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Search: WFRF:(Sideris I)

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  • Anastasiadis, Nikolaos, et al. (author)
  • A fast multiplier-less edge detection accelerator for FPGAs
  • 2010
  • In: SAC '10 Proceedings of the 2010 ACM Symposium on Applied Computing. - New York, NY, USA : ACM. - 9781605586380 ; , s. 510-515
  • Conference paper (peer-reviewed)abstract
    • Real time video is used in a wide variety of applications, ranging from video surveillance to medical imaging. These operations require significant amounts of processing power, especially when high resolution frames are used. A large percentage of processing time is used in edge detection kernels. Thus, accelerating these kernels is of vital importance in achieving satisfactory frame rates for real time performance, even in high resolutions. This paper proposes a hardware coprocessor to the Xilinx Microblaze processor which accelerates edge detection significantly, while keeping the hardware requirements low, by using no multipliers at all. Using a Xilinx Spartan 3E FPGA, we have reported a frame rate of 157 frames per second in 4CIF format, which corresponds to a 4x speedup over the software only solution. The speedup was achieved with only 1131 slices and 5 block RAMs hardware occupation, which makes the solution very attractable.
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3.
  • De, S., et al. (author)
  • Soluble aggregates present in cerebrospinal fluid change in size and mechanism of toxicity during Alzheimer's disease progression
  • 2019
  • In: Acta Neuropathologica Communications. - : Springer Science and Business Media LLC. - 2051-5960. ; 7
  • Journal article (peer-reviewed)abstract
    • Soluble aggregates of amyloid-beta (A beta) have been associated with neuronal and synaptic loss in Alzheimer's disease (AD). However, despite significant recent progress, the mechanisms by which these aggregated species contribute to disease progression are not fully determined. As the analysis of human cerebrospinal fluid (CSF) provides an accessible window into the molecular changes associated with the disease progression, we characterised soluble aggregates present in CSF samples from individuals with AD, mild cognitive impairment (MCI) and healthy controls using a range of sensitive biophysical methods. We used super-resolution imaging and atomic force microscopy to characterise the size and structure of the aggregates present in CSF and correlate this with their ability to permeabilise lipid membranes and induce an inflammatory response. We found that these aggregates are extremely heterogeneous and exist in a range of sizes, varying both structurally and in their mechanisms of toxicity during the disease progression. A higher proportion of small aggregates of A beta that can cause membrane permeabilization are found in MCI CSF; in established AD, a higher proportion of the aggregates were larger and more prone to elicit a pro-inflammatory response in glial cells, while there was no detectable change in aggregate concentration. These results show that large aggregates, some longer than 100nm, are present in the CSF of AD patients and suggest that different neurotoxic mechanisms are prevalent at different stages of AD.
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