Constraints on magnetic field and particle content in blazar jets through optical circular polarization

Polarization offers a unique view in the physical processes of astrophysical jets. We report on optical circular polarization (CP) observations of two famous blazars, namely 3C 279 and PKS 1510−089, at high linearly polarized states. This is the first time PKS 1510−089 is observed in optical CP. While only upper limits can be extracted from our observing campaign, the non-detection of optical CP allows us to provide meaningful constraints on their magnetic field strength and jet composition. We find that high-energy emission models requiring high magnetic field strength and a low positron fraction can be excluded.</p

Hadronic origin of the TeV flare of M87 in April 2010

M87 is a giant radio galaxy with FR-I morphology. It underwent three episodes of TeV flaring in recent years with the strongest one in April 2010 which was jointly monitored by MAGIC, VERITAS and H.E.S.S. We explain its spectral energy distribution in the energy range 0.3–5 TeV by assuming that the flaring occurs in the innermost region of the jet. In this region the low energy SSC photons serve as the target for the Fermi-accelerated high energy protons of energy $${\le }30$$ TeV to form a delta resonance. The TeV photons are produced from the subsequent decay of the delta resonance to neutral pions. In this scenario the observed TeV flux of April 2010 flare is fitted very well

X-ray Time Lags in TeV Blazars

We use Monte Carlo/Fokker-Planck simulations to study the X-ray time lags. Our results show that soft lags will be observed as long as the decay of the flare is dominated by radiative cooling, even when acceleration and cooling timescales are similar. Hard lags can be produced in presence of a competitive achromatic particle energy loss mechanism if the acceleration process operates on a timescale such that particles are slowly moved towards higher energy while the flare evolves. In this type of scenario, the {\gamma} -ray/X-ray quadratic relation is also reproduced.Comment: 4 pages, 6 figures, Proceeding of `Multiwavelength Variability of Blazars', Guangzhou, Chin

Analysis of RNA splicing defects in PITX2 mutants supports a gene dosage model of Axenfeld-Rieger syndrome

BACKGROUND: Axenfeld-Rieger syndrome (ARS) is associated with mutations in the PITX2 gene that encodes a homeobox transcription factor. Several intronic PITX2 mutations have been reported in Axenfeld-Rieger patients but their effects on gene expression have not been tested. METHODS: We present two new families with recurrent PITX2 intronic mutations and use PITX2c minigenes and transfected cells to address the hypothesis that intronic mutations effect RNA splicing. Three PITX2 mutations have been analyzed: a G>T mutation within the AG 3' splice site (ss) junction associated with exon 4 (IVS4-1G>T), a G>C mutation at position +5 of the 5' (ss) of exon 4 (IVS4+5G>C), and a previously reported A>G substitution at position -11 of 3'ss of exon 5 (IVS5-11A>G). RESULTS: Mutation IVS4+5G>C showed 71% retention of the intron between exons 4 and 5, and poorly expressed protein. Wild-type protein levels were proportionally expressed from correctly spliced mRNA. The G>T mutation within the exon 4 AG 3'ss junction shifted splicing exclusively to a new AG and resulted in a severely truncated, poorly expressed protein. Finally, the A>G substitution at position -11 of the 3'ss of exon 5 shifted splicing exclusively to a newly created upstream AG and resulted in generation of a protein with a truncated homeodomain. CONCLUSION: This is the first direct evidence to support aberrant RNA splicing as the mechanism underlying the disorder in some patients and suggests that the magnitude of the splicing defect may contribute to the variability of ARS phenotypes, in support of a gene dosage model of Axenfeld-Rieger syndrome

Search for direct pair production of the top squark in all-hadronic final states in proton-proton collisions at s√=8 TeV with the ATLAS detector

The results of a search for direct pair production of the scalar partner to the top quark using an integrated luminosity of 20.1fb−1 of proton–proton collision data at √s = 8 TeV recorded with the ATLAS detector at the LHC are reported. The top squark is assumed to decay via t˜→tχ˜01 or t˜→ bχ˜±1 →bW(∗)χ˜01 , where χ˜01 (χ˜±1 ) denotes the lightest neutralino (chargino) in supersymmetric models. The search targets a fully-hadronic final state in events with four or more jets and large missing transverse momentum. No significant excess over the Standard Model background prediction is observed, and exclusion limits are reported in terms of the top squark and neutralino masses and as a function of the branching fraction of t˜ → tχ˜01 . For a branching fraction of 100%, top squark masses in the range 270–645 GeV are excluded for χ˜01 masses below 30 GeV. For a branching fraction of 50% to either t˜ → tχ˜01 or t˜ → bχ˜±1 , and assuming the χ˜±1 mass to be twice the χ˜01 mass, top squark masses in the range 250–550 GeV are excluded for χ˜01 masses below 60 GeV

Search for pair-produced long-lived neutral particles decaying to jets in the ATLAS hadronic calorimeter in ppcollisions at √s=8TeV

The ATLAS detector at the Large Hadron Collider at CERN is used to search for the decay of a scalar boson to a pair of long-lived particles, neutral under the Standard Model gauge group, in 20.3fb−1of data collected in proton–proton collisions at √s=8TeV. This search is sensitive to long-lived particles that decay to Standard Model particles producing jets at the outer edge of the ATLAS electromagnetic calorimeter or inside the hadronic calorimeter. No significant excess of events is observed. Limits are reported on the product of the scalar boson production cross section times branching ratio into long-lived neutral particles as a function of the proper lifetime of the particles. Limits are reported for boson masses from 100 GeVto 900 GeV, and a long-lived neutral particle mass from 10 GeVto 150 GeV

AWAKE: A Proton-Driven Plasma Wakefield Acceleration Experiment at CERN

The AWAKE Collaboration has been formed in order to demonstrate proton-driven plasma wakefield acceleration for the first time. This acceleration technique could lead to future colliders of high energy but of a much reduced length when compared to proposed linear accelerators. The CERN SPS proton beam in the CNGS facility will be injected into a 10 m plasma cell where the long proton bunches will be modulated into significantly shorter micro-bunches. These micro-bunches will then initiate a strong wakefield in the plasma with peak fields above 1 GV/m that will be harnessed to accelerate a bunch of electrons from about 20 MeV to the GeV scale within a few meters. The experimental program is based on detailed numerical simulations of beam and plasma interactions. The main accelerator components, the experimental area and infrastructure required as well as the plasma cell and the diagnostic equipment are discussed in detail. First protons to the experiment are expected at the end of 2016 and this will be followed by an initial three-four years experimental program. The experiment will inform future larger-scale tests of proton-driven plasma wakefield acceleration and applications to high energy colliders

A multicenter, randomized controlled trial of immediate total-body CT scanning in trauma patients (REACT-2)

Contains fulltext : 110874.pdf (publisher's version ) (Open Access)BACKGROUND: Computed tomography (CT) scanning has become essential in the early diagnostic phase of trauma care because of its high diagnostic accuracy. The introduction of multi-slice CT scanners and infrastructural improvements made total-body CT scanning technically feasible and its usage is currently becoming common practice in several trauma centers. However, literature provides limited evidence whether immediate total-body CT leads to better clinical outcome then conventional radiographic imaging supplemented with selective CT scanning in trauma patients. The aim of the REACT-2 trial is to determine the value of immediate total-body CT scanning in trauma patients. METHODS/DESIGN: The REACT-2 trial is an international, multicenter randomized clinical trial. All participating trauma centers have a multi-slice CT scanner located in the trauma room or at the Emergency Department (ED). All adult, non-pregnant, severely injured trauma patients according to predefined criteria will be included. Patients in whom direct scanning will hamper necessary cardiopulmonary resuscitation or who require an immediate operation because of imminent death (both as judged by the trauma team leader) are excluded. Randomization will be computer assisted. The intervention group will receive a contrast-enhanced total-body CT scan (head to pelvis) during the primary survey. The control group will be evaluated according to local conventional trauma imaging protocols (based on ATLS guidelines) supplemented with selective CT scanning. Primary outcome will be in-hospital mortality. Secondary outcomes are differences in mortality and morbidity during the first year post trauma, several trauma work-up time intervals, radiation exposure, general health and quality of life at 6 and 12 months post trauma and cost-effectiveness. DISCUSSION: The REACT-2 trial is a multicenter randomized clinical trial that will provide evidence on the value of immediate total-body CT scanning during the primary survey of severely injured trauma patients. If immediate total-body CT scanning is found to be the best imaging strategy in severely injured trauma patients it could replace conventional imaging supplemented with CT in this specific group. TRIAL REGISTRATION: ClinicalTrials.gov: (NCT01523626)

Phosphatidylinositol 3-kinase (PI3K) pathway activation in bladder cancer

The phosphatidylinositol 3-kinase (PI3K) pathway is a critical signal transduction pathway that regulates multiple cellular functions. Aberrant activation of this pathway has been identified in a wide range of cancers. Several pathway components including AKT, PI3K and mTOR represent potential therapeutic targets and many small molecule inhibitors are in development or early clinical trials. The complex regulation of the pathway, together with the multiple mechanisms by which it can be activated, make this a highly challenging pathway to target. For successful inhibition, detailed molecular information on individual tumours will be required and it is already clear that different tumour types show distinct combinations of alterations. Recent results have identified alterations in pathway components PIK3CA, PTEN, AKT1 and TSC1 in bladder cancer, some of which are significantly related to tumour phenotype and clinical behaviour. Co-existence of alterations to several PI3K pathway genes in some bladder tumours indicates that these proteins may have functions that are not related solely to the known canonical pathway