247 research outputs found

    Two years of AD operation: Experience and progress

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    The antiproton decelerator (AD) has been running successfully for physics for the past two years. After the end of the commissioning period [1] that finished in 2000, the machine has gradually been improved. The main efforts were concentrated on increasing the beam intensity, reducing the cycle length and improving the machine stability. The intensity of the injected beam has been significantly increased due to a higher beam intensity from the PS complex and also due to increased transverse acceptances in the AD machine. The beam losses during deceleration were reduced from 30-40 % down to a few percent, mainly due to improvements of the operation of the deceleration RF cavity. Altogether these improvements increased the intensity of the ejected beam by a factor of two. Improvements of the electron cooling were followed by a reduction of emittances and cycle duration (about 15%). Progress in beam diagnostics now allows the monitoring of the machine performance during the whole cycle. The stability of the machine at the ejection momentum 100 MeV/c remains a crucial point and the identification of the causes of fluctuations in the ejected beam parameters are now under investigation

    ELENA, a preliminary cost and feasibility study

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    To produce dense pbar beams at very low energies (100-200 keV), a small decelerator ring could be built and installed between the existing AD ring and the experimental area. Phase-space blowup during deceleration would be compensated by electron cooling in order to obtain final emittances comparable to the 5MeV beam presently delivered by the AD. This report describes preliminary machine parameters and layout of ELENA and also gives an approximate estimate of cost and manpower needs

    LEIR Commissioning

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    The Low Energy Ion Ring (LEIR) is a central piece of the injector chain for LHC ion operation, transforming long Linac 3 pulses into high density bunches needed for LHC. LEIR commissioning is scheduled to be completed at the time of the conference. A review of LEIR commissioning highlighting expected and unexpected problems and actions to tackle them will be given

    Commissioning and First Operation of the Antiproton Decelerator (AD)

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    The Antiproton Decelerator (AD) is a simplified source of antiprotons which provides low energy antiprotons for experiments, replacing four machines: AC (Antiproton Collector), AA (Antiproton Accumulator), PS and LEAR (Low Energy Antiproton Ring), shutdown in 1996. The former AC was modified to include deceleration and electron cooling. The AD started operation in July 2000 and has since delivered cooled beam at 100 MeV/c (kinetic energy of 5.3 MeV) to 3 experiments (ASACUSA, ATHENA and ATRAP) for 1500 h. The flux (up to 2.5´105pbars /s delivered in short pulses of 330 ns every 110 s) and the quality of the ejected beam are not far from the design specifications. A linear RF Quadrupole Decelerator (RFQD) was commissioned in November 2000 to post-decelerate the beam for ASACUSA from 5.3 MeV to about 15 keV. Problems encountered in converting the fixed energy AC into a decelerating machine will be outlined, and the present status of the AD, including the performance of the cooling systems and the special diagnostics to cope with beams of less than 107 pbars, will be reviewed. Possible future developments will be sketche

    Mitochondrial abnormalities and low grade inflammation are present in the skeletal muscle of a minority of patients with amyotrophic lateral sclerosis; an observational myopathology study

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    BACKGROUND Amyotrophic lateral sclerosis (ALS) is a primary progressive neurodegenerative disease characterised by neuronal loss of lower motor neurons (in the spinal cord and brainstem) and/or upper motor neurons (in the motor cortex) and subsequent denervation atrophy of skeletal muscle. AIM A comprehensive examination of muscle pathology from a cohort of clinically confirmed ALS patients, including an investigation of inflammation, complement activation, and deposition of abnormal proteins in order to compare them with findings from an age-matched, control group. MATERIAL AND METHODS 31 muscle biopsies from clinically confirmed ALS patients and 20 normal controls underwent a comprehensive protocol of histochemical and immunohistochemical stains, including HLA-ABC, C5b-9, p62, and TDP-43. RESULTS Neurogenic changes were confirmed in 30/31 ALS cases. In one case, no neurogenic changes could be detected. Muscle fibre necrosis was seen in 5/31 cases and chronic mononuclear inflammatory cell infiltration in 5/31 (2 of them overlapped with those showing muscle necrosis). In four biopsies there was an increase in the proportion of cytochrome oxidase (COX) negative fibres (2-3%). p62 faintly stained cytoplasmic bodies in eight cases and none were immunoreactive to TDP-43. CONCLUSION This large series of muscle biopsies from patients with ALS demonstrates neurogenic atrophy is a nearly uniform finding and that mild mitochondrial abnormalities and low-grade inflammation can be seen and do not rule out the diagnosis of ALS. These findings could lend support to the notion that ALS is a complex and heterogeneous disorder

    IONS FOR LHC: STATUS OF THE INJECTOR CHAIN

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    The LHC will, in addition to proton runs, be operated with Pb ions and provide collisions at energies of 5.5 TeV per nucleon pair, i.e. more than 1.1 PeV per event, to experiments. The transformation of CERN's ion injector complex (Linac3-LEIR-PS-SPS) to allow collision of ions in LHC in 2008 is well under way. The status of these modifications and the latest results of commissioning will be presented. The remaining challenges are reviewed

    Ions for LHC: Towards Completion of the Injector Chain

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    The commissioning of CERN's ion injector complex [1] to allow 1.1 PeV collisions of ions in LHC is well under way. After the Low Energy Ion Ring (LEIR) in 2005 [2] and the Proton Synchrotron (PS) in 2006 [3], the Super Proton Synchrotron (SPS) has now been commissioned with the 'Early' ion beam, which should give a luminosity of 5×1025cm2s15×10^{25}cm^{-2}s^{-1} in the LHC. This paper summarizes the operation in 2007 of all the machines involved in the ion injection chain

    Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS.

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    Many mutations confer one or more toxic function(s) on copper/zinc superoxide dismutase 1 (SOD1) that impair motor neuron viability and cause familial amyotrophic lateral sclerosis (FALS). Using a conformation-specific antibody that detects misfolded SOD1 (C4F6), we found that oxidized wild-type SOD1 and mutant SOD1 share a conformational epitope that is not present in normal wild-type SOD1. In a subset of human sporadic ALS (SALS) cases, motor neurons in the lumbosacral spinal cord were markedly C4F6 immunoreactive, indicating that an aberrant wild-type SOD1 species was present. Recombinant, oxidized wild-type SOD1 and wild-type SOD1 immunopurified from SALS tissues inhibited kinesin-based fast axonal transport in a manner similar to that of FALS-linked mutant SOD1. Our findings suggest that wild-type SOD1 can be pathogenic in SALS and identify an SOD1-dependent pathogenic mechanism common to FALS and SALS
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