150 research outputs found
From state to market revisited: more empirical evidence on the efficiency of public (and privately-owned) enterprises
For several decades public enterprises have been criticised for their poor economic performance. Many economists take it as “conventional wisdom” that publicly owned enterprises are inefficient by their very nature. This seemed to be proved by what is probably the most cited survey worldwide, that was written by Megginson and Netter (2001). They claim: “Research now supports the proposition that privately owned firms are more efficient and more profitable than otherwise-comparable state-owned firms” (p. 380). The objective of this paper is to question the proposition that public enterprises are necessarily less efficient as their private counterparts. In doing so, we argue that profits are not a reasonable performance measure for public enterprises. However, our main focus is to present a much more comprehensive review of the empirical evidence than was provided by Megginson and Netter. The evidence indicates that these authors’ conclusions were biased in favour of privatization despite the evidence indicating that the true picture is much more differentiated
From state to market revisited: more empirical evidence on the efficiency of public (and privately-owned) enterprises
For several decades public enterprises have been criticised for their poor economic performance. Many economists take it as “conventional wisdom” that publicly owned enterprises are inefficient by their very nature. This seemed to be proved by what is probably the most cited survey worldwide, that was written by Megginson and Netter (2001). They claim: “Research now supports the proposition that privately owned firms are more efficient and more profitable than otherwise-comparable state-owned firms” (p. 380). The objective of this paper is to question the proposition that public enterprises are necessarily less efficient as their private counterparts. In doing so, we argue that profits are not a reasonable performance measure for public enterprises. However, our main focus is to present a much more comprehensive review of the empirical evidence than was provided by Megginson and Netter. The evidence indicates that these authors’ conclusions were biased in favour of privatization despite the evidence indicating that the true picture is much more differentiated
Grundsätze und (best-)mögliche Ansätze zur Bewertung des Vermögens von öffentlichen Gebietskörperschaften
Was Sie schon immer über Public Private Partnerships wissen wollten… Vorstellung des Projektverbunds "Public Private Partnership" des Deutschen Forschungsinstituts für öffentliche Verwaltung
Der vorliegende Beitrag skizziert, nach einem Überblick über die mit der Einführung von Public Private Partnerships verbundenen Herausforderungen, den interdisziplinären Projektverbund "Public Private Partnership" des Deutschen Forschungsinstituts für öffentliche Verwaltung. Ziel des Verbunds ist es, Forschungslücken zu schließen, belastbare Daten zu PPPs in Deutschland zu generieren und ein besseres Verständnis für die institutionellen Rahmenbedingungen und Akteure zu gewinnen, die über das Zustandekommen oder Nicht-Zustandekommen von PPPs in Deutschland entscheiden.The following article, after addressing current challenges related to the successful introduction of public- private partnerships, summarizes the research agenda of the interdisciplinary project group on "public-private partnership" at the German Research. Institute for Public Administration. The overall research goal of the project group is to close research gaps in the context of public-private partnerships, to gather reliable data on public-private partnerships in Germany and to gain a better understanding of the institutional framework and of how actors decide about the establishment or rejection of public-private partnerships in Germany
Catching a SPY: using the SpyCatcher-SpyTag and related systems for labeling and localizing bacterial proteins
The SpyCatcher-SpyTag system was developed seven years ago as a method for protein ligation. It is based on a modified domain from a Streptococcus pyogenes surface protein (SpyCatcher), which recognizes a cognate 13-amino-acid peptide (SpyTag). Upon recognition, the two form a covalent isopeptide bond between the side chains of a lysine in SpyCatcher and an aspartate in SpyTag. This technology has been used, among other applications, to create covalently stabilized multi-protein complexes, for modular vaccine production, and to label proteins (e.g., for microscopy). The SpyTag system is versatile as the tag is a short, unfolded peptide that can be genetically fused to exposed positions in target proteins; similarly, SpyCatcher can be fused to reporter proteins such as GFP, and to epitope or purification tags. Additionally, an orthogonal system called SnoopTag-SnoopCatcher has been developed from an S. pneumoniae pilin that can be combined with SpyCatcher-SpyTag to produce protein fusions with multiple components. Furthermore, tripartite applications have been produced from both systems allowing the fusion of two peptides by a separate, catalytically active protein unit, SpyLigase or SnoopLigase. Here, we review the current state of the SpyCatcher-SpyTag and related technologies, with a particular emphasis on their use in vaccine development and in determining outer membrane protein localization and topology of surface proteins in bacteria
Yersinia enterocolitica exploits different pathways to accomplish adhesion and toxin injection into host cells.
The current paradigm suggests that Yersinia enterocolitica (Ye) adheres to host cells via the outer membrane proteins Yersinia adhesin A (YadA) or invasin (Inv) to facilitate injection of Yops by the type III secretion system. In this process Inv binds directly to β1 integrins of host cells while YadA may bind indirectly via extracellular matrix proteins to β1 integrins. Here we challenged this paradigm and investigated the requirements for Yop injection. We demonstrate that Inv- but not YadA-mediated adhesion depends on β1 integrin binding and activation, and that tight adhesion is a prerequisite for Yop injection. By means of novel transgenic cell lines, shRNA approaches and RGD peptides, we found that YadA, in contrast to Inv, may use a broad host cell receptor repertoire for host cell adhesion. In the absence of β1 integrins, YadA mediates Yop injection by interaction with αV integrins in cooperation with yet unknown cofactors expressed by epithelial cells, but not fibroblasts. Electron microscopic and flow chamber studies revealed that a defined intimate contact area between Ye and host cells resulting in adhesion forces resisting shear stress is required for Yop injection. Thus, the indirect binding of YadA to a broad extracellular matrix (ECM) binding host cell receptor repertoire of different cell types makes YadA a versatile tool to ensure Yop injection. In conclusion, given the differential expression of the outer membrane proteins Inv and YadA in the course of Ye infection and differential expression of integrins by various host cell populations, the data demonstrate that Ye is flexibly armed to accomplish Yop injection in different host cell types, a central event in its immune evasion strategy
Vitronectin binds to a specific stretch within the head region of Yersinia adhesin A and thereby modulates Yersinia enterocolitica host interaction
Complement resistance is an important virulence trait of Yersinia enterocolitica (Ye) . The predominant virulence factor expressed by Ye is Yersinia adhesin A (YadA), which enables bacterial attachment to host cells and extracellular matrix and additionally allows the acquisition of soluble serum factors. The serum glycoprotein vitronectin (Vn) acts as an inhibitory regulator of the terminal complement complex by inhibiting the lytic pore formation. Here, we show YadA-mediated direct interaction of Ye with Vn and investigated the role of this Vn binding during mouse infection in vivo. Using different Yersinia strains, we identified a short stretch in the YadA head domain of Ye O:9 E40, similar to the ‘uptake region’ of Y. pseudotuberculosis YPIII YadA, as crucial for efficient Vn binding. Using recombinant fragments of Vn, we found the C-terminal part of Vn, including heparin-binding domain 3, to be responsible for binding to YadA. Moreover, we found that Vn bound to the bacterial surface is still functionally active and thus inhibits C5b-9 formation. In a mouse infection model, we demonstrate that Vn reduces complement-mediated killing of Ye O:9 E40 and, thus, improved bacterial survival. Taken together, these findings show that YadA-mediated Vn binding influences Ye pathogenesis
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