Actuariële bedenkingen bij een eenvormig opgelegd bonus-malus stelsel.

Verscheidene actoren van het verzekeringswezen dringen sterk aan om het verplicht eenvormig bonus-malus stelsel in de verzekering B.A.-auto te behouden. In deze nota wordt aan de hand van een theoretisch voorbeeld aangetoond dat dit standpunt vanuit actuariëel oogpunt onhoudbaar is.

Actuariële bedenkingen bij een eenvormig opgelegd bonus-malus stelsel

Verscheidene actoren van het verzekeringswezen dringen sterk aan om het verplicht eenvormig bonus-malus stelsel in de verzekering B.A.-auto te behouden. In deze nota wordt aan de hand van een theoretisch voorbeeld aangetoond dat dit standpunt vanuit actuariëel oogpunt onhoudbaar is.status: publishe

Lysyl oxidase‐like 2 is a regulator of angiogenesis through modulation of endothelial‐to‐mesenchymal transition

Lysyl oxidase‐like 2 (LOXL2) belongs to the family of lysyl oxidases, and as such promotes crosslinking of collagens and elastin by oxidative deamination of lysine residues. In endothelial cells (ECs), LOXL2 is involved in crosslinking and scaffolding of collagen IV. Additionally, several reports have shown a role for LOXL2 in other processes, including regulation of gene expression, tumor metastasis, and epithelial‐to‐mesenchymal transition (EMT). Here, we demonstrate an additional role for LOXL2 in the regulation of angiogenesis by modulation of endothelial‐to‐mesenchymal transition (EndMT). LOXL2 knockdown in ECs results in decreased migration and sprouting, and concordantly, LOXL2 overexpression leads to an increase in migration and sprouting, independent of its catalytic activity. Furthermore, LOXL2 knockdown resulted in a reduced expression of EndMT markers, and inhibition of transforming growth factor‐β (TGF‐β)‐mediated induction of EndMT. Interestingly, unlike in EMT, overexpression of LOXL2 alone is insufficient to induce EndMT. Further investigation revealed that LOXL2 expression regulates protein kinase B (PKB)/Akt and focal adhesion kinase (FAK) signaling, both pathways that have been implicated in the regulation of EMT. Altogether, our studies reveal a role for LOXL2 in angiogenesis through the modulation of EndMT in ECs, independent of its enzymatic crosslinking activity

Lysyl oxidase‐like 2 is a regulator of angiogenesis through modulation of endothelial‐to‐mesenchymal transition

Lysyl oxidase‐like 2 (LOXL2) belongs to the family of lysyl oxidases, and as such promotes crosslinking of collagens and elastin by oxidative deamination of lysine residues. In endothelial cells (ECs), LOXL2 is involved in crosslinking and scaffolding of collagen IV. Additionally, several reports have shown a role for LOXL2 in other processes, including regulation of gene expression, tumor metastasis, and epithelial‐to‐mesenchymal transition (EMT). Here, we demonstrate an additional role for LOXL2 in the regulation of angiogenesis by modulation of endothelial‐to‐mesenchymal transition (EndMT). LOXL2 knockdown in ECs results in decreased migration and sprouting, and concordantly, LOXL2 overexpression leads to an increase in migration and sprouting, independent of its catalytic activity. Furthermore, LOXL2 knockdown resulted in a reduced expression of EndMT markers, and inhibition of transforming growth factor‐β (TGF‐β)‐mediated induction of EndMT. Interestingly, unlike in EMT, overexpression of LOXL2 alone is insufficient to induce EndMT. Further investigation revealed that LOXL2 expression regulates protein kinase B (PKB)/Akt and focal adhesion kinase (FAK) signaling, both pathways that have been implicated in the regulation of EMT. Altogether, our studies reveal a role for LOXL2 in angiogenesis through the modulation of EndMT in ECs, independent of its enzymatic crosslinking activity

Enhancement of coercivity and saturation magnetization of Al3+ substituted M-type Sr-hexaferrites

Hexagonal SrFe12-xAlxO19 (x = 0, 0.2, 1, 2, 4) powders were prepared via mechanochemical activation and subsequently calcined at different temperatures (between 900 °C and 1300 °C). Afterwards the powders were milled by high energy milling and annealed at 1000 °C in NaCl to obtain ultrafine nano-particles. The particle size, measured by scanning electron microscopy (SEM), varied between 50 nm and few micrometers depending on Al3+ substitution and calcination temperature. Average crystallite size, determined by X-ray diffraction (XRD), decreases from 330 nm ± 30 nm (x = 0) to 70 nm ± 10 nm (x = 4) by substitution of Fe3+ by Al3+ for optimized calcination temperature of 1100 °C. Furthermore coercivity measured by SQUID magnetometry increases from 420 kA/m (x = 0) to 970 kA/m (x = 4). A maximum saturation magnetization of 74 Am2/kg (x = 0) was observed. With substitution of Fe3+ by Al3+ saturation magnetization decreases monotonously to 28 Am2/kg (x = 4). Annealing in NaCl matrix at lower temperatures compared to calcination temperatures leads to a further increase of coercivity. At the same time saturation magnetization increases for SrFe12-xAlxO19 (x = 0, 1) by NaCl annealing treatment. Additionally, we discuss the initial magnetization curves of SrFe12O19 and SrFe8Al4O19 after different processing steps with respect to the specific reversal mechanism of hexaferrites. The here proposed processing route enables a simultaneous enhancement of coercivity and saturation magnetization as compared to conventional ceramic method [1] and [2]. The presented processing route can solve challenges of conventional manufacturing steps towards single domain grains in rare earth free SrFe12-xAlxO19 for higher coercivity and could enable an improved industrial production process

Lysyl oxidase‐like 2 is a regulator of angiogenesis through modulation of endothelial‐to‐mesenchymal transition

Lysyl oxidase-like 2 (LOXL2) belongs to the family of lysyl oxidases, and as such promotes crosslinking of collagens and elastin by oxidative deamination of lysine residues. In endothelial cells (ECs), LOXL2 is involved in crosslinking and scaffolding of collagen IV. Additionally, several reports have shown a role for LOXL2 in other processes, including regulation of gene expression, tumor metastasis, and epithelial-to-mesenchymal transition (EMT). Here, we demonstrate an additional role for LOXL2 in the regulation of angiogenesis by modulation of endothelial-to-mesenchymal transition (EndMT). LOXL2 knockdown in ECs results in decreased migration and sprouting, and concordantly, LOXL2 overexpression leads to an increase in migration and sprouting, independent of its catalytic activity. Furthermore, LOXL2 knockdown resulted in a reduced expression of EndMT markers, and inhibition of transforming growth factor-β (TGF-β)-mediated induction of EndMT. Interestingly, unlike in EMT, overexpression of LOXL2 alone is insufficient to induce EndMT. Further investigation revealed that LOXL2 expression regulates protein kinase B (PKB)/Akt and focal adhesion kinase (FAK) signaling, both pathways that have been implicated in the regulation of EMT. Altogether, our studies reveal a role for LOXL2 in angiogenesis through the modulation of EndMT in ECs, independent of its enzymatic crosslinking activity

Self-Healing Glassy Thin Coating for High-Temperature Applications

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