Preliminary results of 3D-DDTC pixel detectors for the ATLAS upgrade

Presented at: 9th International Conference on Large Scale Applications and Radiation Hardness of Semiconductor Detectors - RD09. Florence, Italy, 30 September - 2 October 20093D Silicon sensors fabricated at FBK-irst with the Double-side Double Type Column (DDTC) approach and columnar electrodes only partially etched through p-type substrates were tested in laboratory and in a 1.35 Tesla magnetic field with a 180GeV pion beam at CERN SPS. The substrate thickness of the sensors is about 200μm, and different column depths are available, with overlaps between junction columns (etched from the front side) and ohmic columns (etched from the back side) in the range from 110μm to 150μm. The devices under test were bump bonded to the ATLAS Pixel readout chip (FEI3) at SELEX SI (Rome, Italy). We report leakage current and noise measurements, results of functional tests with Am241 γ-ray sources, charge collection tests with Sr90 β-source and an overview of preliminary results from the CERN beam test.publishedVersio

The pharmacological effect of BGC20-1531, a novel prostanoid EP4 receptor antagonist, in the Prostaglandin E2 human model of headache

Using a human Prostaglandin E2 (PGE2) model of headache, we examined whether a novel potent and selective EP4 receptor antagonist, BGC20-1531, may prevent headache and dilatation of the middle cerebral (MCA) and superficial temporal artery (STA). In a three-way cross-over trial, eight healthy volunteers were randomly allocated to receive 200 and 400 mg BGC20-1531 and placebo, followed by a 25-min infusion of PGE2. We recorded headache intensity on a verbal rating scale, MCA blood flow velocity and STA diameter. There was no difference in headache response or prevention of the dilation of the MCA or the STA (P > 0.05) with either dose of BGC20-1531 relative to placebo, although putative therapeutic exposures were not reached in all volunteers. In conclusion, these data suggest that the other EP receptors may be involved in PGE2 induced headache and dilatation in normal subjects

Measurement of the b-hadron production cross section using decays to D*+ μ − X final states in pp collisions at √s = 7 TeV with the ATLAS detector

The b-hadron production cross section is measured with the ATLAS detector in pp collisions at √s = 7 TeV, using 3.3 pb−1 of integrated luminosity, collected during the 2010 LHC run. The b-hadrons are selected by partially reconstructing D*+μ−X final states. Differential cross sections are measured as functions of the transverse momentum and pseudorapidity. The measured production cross section for a b-hadron with pT > 9 GeV and |η| < 2.5 is 32.7±0.8(stat.)+4.5−6.8(syst.) μb, higher than the next-to-leadingorder QCD predictions but consistent within the experimental and theoretical uncertainties

Measurement of the production cross section of prompt J/ψ mesons in association with a W ± boson in pp collisions at √s = 7 TeV with the ATLAS detector

The process pp → W ± J/ψ provides a powerful probe of the production mechanism of charmonium in hadronic collisions, and is also sensitive to multiple parton interactions in the colliding protons. Using the 2011 ATLAS dataset of 4.5 fb−1 of s√ = 7 TeV pp collisions at the LHC, the first observation is made of the production of W ± + prompt J/ψ events in hadronic collisions, using W ± → μν μ and J/ψ → μ + μ −. A yield of 27.4+7.5−6.5 W ± + prompt J/ψ events is observed, with a statistical significance of 5.1σ. The production rate as a ratio to the inclusive W ± boson production rate is measured, and the double parton scattering contribution to the cross section is estimated.publishedVersio

ATLAS search for new phenomena in dijet mass and angular distributions using pp collisions at s\sqrt{s}=7 TeV

Mass and angular distributions of dijets produced in LHC proton-proton collisions at a centre-of-mass energy $\sqrt{s}$=7 TeV have been studied with the ATLAS detector using the full 2011 data set with an integrated luminosity of 4.8/fb. Dijet masses up to 4.0 TeV have been probed. No resonance-like features have been observed in the dijet mass spectrum, and all angular distributions are consistent with the predictions of QCD. Exclusion limits on six hypotheses of new phenomena have been set at 95% CL in terms of mass or energy scale, as appropriate. These hypotheses include excited quarks below 2.83 TeV, colour octet scalars below 1.86 TeV, heavy W bosons below 1.68 TeV, string resonances below 3.61 TeV, quantum black holes with six extra space-time dimensions for quantum gravity scales below 4.11 TeV, and quark contact interactions below a compositeness scale of 7.6 TeV in a destructive interference scenario.publishedVersio

Loss of glutamate transporter eaat2a leads to aberrant neuronal excitability, recurrent epileptic seizures, and basal hypoactivity

Astroglial excitatory amino acid transporter 2 (EAAT2, GLT-1, and SLC1A2) regulates the duration and extent of neuronal excitation by removing glutamate from the synaptic cleft. Hence, an impairment in EAAT2 function could lead to an imbalanced brain network excitability. Here, we investigated the functional alterations of neuronal and astroglial networks associated with the loss of function in the astroglia predominant eaat2a gene in zebrafish. We observed that eaat2a-/- mutant zebrafish larvae display recurrent spontaneous and light-induced seizures in neurons and astroglia, which coincide with an abrupt increase in extracellular glutamate levels. In stark contrast to this hyperexcitability, basal neuronal and astroglial activity was surprisingly reduced in eaat2a-/- mutant animals, which manifested in decreased overall locomotion. Our results reveal an essential and mechanistic contribution of EAAT2a in balancing brain excitability, and its direct link to epileptic seizures. Keywords: astroglia; brain excitability; calcium imaging; eaat2; epilepsy; glutamate; zebrafish

Loss of glutamate transporter eaat2a leads to aberrant neuronal excitability, recurrent epileptic seizures, and basal hypoactivity

Astroglial excitatory amino acid transporter 2 (EAAT2, GLT-1, and SLC1A2) regulates the duration and extent of neuronal excitation by removing glutamate from the synaptic cleft. Hence, an impairment in EAAT2 function could lead to an imbalanced brain network excitability. Here, we investigated the functional alterations of neuronal and astroglial networks associated with the loss of function in the astroglia predominant eaat2a gene in zebrafish. We observed that eaat2a−/− mutant zebrafish larvae display recurrent spontaneous and light-induced seizures in neurons and astroglia, which coincide with an abrupt increase in extracellular glutamate levels. In stark contrast to this hyperexcitability, basal neuronal and astroglial activity was surprisingly reduced in eaat2a−/− mutant animals, which manifested in decreased overall locomotion. Our results reveal an essential and mechanistic contribution of EAAT2a in balancing brain excitability, and its direct link to epileptic seizures