K. Theofilatos

This Report summarizes the proceedings of the 2019 Les Houches workshop on Physics at TeV Colliders. Session 1 dealt with (I) new developments for high precision Standard Model calculations, (II) the sensitivity of parton distribution functions to the experimental inputs, (III) new developments in jet substructure techniques and a detailed examination of gluon fragmentation at the LHC, (IV) issues in the theoretical description of the production of Standard Model Higgs bosons and how to relate experimental measurements, and (V) Monte Carlo event generator studies relating to PDF evolution and comparisons of important processes at the LHC.

This Report summarizes the proceedings of the 2017 Les Houches workshop on Physics at TeV Colliders. Session 1 dealt with (I) new developments relevant for high precision Standard Model calculations, (II) theoretical uncertainties and dataset dependence of parton distribution functions, (III) new developments in jet substructure techniques, (IV) issues in the theoretical description of the production of Standard Model Higgs bosons and how to relate experimental measurements, (V) phenomenological studies essential for comparing LHC data from Run II with theoretical predictions and projections for future measurements, and (VI) new developments in Monte Carlo event generators.

The Electromagnetic Calorimeter (ECAL) of the Compact Muon Solenoid (CMS) detector will play a crucial role in new physics searches at the Large Hadron Collider (LHC) as well as in Standard Model precision measurements. The first LHC beams have been used to finalize the commissioning of ECAL read-out and trigger. The precision of the inter-channel synchronization and calibration has been verified and improved with in-situ data. The quality of the offline data reconstruction has been investigated with physics signals, in particular with di-photon states. A review of the CMS ECAL detector status and performance is presented in this note.

We present a search for a kinematic edge in the invariant mass distribution of two opposite-sign same-flavor leptons, in final states with jets and missing transverse energy. The analysis makes use of 19.4 fb−1 proton-proton collision data at √s = 8 TeV. The data have been recorded with the CMS experiment. Complementary methods have been used for the background estimation, which when combined achieve a total uncertainty of 5% (10%) for leptons in the central (forward) rapidity of the detector. We do not observe a statistically significant signal and the results are consistent with the background-only hypothesis.

We present a search for a kinematic edge in the invariant mass distribution of two opposite-sign same-flavor leptons, in final states with jets and missing transverse energy. The analysis makes use of 19.4 fb−1 proton-proton collision data at √s = 8 TeV. The data have been recorded with the CMS experiment. Complementary methods have been used for the background estimation, which when combined achieve a total uncertainty of 5% (10%) for leptons in the central (forward) rapidity of the detector. We do not observe a statistically significant signal and the results are consistent with the background-only hypothesis.

We present results of searches for Supersymmetry in signatures involving lepton or photon final states. These searches are performed with data collected by the CMS experiment at the LHC in pp-collisions at a center of mass energy of 7 TeV. Various data driven techniques used to measure the Standard Model background are demonstrated. The results are interpreted within the CMSSM as well as more general, simplified models.

Anomalous, large signals are observed in the barrel region of the CMS electromagnetic calorimeter during pp collisions at the LHC. Laboratory and beam-test studies, as well as Monte Carlo simulations, have been used to understand their origin. They are ascribed to direct energy depositions by particles in the Avalanche Photo-Diodes used for the scintillation light readout. Their properties and rates are summarized. The methods employed to reject these signals in the online trigger selection and in the offline event reconstruction are presented.

Abstract Background Antiplatelet therapy (APT) has improved cardiovascular outcomes, but some patients develop thrombosis despite APT. Adjusting APT to platelet reactivity with conventional platelet reactivity tests has proven unsuccessful. Many circulating noncoding RNAs (ncRNAs) are derived from platelets and could serve as novel platelet function markers. Material and methods Platelet reactivity was assessed using light transmission aggregometry (LTA) in the Bruneck 2015 study (N = 338), using the agonists arachidonic acid, adenosine diphosphate, collagen, TRAP-6 amide and U46619. LTA platelet releasates were then used for RT-qPCR of five platelet-enriched microRNAs, three circular RNAs and two long non-coding RNAs. Platelet-poor plasma (PPP) was used as negative control. Results and conclusions Platelet agonists induced aggregation and ncRNA release, with aspirin takers (N = 155) showing lower ncRNA release than individuals not on aspirin (N = 183). Agonist responsiveness differed among ncRNAs, with miR-150 being hyperresponsive to adenosine diphosphate and miR-21 being hyperresponsive to arachidonic acid, whereas other ncRNAs were most strongly released to collagen, suggesting a selective release mechanism. In individuals not on aspirin, the inflammation markers C-reactive protein and granulocyte counts correlated positively with platelet-derived ncRNAs in PPP, while they correlated inversely with platelet-derived ncRNAs in releasates. These correlations were not present in aspirin takers. Higher PPP levels and lower releasate levels of platelet-derived ncRNAs in inflammation suggest platelet exhaustion ex vivo due to platelet pre-activation in vivo. Funding sources British Heart Foundation, VASCage (Centre for Promoting Vascular Health in the Ageing Community) of the Austrian Research Promotion Agency FFG (COMET program - Competence Centers for Excellent Technologies).

This Report summarizes the proceedings of the 2017 Les Houches workshop on Physics at TeV Colliders. Session 1 dealt with (I) new developments relevant for high precision Standard Model calculations, (II) theoretical uncertainties and dataset dependence of parton distribution functions, (III) new developments in jet substructure techniques, (IV) issues in the theoretical description of the production of Standard Model Higgs bosons and how to relate experimental measurements, (V) phenomenological studies essential for comparing LHC data from Run II with theoretical predictions and projections for future measurements, and (VI) new developments in Monte Carlo event generators.

This Report summarizes the proceedings of the 2017 Les Houches workshop on Physics at TeV Colliders. Session 1 dealt with (I) new developments relevant for high precision Standard Model calculations, (II) theoretical uncertainties and dataset dependence of parton distribution functions, (III) new developments in jet substructure techniques, (IV) issues in the theoretical description of the production of Standard Model Higgs bosons and how to relate experimental measurements, (V) phenomenological studies essential for comparing LHC data from Run II with theoretical predictions and projections for future measurements, and (VI) new developments in Monte Carlo event generators.

<b>Objectives:</b> To discover the mechanisms underlying the oncogenic properties of CREB in KRAS-mutant lung adenocarcinoma (LUAD). <b>Materials and Methods:</b> We used conditional deletion, focal overexpression, and pharmacologic inhibition of CREB in different mouse and cellular models of early-stage and metastatic KRAS-mutant LUAD. We determined the neutrophil (ΝΦ) influx in the bronchoalveolar lavage (BAL) from LUAD-affected conditionally Creb1-deleted lungs. We employed The Cancer Genome Atlas, the GEO dataset GSE43458, and the human protein atlas to examine CREB and CXCR1 in human LUAD. <b>Results:</b> CREB is overexpressed in murine KRAS-mutant LUAD, pulmonary deletion of Creb1 (encoding murine CREB) inhibits LUAD development, and Creb1-overexpression augments the tumorigenicity of KRAS-mutant cells. Conditional Creb1 deletion in KRAS -mutant LUAD cells causes overexpression of CXCR1 ligands, and LUAD-bearing Creb1-deleted mice display increased pulmonary ΝΦ. Cxcr1-deficient mice are selectively permissive to KRAS-mutant tumor growth and show defective ΝΦ recruitment. The pro-tumor effects of CREB require intact host Cxcr1 and those of host Cxcr1 necessitate mutant KRAS in cancer cells. Pharmacologic CREB blockade prevents tumor growth and restores ΝΦ recruitment only when initiated before immune-evasion of KRAS-mutant LUAD. CREB and CXCR1 expression of human LUAD are compartmentalized to tumor and stromal cells, respectively, while CREB-controlled genes profoundly impact survival. <b>Conclusions:</b> CREB-mediated immune evasion of KRAS-mutant LUAD rests on signaling to ΝΦ CXCR1 and is actionable.