Collider signals of a composite Higgs in the Standard Model with four generations

Recent fits of electroweak precision data to the Standard Model (SM) with a 4th sequential family (SM4) point to a possible "three-prong composite solution": (1) the Higgs mass is at the TeV-scale, (2) the masses of the 4th family quarks t',b' are of O(500) GeV and (3) the mixing angle between the 4th and 3rd generation quarks is of the order of the Cabibbo angle, \theta_{34} ~ O(0.1). Such a manifestation of the SM4 is of particular interest as it may suggest that the Higgs is a composite state, predominantly of the 4th generation heavy quarks. Motivated by the above, we show that the three-prong composite solution to the SM4 can have interesting new implications for Higgs phenomenology. For example, the Higgs can decay to a single heavy 4th generation quark via the 3-body decays (through an off-shell t' or b') H -> t'(bar) t'* -> t'(bar) b W+ and H -> b'(bar) b'* -> b'(bar) t W-. These flavor diagonal decays can be dramatically enhanced at the LHC (by several orders of magnitudes) due to the large width effects of the resonating heavy Higgs in the processes gg -> H -> t'(bar) t'* -> t'(bar) b W+ and gg -> H -> b'(bar) b'* -> b'(bar) t W-, thus yielding a viable signal above the corresponding continuum QCD production rates. In addition, the Higgs can decay to a single t' and b' in the loop-generated flavor changing (FC) channels H -> b' b(bar), t' t(bar). These FC decays are essentially "GIM-free" and can, therefore, have branching ratios as large as 10^{-4} - 10^{-3}.Comment: As published in Phys.Lett.B688:195-201,201

Animal Models of Tourette Syndrome—From Proliferation to Standardization

Tourette syndrome (TS) is a childhood onset disorder characterized by motor and vocal tics and associated with multiple comorbid symptoms. Over the last decade, the accumulation of findings from TS patients and the emergence of new technologies have led to the development of novel animal models with high construct validity. In addition, animal models which were previously associated with other disorders were recently attributed to TS. The proliferation of TS animal models has accelerated TS research and provided a better understanding of the mechanism underlying the disorder. This newfound success generates novel challenges, since the conclusions that can be drawn from TS animal model studies are constrained by the considerable variation across models. Typically, each animal model examines a specific subset of deficits and centers on one field of research (physiology/genetics/pharmacology/etc.). Moreover, different studies do not use a standard lexicon to characterize different properties of the model. These factors hinder the evaluation of individual model validity as well as the comparison across models, leading to a formation of a fuzzy, segregated landscape of TS pathophysiology. Here, we call for a standardization process in the study of TS animal models as the next logical step. We believe that a generation of standard examination criteria will improve the utility of these models and enable their consolidation into a general framework. This should lead to a better understanding of these models and their relationship to TS, thereby improving the research of the mechanism underlying this disorder and aiding the development of new treatments

The Impact of Stimulation Induced Short-Term Synaptic Plasticity on Firing Patterns in the Globus Pallidus of the Rat

Electrical stimulation in the globus pallidus (GP) leads to complex modulations of neuronal activity in the stimulated nucleus. Multiple in vivo studies have demonstrated the modulation of both firing rates and patterns during and immediately following the GP stimulation. Previous in vitro studies, together with computational studies, have suggested the involvement of short-term synaptic plasticity (STP) during the stimulation. The aim of the current study was to explore in vitro the effects of STP on neuronal activity of GP neurons during local repetitive stimulation. We recorded synaptic potentials and assessed the modulations of spontaneous firing in a postsynaptic neuron in acute brain slices via a whole-cell pipette. Low-frequency repetitive stimulation locked the firing of the neuron to the stimulus. However, high-frequency repetitive stimulation in the GP generated a biphasic modulation of the firing frequency consisting of inhibitory and excitatory phases. Using blockers of synaptic transmission, we show that GABAergic synapses mediated the inhibitory and glutamatergic synapses the excitatory part of the response. Furthermore, we report that at high stimulation frequencies both types of synapses undergo short-term depression leading to a time dependent modulation of the neuronal firing. These findings indicate that STP modulates the dynamic responses of pallidal activity during electrical stimulation, and may contribute to a better understanding of the mechanism underlying deep brain stimulation like protocols

Scalar FCNC and rare top decays in a two Higgs doublet model "for the top"

In the so called two Higgs doublet model for the top-quark (T2HDM), first suggested by Das and Kao, the top quark receives a special status, which endows it with a naturally large mass, and also potentially gives rise to large flavor changing neutral currents (FCNC) only in the up-quark sector. In this paper we calculate the branching ratio (BR) for the rare decays t->ch and h->tc (h is a neutral Higgs) in the T2HDM, at tree level and at 1-loop when it exceeds the tree-level. We compare our results to predictions from other versions of 2HDM's and find that the scalar FCNC in the T2HDM can play a significant role in these decays. In particular, the 1-loop mediated decays can be significantly enhanced in the T2HDM compared to the 2HDM of types I and II, in some instances reaching BR~10^-4 which is within the detectable level at the LHC.Comment: added two references. 15 pages, 14 figure

Second order direct CP asymmetry in B_(s) -> X l nu

A direct CP asymmetry in inclusive semileptonic B_(s) decays vanishes by CPT to lowest order in weak interactions. Calculating the asymmetry at second order weak interactions in the Cabibbo-Kobayashi-Maskawa framework we find A_{sl} = (-3.2 \pm 0.9) x 10^{-9}. A maximal asymmetry which is two orders of magnitude larger is estimated in a left-right symmetric model. This quite generic upper bound implies negligible effects on wrong-sign lepton asymmetries in B^0 and B_s decays.Comment: 13 pages, 3 figures. A few changes and new references, separate section on decays to wrong-sign leptons; some clarification