Electron and neutron electric dipole moment in the 3-3-1 model with heavy leptons

We calculate the electric dipole moment for the electron and neutron in the framework of the 3-3-1 model with heavy charged leptons. We assume that the only source of $CP$ violation arises from a complex trilinear coupling constant and the three complex vacuum expectation values. However, two of the vacua phases are absorbed and the other two are equal up to a minus sign. Hence only one physical phase survives. In order to be compatible with the experimental data this phase has to be smaller than $10^{-6}$.Comment: 21 pages, 4 figures. Version published in PR

Electron and muon anomalous magnetic dipole moment in a 3-3-1 model

We calculate, in the context of a 3-3-1 model with heavy charged leptons, constraints on some parameters of the extra particles in the model by imposing that their contributions to both the electron and muon $(g-2)$ factors are in agreement with experimental data up to 1$\sigma$-3$\sigma$. In order to obtain realistic results we use some of the possible solutions of the left- and right- unitary matrices that diagonalize the lepton mass matrices, giving the observed lepton masses and at the same time allowing to accommodate the Pontecorvo-Maki-Nakagawa-Sakata (PMNS) mixing matrix. We show that, at least up to 1-loop order, in the particular range of the space parameter that we have explored, it is not possible to fit the observed electron and muon $(g-2)$ factors at the same time unless one of the extra leptons has a mass of the order of 20-40 GeVs and the energy scale of the 331 symmetry to be of around 60-80 TeVs.Comment: 34 pages, 19 figure

Charged scalar production at the Compact Linear Collider for the S3⊗Z2S_3 \otimes \mathbb{Z}_2 model

We present a model with $S_3 \otimes \mathbb{Z}_2$ model plus a sterile neutrino and its phenomenological expectations for the production of charged scalars at the Compact Linear Collider. At tree level, our model predicts a total cross section in between 0.1 and $10^{-5}$ pb for the $e^- e^+ \to H^+ H^-$ process, considering all possible mass values for the charged scalar in the CLIC experiment. We also show that this prediction holds regardless of the masses of the other exotic particles and their couplings.Comment: arXiv admin note: substantial text overlap with arXiv:1810.02818; text overlap with arXiv:0808.3902 by other author

Modulation of micrornome by human cytomegalovirus and human herpesvirus 6 infection in human dermal fibroblasts: Possible significance in the induction of fibrosis in systemic sclerosis

Human cytomegalovirus (HCMV) and Human herpesvirus 6 (HHV‐6) have been report-edly suggested as triggers of the onset and/or progression of systemic sclerosis (SSc), a severe autoimmune disorder characterized by multi‐organ fibrosis. The etiology and pathogenesis of SSc are still largely unknown but virological and immunological observations support a role for these beta-herpesviruses, and we recently observed a direct impact of HCMV and HHV‐6 infection on the expression of cell factors associated with fibrosis at the cell level. Since miRNA expression has been found profoundly deregulated at the tissue level, here we aimed to investigate the impact on cell microRNome (miRNome) of HCMV and HHV‐6 infection in in vitro infected primary human dermal fibroblasts, which represent one of the main SSc target cells. The analysis, performed by Taq-man arrays detecting and quantifying 754 microRNAs (miRNAs), showed that both herpesviruses significantly modulated miRNA expression in infected cells, with evident early and late effects and deep modulation (>10 fold) of >40 miRNAs at each time post infection, including those previously recognized for their key function in fibrosis. The correlation between these in vitro results with in vivo observations is strongly suggestive of a role of HCMV and/or HHV‐6 in the multistep patho-genesis of fibrosis in SSc and in the induction of fibrosis‐signaling pathways finally leading to tissue fibrosis. The identification of specific miRNAs may open the way to their use as biomarkers for SSc diagnosis, assessment of disease progression and possible antifibrotic therapies