Search for triboson [Formula: see text] production in collisions at [Formula: see text] [Formula: see text] with the ATLAS detector.

This paper reports a search for triboson [Formula: see text] production in two decay channels ([Formula: see text] and [Formula: see text] with [Formula: see text]) in proton-proton collision data corresponding to an integrated luminosity of 20.3 [Formula: see text] at a centre-of-mass energy of 8 [Formula: see text] with the ATLAS detector at the Large Hadron Collider. Events with exactly three charged leptons, or two leptons with the same electric charge in association with two jets, are selected.

Measurement of the prompt /[Formula: see text] pair production cross-section in collisions at [Formula: see text] TeV with the ATLAS detector.

The production of two prompt [Formula: see text] mesons, each with transverse momenta [Formula: see text] GeV and rapidity [Formula: see text], is studied using a sample of proton-proton collisions at [Formula: see text] TeV, corresponding to an integrated luminosity of 11.4 fb[Formula: see text] collected in 2012 with the ATLAS detector at the LHC. The differential cross-section, assuming unpolarised [Formula: see text] production, is measured as a function of the transverse momentum of the lower-[Formula: see text] [Formula: see text] meson, di-[Formula: see text] [Formula: see text] and mass, the difference in rapidity between the two [Formula: see text] mesons, and the azimuthal angle between the two [Formula: see text] mesons.

Measurement of the [Formula: see text] and [Formula: see text] production cross sections in multilepton final states using 3.2 fb[Formula: see text] of [Formula: see text] collisions at [Formula: see text] = 13 TeV with the ATLAS detector.

A measurement of the [Formula: see text] and [Formula: see text] production cross sections in final states with either two same-charge muons, or three or four leptons (electrons or muons) is presented. The analysis uses a data sample of proton-proton collisions at [Formula: see text] TeV recorded with the ATLAS detector at the Large Hadron Collider in 2015, corresponding to a total integrated luminosity of 3.2 fb[Formula: see text].

A measurement of the calorimeter response to single hadrons and determination of the jet energy scale uncertainty using LHC Run-1 -collision data with the ATLAS detector.

A measurement of the calorimeter response to isolated charged hadrons in the ATLAS detector at the LHC is presented. This measurement is performed with 3.2 nb[Formula: see text] of proton-proton collision data at [Formula: see text] [Formula: see text] from 2010 and 0.

imaging of skeletal muscle in mice highlights muscle defects in a model of myotubular myopathy.

Skeletal muscle structure and function are altered in different myopathies. However, the understanding of the molecular and cellular mechanisms mainly rely on and investigations in mammalian models. In order to monitor the intracellular structure of the neuromuscular system in its environment under normal and pathological conditions, we set-up and validated non-invasive imaging of ear and leg muscles in mice.

Recessive MYPN mutations cause cap myopathy with occasional nemaline rods.

Congenital myopathies are phenotypically and genetically heterogeneous. We describe homozygous truncating mutations in MYPN in 2 unrelated families with a slowly progressive congenital cap myopathy. MYPN encodes the Z-line protein myopalladin implicated in sarcomere integrity.

ORAI1 Mutations with Distinct Channel Gating Defects in Tubular Aggregate Myopathy.

Calcium (Ca ) is a physiological key factor, and the precise modulation of free cytosolic Ca levels regulates multiple cellular functions. Store-operated Ca entry (SOCE) is a major mechanism controlling Ca homeostasis, and is mediated by the concerted activity of the Ca sensor STIM1 and the Ca channel ORAI1. Dominant gain-of-function mutations in STIM1 or ORAI1 cause tubular aggregate myopathy (TAM) or Stormorken syndrome, whereas recessive loss-of-function mutations are associated with immunodeficiency.

Identification and rejection of pile-up jets at high pseudorapidity with the ATLAS detector.

The rejection of forward jets originating from additional proton-proton interactions (pile-up) is crucial for a variety of physics analyses at the LHC, including Standard Model measurements and searches for physics beyond the Standard Model. The identification of such jets is challenging due to the lack of track and vertex information in the pseudorapidity range . This paper presents a novel strategy for forward pile-up jet tagging that exploits jet shapes and topological jet correlations in pile-up interactions.

Study of and production in collisions at and search for anomalous quartic gauge couplings with the ATLAS experiment.

This paper presents a study of and triboson production using events from proton-proton collisions at a centre-of-mass energy of recorded with the ATLAS detector at the LHC and corresponding to an integrated luminosity of 20.2 fb . The production cross-section is determined using a final state containing an electron, a muon, a photon, and neutrinos ( ).

Measurement of production with the hadronically decaying boson reconstructed as one or two jets in collisions at with ATLAS, and constraints on anomalous gauge couplings.

This paper presents a study of the production of or boson pairs, with one boson decaying to or and one or boson decaying hadronically. The analysis uses of collision data, collected by the ATLAS detector at the Large Hadron Collider. Cross-sections for  /  production are measured in high- fiducial regions defined close to the experimental event selection.

Measurement of lepton differential distributions and the top quark mass in production in collisions at TeV with the ATLAS detector.

This paper presents single lepton and dilepton kinematic distributions measured in dileptonic events produced in 20.2 of  TeV collisions recorded by the ATLAS experiment at the LHC. Both absolute and normalised differential cross-sections are measured, using events with an opposite-charge pair and one or two -tagged jets.

Measurement of detector-corrected observables sensitive to the anomalous production of events with jets and large missing transverse momentum in collisions at TeV using the ATLAS detector.

Observables sensitive to the anomalous production of events containing hadronic jets and missing momentum in the plane transverse to the proton beams at the Large Hadron Collider are presented. The observables are defined as a ratio of cross sections, for events containing jets and large missing transverse momentum to events containing jets and a pair of charged leptons from the decay of a boson. This definition minimises experimental and theoretical systematic uncertainties in the measurements.

Determination of the strong coupling constant from transverse energy-energy correlations in multijet events at using the ATLAS detector.

Measurements of transverse energy-energy correlations and their associated asymmetries in multi-jet events using the ATLAS detector at the LHC are presented. The data used correspond to proton-proton collisions with an integrated luminosity of 20.2 .

Search for direct top squark pair production in final states with two leptons in TeV collisions with the ATLAS detector.

The results of a search for direct pair production of top squarks in events with two opposite-charge leptons (electrons or muons) are reported, using of integrated luminosity from proton-proton collisions at TeV collected by the ATLAS detector at the Large Hadron Collider. To cover a range of mass differences between the top squark and lighter supersymmetric particles, four possible decay modes of the top squark are targeted with dedicated selections: the decay into a -quark and the lightest chargino with , the decay into an on-shell top quark and the lightest neutralino, the three-body decay and the four-body decay . No significant excess of events is observed above the Standard Model background for any selection, and limits on top squarks are set as a function of the and masses.

Precision measurement and interpretation of inclusive , and production cross sections with the ATLAS detector.

High-precision measurements by the ATLAS Collaboration are presented of inclusive , and ( ) Drell-Yan production cross sections at the LHC. The data were collected in proton-proton collisions at with an integrated luminosity of . Differential and cross sections are measured in a lepton pseudorapidity range .

Measurement of jet fragmentation in Pb+Pb and collisions at TeV with the ATLAS detector at the LHC.

The distributions of transverse momentum and longitudinal momentum fraction of charged particles in jets are measured in Pb+Pb and collisions with the ATLAS detector at the LHC. The distributions are measured as a function of jet transverse momentum and rapidity. The analysis utilises an integrated luminosity of 0.

Dihydropyridine receptor (DHPR, CACNA1S) congenital myopathy.

Muscle contraction upon nerve stimulation relies on excitation-contraction coupling (ECC) to promote the rapid and generalized release of calcium within myofibers. In skeletal muscle, ECC is performed by the direct coupling of a voltage-gated L-type Ca channel (dihydropyridine receptor; DHPR) located on the T-tubule with a Ca release channel (ryanodine receptor; RYR1) on the sarcoplasmic reticulum (SR) component of the triad. Here, we characterize a novel class of congenital myopathy at the morphological, molecular, and functional levels.

Progressive Structural Defects in Canine Centronuclear Myopathy Indicate a Role for HACD1 in Maintaining Skeletal Muscle Membrane Systems.

Mutations in HACD1/PTPLA cause recessive congenital myopathies in humans and dogs. Hydroxyacyl-coA dehydratases are required for elongation of very long chain fatty acids, and HACD1 has a role in early myogenesis, but the functions of this striated muscle-specific enzyme in more differentiated skeletal muscle remain unknown. Canine HACD1 deficiency is histopathologically classified as a centronuclear myopathy (CNM).

Novel Dominant Mutation in BIN1 Gene Causing Mild Centronuclear Myopathy Revealed by Myalgias and CK Elevation.

We present the clinical, morphological and molecular data of an Italian family with centronuclear myopathy, carrying a novel pathogenic mutation of BIN1 gene in heterozygous state, consistent with autosomal dominant inheritance. The proband, a 56-years-old man suffered of lower limbs myalgia and slight CK elevation. Clinical examination revealed no muscle weakness, short stature, mild symmetric eyelid ptosis, scapular winging, ankle retraction and well-developed muscles.

Measurement of the Inelastic Proton-Proton Cross Section at sqrt[s]=13 TeV with the ATLAS Detector at the LHC.

This Letter presents a measurement of the inelastic proton-proton cross section using 60  μb^{-1} of pp collisions at a center-of-mass energy sqrt[s] of 13 TeV with the ATLAS detector at the LHC. Inelastic interactions are selected using rings of plastic scintillators in the forward region (2.07<|η|<3.

Characteristics, aetiology, antimicrobial resistance and outcomes of bacteraemic cholangitis in patients with solid tumours: A prospective cohort study.

Objectives: To asses the clinical features, aetiology, antimicrobial resistance and outcomes of bacteraemic cholangitis in patients with solid tumours (ST).

Methods: All consecutive episodes of bacteraemia in hospitalized patients were prospectively analysed (2006-2015).

Results: Of 1852 episodes of bacteraemia, 750 involved patients with ST.

Recessive mutations in the kinase ZAK cause a congenital myopathy with fibre type disproportion.

Congenital myopathies define a heterogeneous group of neuromuscular diseases with neonatal or childhood hypotonia and muscle weakness. The genetic cause is still unknown in many patients, precluding genetic counselling and better understanding of the physiopathology. To identify novel genetic causes of congenital myopathies, exome sequencing was performed in three consanguineous families.

Variants in the Oxidoreductase PYROXD1 Cause Early-Onset Myopathy with Internalized Nuclei and Myofibrillar Disorganization.

This study establishes PYROXD1 variants as a cause of early-onset myopathy and uses biospecimens and cell lines, yeast, and zebrafish models to elucidate the fundamental role of PYROXD1 in skeletal muscle. Exome sequencing identified recessive variants in PYROXD1 in nine probands from five families. Affected individuals presented in infancy or childhood with slowly progressive proximal and distal weakness, facial weakness, nasal speech, swallowing difficulties, and normal to moderately elevated creatine kinase.