The Υ(1S)\Upsilon(1S) leptonic decay using the principle of maximum conformality

In the paper, we study the $\Upsilon(1S)$ leptonic decay width $\Gamma(\Upsilon(1S)\to \ell^+\ell^-)$ by using the principle of maximum conformality (PMC) scale-setting approach. The PMC adopts the renormalization group equation to set the correct momentum flow of the process, whose value is independent to the choice of the renormalization scale and its prediction thus avoids the conventional renormalization scale ambiguities. Using the known next-to-next-to-next-to-leading order perturbative series together with the PMC single scale-setting approach, we do obtain a renormalization scale independent decay width, $\Gamma_{\Upsilon(1S) \to e^+ e^-} = 1.262^{+0.195}_{-0.175}$ keV, where the error is squared average of those from $\alpha_s(M_{Z})=0.1181\pm0.0011$, $m_b=4.93\pm0.03$ GeV and the choices of factorization scales within $\pm 10\%$ of their central values. To compare with the result under conventional scale-setting approach, this decay width agrees with the experimental value within errors, indicating the importance of a proper scale-setting approach.Comment: 6 pages, 4 figure

Sequential Wnt Agonist then Antagonist Treatment Accelerates Tissue Repair and Minimizes Fibrosis

Tissue fibrosis compromises organ function and occurs as a potential long-term outcome in response to acute tissue injuries. Currently, lack of mechanistic understanding prevents effective prevention and treatment of the progression from acute injury to fibrosis. Here, we combined quantitative experimental studies with a mouse kidney injury model and a computational approach to determine how the physiological consequences are determined by the severity of ischemia injury, and to identify how to manipulate Wnt signaling to accelerate repair of ischemic tissue damage while minimizing fibrosis. The study reveals that Wnt-mediated memory of prior injury contributes to fibrosis progression, and ischemic preconditioning reduces the risk of death but increases the risk of fibrosis. Furthermore, we validated the prediction that sequential combination therapy of initial treatment with a Wnt agonist followed by treatment with a Wnt antagonist can reduce both the risk of death and fibrosis in response to acute injuries

Methyl 2-[2-(tert-but­oxy­carbonyl­amino)-1,3-benzothia­zole-6-carboxamido]­acetate

In the title compound, C16H19N3O5S, the dihedral angle between the benzene ring and the carbonyl­amino group is 18.18 (2)°. In the crystal, mol­ecules form centrosymmetric dimers via pairs of N—H⋯N hydrogen bonds. The dimers are connected via N—H⋯O hydrogen bonds into a three-dimensional network.