544 research outputs found
Search for lepton flavor violation via the intense high-energy muon beam
A deep inerastic scattering process \mutau is discussed to study lepton
flavor violation between muons and tau leptons. In supersymmetric models, the
Higgs boson mediated diagrams could be important for this reaction. We find
that at a muon energy () higher than 50 GeV, the predicted cross
section significantly increases due to the contribution from sea -quarks.
The number of produced tau leptons can be at = 300
GeV from muons, whereas events are given at
GeV.Comment: Contribution to the 6th International Workshop on Neutrino Factories
& Superbeams(NuFact04), Jul. 26-Aug. 1, 2004, Osaka Univerisity, Osaka,
Japan, talk given by S.K., to appear in the Proceedings, 3 pages, 4 figure
Large Solar Neutrino Mixing in an Extended Zee Model
The Zee model, which employs the standard Higgs scalar () with its
duplicate () and a singly charged scalar (), can utilize two
global symmetries associated with the conservation of the numbers of and
, , where coincides
with the hypercharge while () is a new
conserved charge, which is identical to for the left-handed
leptons. Charged leptons turn out to have - and - mixing
masses, which are found to be crucial for the large solar neutrino mixing. In
an extended version of the Zee model with an extra triplet Higgs scalar (s),
neutrino oscillations are described by three steps: 1) the maximal atmospheric
mixing is induced by democratic mass terms supplied by with =2 that can
initiate the type II seesaw mechanism for the smallness of these masses; 2) the
maximal solar neutrino mixing is triggered by the creation of radiative masses
by with = 0; 3) the large solar neutrino mixing is finally induced by
a - mixing arising from the rotation of the radiative mass
terms as a result of the diagonalization that converts - and -
mixing masses into the electron mass.Comment: RevTex, 10 pages including one figure page, to be published in Int.
J. Mod. Phys. A (2002
Phenomenology of Higgs bosons in the Zee-Model
To generate small neutrino masses radiatively, the Zee-model introduces two
Higgs doublets and one weak-singlet charged Higgs boson to its Higgs sector.
From analyzing the renormalization group equations, we determine the
possibile range of the lightest CP-even Higgs boson () mass and the Higgs
boson self-couplings as a function of the cut-off scale beyond which either
some of the coupling constants are strong enough to invalidate the perturbative
analysis or the stability of the electroweak vacuum is no longer guaranteed.
Using the results obtained from the above analysis, we find that the singlet
charged Higgs boson can significantly modify the partial decay width of via radiative corrections, and its collider phenomenology can
also be drastically different from that of the charged Higgs bosons in the
usual two-Higgs-doublet models.Comment: Added a paragraph and a figure in Section V, corrected typos, added
references. (RevTeX, 45 pages, 16 figures included.) To appear in Physical
Review
Neurologic phenotype of Schimke immuno-osseous dysplasia and neurodevelopmental expression of SMARCAL1
Schimke immuno-osseous dysplasia (OMIM 242900) is an uncommon autosomal-recessive multisystem disease caused by mutations in SMARCAL1 (swi/snf-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a-like 1), a gene encoding a putative chromatin remodeling protein. Neurologic manifestations identified to date relate to enhanced atherosclerosis and cerebrovascular disease. Based on a clinical survey, we determined that half of Schimke immuno-osseous dysplasia patients have a small head circumference, and 15% have social, language, motor, or cognitive abnormalities. Postmortem examination of 2 Schimke immuno-osseous dysplasia patients showed low brain weights and subtle brain histologic abnormalities suggestive of perturbed neuron-glial migration such as heterotopia, irregular cortical thickness, incomplete gyral formation, and poor definition of cortical layers. We found that SMARCAL1 is highly expressed in the developing and adult mouse and human brain, including neural precursors and neuronal lineage cells. These observations suggest that SMARCAL1 deficiency may influence brain development and function in addition to its previously recognized effect on cerebral circulation
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