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Träfflista för sökning "WFRF:(Mayer E.) srt2:(2005-2009)"

Sökning: WFRF:(Mayer E.) > (2005-2009)

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2.
  • Aamodt, K., et al. (författare)
  • The ALICE experiment at the CERN LHC
  • 2008
  • Ingår i: Journal of Instrumentation. - 1748-0221. ; 3:S08002
  • Forskningsöversikt (refereegranskat)abstract
    • ALICE (A Large Ion Collider Experiment) is a general-purpose, heavy-ion detector at the CERN LHC which focuses on QCD, the strong-interaction sector of the Standard Model. It is designed to address the physics of strongly interacting matter and the quark-gluon plasma at extreme values of energy density and temperature in nucleus-nucleus collisions. Besides running with Pb ions, the physics programme includes collisions with lighter ions, lower energy running and dedicated proton-nucleus runs. ALICE will also take data with proton beams at the top LHC energy to collect reference data for the heavy-ion programme and to address several QCD topics for which ALICE is complementary to the other LHC detectors. The ALICE detector has been built by a collaboration including currently over 1000 physicists and engineers from 105 Institutes in 30 countries, Its overall dimensions are 16 x 16 x 26 m(3) with a total weight of approximately 10 000 t. The experiment consists of 18 different detector systems each with its own specific technology choice and design constraints, driven both by the physics requirements and the experimental conditions expected at LHC. The most stringent design constraint is to cope with the extreme particle multiplicity anticipated in central Pb-Pb collisions. The different subsystems were optimized to provide high-momentum resolution as well as excellent Particle Identification (PID) over a broad range in momentum, up to the highest multiplicities predicted for LHC. This will allow for comprehensive studies of hadrons, electrons, muons, and photons produced in the collision of heavy nuclei. Most detector systems are scheduled to be installed and ready for data taking by mid-2008 when the LHC is scheduled to start operation, with the exception of parts of the Photon Spectrometer (PHOS), Transition Radiation Detector (TRD) and Electro Magnetic Calorimeter (EMCal). These detectors will be completed for the high-luminosity ion run expected in 2010. This paper describes in detail the detector components as installed for the first data taking in the summer of 2008.
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3.
  • Aumailley, M, et al. (författare)
  • A simplified laminin nomenclature
  • 2005
  • Ingår i: Matrix Biology. - : Elsevier BV. - 1569-1802 .- 0945-053X. ; 24:5, s. 326-332
  • Forskningsöversikt (refereegranskat)abstract
    • A simplification of the laminin nomenclature is presented. Laminins are multidomain heterotrimers composed of alpha, beta and gamma chains. Previously, laminin trimers were numbered with Arabic numerals in the order discovered, that is laminins-1 to -5. We introduce a new identification system for a trimer using three Arabic numerals, based on the alpha, beta and gamma chain numbers. For example, the laminin with the chain composition alpha 5 beta 1 gamma 1 is termed laminin-511, and not laminin-10. The current practice is also to mix two overlapping domain and module nomenclatures. Instead of the older Roman numeral nomenclature and mixed nomenclature, all modules are now called domains. Some domains are renamed or renumbered. Laminin epidermal growth factor-like (LE) domains are renumbered starting at the N-termini, to be consistent with general protein nomenclature. Domain IVb of alpha chains is named laminin 4a (L4a), domain IVa of alpha chains is named L4b, domain IV of gamma chains is named L4, and domain IV of beta chains is named laminin four (LF). The two coiled-coil domains I and II are now considered one laminin coiled-coil domain (LCC). The interruption in the coiled-coil of 13 chains is named laminin beta-knob (L beta) domain. The chain origin of a domain is specified by the chain nomenclature, such as alpha IL4a. The abbreviation LM is suggested for laminin. Otherwise, the nomenclature remains unaltered.
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4.
  • Coad, J. P., et al. (författare)
  • Erosion and deposition in the JET MkII-SRP divertor
  • 2007
  • Ingår i: Journal of Nuclear Materials. - : Elsevier BV. - 0022-3115 .- 1873-4820. ; 363, s. 287-293
  • Tidskriftsartikel (refereegranskat)abstract
    • Carbon-13 labelled methane was injected into the outer divertor during a series of H-mode discharges on the last day of operations with the JET MkII-SRP divertor. Tiles from around the vessel were removed during the subsequent shutdown and surface deposits were analysed by IBA techniques and SIMS. First attempts to model the pattern of 13 C deposition using EDGE2D are reported. Erosion of W markers at the outer divertor was observed, with implications for the ITER-like wall experiment planned for JET, whilst thin film growth in the same region has been followed by the effect on infrared measurements. The composition of thick films deposited at the inner divertor during the MkII-SRP campaign, and the migration to the inner corner of the divertor observed by a quartz micro-balance, provide further information on divertor transport. Crown
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6.
  • Kamm, C, et al. (författare)
  • The fragile X tremor ataxia syndrome in the differential diagnosis of multiple system atrophy: data from the EMSA Study Group
  • 2005
  • Ingår i: Brain. - : Oxford University Press (OUP). - 1460-2156 .- 0006-8950. ; 128:8, s. 1855-1860
  • Tidskriftsartikel (refereegranskat)abstract
    • The recent identification of fragile X-associated tremor ataxia syndrome (FXTAS) associated with premutations in the FMR1 gene and the possibility of clinical overlap with multiple system atrophy (MSA) has raised important questions, such as whether genetic testing for FXTAS should be performed routinely in MSA and whether positive cases might affect the specificity of current MSA diagnostic criteria. We genotyped 507 patients with clinically diagnosed or pathologically proven MSA for FMR1 repeat length. Among the 426 clinically diagnosed cases, we identified four patients carrying FMR1 premutations (0.94%). Within the subgroup of patients with probable MSA-C, three of 76 patients (3.95%) carried premutations. We identified no premutation carriers among 81 patients with pathologically proven MSA and only one carrier among 622 controls (0.16%). Our results suggest that, with proper application of current diagnostic criteria, FXTAS is very unlikely to be confused with MSA. However, slowly progressive disease or predominant tremor are useful red flags and should prompt the consideration of FXTAS. On the basis of our data, the EMSA Study Group does not recommend routine FMR1 genotyping in typical MSA patients.
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7.
  • Aguilar, Maria I., et al. (författare)
  • Treatment of warfarin-associated intracerebral hemorrhage: Literature review and expert opinion
  • 2007
  • Ingår i: Mayo Clinic Proceedings. - 0025-6196. ; 82:1, s. 82-92
  • Forskningsöversikt (refereegranskat)abstract
    • Wider use of oral anticoagulants has led to an increasing frequency of warfarin-related intracerebral hemorrhage (ICH). The high early mortality of approximately 50% has remained stable in recent decades. In contrast to spontaneous ICH, the duration of bleeding is, 12 to 24 hours in many patients, offering a longer opportunity for Intervention. Treatment varies widely, and optimal therapy has yet to be defined. An OVID search was conducted from January 1996 to January 2006, combining the terms warfarin or anticoagulation with intracranial hemorrhage or intracerebral hemorrhage. Seven experts on clinical stroke, neurologic intensive care, and hematology were provided with the available information and were asked to independently address 3 clinical scenarios about acute reversal and resumption of anticoagulation in the setting of warfarin-associated ICH. No randomized trials assessing clinical outcomes were found on management of warfarin-associated ICH. All experts agreed that anticoagulation should be urgently reversed, but how to achieve it varied from use of prothrombin complex concentrates only (3 experts) to recombinant factor Vila only (2 experts) to recombinant factor Vila along with fresh frozen plasma (1 expert) and prothrombin complex concentrates or fresh frozen plasma (1 expert). All experts favored resumption of warfarin therapy within 3 to 10 days of ICH in stable patients in whom subsequent anticoagulation is mandatory. No general agreement occurred regarding subsequent anticoagulation of patients with atrial fibrillation who survived warfarin-associated ICH. For warfarin-associated ICH, discontinuing warfarin therapy with administration of vitamin K does not reverse the hemostatic defect for many hours and is inadequate. Reasonable management based on expert opinion includes a wide range of additional measures to reverse anticoagulation in the absence of solid evidence.
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8.
  • Eisenacher, Martin, et al. (författare)
  • Proteomics Data Collection - 2nd ProDaC Workshop 5 October 2007, Seoul, Korea
  • 2008
  • Ingår i: Proteomics. - : Wiley. - 1615-9861 .- 1615-9853. ; 8:7, s. 1326-1330
  • Tidskriftsartikel (refereegranskat)abstract
    • Proteomics Data Collection (ProDaC) is an EU-funded Coordination Action within the 6th framework programme. It aims to simplify the publication, dissemination and utilization of proteomics data by establishing standards that will support broad data collection from the research community. As a part of ProDaC, regular workshops are organized on a half-yearly basis to enable communication and discussion of the involved partners and to report on project progress. After the kick-off meeting (October 2006) in Long Beach, CA, USA and the 1st workshop in Lyon, France (April 2007), the 2nd ProDaC workshop took place at the COEX InterContinental Hotel in Seoul, Korea, on 5th October 2007, shortly before the HUPO World Congress. The progress achieved within the first year was presented by the leaders of the work packages. Additionally, a Journal's representative talked about his experiences and future plans concerning Proteomics standards; and two further external speakers presented their research related to data handling and Proteomics repositories.
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10.
  • Fellström, Bengt, et al. (författare)
  • Rosuvastatin and cardiovascular events in patients undergoing hemodialysis.
  • 2009
  • Ingår i: The New England journal of medicine. - 1533-4406 .- 0028-4793. ; 360:14, s. 1395-407
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Statins reduce the incidence of cardiovascular events in patients at high cardiovascular risk. However, a benefit of statins in such patients who are undergoing hemodialysis has not been proved. METHODS: We conducted an international, multicenter, randomized, double-blind, prospective trial involving 2776 patients, 50 to 80 years of age, who were undergoing maintenance hemodialysis. We randomly assigned patients to receive rosuvastatin, 10 mg daily, or placebo. The combined primary end point was death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke. Secondary end points included death from all causes and individual cardiac and vascular events. RESULTS: After 3 months, the mean reduction in low-density lipoprotein (LDL) cholesterol levels was 43% in patients receiving rosuvastatin, from a mean baseline level of 100 mg per deciliter (2.6 mmol per liter). During a median follow-up period of 3.8 years, 396 patients in the rosuvastatin group and 408 patients in the placebo group reached the primary end point (9.2 and 9.5 events per 100 patient-years, respectively; hazard ratio for the combined end point in the rosuvastatin group vs. the placebo group, 0.96; 95% confidence interval [CI], 0.84 to 1.11; P=0.59). Rosuvastatin had no effect on individual components of the primary end point. There was also no significant effect on all-cause mortality (13.5 vs. 14.0 events per 100 patient-years; hazard ratio, 0.96; 95% CI, 0.86 to 1.07; P=0.51). CONCLUSIONS: In patients undergoing hemodialysis, the initiation of treatment with rosuvastatin lowered the LDL cholesterol level but had no significant effect on the composite primary end point of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke. (ClinicalTrials.gov number, NCT00240331.)
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