64 research outputs found
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 -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 -theory
on a De Sitter background.Comment: 18 pages, LaTeX file, UB-ECM-PF 93/2
The Landau Pole and decays in the 331 bilepton model
We calculate the decay widths and branching ratios of the extra neutral boson
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 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
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