A measurement of the Higgs boson mass is presented based on the combined data samples of the ATLAS and CMS experiments at the CERN LHC in the H → γγ and H → ZZ → 4l decay channels. The results are obtained from a simultaneous fit to the reconstructed invariant mass peaks in the two channels and for the two experiments. The measured masses from the individual channels and the two experiments are found to be consistent among themselves. The combined measured mass of the Higgs boson is m H ¼ 125.09 AE 0.21 ðstatÞ AE 0.11 ðsystÞ GeV. DOI: 10.1103/PhysRevLett.114.191803 PACS numbers: 14.80.Bn, 13.85.Qk The study of the mechanism of electroweak symmetry breaking is one of the principal goals of the CERN LHC program. In the standard model (SM), this symmetry breaking is achieved through the introduction of a complex doublet scalar field, leading to the prediction of the Higgs boson H [1-6], whose mass m H is, however, not predicted by the theory. In 2012, the ATLAS and CMS Collaborations at the LHC announced the discovery of a particle with Higgs-boson-like properties and a mass of about 125 GeV [7][8][9]. The discovery was based primarily on mass peaks observed in the γγ and ZZ → l þ l − l 0þ l 0−(denoted H → ZZ → 4l for simplicity) decay channels, where one or both of the Z bosons can be off shell and where l and l 0 denote an electron or muon. With m H known, all properties of the SM Higgs boson, such as its production cross section and partial decay widths, can be predicted. Increasingly precise measurements [10][11][12][13] have established that all observed properties of the new particle, including its spin, parity, and coupling strengths to SM particles are consistent within the uncertainties with those expected for the SM Higgs boson.The ATLAS and CMS Collaborations have independently measured m H using the samples of proton-proton collision data collected in 2011 and 2012, commonly referred to as LHC Run 1. The analyzed samples correspond to approximately 5 fb −1 of integrated luminosity at ffiffi ffi s p ¼ 7 TeV, and 20 fb −1 at ffiffi ffi s p ¼ 8 TeV, for each experiment. Combined results in the context of the separate experiments, as well as those in the individual channels, are presented in Refs. [12,[14][15][16].This Letter describes a combination of the Run 1 data from the two experiments, leading to improved precision for m H . Besides its intrinsic importance as a fundamental parameter, improved knowledge of m H yields more precise predictions for the other Higgs boson properties. Furthermore, the combined mass measurement provides a first step towards combinations of other quantities, such as the couplings. In the SM, m H is related to the values of the masses of the W boson and top quark through loopinduced effects. Taking into account other measured SM quantities, the comparison of the measurements of the Higgs boson, W boson, and top quark masses can be used to directly test the consistency of the SM [17] and thus to search for evidence of physics beyond the SM.The combination is performed usin...

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SUMMARY Proinflammatory stimuli elicit rapid transcriptional responses via transduced signals to master regulatory transcription factors. To explore the role of chromatin-dependent signal transduction in the atherogenic inflammatory response, we characterized the dynamics, structure and function of regulatory elements in the activated endothelial cell epigenome. Stimulation with tumor necrosis factor alpha prompted a dramatic and rapid global redistribution of chromatin activators to massive de novo clustered enhancer domains. Inflammatory super enhancers formed by NF-κB accumulate at the expense of immediately decommissioned, basal endothelial super enhancers, despite persistent histone hyperacetylation. Mass action of enhancer factor redistribution causes momentous swings in transcriptional initiation and elongation. A chemical genetic approach reveals a requirement for BET bromodomains in communicating enhancer remodeling to RNA polymerase and orchestrating the transition to the inflammatory cell state, demonstrated in activated endothelium and macrophages. BET bromodomain inhibition abrogates super enhancer mediated inflammatory transcription, atherogenic endothelial responses and atherosclerosis in vivo.

Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy1-3. BET bromodomain inhibitors, which have shown efficacy in several models of cancer4-6, have not been evaluated in TNBC. These inhibitors displace BET bromodomain proteins such as BRD4 from chromatin by competing with their acetyllysine recognition modules, leading to inhibition of oncogenic transcriptional programs7-9. Here we report the preferential sensitivity of TNBCs to BET bromodomain inhibition in vitro and in vivo, establishing a rationale for clinical investigation and further motivation to understand mechanisms of resistance. In paired cell lines selected for acquired resistance to BET inhibition from previously sensitive TNBCs, we failed to identify gatekeeper mutations, new driver events or drug pump activation. BET-resistant TNBC cells remain dependent on wild-type BRD4, which supports transcription and cell proliferation in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify strong association with MED1 and hyper-phosphorylation of BRD4 attributable to decreased activity of PP2A, identified here as a principal BRD4 serine phosphatase. Together, these studies provide a rationale for BET inhibition in TNBC and present mechanism-based combination strategies to anticipate clinical drug resistance.