LHC diphoton Higgs signal and top quark forward-backward asymmetry in quasi-inert Higgs doublet model

In the quasi-inert Higgs doublet model, we study the LHC diphoton rate for a standard model-like Higgs boson and the top quark forward-backward asymmetry at Tevatron. Taking into account the constraints from the vacuum stability, unitarity, electroweak precision tests, flavor physics and the related experimental data of top quark, we find that compared with the standard model prediction, the diphoton rate of Higgs boson at LHC can be enhanced due to the light charged Higgs contributions, while the measurement of the top quark forward-backward asymmetry at Tevatron can be explained to within $1\sigma$ due to the non-standard model neutral Higgs bosons contributions. Finally, the correlations between the two observables are discussed.Comment: 14 pages, 5 figues. Version to appear in JHEP, some references adde

Novel signatures for vector-like quarks

We consider supersymmetric extensions of the standard model with a vector-like doublet (T B) of quarks with charge 2/3 and −1/3, respectively. Compared to non-supersymmetric models, there is a variety of new decay modes for the vector-like quarks, involving the extra scalars present in supersymmetry. The importance of these new modes, yielding multi-top, multi-bottom and also multi-Higgs signals, is highlighted by the analysis of several benchmark scenarios. We show how the triangles commonly used to represent the branching ratios of the ‘standard’ decay modes of the vector-like quarks involving W, Z or Higgs bosons can be generalised to include additional channels. We give an example by recasting the limits of a recent heavy quark search for this more general case.The work of J.A. Aguilar-Saavedra has been supported by MINECO Projects FPA 2016- 78220-C3-1-P and FPA 2013-47836-C3-2-P (including ERDF), and by Junta de Andaluc a Project FQM-101. The work of D.E. L opez-Fogliani has been supported by the Argentinian CONICET. The work of C. Mu~noz has been supported in part by the Programme SEV- 2012-0249 `Centro de Excelencia Severo Ochoa'. D.E. L opez-Fogliani and C. Mu~noz also acknowledge the support of the Spanish grant FPA2015-65929-P (MINECO/FEDER, UE), and MINECO's Consolider-Ingenio 2010 Programme under grant MultiDark CSD2009- 00064

Activation of canonical Wnt signalling is required for TGF-β-mediated fibrosis

The transforming growth factor-β (TGF-β) signalling pathway is a key mediator of fibroblast activation that drives the aberrant synthesis of extracellular matrix in fibrotic diseases. Here we demonstrate a novel link between transforming growth factor-β and the canonical Wnt pathway. TGF-β stimulates canonical Wnt signalling in a p38-dependent manner by decreasing the expression of the Wnt antagonist Dickkopf-1. Tissue samples from human fibrotic diseases show enhanced expression of Wnt proteins and decreased expression of Dickkopf-1. Activation of the canonical Wnt pathway stimulates fibroblasts in vitro and induces fibrosis in vivo. Transgenic overexpression of Dickkopf-1 ameliorates skin fibrosis induced by constitutively active TGF-β receptor type I signalling and also prevents fibrosis in other TGF-β-dependent animal models. These findings demonstrate that canonical Wnt signalling is necessary for TGF-β-mediated fibrosis and highlight a key role for the interaction of both pathways in the pathogenesis of fibrotic diseases