Renormalization-Group Improved Effective Potential for Interacting Theories with Several Mass Scales in Curved Spacetime

The renormalization group (RG) is used in order to obtain the RG improved effective potential in curved spacetime. This potential is explicitly calculated for the Yukawa model and for scalar electrodynamics, i.e. theories with several (namely, more than one) mass scales, in a space of constant curvature. Using the $\lambda \varphi^4$-theory on a general curved spacetime as an example, we show how it is possible to find the RG improved effective Lagrangian in curved spacetime. As specific applications, we discuss the possibility of curvature induced phase transitions in the Yukawa model and the effective equations (back-reaction problem) for the $\lambda \varphi^4$-theory on a De Sitter background.Comment: 18 pages, LaTeX file, UB-ECM-PF 93/2

The Landau Pole and Z′Z^{\prime} decays in the 331 bilepton model

We calculate the decay widths and branching ratios of the extra neutral boson $Z^{\prime}$ predicted by the 331 bilepton model in the framework of two different particle contents. These calculations are performed taken into account oblique radiative corrections, and Flavor Changing Neutral Currents (FCNC) under the ansatz of Matsuda as a texture for the quark mass matrices. Contributions of the order of $10^{-1}-10^{-2}$ are obtained in the branching ratios, and partial widths about one order of magnitude bigger in relation with other non- and bilepton models are also obtained. A Landau-like pole arise at 3.5 TeV considering the full particle content of the minimal model (MM), where the exotic sector is considered as a degenerated spectrum at 3 TeV scale. The Landau pole problem can be avoid at the TeV scales if a new leptonic content running below the threshold at $$ TeV is implemented as suggested by other authors.Comment: 20 pages, 5 figures, LaTeX2

Search for Lepton-Flavor-Violating tau Decays into a Lepton and an f0(980) Meson

We search for lepton-flavor-violating tau decays into a lepton (electron or muon) and an f0(980) meson using 671 fb-1 of data collected with the Belle detector at the KEKB asymmetric-energy e+e- collider. No events are observed and we set the following 90% C.L. upper limits on the branching fraction products: B(tau- -> e-f0(980))*B(f0(980)->pi+pi-) mu-f0(980))*B(f0(980) -> pi+pi-)<3.4x10^-8. This is the first search performed for these modes.Comment: 10 pages, 4 figures, submitted to Phys. Lett.

Search for lepton flavor violating decays tau- -> l- pi0, l- eta, l- eta'

We have searched for lepton flavor violating semileptonic tau decays using a data sample of 153.8/fb accumulated with the Belle detector at the KEKB e+e- collider. For the six decay modes studied, the observed yield is compatible with the estimated background and the following upper limits are set at the 90% confidence level: B(tau- -> e- eta) mu- eta) < 1.5 x 10^-7, B(tau- -> e- pi0) mu- pi0) < 4.1 x 10^-7, B(tau- -> e- eta') mu- eta') < 4.7 x 10^-7. These results are 10 to 64 times more restrictive than previous limits.Comment: 14 pages, 13 figures, RevTex

Linkage analysis of a kindred with inherited 46,XY partial gonadal dysgenesis

We have reported a kindred in which 46,XY gonadal dysgenesis was inherited in an X-linked (or autosomal dominant sex-limited) manner and in which affected subjects did not have a large duplication of the short arm of the X-chromosome. In the present study we used linkage and sequence analyses to test the role of X-linked and various autosomal genes in the etiology of the familial 46,XY partial gonadal dysgenesis. For analysis of X-linkage, 28 microsatellite polymorphisms and 1 restriction fragment length polymorphism were studied. The genotypes of informative family members were determined at each locus, and data were analyzed. Despite the large number of loci tested, our studies did not establish linkage between the trait and an X-chromosomal locus. With respect to the study of autosomal genes, linkage analysis using a polymorphism within the 3'-untranslated region of the WT1 gene excluded involvement of WT-1 in the etiology of the abnormal gonadal differentiation of the family in this study. Similarly, linkage analysis using four microsatellites on the distal short arm of chromosome 9 was not consistent with linkage. Linkage analysis of a locus close to the SOX9 gene as well as analysis of the coding region of the SOX9 gene suggested that this gene was not associated with the trait in the affected subjects we studied. Our data suggest the role of an autosomal gene in the abnormal gonadal differentiation in the family in the study, but do not formally exclude the role of an X-chromosome gene