This document proposes a collection of simplified models relevant to the design of new-physics searches at the Large Hadron Collider (LHC) and the characterization of their results. Both ATLAS and CMS have already presented some results in terms of simplified models, and we encourage them to continue and expand this effort, which supplements both signature-based results and benchmark model interpretations. A simplified model is defined by an effective Lagrangian describing the interactions of a small number of new particles. Simplified models can equally well be described by a small number of masses and cross-sections. These parameters are directly related to collider physics observables, making simplified models a particularly effective framework for evaluating searches and a useful starting point for characterizing positive signals of new physics. This document serves as an official summary of the results from the 'Topologies for Early LHC Searches' workshop, held at SLAC in September

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Increasing evidence points to the importance of local protein synthesis for axonal growth and responses to axotomy, yet there is little insight into the functions of individual locally synthesized proteins. We recently showed that expression of a reporter mRNA with the axonally localizing β-actin mRNA 3′UTR competes with endogenous β-actin and GAP-43 mRNAs for binding to ZBP1 and axonal localization in adult sensory neurons (Donnelly et al., 2011). Here, we show that the 3′UTR of GAP-43 mRNA can deplete axons of endogenous β-actin mRNA. We took advantage of this 3′UTR competition to address the functions of axonally synthesized β-actin and GAP-43 proteins. In cultured rat neurons, increasing axonal synthesis of β-actin protein while decreasing axonal synthesis of GAP-43 protein resulted in short highly branched axons. Decreasing axonal synthesis of β-actin protein while increasing axonal synthesis of GAP-43 protein resulted in long axons with few branches. siRNA-mediated depletion of overall GAP-43 mRNA from dorsal root ganglia (DRGs) decreased the length of axons, while overall depletion of β-actin mRNA from DRGs decreased the number of axon branches. These deficits in axon growth could be rescued by transfecting with siRNA-resistant constructs encoding β-actin or GAP-43 proteins, but only if the mRNAs were targeted for axonal transport. Finally, in ovo electroporation of axonally targeted GAP-43 mRNA increased length and axonally targeted β-actin mRNA increased branching of sensory axons growing into the chick spinal cord. These studies indicate that axonal translation of β-actin mRNA supports axon branching and axonal translation of GAP-43 mRNA supports elongating growth.

A search for neutral Higgs bosons in the minimal supersymmetric extension of the standard model (MSSM) decaying to tau-lepton pairs in pp collisions is performed, using events recorded by the CMS experiment at the LHC. The dataset corresponds to an integrated luminosity of 24.6 fb −1 , with 4.9 fb −1 at 7 TeV and 19.7 fb −1 at 8 TeV. To enhance the sensitivity to neutral MSSM Higgs bosons, the search includes the case where the Higgs boson is produced in association with a b-quark jet. No excess is observed in the tau-lepton-pair invariant mass spectrum. Exclusion limits are presented in the MSSM parameter space for different benchmark scenarios, m max h , m mod+ h , m mod− h , light-stop, lightstau, τ -phobic, and low-m H . Upper limits on the cross section times branching fraction for gluon fusion and b-quark associated Higgs boson production are also given. A Exclusion limits 23The CMS collaboration 37 IntroductionA broad variety of precision measurements have shown the overwhelming success of the standard model (SM) [1][2][3] of fundamental interactions, which includes an explanation for the origin of the mass of the weak force carriers, as well as for the quark and lepton masses. In the SM, this is achieved via the Brout-Englert-Higgs mechanism [4][5][6][7][8][9], which predicts the existence of a scalar boson, the Higgs boson. However, the Higgs boson mass in the SM is not protected against quadratically divergent quantum-loop corrections at high energy, known as the hierarchy problem. In the model of supersymmetry (SUSY) [10,11], which postulates a symmetry between the fundamental bosons and fermions, a cancellation of these divergences occurs naturally. The Higgs sector of the minimal supersymmetric extension of the standard model (MSSM) [12,13] The dominant neutral MSSM Higgs boson production mechanism is the gluon fusion process for small and moderate values of tan β. At large values of tan β b-quark associated production is the dominant contribution, due to the enhanced Higgs boson Yukawa coupling to b quarks. Figure 1 shows the leading-order diagrams for the gluon fusion and b-quark associated Higgs boson production, in the four-flavor and in the five-flavor scheme. In the region of large tan β the branching fraction to tau leptons is also enhanced, making the search for neutral MSSM Higgs bosons in the τ τ final state particularly interesting. This paper reports a search for neutral MSSM Higgs bosons in pp collisions at √ s = 7 TeV and 8 TeV in the τ τ decay channel. The data were recorded with the CMS detector [14] at the CERN LHC and correspond to an integrated luminosity of 24.6 fb −1 , with 4.9 fb −1 at 7 TeV and 19.7 fb −1 at 8 TeV. Five different τ τ signatures are studied, eτ h , µτ h , eµ, µµ, and τ h τ h , where τ h denotes a hadronically decaying τ . These results are an extension of previous searches by the The results are interpreted in the context of the MSSM with different benchmark scenarios described in section 1.1 and also in a model independent way, in terms of upper...

Localized translation of axonal mRNAs contributes to developmental and regenerative axon growth. Although untranslated regions (UTRs) of many different axonal mRNAs appear to drive their localization, there has been no consensus RNA structure responsible for this localization. We recently showed that limited expression of ZBP1 protein restricts axonal localization of both β-actin and GAP-43 mRNAs. β-actin 3′UTR has a defined element for interaction with ZBP1, but GAP-43 mRNA shows no homology to this RNA sequence. Here, we show that an AU-rich element (ARE) in GAP-43’s 3′UTR is necessary and sufficient for its axonal localization. Axonal GAP-43 mRNA levels increase after in vivo injury, and GAP-43 mRNA shows an increased half-life in regenerating axons. GAP-43 mRNA interacts with both HuD and ZBP1, and HuD and ZBP1 coimmunoprecipitate in an RNA-dependent fashion. Reporter mRNA with the GAP-43 ARE competes with endogenous β-actin mRNA for axonal localization and decreases axon length and branching similar to the β-actin 3′UTR competing with endogenous GAP-43 mRNA. Conversely, overexpressing GAP-43 coding sequence with it’s 3′UTR ARE increases axonal elongation and this effect is lost when just the ARE is deleted from GAP-43’s 3′UTR.