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Träfflista för sökning "WFRF:(Keskin M) srt2:(2011-2014)"

Search: WFRF:(Keskin M) > (2011-2014)

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1.
  • Keskin, U., et al. (author)
  • An engineering approach to synchronization based on overrun for compositional real-time systems
  • 2011
  • In: SIES 2011 - 6th IEEE International Symposium on Industrial Embedded Systems, Conference Proceedings. - 9781612848204 ; , s. 274-283
  • Conference paper (peer-reviewed)abstract
    • Hierarchical scheduling frameworks (HSFs) provide means for composing complex real-time systems from well-defined independently developed and analyzed subsystems. To support shared logical resources requiring mutual exclusive access in two-level HSFs, overrun without payback has been proposed as a mechanism to prevent budget depletion during resource access arbitrated by the stack resource policy (SRP). In this paper, we revisit the global schedulability analysis of synchronization protocols based on SRP and overrun without payback for fixed-priority scheduled HSFs. We derive a new global schedulability analysis based on the observation that the overrun budget is merely meant to prevent budget depletion during global resource access. The deadline of a subsystem therefore only needs to hold for its normal budget rather than the sum of the normal and overrun budget. Our novel analysis is considerably simpler than an earlier, initially improved analysis, which improved both the original local and global schedulability analyses. We evaluate the new analysis based on an extensive simulation study and compare the results with the existing analysis. Our simplified analysis does not significantly affect schedulability compared to the initially improved analysis. It is therefore proposed as a preferable engineering approach to synchronization protocols for compositional real-time systems. We accordingly present the implementation of our improvement in an OSEK-compliant real-time operating system to sketch its applicability in today's industrial automotive standards. Both implementation and run-time overheads are discussed providing measured results1. © 2011 IEEE.
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3.
  • Piwowar, A. M., et al. (author)
  • C60-ToF SIMS imaging of frozen hydrated HeLa cells
  • 2013
  • In: Surface and Interface Analysis. - : Wiley. - 0142-2421 .- 1096-9918. ; 45:1, s. 302-304
  • Journal article (peer-reviewed)abstract
    • Sample preparation continues to be a major challenge for SIMS studies of biological materials. Maintaining the native hydrated state of the material is important for preserving both chemical and spatial information. Here, we discuss a method that combines a sample wash and dry protocol followed by plunge-freezing in liquid ethane for a frozen-hydrated analysis of mammalian cells (HeLa). This method allows for the removal of the growth medium and maintains the hydrated state of the cells so that they can be prepared frozen-hydrated without the need for a freeze-fracture device. The cells, which were grown on silicon, were successfully regrown after the cleaning procedure, confirming that a significant portion of the cells remain undamaged during the wash and dry procedure. Results from preliminary SIMS measurements show that is it possible to detect a large variety of biomolecular signals, including intact lipids from the plasma membrane in the mass range of 700–900Da from single cells, with little external water interference at the surface.
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4.
  • Synofzik, M., et al. (author)
  • Mutant superoxide dismutase-1 indistinguishable from wild-type causes ALS
  • 2012
  • In: Human Molecular Genetics. - : Oxford University Press (OUP): Policy B - Oxford Open Option B. - 0964-6906 .- 1460-2083. ; 21:16, s. 3568-3574
  • Journal article (peer-reviewed)abstract
    • A reason for screening amyotrophic lateral sclerosis (ALS) patients for mutations in the superoxide dismutase-1 (SOD1) gene is the opportunity to find novel mutations with properties that can give information on pathogenesis. A novel c.352Cgreater thanG (L117V) SOD1 mutation was found in two Syrian ALS families living in Europe. The disease showed unusually low penetrance and slow progression. In erythrocytes, the total SOD1 activity, as well as specific activity of the mutant protein, was equal in carriers of the mutation and family controls lacking SOD1 mutations. The structural stabilities of the L117V mutant and wild-type SOD1 under denaturing conditions were likewise equal, but considerably lower than that of murine SOD1. As analyzed with an ELISA specific for misfolded SOD1 species, no differences were found in the content of misfolded SOD1 protein between extracts of fibroblasts from wild-type controls and from an L117V patient. In contrast, elevated levels of misfolded SOD1 protein were found in fibroblasts from ALS patients carrying seven other mutations in the SOD1 gene. We conclude that mutations in SOD1 that result in a fully stable protein are associated with low disease penetrance for ALS and may be found in cases of apparently sporadic ALS. Wild-type human SOD1 is moderately stable, and was found here to be within the stability range of ALS-causing SOD1 variants, lending support to the hypothesis that wild-type SOD1 could be more generally involved in ALS pathogenesis.
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