CP Violation in a Supersymmetric SO(10) x U(2)_{F} Model

A model based on SUSY SO(10) combined with U(2) family symmetry constructed recently by the authors is generalized to include phases in the mass matrices leading to CP violation. In contrast with the commonly used effective operator approach, $\bar{126}$-dimensional Higgs fields are utilized to construct the Yukawa sector. R-parity symmetry is thus preserved at low energies. The symmetric mass textures arising from the left-right symmetry breaking chain of SO(10) give rise to very good predictions for quark and lepton masses and mixings. The prediction for $\sin 2\beta$ agrees with the average of current bounds from BaBar and Belle. In the neutrino sector, our predictions are in good agreement with results from atmospheric neutrino experiments. Our model favors both the LOW and QVO solutions to the solar neutrino anomaly; the matrix element for neutrinoless double beta decay is highly suppressed. The leptonic analog of the Jarlskog invariant, $J_{CP}^{l}$, is predicted to be of $O(10^{-2})$.Comment: RevTeX4; 7 pages; typos corrected; clarification remarks added; more references added. To appear in Physical Review

Charged lepton electric dipole moments with the localized leptons and the new Higgs doublet in the two Higgs doublet model

We study the lepton electric dipole moments in the split fermion scenario, in the two Higgs doublet model, where the new Higgs scalars are localized around the origin in the extra dimension, with the help of the localizer field. We observe that the numerical value of the electron (muon, tau) electric dipole moment is at the order of the magnitude of 10^{-31} (10^{-24}, 10^{-22}) (e-cm) and this quantity is sensitive the new Higgs localization in the extra dimension.Comment: 20 pages, 7 figure

B decays and models for CP violation

The decay modes $B$ to $\pi\pi$, $\psi K_S$, $K^- D$, $\pi K$ and $\eta K$ are promising channels to study the unitarity triangle of the CP violating CKM matrix. In this paper I study the consequences of these measurements in the Weinberg model. I show that using the same set of measurements, the following different mechanisms for CP violation can be distinguished: 1) CP is violated in the CKM sector only; 2) CP is violated spontaneously in the Higgs sector only; And 3) CP is violated in both the CKM and Higgs sectors.Comment: 18 pagers, Revtex, Four compressed figures. Some typos in the figure captions are correcte

CP Violation in τ→3πντ\tau\rightarrow 3\pi\nu_\tau

We consider CP violating effects in the decays $\tau\rightarrow (3\pi)\nu_\tau$ where both the ${\rm J}^{\rm P}=1^+$ resonance, $a_1$, and ${\rm J}^{\rm P}=0^-$ resonance, $\pi^\prime$, can contribute. The interference between the $a_1$ and $\pi^\prime$ resonances can lead to enhanced CP-violating asymmetries whose magnitudes depend crucially on the $\pi^\prime$ decay constant, $f_{\pi^\prime}$. We make an estimate of $f_{\pi^\prime}$ with a simplified chiral Lagrangian coupled to a massive pseudoscalar field, and we compare the estimates from the non-relativistic quark model and from the QCD sum rule with the estimate from the `mock' meson model. We then estimate quantitatively the size of CP-violating effects in a multi-Higgs-doublet model and scalar-leptoquark models. We find that, while CP-violating effects in the scalar-leptoquark models may require more than $10^{10}$ $\tau$ leptons, CP-violating effects from the multi-Higgs-doublet model can be seen at the $2\sigma$ level with about $10^7$ $\tau$ leptons using the chiral Lagrangian estimate of $f_{\pi^\prime}=(1\sim 5)\times 10^{-3}$ GeV.Comment: Latex, 30 pages, 2 figures (not included). Three compressed postscript files of the paper available at ftp://ftp.kek.jp/kek/preprints/TH/TH-419/kekth419.ps.gz, Tau1.ps.gz, Tau2.ps.g

Distinct germline genetic susceptibility profiles identified for common non-Hodgkin lymphoma subtypes

Lymphoma risk is elevated for relatives with common non-Hodgkin lymphoma (NHL) subtypes, suggesting shared genetic susceptibility across subtypes. To evaluate the extent of mutual heritability among NHL subtypes and discover novel loci shared among subtypes, we analyzed data from eight genome-wide association studies within the InterLymph Consortium, including 10,629 cases and 9505 controls. We utilized Association analysis based on SubSETs (ASSET) to discover loci for subsets of NHL subtypes and evaluated shared heritability across the genome using Genome-wide Complex Trait Analysis (GCTA) and polygenic risk scores. We discovered 17 genome-wide significant loci (P < 5 × 10−8) for subsets of NHL subtypes, including a novel locus at 10q23.33 (HHEX) (P = 3.27 × 10−9). Most subset associations were driven primarily by only one subtype. Genome-wide genetic correlations between pairs of subtypes varied broadly from 0.20 to 0.86, suggesting substantial heterogeneity in the extent of shared heritability among subtypes. Polygenic risk score analyses of established loci for different lymphoid malignancies identified strong associations with some NHL subtypes (P < 5 × 10−8), but weak or null associations with others. Although our analyses suggest partially shared heritability and biological pathways, they reveal substantial heterogeneity among NHL subtypes with each having its own distinct germline genetic architecture