflR expression was delayed (brlA) or eliminated (aflR) in a DrcoA strain. Overexpression of aflR in a DrcoA strain could not rescue normal expression of downstream targets of AflR. CreAdependent carbon catabolite repression of starch and ethanol utilization was only weakly affected in a DrcoA strain. The strong role of RcoA in development, vegetative growth and ST production, compared with a relatively weak role in carbon catabolite repression, is similar to the role of RCO1 in N. crassa.Julie Hicks, Robin A. Lockington, Joseph Strauss, Daniel Dieringer, Christian P. Kubicek, Joan Kelly and Nancy Kelle