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Sökning: WFRF:(Relini A.)

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1.
  • Bolognesi, A., et al. (författare)
  • High photoluminescence efficiency in substituted polythiophene aggregates
  • 2003
  • Ingår i: Synthetic metals. - 0379-6779 .- 1879-3290. ; 139:2, s. 303-310
  • Tidskriftsartikel (refereegranskat)abstract
    • In this paper we discuss the optical (absorption and photoluminescence) and solvatochromic properties of a newly synthesized alternating copolymer based on poly(3-alkylthiophene) structure. In this copolymer an unsubstituted thiophene ring is linked to a 3-alkyl-substituted thiophene, the two repeating units being alternated in the copolymer chains. Moreover, a bulky group, THP, with high steric hindrance has been introduced in the side chain. This copolymer, designed to preserve the backbone planarity of polythiophenes and to prevent a close packing arrangement through the non-regioregular insertion of the bulky substituted monomer, shows high PL quantum yield in the solid state and in solution aggregates. The electroluminescence of this copolymer is reported for a simple single layer device. © 2003 Elsevier Science B.V. All rights reserved.
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2.
  • Valleix, Sophie, et al. (författare)
  • D25V apolipoprotein C-III variant causes dominant hereditary systemic amyloidosis and confers cardiovascular protective lipoprotein profile
  • 2016
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7
  • Tidskriftsartikel (refereegranskat)abstract
    • Apolipoprotein C-III deficiency provides cardiovascular protection, but apolipoprotein C-III is not known to be associated with human amyloidosis. Here we report a form of amyloidosis characterized by renal insufficiency caused by a new apolipoprotein C-III variant, D25V. Despite their uremic state, the D25V-carriers exhibit low triglyceride (TG) and apolipoprotein C-III levels, and low very-low-density lipoprotein (VLDL)/high high-density lipoprotein (HDL) profile. Amyloid fibrils comprise the D25V-variant only, showing that wild-type apolipoprotein C-III does not contribute to amyloid deposition in vivo. The mutation profoundly impacts helical structure stability of D25V-variant, which is remarkably fibrillogenic under physiological conditions in vitro producing typical amyloid fibrils in its lipid-free form. D25V apolipoprotein C-III is a new human amyloidogenic protein and the first conferring cardioprotection even in the unfavourable context of renal failure, extending the evidence for an important cardiovascular protective role of apolipoprotein C-III deficiency. Thus, fibrate therapy, which reduces hepatic APOC3 transcription, may delay amyloid deposition in affected patients.
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