Mechanical properties and in vitro degradation behavior of additively manufactured phosphate glass particles/fibers reinforced polylactide

Phosphate glass/polylactide (PG/PLA) composites were additively manufactured via fused deposition modeling. The incorporation of 10 wt % PG particles improved the flexural modulus of composites by ~14% (3.53 GPa) but led to 5% reduction in flexural strength (92.4 MPa). The trend was more pronounced as the particle loading doubled. Comparing to a particulate composite of the same weight fraction, milled PG fibers (PGFs) reinforcement led to more effectively improved flexural modulus (~30%, 4.10 GPa). After 28 days of in vitro degradation in phosphate buffered saline, the particulate composites lost more than 30% of their initial mechanical properties, in contrast to less than 10% reduction of strength/modulus reported from fiber reinforced composites. The additively manufactured PG/PLA matrix composites have potential for application as customized bone fixation plates to repair the fractures under modest load‐bearing applications. © 2019 The Authors. Journal of Applied Polymer Science published by Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2019, 136, 48171

Rentabilitätsvergleiche im Umlage- und Kapitaldeckungsverfahren : Konzepte, empirische Ergebnisse, sozialpolitische Konsequenzen

Die demographischen Veränderungen sind Auslöser einer grundsätzlicheren Debatte über Alterssicherungsverfahren, nämlich der Wahl eines effizienten Finanzierungsverfahrens der Altersvorsorge. Im Zentrum der Debatte steht immer wieder der Renditevergleich zwischen dem Umlage- und dem Kapitaldeckungsverfahren. Ihm gilt dieses Papier. Er ist keineswegs so einfach, wie es oft suggeriert wird, da Versicherungs- und Risikoaspekte, vor allem aber das Übergangsproblem berücksichtigt werden müssen. Der vorliegende Beitrag stellt den wirtschaftstheoretischen Hintergrund mit den wichtigsten relevanten Konzepten dar und präsentiert empirische Schätzungen zur heutigen und Simulationsergebnisse zur zukünftigen Entwicklung der relevanten Renditen. Wir schließen mit den sozialpolitischen Konsequenzen für eine reformierte Altersvorsorge

The proteoglycan osteoglycin/mimecan is correlated with arteriogenesis

Arteriogenesis or collateral growth is able to compensate for the stenosis of major arteries. Using differential display RT-PCR on growing and quiescent collateral arteries in a rabbit femoral artery ligation model, we cloned the rabbit full-length cDNA of osteoglycin/mimecan. Osteoglycin was present in the adventitia of collateral arteries as a glycosylated protein without keratan sulfate side chains, mainly produced by smooth muscle cells (SMCs) and perivascular fibroblasts. Northern blot, Western blot, and immunohistochemistry confirmed a collateral artery-specific downregulation of osteoglycin from 6 h to 3 weeks after the onset of arteriogenesis. Treatment of primary SMCs with the arteriogenic protein fibroblast growth factor-2 (FGF-2) resulted in a similar reduction of osteoglycin expression as observed in vivo. Application of the FGF-2 inhibitor polyanethole sulfonic acid (PAS) blocked the downregulation of osteoglycin and interfered with arteriogenesis. From our study we conclude that downregulation of osteoglycin is a fundamental requirement for proper arteriogenesis

The range of adaptation by collateral vessels after femoral artery occlusion

Natural adaptation to femoral artery occlusion in animals by collateral artery growth restores only approximately 35% of adenosine-recruitable maximal conductance (C(max)) probably because initially elevated fluid shear stress (FSS) quickly normalizes. We tested the hypothesis whether this deficit can be mended by artificially increasing FSS or whether anatomical restraints prevent complete restitution. We chronically increased FSS by draining the collateral flow directly into the venous system by a side-to-side anastomosis between the distal stump of the occluded femoral artery and the accompanying vein. After reclosure of the shunt collateral flow was measured at maximal vasodilatation. C(max) reached 100% already at day 7 and had, after 4 weeks, surpassed (2-fold) the C(max) of the normal vasculature before occlusion. Expression profiling showed upregulation of members of the Rho-pathway (RhoA, cofilin, focal adhesion kinase, vimentin) and the Rho-antagonist Fasudil markedly inhibited arteriogenesis. The activities of Ras and ERK-1,-2 were markedly increased in collateral vessels of the shunt experiment, and infusions of L-NAME and L-NNA strongly inhibited MAPK activity as well as shunt-induced arteriogenesis. Infusions of the peroxinitrite donor Sin-1 inhibited arteriogenesis. The radical scavengers urate, ebselen, SOD, and catalase had no effect. We conclude that increased FSS can overcome the anatomical restrictions of collateral arteries and is potentially able to completely restore maximal collateral conductance. Increased FSS activates the Ras-ERK-, the Rho-, and the NO- (but not the Akt-) pathway enabling collateral artery growt