Results are presented from searches for the standard model Higgs boson in proton-proton collisions at root s = 7 and 8 TeV in the Compact Muon Solenoid experiment at the LHC, using data samples corresponding to integrated luminosities of up to 5.1 fb(-1) at 7 TeV and 5.3 fb(-1) at 8 TeV. The search is performed in five decay modes: gamma gamma, ZZ, W+W-, tau(+)tau(-), and b (b) over bar. An excess of events is observed above the expected background, with a local significance of 5.0 standard deviations, at a mass near 125 GeV, signalling the production of a new particle. The expected significance for a standard model Higgs boson of that mass is 5.8 standard deviations. The excess is most significant in the two decay modes with the best mass resolution, gamma gamma and ZZ; a fit to these signals gives a mass of 125.3 +/- 0.4(stat.) +/- 0.5(syst.) GeV. The decay to two photons indicates that the new particle is a boson with spin different from one. (C) 2012 CERN. Published by Elsevier B.V. All rights reserved

Recent results of the searches for Supersymmetry in final states with one or two leptons at CMS are presented. Many Supersymmetry scenarios, including the Constrained Minimal Supersymmetric extension of the Standard Model (CMSSM), predict a substantial amount of events containing leptons, while the largest fraction of Standard Model background events -which are QCD interactions -gets strongly reduced by requiring isolated leptons. The analyzed data was taken in 2011 and corresponds to an integrated luminosity of approximately L = 1 fb −1 . The center-of-mass energy of the pp collisions was √ s = 7 TeV.

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Patients with type 2 diabetes (T2D) have disease-associated changes in B-cell function, but the role these changes play in disease pathogenesis is not well established. Data herein show B cells from obese mice produce a proinflammatory cytokine profile compared with B cells from lean mice. Complementary in vivo studies show that obese B cell-null mice have decreased systemic inflammation, inflammatory B-and T-cell cytokines, adipose tissue inflammation, and insulin resistance (IR) compared with obese WT mice. Reduced inflammation in obese/insulin resistant B cell-null mice associates with an increased percentage of anti-inflammatory regulatory T cells (Tregs). This increase contrasts with the sharply decreased percentage of Tregs in obese compared with lean WT mice and suggests that B cells may be critical regulators of T-cell functions previously shown to play important roles in IR. We demonstrate that B cells from T2D (but not non-T2D) subjects support proinflammatory T-cell function in obesity/T2D through contact-dependent mechanisms. In contrast, human monocytes increase proinflammatory T-cell cytokines in both T2D and non-T2D analyses. These data support the conclusion that B cells are critical regulators of inflammation in T2D due to their direct ability to promote proinflammatory T-cell function and secrete a proinflammatory cytokine profile. Thus, B cells are potential therapeutic targets for T2D.immunometabolism | lymphocytes M ultiple studies support the concept that inflammation strongly associates with insulin resistance (IR), which, in addition to loss of islet function, defines type 2 diabetes (T2D) (1). Work implicating B cells in IR/T2D is limited. We showed B cells from T2D subjects secrete a proinflammatory cytokine profile, including an extraordinary inability to secrete the potent anti-inflammatory cytokine IL-10 and an elevated production of proinflammatory IL-8 compared with B cells from non-T2D subjects (2). Given the importance of B-cell IL-10 in preventing numerous inflammatory diseases (3, 4) and the links between IL-8 and T2D (5, 6), these data suggest that altered B-cell cytokine production plays an important role in initiating or promoting IR/T2D. Published analyses further support a role for B cells in IR and include studies of B cell-null New Zealand Obese (NZO) mice, which, in contrast to B cell-sufficient NZOs, fail to develop IR in response to obesity (7). These findings have been recently reproduced in studies showing obese B cell-null or B cell-depleted mice have less inflammation and IR than obese WT mice (8). Interestingly, T-cell cytokine production is decreased in obese B cell-null mouse adipose tissue (AT) (8), which raises the possibility that, in addition to production of a proinflammatory cytokine profile, B cells may function in IR by regulating the T cell-mediated inflammation known to drive disease pathogenesis (9, 10). We identified a proinflammatory T-cell ratio [defined by increased Th17 cells plus decreased regulatory T cells (Tregs)] in T2D patients that mirror...