Flavour changing neutral currents and CP violating processes in generalized supersymmetric theories

We consider supersymmetric extensions of the standard model with general non-universal soft breaking terms. We analyse in a model-independent way the constraints on these terms at the electroweak energy scale coming from gluino mediated flavour (F) changing neutral current and CP-violating processes. We have computed the complete $\Delta F=1$ and $\Delta F=2$ effective hamiltonian for gluino mediated processes, including for the first time the effect of box diagrams in the evaluation of $\epsilon^{\prime}/\epsilon$. We present numerical results for the constraints on these non-universal soft breaking terms for different values of the parameters, extending the analysis also to the leptonic sector. A comparison with previous results in the literature is given.Comment: LaTeX, 17 pages, 3 uuencoded figure

Phenomenology on a Slice of AdS5×MδAdS_5 \times {\cal M}^\delta Spacetime

We study the phenomenology resulting from backgrounds of the form $AdS_5 \times {\cal M}^\delta$, where ${\cal M}^\delta$ denotes a generic manifold of dimension $\delta \geq 1$, and $AdS_5$ is the slice of 5-dimensional anti-de Sitter space which generates the hierarchy in the Randall-Sundrum (RS) model. The $\delta$ additional dimensions may be required when the RS model is embedded into a more fundamental theory. We analyze two classes of $\delta-$dimensional manifolds: flat and curved geometries. In the first case, the additional flat dimensions may accommodate localized fermions which in turn could resolve issues, such as proton decay and flavor, that were not addressed in the original RS proposal. In the latter case, the positive curvature of an $S^\delta$ manifold with $\delta> 1$ can geometrically provide the 5-dimensional warping of the RS model. We demonstrate the key features of these two classes of models by presenting the background solutions, the spectra of the Kaluza-Klein (KK) gravitons, and their 4-dimensional couplings, for the sample manifolds $S^1/Z_2$, $S^1$, and $S^2$. The resulting phenomenology is distinct from that of the original RS scenario due to the appearance of a multitude of new KK graviton states at the weak scale with couplings that are predicted to be measurably non-universal within the KK tower. In addition, in the case of flat compactifications, fermion localization can result in KK graviton and gauge field flavor changing interactions.Comment: 30 pages, 8 figures. Small corrections included to agree with published versio

Supersymmetric Relations Among Electromagnetic Dipole Operators

Supersymmetric contributions to all leptonic electromagnetic dipole operators have essentially identical diagramatic structure. With approximate slepton universality this allows the muon anomalous magnetic moment to be related to the electron electric dipole moment in terms of supersymmetric phases, and to radiative flavor changing lepton decays in terms of small violations of slepton universality. If the current discrepancy between the measured and Standard Model values of the muon anomalous magnetic moment is due to supersymmetry, the current bound on the electron electric dipole moment then implies that the phase of the electric dipole operator is less than $2 \times 10^{-3}$. Likewise the current bound on $\mu \to e \gamma$ decay implies that the fractional selectron-smuon mixing in the left-left mass squared matrix, \delta m_{\smuon \selectron}^2 / m_{\slepton}^2, is less than $10^{-4}$. These relations and constraints are fairly insensitive to details of the superpartner spectrum for moderate to large $\tan \beta$.Comment: Latex, 38 pages, 2 figure

Electric Dipole Moments Do Not Require the CP-violating Phases of Supersymmetry To Be Small

We report the first fully general numerical calculation of the neutron and electron dipole moments, including the seven significant phases. We find that there are major regions in the parameter space where none of the phases are required to be small, contrary to the conventional wisdom. The electric dipole moments (EDM's) do provide useful constraints, allowing other regions of parameter space to be carved away. We keep all superpartner masses light so agreement with experimental limits arises purely from interesting relations among soft breaking parameters.Comment: 23 pages, 7 figures; 2 references adde

Collider aspects of flavour physics at high Q

This review presents flavour related issues in the production and decays of heavy states at LHC, both from the experimental side and from the theoretical side. We review top quark physics and discuss flavour aspects of several extensions of the Standard Model, such as supersymmetry, little Higgs model or models with extra dimensions. This includes discovery aspects as well as measurement of several properties of these heavy states. We also present public available computational tools related to this topic.Comment: Report of Working Group 1 of the CERN Workshop ``Flavour in the era of the LHC'', Geneva, Switzerland, November 2005 -- March 200

Genome-wide association study identifies four novel loci associated with Alzheimer's endophenotypes and disease modifiers

More than 20 genetic loci have been associated with risk for Alzheimer's disease (AD), but reported genome-wide significant loci do not account for all the estimated heritability and provide little information about underlying biological mechanisms. Genetic studies using intermediate quantitative traits such as biomarkers, or endophenotypes, benefit from increased statistical power to identify variants that may not pass the stringent multiple test correction in case-control studies. Endophenotypes also contain additional information helpful for identifying variants and genes associated with other aspects of disease, such as rate of progression or onset, and provide context to interpret the results from genome-wide association studies (GWAS). We conducted GWAS of amyloid beta (Aβ42), tau, and phosphorylated tau (ptau181) levels in cerebrospinal fluid (CSF) from 3146 participants across nine studies to identify novel variants associated with AD. Five genome-wide significant loci (two novel) were associated with ptau181, including loci that have also been associated with AD risk or brain-related phenotypes. Two novel loci associated with Aβ42 near GLIS1 on 1p32.3 (β = -0.059, P = 2.08 × 10-8) and within SERPINB1 on 6p25 (β = -0.025, P = 1.72 × 10-8) were also associated with AD risk (GLIS1: OR = 1.105, P = 3.43 × 10-2), disease progression (GLIS1: β = 0.277, P = 1.92 × 10-2), and age at onset (SERPINB1: β = 0.043, P = 4.62 × 10-3). Bioinformatics indicate that the intronic SERPINB1 variant (rs316341) affects expression of SERPINB1 in various tissues, including the hippocampus, suggesting that SERPINB1 influences AD through an Aβ-associated mechanism. Analyses of known AD risk loci suggest CLU and FERMT2 may influence CSF Aβ42 (P = 0.001 and P = 0.009, respectively) and the INPP5D locus may affect ptau181 levels (P = 0.009); larger studies are necessary to verify these results. Together the findings from this study can be used to inform future AD studies

A common haplotype lowers PU.1 expression in myeloid cells and delays onset of Alzheimer's disease

A genome-wide survival analysis of 14,406 Alzheimer's disease (AD) cases and 25,849 controls identified eight previously reported AD risk loci and 14 novel loci associated with age at onset. Linkage disequilibrium score regression of 220 cell types implicated the regulation of myeloid gene expression in AD risk. The minor allele of rs1057233 (G), within the previously reported CELF1 AD risk locus, showed association with delayed AD onset and lower expression of SPI1 in monocytes and macrophages. SPI1 encodes PU.1, a transcription factor critical for myeloid cell development and function. AD heritability was enriched within the PU.1 cistrome, implicating a myeloid PU.1 target gene network in AD. Finally, experimentally altered PU.1 levels affected the expression of mouse orthologs of many AD risk genes and the phagocytic activity of mouse microglial cells. Our results suggest that lower SPI1 expression reduces AD risk by regulating myeloid gene expression and cell function