Testing Electroweak Baryogenesis with Future Colliders

Electroweak Baryogenesis (EWBG) is a compelling scenario for explaining the matter-antimatter asymmetry in the universe. Its connection to the electroweak phase transition makes it inherently testable. However, completely excluding this scenario can seem difficult in practice, due to the sheer number of proposed models. We investigate the possibility of postulating a "no-lose" theorem for testing EWBG in future e+e- or hadron colliders. As a first step we focus on a factorized picture of EWBG which separates the sources of a stronger phase transition from those that provide new sources of CP violation. We then construct a "nightmare scenario" that generates a strong first-order phase transition as required by EWBG, but is very difficult to test experimentally. We show that a 100 TeV hadron collider is both necessary and possibly sufficient for testing the parameter space of the nightmare scenario that is consistent with EWBG.Comment: 26 pages + references, 10 figures. Fixed minor typos, updated TLEP and 100 TeV projections. Conclusions unchange

Taking a Razor to Dark Matter Parameter Space at the LHC

Dark matter (DM) has been searched for at colliders in a largely model independent fashion by looking for an excess number of events involving a single jet, or photon, and missing energy. We investigate the possibility of looking for excesses in more inclusive jet channels. Events with multiple jets contain more information and thus more handles to increase the signal to background ratio. In particular, we adapt the recent CMS "razor" analysis from a search for supersymmetry to a search for DM. We consider simplified models where DM is a Dirac fermion that couples to the quarks of the Standard Model (SM) through exchange of vector or axial-vector mediators or to gluons through scalar exchange. We consider both light and heavy (leading to effective contact interactions) mediators. Since the razor analysis requires multiple jets in the final state, the data set is complementary to that used for the monojet search and thus the bounds can be combined.Comment: 25 pages, 10 figures; v2 published version; v3 removes duplication of manuscript in pd

Parity Nonconservation in Strong Interactions

For top-quarks produced via the subprocess $q\bar q\to t\bar t$, the longitudinal t-quark polarization ($P_{\parallel}$) vanishes in QCD. $P_{\parallel}$ can be measured by the angular distribution of the lepton in $t$-quark semileptonic decay. New physics contributions that are parity nonconserving will be manifest by non-vanishing $P_{\parallel}$, which may be large. We illustrate this with the s-channel exchange of a massive $X$-gluon with chiral quark couplings.Comment: 4 pages, 3 figures; v2 references added, typos in eqs. 13-15 corrected, Fig. 2 change

Asymmetric Left-Right Model and the Top Pair Forward-Backward Asymmetry

The forward-backward asymmetry measurement in top-pair production at the Tevatron is about $2\sigma$ from the Standard Model prediction. We propose an asymmetric left-right model, which includes a $W'$ boson with a right-handed coupling of down to top quark, and a $Z'$ boson with diagonal couplings to the up, top, and down quarks with $M_{W'}\approx175$ GeV and $M_{Z'}\approx 900$ GeV. The model accounts for the asymmetry while remaining consistent with the top-pair total cross-section and invariant mass distribution.Comment: 7 pages, 6 figures; version published in Phys. Rev.

The Adaptor Protein SH2B3 (Lnk) Negatively Regulates Neurite Outgrowth of PC12 Cells and Cortical Neurons

SH2B adaptor protein family members (SH2B1-3) regulate various physiological responses through affecting signaling, gene expression, and cell adhesion. SH2B1 and SH2B2 were reported to enhance nerve growth factor (NGF)-induced neuronal differentiation in PC12 cells, a well-established neuronal model system. In contrast, SH2B3 was reported to inhibit cell proliferation during the development of immune system. No study so far addresses the role of SH2B3 in the nervous system. In this study, we provide evidence suggesting that SH2B3 is expressed in the cortex of embryonic rat brain. Overexpression of SH2B3 not only inhibits NGF-induced differentiation of PC12 cells but also reduces neurite outgrowth of primary cortical neurons. SH2B3 does so by repressing NGF-induced activation of PLCγ, MEK-ERK1/2 and PI3K-AKT pathways and the expression of Egr-1. SH2B3 is capable of binding to phosphorylated NGF receptor, TrkA, as well as SH2B1β. Our data further demonstrate that overexpression of SH2B3 reduces the interaction between SH2B1β and TrkA. Consistent with this finding, overexpressing the SH2 domain of SH2B3 is sufficient to inhibit NGF-induced neurite outgrowth. Together, our data demonstrate that SH2B3, unlike the other two family members, inhibits neuronal differentiation of PC12 cells and primary cortical neurons. Its inhibitory mechanism is likely through the competition of TrkA binding with the positive-acting SH2B1 and SH2B2

Stops and MET: the shape of things to come

LHC experiments have placed strong bounds on the production of supersymmetric colored particles (squarks and gluinos), under the assumption that all flavors of squarks are nearly degenerate. However, the current experimental constraints on stop squarks are much weaker, due to the smaller production cross section and difficult backgrounds. While light stops are motivated by naturalness arguments, it has been suggested that such particles become nearly impossible to detect near the limit where their mass is degenerate with the sum of the masses of their decay products. We show that this is not the case, and that searches based on missing transverse energy (MET) have significant reach for stop masses above 175 GeV, even in the degenerate limit. We consider direct pair production of stops, decaying to invisible LSPs and tops with either hadronic or semi-leptonic final states. Modest intrinsic differences in MET are magnified by boosted kinematics and by shape analyses of MET or suitably-chosen observables related to MET. For these observables we show that the distributions of the relevant backgrounds and signals are well-described by simple analytic functions, in the kinematic regime where signal is enhanced. Shape analyses of MET-related distributions will allow the LHC experiments to place significantly improved bounds on stop squarks, even in scenarios where the stop-LSP mass difference is degenerate with the top mass. Assuming 20/fb of luminosity at 8 TeV, we conservatively estimate that experiments can exclude or discover degenerate stops with mass as large as ~ 360 GeV and 560 GeV for massless LSPs.Comment: Version submitted to journal with improved analysis and small fixes, 27 pages, 11 figures, 2 table

EBV-encoded small RNA1 and nonresolving inflammation in rheumatoid arthritis

AbstractRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by perpetuated inflammation in multiple joints. To date, there is no cure for RA, and the causal factor for non-resolving inflammation in RA remains unclear. In this study, we initially observed expression of Epstein–Barr virus-encoded small RNA1 (EBER1) in the synovial tissue of all five patients who showed nonresolving RA inflammation. By contrast, EBER1 was detected in the synovial tissue of only one out of seven patients with advanced osteoarthritis (OA; p < 0.01, Fisher’s exact test). To confirm this finding, we conducted a second study on synovial tissue samples taken from 23 patients with nonresolving RA inflammation and 13 patients with OA. All synovial samples from patients with nonresolving inflammation of RA showed positive expression of EBER1 (23/23, 100%), whereas none of the synovial samples from patients with OA showed expression of EBER1 (0/13, 0%; p < 0.001, by Fisher’s exact test). In vitro, transfection of RA synovial fibroblasts with EBER1 induced the production of interleukin-6. Taken together, these data strongly suggest that nonresolving RA inflammation is strongly related to the presence of EBER1, which might be, at least partially, responsible for synovial fibroblast interleukin-6 production