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The operation and performance of the Compact Muon Solenoid (CMS) electromagnetic calorimeter (ECAL) are presented, based on data collected in pp collisions at root s = 13 TeV at the CERN LHC, in the years from 2015 to 2018 (LHC Run 2), corresponding to an integrated luminosity of 151 fb(-1). The CMS ECAL is a scintillating lead-tungstate crystal calorimeter, with a silicon strip preshower detector in the forward region that provides precise measurements of the energy and the time-of-arrival of electrons and photons. The successful operation of the ECAL is crucial for a broad range of physics goals, ranging from observing the Higgs boson and measuring its properties, to other standard model measurements and searches for new phenomena. Precise calibration, alignment, and monitoring of the ECAL response are important ingredients to achieve these goals. To face the challenges posed by the higher luminosity, which characterized the operation of the LHC in Run 2, the procedures established during the 2011-2012 run of the LHC have been revisited and new methods have been developed for the energy measurement and for the ECAL calibration. The energy resolution of the calorimeter, for electrons from Z boson decays reaching the ECAL without significant loss of energy by bremsstrahlung, was better than 1.8%, 3.0%, and 4.5% in the vertical bar eta vertical bar intervals [ 0.0, 0.8], [0.8, 1.5], [1.5, 2.5], respectively. This resulting performance is similar to that achieved during Run 1 in 2011-2012, in spite of the more severe running conditions.

Cancer cells frequently alter their lipids to grow and adapt to their environment(1-3). Despite the critical functions of lipid metabolism in membrane physiology, signalling and energy production, how specific lipids contribute to tumorigenesis remains incompletely understood. Here, using functional genomics and lipidomic approaches, we identified de novo sphingolipid synthesis as an essential pathway for cancer immune evasion. Synthesis of sphingolipids is surprisingly dispensable for cancer cell proliferation in culture or in immunodeficient mice but required for tumour growth in multiple syngeneic models. Blocking sphingolipid production in cancer cells enhances the anti-proliferative effects of natural killer and CD8(+) T cells partly via interferon-gamma (IFN gamma) signalling. Mechanistically, depletion of glycosphingolipids increases surface levels of IFN gamma receptor subunit 1 (IFNGR1), which mediates IFN gamma-induced growth arrest and pro-inflammatory signalling. Finally, pharmacological inhibition of glycosphingolipid synthesis synergizes with checkpoint blockade therapy to enhance anti-tumour immune response. Altogether, our work identifies glycosphingolipids as necessary and limiting metabolites for cancer immune evasion.