Radiation Tolerance Qualification Tests of the Final Source Interface Unit for the ALICE Experiment

The ALICE Detector Data Link (DDL) is a high-speed optical link designed to interface the readout electronics of ALICE sub-detectors to the DAQ computers. The Source Interface Unit (SIU) of the DDL will operate in radiation environment. Previous tests showed that a configuration loss of SRAM-based FPGA devices may happen and the frequency of undetected data errors in the FPGA user memory area is also not acceptable. Therefore, we redesigned the SIU card using another FPGA based on flash technology. In order to detect bit errors in the user memory we added parity check logic to the design. The new SIU has been extensively tested using neutron and proton irradiation to verify its radiation tolerance. In this paper we summarize the design changes, introduce the final design, and the results of the radiation tolerance measurements on the final card

VHMPID: a new detector for the ALICE experiment at LHC

This article presents the basic idea of VHMPID, an upgrade detector for the ALICE experiment at LHC, CERN. The main goal of this detector is to extend the particle identification capabilities of ALICE to give more insight into the evolution of the hot and dense matter created in Pb-Pb collisions. Starting from the physics motivations and working principles the challenges and current status of development is detailed.Comment: 4 pages, 6 figures. To be published in EPJ Web of Conference

Evaluation of Brain Nuclear Medicine Imaging Tracers in a Murine Model of Sepsis-Associated Encephalopathy

PURPOSE: The purpose of this study was to evaluate a set of widely used nuclear medicine imaging agents as possible methods to study the early effects of systemic inflammation on the living brain in a mouse model of sepsis-associated encephalopathy (SAE). The lipopolysaccharide (LPS)-induced murine systemic inflammation model was selected as a model of SAE. PROCEDURES: C57BL/6 mice were used. A multimodal imaging protocol was carried out on each animal 4 h following the intravenous administration of LPS using the following tracers: [(99m)Tc][2,2-dimethyl-3-[(3E)-3-oxidoiminobutan-2-yl]azanidylpropyl]-[(3E)-3-hyd roxyiminobutan-2-yl]azanide ([(99m)Tc]HMPAO) and ethyl-7-[(125)I]iodo-5-methyl-6-oxo-4H-imidazo[1,5-a][1,4]benzodiazepine-3-carbox ylate ([(125)I]iomazenil) to measure brain perfusion and neuronal damage, respectively; 2-deoxy-2-[(18)F]fluoro-D-glucose ([(18)F]FDG) to measure cerebral glucose uptake. We assessed microglia activity on another group of mice using 2-[6-chloro-2-(4-[(125)I]iodophenyl)-imidazo[1,2-a]pyridin-3-yl]-N-ethyl-N-methyl -acetamide ([(125)I]CLINME). Radiotracer uptakes were measured in different brain regions and correlated. Microglia activity was also assessed using immunohistochemistry. Brain glutathione levels were measured to investigate oxidative stress. RESULTS: Significantly reduced perfusion values and significantly enhanced [(18)F]FDG and [(125)I]CLINME uptake was measured in the LPS-treated group. Following perfusion compensation, enhanced [(125)I]iomazenil uptake was measured in the LPS-treated group's hippocampus and cerebellum. In this group, both [(18)F]FDG and [(125)I]iomazenil uptake showed highly negative correlation to perfusion measured with ([(99m)Tc]HMPAO uptake in all brain regions. No significant differences were detected in brain glutathione levels between the groups. The CD45 and P2Y12 double-labeling immunohistochemistry showed widespread microglia activation in the LPS-treated group. CONCLUSIONS: Our results suggest that [(125)I]CLINME and [(99m)Tc]HMPAO SPECT can be used to detect microglia activation and brain hypoperfusion, respectively, in the early phase (4 h post injection) of systemic inflammation. We suspect that the enhancement of [(18)F]FDG and [(125)I]iomazenil uptake in the LPS-treated group does not necessarily reflect neural hypermetabolism and the lack of neuronal damage. They are most likely caused by processes emerging during neuroinflammation, e.g., microglia activation and/or immune cell infiltration

ALICE: Physics Performance Report, Volume I

ALICE is a general-purpose heavy-ion experiment designed to study the physics of strongly interacting matter and the quark-gluon plasma in nucleus-nucleus collisions at the LHC. It currently includes more than 900 physicists and senior engineers, from both nuclear and high-energy physics, from about 80 institutions in 28 countries. The experiment was approved in February 1997. The detailed design of the different detector systems has been laid down in a number of Technical Design Reports issued between mid-1998 and the end of 2001 and construction has started for most detectors. Since the last comprehensive information on detector and physics performance was published in the ALICE Technical Proposal in 1996, the detector as well as simulation, reconstruction and analysis software have undergone significant development. The Physics Performance Report (PPR) will give an updated and comprehensive summary of the current status and performance of the various ALICE subsystems, including updates to the Technical Design Reports, where appropriate, as well as a description of systems which have not been published in a Technical Design Report. The PPR will be published in two volumes. The current Volume I contains: 1. a short theoretical overview and an extensive reference list concerning the physics topics of interest to ALICE, 2. relevant experimental conditions at the LHC, 3. a short summary and update of the subsystem designs, and 4. a description of the offline framework and Monte Carlo generators. Volume II, which will be published separately, will contain detailed simulations of combined detector performance, event reconstruction, and analysis of a representative sample of relevant physics observables from global event characteristics to hard processes

Geastrum minimum

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Geastrum melanocephalum

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Geastrum saccatum

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Myriostoma coliforme

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Geastrum fornicatum

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Geastrum rufescens

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