The NLO contributions to the scalar pion form factors and the O(αs2){\cal O}(\alpha_s^2) annihilation corrections to the B→ππB\to \pi\pi decays

In this paper, by employing the $k_{T}$ factorization theorem, we made the first calculation for the space-like scalar pion form factor $Q^2 F(Q^2)$ at the leading order (LO) and the next-to-leading order (NLO) level, and then found the time-like scalar pion form factor $F'^{(1)}_{\rm a,I}$ by analytic continuation from the space-like one. From the analytical evaluations and the numerical results, we found the following points: (a) the NLO correction to the space-like scalar pion form factor has an opposite sign with the LO one but is very small in magnitude, can produce at most $10\%$ decrease to LO result in the considered $Q^2$ region; (b) the NLO time-like scalar pion form factor $F'^{(1)}_{\rm a,I}$ describes the ${\cal O}(\alpha_s^2)$ contribution to the factorizable annihilation diagrams of the considered $B \to \pi\pi$ decays, i.e. the NLO annihilation correction; (c) the NLO part of the form factor $F'^{(1)}_{\rm a,I}$ is very small in size, and is almost independent with the variation of cutoff scale $\mu_0$, but this form factor has a large strong phase around $-55^\circ$ and may play an important role in producing large CP violation for $B\to \pi\pi$ decays; and (d) for $B^0 \to \pi^+\pi^-$ and $\pi^0\pi^0$ decays, the newly known NLO annihilation correction can produce only a very small enhancement to their branching ratios, less than $3\%$ in magnitude, and therefore we could not interpret the well-known $\pi\pi$-puzzle by the inclusion of this NLO correction to the factorizable annihilation diagrams.Comment: 26 pages, 12 figures, 1 Table; Minor correction

Phenomenological discriminations of the Yukawa interactions in two-Higgs doublet models with Z2Z_2 symmetry

There are four types of two-Higgs doublet models under a discrete $Z_2$ symmetry imposed to avoid tree-level flavour-changing neutral current, i.e. type-I, type-II, type-X and type-Y models. We investigate the possibility to discriminate the four models in the light of the flavour physics data, including $B_s-\bar B_s$ mixing, $B_{s,d} \to \mu^+ \mu^-$, $B\to \tau\nu$ and $\bar B \to X_s \gamma$ decays, the recent LHC Higgs data, the direct search for charged Higgs at LEP, and the constraints from perturbative unitarity and vacuum stability. After deriving the combined constraints on the Yukawa interaction parameters, we have shown that the correlation between the mass eigenstate rate asymmetry $A_{\Delta\Gamma}$ of $B_{s} \to \mu^+ \mu^-$ and the ratio $R={\cal B}(B_{s} \to \mu^+ \mu^-)_{exp}/ {\cal B}(B_{s} \to \mu^+ \mu^-)_{SM}$ could be sensitive probe to discriminate the four models with future precise measurements of the observables in the $B_{s} \to \mu^+ \mu^-$ decay at LHCb.Comment: 29 pages, 4 tables, 11 figures. v3: minor corrections included, matches published version in EPJ

Elucidation of Emergent Regional Mechanisms of Heart Muscle Dysfunction in the Mouse Model of Duchenne Muscular Dystrophy

Cardiac dysfunction is a primary cause of mortality in Duchenne Muscular Dystrophy (DMD), potentially related to elevated cytosolic calcium. However, the regional versus global functional consequences of cellular calcium mishandling have not been defined in the whole heart. Here, we elucidate, for the first time, loci- and age-dependencies between calcium mishandling and myocardial sheet function as a manifestation of dystrophin-deficient cardiomyopathy. We also map calcium transients to illustrate the regional dependence of ion flux disturbances in the dystrophin-deficient (mdx) mouse heart. Furthermore, we elucidate abnormalities in autophagic processes that can be corrected with nanoparticle therapeutics delivering rapamycin to heart tissues to improve ventricular function in affected older mice with incipient cardiomyopathy. We conclude that the rapid reversibility of functional defects by reducing cytosolic calcium or by impacting impaired autophagy points to the significance of regional mechanical factors in the progression of the disease