Radiative Symmetry Breaking of the Minimal Left-Right Symmetric Model

Under the assumption of classical conformal invariance, we study the Coleman-Weinberg symmetry breaking mechanism in the minimal left-right symmetric model. This model is attractive as it provides a natural framework for small neutrino masses and the restoration of parity as a good symmetry of nature. We find that, in a large fraction of the parameter space, the parity symmetry is maximally broken by quantum corrections in the Coleman-Weinberg potential, which are a consequence of the conformal anomaly. As the left-right symmetry breaking scale is connected to the Planck scale through the logarithmic running of the dimensionless couplings of the scalar potential, a large separation of the two scales can be dynamically generated. The symmetry breaking dynamics of the model was studied using a renormalization group analysis. Electroweak symmetry breaking is triggered by the breakdown of left-right symmetry, and the left-right breaking scale is therefore expected in the few TeV range. The phenomenological implications of the symmetry breaking mechanism are discussed.Comment: 23 pages, 1 figure; version as published in journal; title changed, changes in abstract, introduction and conclusion

Glucose transporter-1 deficiency syndrome: the expanding clinical and genetic spectrum of a treatable disorder

Glucose transporter-1 deficiency syndrome is caused by mutations in the SLC2A1 gene in the majority of patients and results in impaired glucose transport into the brain. From 2004-2008, 132 requests for mutational analysis of the SLC2A1 gene were studied by automated Sanger sequencing and multiplex ligation-dependent probe amplification. Mutations in the SLC2A1 gene were detected in 54 patients (41%) and subsequently in three clinically affected family members. In these 57 patients we identified 49 different mutations, including six multiple exon deletions, six known mutations and 37 novel mutations (13 missense, five nonsense, 13 frame shift, four splice site and two translation initiation mutations). Clinical data were retrospectively collected from referring physicians by means of a questionnaire. Three different phenotypes were recognized: (i) the classical phenotype (84%), subdivided into early-onset (<2 years) (65%) and late-onset (18%); (ii) a non-classical phenotype, with mental retardation and movement disorder, without epilepsy (15%); and (iii) one adult case of glucose transporter-1 deficiency syndrome with minimal symptoms. Recognizing glucose transporter-1 deficiency syndrome is important, since a ketogenic diet was effective in most of the patients with epilepsy (86%) and also reduced movement disorders in 48% of the patients with a classical phenotype and 71% of the patients with a non-classical phenotype. The average delay in diagnosing classical glucose transporter-1 deficiency syndrome was 6.6 years (range 1 month-16 years). Cerebrospinal fluid glucose was below 2.5 mmol/l (range 0.9-2.4 mmol/l) in all patients and cerebrospinal fluid : blood glucose ratio was below 0.50 in all but one patient (range 0.19-0.52). Cerebrospinal fluid lactate was low to normal in all patients. Our relatively large series of 57 patients with glucose transporter-1 deficiency syndrome allowed us to identify correlations between genotype, phenotype and biochemical data. Type of mutation was related to the severity of mental retardation and the presence of complex movement disorders. Cerebrospinal fluid : blood glucose ratio was related to type of mutation and phenotype. In conclusion, a substantial number of the patients with glucose transporter-1 deficiency syndrome do not have epilepsy. Our study demonstrates that a lumbar puncture provides the diagnostic clue to glucose transporter-1 deficiency syndrome and can thereby dramatically reduce diagnostic delay to allow early start of the ketogenic die

Natural Vacuum Alignment from Group Theory: The Minimal Case

Discrete flavour symmetries have been proven successful in explaining the leptonic flavour structure. To account for the observed mixing pattern, the flavour symmetry has to be broken to different subgroups in the charged and neutral lepton sector. However, cross-couplings via non-trivial contractions in the scalar potential force the group to break to the same subgroup. We present a solution to this problem by extending the flavour group in such a way that it preserves the flavour structure, but leads to an 'accidental' symmetry in the flavon potential. We have searched for symmetry groups up to order 1000, which forbid all dangerous cross-couplings and extend one of the interesting groups A4, T7, S4, T' or \Delta(27). We have found a number of candidate groups and present a model based on one of the smallest extension of A4, namely Q8 \rtimes A4. We show that the most general non-supersymmetric potential allows for the correct vacuum alignment. We investigate the effects of higher dimensional operators on the vacuum configuration and mixing angles, and give a see-saw-like UV completion. Finally, we discuss the supersymmetrization of the model. Additionally, we release the Mathematica package "Discrete" providing various useful tools for model building such as easily calculating invariants of discrete groups and flavon potentials.Comment: 33 pages, 7 figures; references added, minor changes, matches version published in JHE