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Search: WFRF:(Saurat D) > (2015-2019)

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1.
  • Lebacq, A L, et al. (author)
  • European intercomparison on the measurement of l-131 in thyroid of adults and children.
  • 2019
  • In: Radiation Measurements. - : Elsevier BV. - 1350-4487. ; 129
  • Journal article (peer-reviewed)abstract
    • In case of a nuclear reactor accident affecting a large population the internal contamination of the workers and the public can be assessed through in vivo measurements. Since iodine-131 is one of the most important releases and since it is of health concern, thyroid monitoring of this radionuclide is of special interest. Intercomparisons of thyroid in vivo measurements usually focus on the adult case. Here we report about a European intercomparison exercise for spectroscopic devices. Three sets of thyroid phantoms of unknown activity were circulated, representing the following ages: 5 years-old, 10 years-old and the adult. Nineteen institutions from twelve countries in Europe took part in an intercomparison exercise. Twenty-nine measurement devices have been tested. In the adult case, 5 results were outside the acceptance criteria and 10 in the 10-years old case. In the 5 years-old case, the result was not reported for one measurement device and 11 results were outside the acceptance criteria. Devices that have been tested during this intercomparison now dispose of calibration coefficients for the three age groups.
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2.
  • Moore, S., et al. (author)
  • APP Metabolism Regulates Tau Proteostasis in Human Cerebral Cortex Neurons
  • 2015
  • In: Cell Reports. - : Elsevier BV. - 2211-1247. ; 11:5, s. 689-696
  • Journal article (peer-reviewed)abstract
    • Accumulation of A beta peptide fragments of the APP protein and neurofibrillary tangles of the microtubule-associated protein tau are the cellular hallmarks of Alzheimer's disease (AD). To investigate the relationship between APP metabolism and tau protein levels and phosphorylation, we studied human-stem-cell-derived forebrain neurons with genetic forms of AD, all of which increase the release of pathogenic A beta peptides. We identified marked increases in intracellular tau in genetic forms of AD that either mutated APP or increased its dosage, suggesting that APP metabolism is coupled to changes in tau proteostasis. Manipulating APP metabolism by beta-secretase and gamma-secretase inhibition, as well as gamma-secretase modulation, results in specific increases and decreases in tau protein levels. These data demonstrate that APP metabolism regulates tau proteostasis and suggest that the relationship between APP processing and tau is not mediated solely through extracellular A beta signaling to neurons.
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