1,379 research outputs found

    ATLAS Pixel Detector status in Run 2

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    The ATLAS Pixel Detector had good performance throughout the first operation of the LHC. During the long shutdown of data taking in 2013 and 2014, the services of the detector have been renovated and a fourth layer of pixels, called Insertable B-Layer (IBL), has been placed around new smaller radius beampipe. The new layer is closer to the interaction point and has a reduced pixel size. It will mitigate some loss of efficiency of the previous innermost layer when increasing the peak luminosity, scheduled to reach 2×1034 cm−2 s−1. The modules production has been completed in the first months of 2014. An overview of the used Technologies and the expected performance of the Pixel Detector is presented

    Some new results on a Lavrentieff phenomenon for problems of homogenization with constraints on the gradient

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    In this paper we analyze, in the context of a Lavrentieff phenomenon, the process of homogenization for Dirichlet problems

    Evaluation of basal ganglia haemodynamic changes with perfusion-weighted magnetic resonance imaging in patients with Parkinson's disease

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    The aim of our study was to assess the regional cerebral blood flow (rCBF) of basal ganglia and thalami in patients with Parkinson’s disease (PD) using perfusion–weighted magnetic resonance imaging (PW–MRI)

    Test with high-energy and high-intensity proton beam on ATLAS silicon detectors towards HL-LHC

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    The ATLAS silicon tracker was designed to sustain a high level of dose integrated over several years of LHC operations. The radiation tolerance should nevertheless guarantee the survival of the detector in the case of accidental beam loss. In 2006, an experiment performed on an ATLAS Pixel module established that they are able to sustain beam losses in the order of 1.5 × 1010 protons/cm2 with a minimal or no performance degradation. Recently, a new experiment was performed with a higher-intensity and -energy proton beam on two IBL Pixel modules and one ITk strip in the HiRadMat area at CERN. Preliminary results are presented along with perspectives of 2018 test beams

    ALS5/SPG11/KIAA1840 mutations cause autosomal recessive axonal Charcot-Marie-Tooth disease

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    Charcot-Marie-Tooth disease is a group of hereditary peripheral neuropathies that share clinical characteristics of progressive distal muscle weakness and atrophy, foot deformities, distal sensory loss, as well as diminished tendon reflexes. Hundreds of causative DNA changes have been found, but much of the genetic basis of the disease is still unexplained. Mutations in the ALS5/SPG11/KIAA1840 gene are a frequent cause of autosomal recessive hereditary spastic paraplegia with thin corpus callosum and peripheral axonal neuropathy, and account for similar to 40% of autosomal recessive juvenile amyotrophic lateral sclerosis. The overlap of axonal Charcot-Marie-Tooth disease with both diseases, as well as the common autosomal recessive inheritance pattern of thin corpus callosum and axonal Charcot-Marie-Tooth disease in three related patients, prompted us to analyse the ALS5/SPG11/KIAA1840 gene in affected individuals with autosomal recessive axonal Charcot-Marie-Tooth disease. We investigated 28 unrelated families with autosomal recessive axonal Charcot-Marie-Tooth disease defined by clinical, electrophysiological, as well as pathological evaluation. Besides, we screened for all the known genes related to axonal autosomal recessive Charcot-Marie-Tooth disease (CMT2A2/HMSN2A2/MFN2, CMT2B1/LMNA, CMT2B2/MED25, CMT2B5/NEFL, ARCMT2F/dHMN2B/HSPB1, CMT2K/GDAP1, CMT2P/LRSAM1, CMT2R/TRIM2, CMT2S/IGHMBP2, CMT2T/HSJ1, CMTRID/COX6A1, ARAN-NM/HINT and GAN/GAN), for the genes related to autosomal recessive hereditary spastic paraplegia with thin corpus callosum and axonal peripheral neuropathy (SPG7/PGN, SPG15/ZFYVE26, SPG21/ACP33, SPG35/FA2H, SPG46/GBA2, SPG55/C12orf65 and SPG56/CYP2U1), as well as for the causative gene of peripheral neuropathy with or without agenesis of the corpus callosum (SLC12A6). Mitochondrial disorders related to Charcot-Marie-Tooth disease type 2 were also excluded by sequencing POLG and TYMP genes. An additional locus for autosomal recessive Charcot-Marie-Tooth disease type 2H on chromosome 8q13-21.1 was excluded by linkage analysis. Pedigrees originated in Italy, Brazil, Canada, England, Iran, and Japan. Interestingly, we identified 15 ALS5/SPG11/KIAA1840 mutations in 12 families (two sequence variants were never reported before, p.Gln198* and p.Pro2212fs*5). No large deletions/duplications were detected in these patients. The novel mutations seemed to be pathogenic since they co-segregated with the disease in all pedigrees and were absent in 300 unrelated controls. Furthermore, in silico analysis predicted their pathogenic effect. Our results indicate that ALS5/SPG11/KIAA1840 is the causative gene of a wide spectrum of clinical features, including autosomal recessive axonal Charcot-Marie-Tooth disease

    The INFN-FBK "Phase-2" R&D program

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    We report on the 3-year INFN ATLAS-CMS joint research activity in collaboration with FBK, started in 2014, and aimed at the development of new thin pixel detectors for the High Luminosity LHC Phase-2 upgrades. The program is concerned with both 3D and planar active-edge pixel sensors to be made on 6" p-type wafers. The technology and the design will be optimized and qualified for extreme radiation hardness (2×1016 neq cm-2). Pixel layouts compatible with present (for testing) and future (RD53 65nm) front-end chips of ATLAS and CMS are considered. The paper covers the main aspects of the research program, from the sensor design and fabrication technology, to the results of initial tests performed on the first prototypes. © 2015 Elsevier B.V
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