Results of a search for new phenomena in final states with an energetic jet and large missing transverse momentum are reported. The search uses proton-proton collision data corresponding to an integrated luminosity of 3.2 fb −1 at ffiffi ffi s p ¼ 13 TeV collected in 2015 with the ATLAS detector at the Large Hadron Collider. Events are required to have at least one jet with a transverse momentum above 250 GeV and no leptons. Several signal regions are considered with increasing missing-transverse-momentum requirements between E miss T > 250 GeV and E miss T > 700 GeV. Good agreement is observed between the number of events in data and Standard Model predictions. The results are translated into exclusion limits in models with large extra spatial dimensions, pair production of weakly interacting dark-matter candidates, and the production of supersymmetric particles in several compressed scenarios.

The luminosity determination for the ATLAS detector at the LHC during pp collisions at  8 TeV in 2012 is presented. The evaluation of the luminosity scale is performed using several luminometers, and comparisons between these luminosity detectors are made to assess the accuracy, consistency and long-term stability of the results. A luminosity uncertainty of is obtained for the of pp collision data delivered to ATLAS at  8 TeV in 2012.

The reconstruction of the signal from hadrons and jets emerging from the proton–proton collisions at the Large Hadron Collider (LHC) and entering the ATLAS calorimeters is based on a three-dimensional topological clustering of individual calorimeter cell signals. The cluster formation follows cell signal-significance patterns generated by electromagnetic and hadronic showers. In this, the clustering algorithm implicitly performs a topological noise suppression by removing cells with insignificant signals which are not in close proximity to cells with significant signals. The resulting topological cell clusters have shape and location information, which is exploited to apply a local energy calibration and corrections depending on the nature of the cluster. Topological cell clustering is established as a well-performing calorimeter signal definition for jet and missing transverse momentum reconstruction in ATLAS.

This paper presents a measurement of the double-differential cross section for the Drell-Yan Z/γ * → + − and photon-induced γγ → + − processes where is an electron or muon. The measurement is performed for invariant masses of the lepton pairs, m , between 116 GeV and 1500 GeV using a sample of 20.3 fb −1 of pp collisions data at centre-of-mass energy of √ s = 8 TeV collected by the ATLAS detector at the LHC in 2012. The data are presented double differentially in invariant mass and absolute dilepton rapidity as well as in invariant mass and absolute pseudorapidity separation of the lepton pair. The single-differential cross section as a function of m is also reported. The electron and muon channel measurements are combined and a total experimental precision of better than 1% is achieved at low m . A comparison to next-to-next-to-leading order perturbative QCD predictions using several recent parton distribution functions and including next-to-leading order electroweak effects indicates the potential of the data to constrain parton distribution functions. In particular, a large impact of the data on the photon PDF is demonstrated. JHEP08(2016)009The ATLAS collaboration 44 IntroductionThe Drell-Yan (DY) process [1] of lepton pair production in hadronic interactions, pp → Z/γ * + X with Z/γ * → + − , is a powerful tool in understanding the nature of partonic interactions and of hadronic structure in detail. The study of this process has been fundamental in developing theoretical perturbative calculations of quantum chromodynamics (QCD) which are now performed at next-to-next-to-leading-order (NNLO) accuracy [2][3][4][5]. Measurements from the Large Hadron Collider (LHC) of neutral-and charged-current Drell-Yan processes mediated by Z/γ * and W exchange respectively at centre-of-mass energies of √ s = 7 TeV and 8 TeV have been recently published by the ATLAS [6-8], CMS [9][10][11][12] and LHCb [13][14][15][16][17] collaborations. These data provide new constraints on the parton distribution functions (PDFs) of the proton, some of which have been used in recent global PDF fits [18][19][20].Although on-shell Z and W boson measurements provide the greatest experimental precision, they are restricted in the kinematic range of partonic momentum fraction x, and four-momentum transfer Q = m , the invariant mass of the dilepton pair. Offshell measurements provide complementary constraints in a wider range of x and Q. In the neutral-current case, the off-shell measurements are dominated by the electromagnetic quark couplings to the virtual photon γ * , whereas the on-shell measurements are dominated by the weak axial and vector couplings of the quarks to the Z boson. Therefore, the measurements have different sensitivity to the up-type and down-type quarks. At large m the measurements offer constraints on the large-x antiquark PDFs which are poorly known. In addition, off-shell measurements may also be sensitive to the largely unconstrained photon PDF [7, 8, 21, 22] through the photon-induced (PI) process γγ → + ...

It is well documented that N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors play a pivotal role in ischaemic brain injury. Recent studies have shown that kainate (KA) receptors are involved in neuronal cell death induced by seizure, which is mediated by the GluR6*PSD-95*MLK3 signalling module and subsequent c-Jun N-terminal kinase (JNK) activation. Here we investigate whether GluR6 mediated JNK activation is correlated with ischaemic brain injury. Our results show that cerebral ischaemia followed by reperfusion can enhance the assembly of the GluR6*PSD-95*MLK3 signalling module and JNK activation. As a result, activated JNK can not only phosphorylate the transcription factor c-Jun and up-regulate Fas L expression but can also phosphorylate 14-3-3 and promote Bax translocation to mitochondria, increase the release of cytochrome c and increase caspase-3 activation. These results indicate that GluR6 mediated JNK activation induced by ischaemia/reperfusion ultimately results in neuronal cell death via nuclear and non-nuclear pathways. Furthermore, the peptides we constructed, Tat-GluR6-9c, show a protective role against neuronal death induced by cerebral ischaemia/reperfusion through inhibiting the GluR6 mediated signal pathway. In summary, our results indicate that the KA receptor subunit GluR6 mediated JNK activation is involved in ischaemic brain injury and provides a new approach for stroke therapy.