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Sökning: WFRF:(Cairns Nigel) > (2020-2024)

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1.
  • Cairns, Mathew J., et al. (författare)
  • Tetraethylorthosilicate-containing barrier dispersion coatings-Mechanism of action
  • 2020
  • Ingår i: Progress in organic coatings. - : Elsevier. - 0300-9440 .- 1873-331X. ; 139
  • Tidskriftsartikel (refereegranskat)abstract
    • We demonstrate the use of tetraethylorthosilicate (TEOS) as a silica precursor for water barrier poly(styrenebutadiene) latex dispersion coating applications. The TEOS is adsorbed at the surface interface by the latex particles in the aqueous dispersion due to the hydrophobic nature of the surface and the TEOS. It then undergoes hydrolysis and condensation to the silica phase in the interstitial sites in the partially dry close-packed polymer structure. The fully cured film exhibits a greater degree of coalescence than films prepared from the unmodified latex binder. Large discrete silica particles are not formed within the cured film; rather the films contain homogenous silica dispersion with a probable particle size no larger than 10 nm. This higher degree of coalescence results in improvements in water vapour barrier performance from 121 - 20 g m(-2) d(-1), with direct water barrier performance (Cobb 120 s) improving from 25 to < 2 g m(-2), compared to the silica-free film.
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2.
  • Levin, Johannes, et al. (författare)
  • α-Synuclein seed amplification assay detects Lewy body co-pathology in autosomal dominant Alzheimer's disease late in the disease course and dependent on Lewy pathology burden
  • 2024
  • Ingår i: Alzheimer's and Dementia. - 1552-5260. ; 20:6, s. 4351-4365
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: Amyloid beta and tau pathology are the hallmarks of sporadic Alzheimer's disease (AD) and autosomal dominant AD (ADAD). However, Lewy body pathology (LBP) is found in ≈ 50% of AD and ADAD brains. METHODS: Using an α-synuclein seed amplification assay (SAA) in cerebrospinal fluid (CSF) from asymptomatic (n = 26) and symptomatic (n = 27) ADAD mutation carriers, including 12 with known neuropathology, we investigated the timing of occurrence and prevalence of SAA positive reactivity in ADAD in vivo. RESULTS: No asymptomatic participant and only 11% (3/27) of the symptomatic patients tested SAA positive. Neuropathology revealed LBP in 10/12 cases, primarily affecting the amygdala or the olfactory areas. In the latter group, only the individual with diffuse LBP reaching the neocortex showed α-synuclein seeding activity in CSF in vivo. DISCUSSION: Results suggest that in ADAD LBP occurs later than AD pathology and often as amygdala- or olfactory-predominant LBP, for which CSF α-synuclein SAA has low sensitivity. Highlights: Cerebrospinal fluid (CSF) real-time quaking-induced conversion (RT-QuIC) detects misfolded α-synuclein in ≈ 10% of symptomatic autosomal dominant Alzheimer's disease (ADAD) patients. CSF RT-QuIC does not detect α-synuclein seeding activity in asymptomatic mutation carriers. Lewy body pathology (LBP) in ADAD mainly occurs as olfactory only or amygdala-predominant variants. LBP develops late in the disease course in ADAD. CSF α-synuclein RT-QuIC has low sensitivity for focal, low-burden LBP.
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