Minimal gauge origin of baryon triality and flavorful signatures at the LHC

Baryon triality (B3) is a Z3 discrete symmetry that can protect the proton from decay. Although its realization does not require supersymmetry, it is particularly appealing in the supersymmetry as an alternative to the popular R-parity. We discuss the issues in gauging B3, and present the minimal supersymmetric model with B3 as the remnant discrete symmetry of a TeV scale U(1) gauge symmetry. A flavor-dependent U(1) charge is necessary to achieve this, and it results in very distinguishable and flavorful predictions for the LHC experiments. We find a complementarity between a 2-lepton sneutrino resonance and a 4-lepton Z' resonance in the supersymmetry search. In addition, we introduce baryon tetrality (B4), which would play an equivalent role if there are four fermion generations.Comment: Version to appear in PL

Generalized Bergman kernels on symplectic manifolds

We study the near diagonal asymptotic expansion of the generalized Bergman kernel of the renormalized Bochner-Laplacian on high tensor powers of a positive line bundle over a compact symplectic manifold. We show how to compute the coefficients of the expansion by recurrence and give a closed formula for the first two of them. As consequence, we calculate the density of states function of the Bochner-Laplacian and establish a symplectic version of the convergence of the induced Fubini-Study metric. We also discuss generalizations of the asymptotic expansion for non-compact or singular manifolds as well as their applications. Our approach is inspired by the analytic localization techniques of Bismut-Lebeau.Comment: 48 pages. Add two references on the Hermitian scalar curvatur

Leptogenesis from Neutralino Decay with Nonholomorphic R-Parity Violation

In supersymmetric models with lepton-number violation, hence also R-parity violation, it is easy to have realistic neutrino masses, but then leptogenesis becomes difficult to achieve. After explaining the general problems involved, we study the details of a model which escapes these constraints and generates a lepton asymmetry, which gets converted into the present observed baryon asymmetry of the Universe through the electroweak sphalerons. This model requires the presence of certain nonholomorphic R-parity violating terms. For completeness we also present the most general R-parity violating Lagrangian with soft nonholomorphic terms and study their consequences for the charged-scalar mass matrix. New contributions to neutrino masses in this scenario are discussed.Comment: 30 pages, 6 figure

Supersymmetric Model of Muon Anomalous Magnetic Moment and Neutrino Masses

We propose the novel lepton-number relationship $L_\tau = L_e + L_\mu$, which is uniquely realized by the interaction $(\hat \nu_e \hat \mu - \hat e \hat \nu_\mu) \hat \tau^c$ in supersymmetry and may account for a possibly large muon anomalous magnetic moment. Neutrino masses (with bimaximal mixing) may be generated from the spontaneous and soft breaking of this lepton symmetry.Comment: 10 pages, including 2 figure

Budding-like division of all-aqueous emulsion droplets modulated by networks of protein nanofibrils.

Networks of natural protein nanofibrils, such as cytoskeletal filaments, control the shape and the division of cells, yet mimicking this functionality in a synthetic setting has proved challenging. Here, we demonstrate that artificial networks of protein nanofibrils can induce controlled deformation and division of all-aqueous emulsion droplets with budding-like morphologies. We show that this process is driven by the difference in the immersional wetting energy of the nanofibril network, and that both the size and the number of the daughter droplets formed during division can be controlled by modulating the fibril concentration and the chemical properties of the fibril network. Our results demonstrate a route for achieving biomimetic division with synthetic self-assembling fibrils and offer an engineered approach to regulate the morphology of protein gels

Leptogenesis from R parity nonconservation

It is known that realistic neutrino masses for neutrino oscillations may be obtained from R parity nonconserving supersymmetry. It is also known that such interactions would erase any preexisting lepton or baryon asymmetry of the Universe because of the inevitable intervention of the electroweak sphalerons. We now show how a crucial subset of these R parity nonconserving terms may in fact create its own successful leptogenesis.Comment: 4 pages latex file with one postscript figur

The Interplay between Neutrinos and Charged Leptons in the Minimal SU(3)_LxU(1)_N Gauge Model

In the minimal SU(3)_LxU(1)_N gauge model with a global L_e-L_mu-L_tau (=L') symmetry and a discrete Z_4 symmetry, it is found that the interplay between neutrinos and charged leptons contained in triplets of \psi^i=(\nu^i_L, \ell^i_L, \ell^{ci}_L) (i=1,2,3) naturally leads to the large mixing angle (LMA) MSW solution. The model includes two (anti)sextet Higgs scalars, S^(0) with L'=0 and S^(+) with L'=2, which, respectively, couple to \psi^1\psi^{2,3} for the electron mass and masses of atmospheric neutrinos and to \psi^{2,3}\psi^{2,3} for the \mu- and \tau-masses and one-loop radiative neutrino masses relevant to solar neutrinos. This mechanism is realized by utilizing an additional residual discrete symmetry supplied by explicitly broken L', which guarantees the absence of tree-level neutrino mass terms of the \psi^{2,3}\psi^{2,3}-type. Pure rotation effects due to the diagonalization of neutrino and charged-lepton mass matrices are estimated to yield \Delta m^2_\odot/\Delta m^2_{atm} \leq (m_e/m_\mu)^{3/2}=O(10^{-4}) but the radiative effects supersede the rotation effects to yield \Delta m^2_\odot/\Delta m^2_{atm}=O(10^{-2}) as the LMA solution.Comment: 16 pages, RevTeX, including 2 figures with typos and misprints corrected and with modifications in sections II-B and V, accepted by Nuclear Physics

Mechanistic relationship among mutagenicity, skin sensitization, and skin carcinogenicity.

Twenty organic Salmonella mutagens, seven of which (including benzo[a]pyrene) are established skin carcinogens, and one of which (2-chloroethanol) is a well-defined noncarcinogen to skin, have been evaluated for skin-sensitizing activity using the local lymph node assay. The relative mutagenicity of the agents to Salmonella was also established. Fourteen of the chemicals were positive in the local lymph node assay, including the seven skin carcinogens. 2-Chloroethanol was inactive as a sensitizing agent. We suggest that a variety of factors contributes to the lack of sensitizing activity of the remaining six bacterial mutagens: extremes of intrinsic chemical reactivity, high water solubility reducing dermal translocation, and inappropriate dermal metabolism. Two reference skin-sensitizing agents (an oxazolinone and fluorescein isothiocyanate) were established as in vitro clastogens after their recognition as nonmutagens to Salmonella. These data imply that mutagenicity, rather than simply activity in the Salmonella assay, is a primary stimulus for electrophilic sensitization and carcinogenic initiation in the skin. We conclude that genotoxicity data for an agent can provide indications of the agent's potential to induce skin sensitization and that genotoxins which are skin-sensitizing agents have an enhanced potential to initiate skin carcinogenesis. We suggest that common, albeit individually distinct, structure-activity relationships underpin genotoxicity, skin sensitization, and the initiation of skin carcinogenesis. These relationships should simplify the hazard evaluation of chemicals and contribute to a reduction in animal usage. Several predictions of skin carcinogenicity are made based on the data presented

Molecular alterations that drive breast cancer metastasis to bone.

Epithelial cancers including breast and prostate commonly progress to form incurable bone metastases. For this to occur, cancer cells must adapt their phenotype and behaviour to enable detachment from the primary tumour, invasion into the vasculature, and homing to and subsequent colonisation of bone. It is widely accepted that the metastatic process is driven by the transformation of cancer cells from a sessile epithelial to a motile mesenchymal phenotype through epithelial-mesenchymal transition (EMT). Dissemination of these motile cells into the circulation provides the conduit for cells to metastasise to distant organs. However, accumulating evidence suggests that EMT is not sufficient for metastasis to occur and that specific tissue-homing factors are required for tumour cells to lodge and grow in bone. Once tumour cells are disseminated in the bone environment, they can revert into an epithelial phenotype through the reverse process of mesenchymal-epithelial transition (MET) and form secondary tumours. In this review, we describe the molecular alterations undertaken by breast cancer cells at each stage of the metastatic cascade and discuss how these changes facilitate bone metastasis