Data Acquisition in the EUDET Project

The goal of the EUDET project is the development and construction of infrastructure to permit detector R&D for the International Linear Collider (ILC) with larger scale prototypes. It encompasses major detector components: the vertex detector, the tracker and the calorimeters. We describe here the status and plans of the project with emphasis on issues related to data acquisition for future test beam experiments.Comment: 4 pages, 2 figures, to appear in the proceedings of Linear Collider Workshop (LCWS06), Bangalore, Indi

Helicopter roll control effectiveness criteria program summary

A study of helicopter roll control effectiveness is summarized for the purpose of defining military helicopter handling qualities requirements. The study is based on an analysis of pilot-in-the-loop task performance of several basic maneuvers. This is extended by a series of piloted simulations using the NASA Ames Vertical Motion Simulator and selected flight data. The main results cover roll control power and short-term response characteristics. In general the handling qualities requirements recommended are set in conjunction with desired levels of flight task and maneuver response which can be directly observed in actual flight. An important aspect of this, however, is that vehicle handling qualities need to be set with regard to some quantitative aspect of mission performance. Specific examples of how this can be accomplished include a lateral unmask/remask maneuver in the presence of a threat and an air tracking maneuver which recognizes the kill probability enhancement connected with decreasing the range to the target. Conclusions and recommendations address not only the handling qualities recommendations, but also the general use of flight simulators and the dependence of mission performance on handling qualities

Modelling and Measurement of Charge Transfer in Multiple GEM Structures

Measurements and numerical simulations on the charge transfer in Gas Electron Multiplier (GEM) foils are presented and their implications for the usage of GEM foils in Time Projection Chambers are discussed. A small test chamber has been constructed and operated with up to three GEM foils. The charge transfer parameters derived from the electrical currents monitored during the irradiation with an Fe-55 source are compared with numerical simulations. The performance in magnetic fields up to 2 T is also investigated.Comment: 21 pages, 16 figures, submitted to NIM-

Charge Transfer and Charge Broadening of GEM Structures in High Magnetic Fields

We report on measurements of charge transfer in GEM structures in high magnetic fields. These were performed in the framework of the R&D work for a Time Projection Chamber at a future Linear Collider. A small test chamber has been installed into the aperture of a superconducting magnet with the GEM structures mounted perpendicular to the B field direction. The charge transfer is derived from the electrical currents monitored during irradiation with an ${}^{55}$Fe source. No severe loss of primary ionisation charge is observed, but an improved ion feedback suppression is achieved for high magnetic fields. Additionally, the width of the charge cloud released by individual ${}^{55}$Fe photons is measured using a finely segmented strip readout after the triple GEM structure. Charge widths between 0.3 and 0.5 mm RMS are observed, which originate from the charge broadening inside the GEM readout. This charge broadening is only partly suppressed at high magnetic fields.Comment: 11 pages, 9 figure

Inhibition by Anandamide of 6-Hydroxydopamine-Induced Cell Death in PC12 Cells

6-hydroxydopamine (6-OHDA) is a selective neurotoxin that is widely used to investigate cell death and protective strategies in models of Parkinson's disease. Here, we investigated the effects of the endogenous cannabinoid, anandamide, on 6-OHDA-induced toxicity in rat adrenal phaeochromocytoma PC12 cells. Morphological analysis and caspase-3 activity assay revealed that anandamide inhibited 6-OHDA-induced apoptosis. The protection was not affected by antagonists of either cannabinoid receptors (CB1 or CB2) or the vanilloid receptor TRPV1. Anandamide-dependent protection was reduced by pretreatment with LY294002 (inhibitor of phosphatidylinositol 3-kinase, PI3K) and unaffected by U0126 (inhibitor of extracellularly-regulated kinase). Interestingly, phosphorylation of c-Jun-NH2-terminal kinase (JNK) in cells exposed to 6-OHDA was strongly reduced by anandamide pre-treatment. Furthermore, 6-OHDA induced c-Jun activation and increased Bim expression, both of which were inhibited by anandamide. Together, these data demonstrate antiapoptotic effects of anandamide and also suggest a role for activation of PI3K and inhibition of JNK signalling in anandamide-mediated protection against 6-OHDA

Precedence-constrained scheduling problems parameterized by partial order width

Negatively answering a question posed by Mnich and Wiese (Math. Program. 154(1-2):533-562), we show that P2|prec,$p_j{\in}\{1,2\}$|$C_{\max}$, the problem of finding a non-preemptive minimum-makespan schedule for precedence-constrained jobs of lengths 1 and 2 on two parallel identical machines, is W[2]-hard parameterized by the width of the partial order giving the precedence constraints. To this end, we show that Shuffle Product, the problem of deciding whether a given word can be obtained by interleaving the letters of $k$ other given words, is W[2]-hard parameterized by $k$, thus additionally answering a question posed by Rizzi and Vialette (CSR 2013). Finally, refining a geometric algorithm due to Servakh (Diskretn. Anal. Issled. Oper. 7(1):75-82), we show that the more general Resource-Constrained Project Scheduling problem is fixed-parameter tractable parameterized by the partial order width combined with the maximum allowed difference between the earliest possible and factual starting time of a job.Comment: 14 pages plus appendi

Physics at the e+ e- Linear Collider

A comprehensive review of physics at an e+e- Linear Collider in the energy range of sqrt{s}=92 GeV--3 TeV is presented in view of recent and expected LHC results, experiments from low energy as well as astroparticle physics.The report focuses in particular on Higgs boson, Top quark and electroweak precision physics, but also discusses several models of beyond the Standard Model physics such as Supersymmetry, little Higgs models and extra gauge bosons. The connection to cosmology has been analyzed as well.Comment: 179 pages, plots and references updated, version to be published at EPJ

Governance of the international linear collider project

PoS(ICHEP 2010)516 - http://pos.sissa.itInternational audienceGovernance models for the International Linear Collider Project are examined in the light of experience from similar international projects around the world. Recommendations for one path which could be followed to realise the ILC successfully are outlined

HSPB1 facilitates ERK-mediated phosphorylation and degradation of BIM to attenuate endoplasmic reticulum stress-induced apoptosis

BIM, a pro-apoptotic BH3-only protein, is a key regulator of the intrinsic (or mitochondrial) apoptosis pathway. Here, we show that BIM induction by endoplasmic reticulum (ER) stress is suppressed in rat PC12 cells overexpressing heat shock protein B1 (HSPB1 or HSP27) and that this is due to enhanced proteasomal degradation of BIM. HSPB1 and BIM form a complex that immunoprecipitates with p-ERK1/2. We found that HSPB1-mediated proteasomal degradation of BIM is dependent on MEK-ERK signaling. Other studies have shown that several missense mutations in HSPB1 cause the peripheral neuropathy, Charcot-Marie-Tooth (CMT) disease, which is associated with nerve degeneration. Here we show that cells overexpressing CMT-related HSPB1 mutants exhibited increased susceptibility to ER stress-induced cell death and high levels of BIM. These findings identify a novel function for HSPB1 as a negative regulator of BIM protein stability leading to protection against ER stress-induced apoptosis, a function that is absent in CMT-associated HSPB1 mutants