49 research outputs found

    What Determines the ZEW Indicator?

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    This paper analyzes which factors are driving the ZEW Indicator of Economic Sentiment. Using the results of a poll among survey participants as well as Granger causality tests we identify three groups of influence factors: other sentiment indicators, financial variables and real economy data. In a second step these factors are used to estimate out-of-sample forecasts for the ZEW Indicator. We find that a simple model that includes German manufacturing order data, the German yield structure and the US Consumer Confidence indicator as explanatory variables is able to outperform a naive univariate benchmark model as well as the consensus forecast for the ZEW Indicator as published by news agencies. --leading indicators,Germany,zew,forecasting

    Auswirkungen der Besteuerung von KapitaleinkĂŒnften und VerĂ€ußerungsgewinnen auf Vermögensbildung und FinanzmĂ€rkte : Status quo und Reformoptionen

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    Die vorliegende Untersuchung analysiert die Auswirkungen einer erweiterten Besteuerung privater VerĂ€ußerungsgewinne im Geldvermögen. In diesem Zusammenhang werden auch weitere in jĂŒngster Zeit diskutierte Reformoptionen analysiert

    What Determines the ZEW Indicator?

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    This paper analyzes which factors are driving the ZEW Indicator of Economic Sentiment. Using the results of a poll among survey participants as well as Granger causality tests we identify three groups of influence factors: other sentiment indicators, financial variables and real economy data. In a second step these factors are used to estimate out-of-sample forecasts for the ZEW Indicator. We find that a simple model that includes German manufacturing order data, the German yield structure and the US Consumer Confidence indicator as explanatory variables is able to outperform a naive univariate benchmark model as well as the consensus forecast for the ZEW Indicator as published by news agencies

    The Impact of Pay-As-You-Throw Schemes on Municipal Solid Waste Management:The Exemplar Case of the County of Aschaffenburg, Germany

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    The “pay-as-you-throw” (PAYT) scheme is an economic instrument for waste management that applies the “polluter pays” principle by charging the inhabitants of municipalities according to the amount of residual, organic, and bulky waste they send for third-party waste management. When combined with well-developed infrastructure to collect the different waste fractions (residual waste, paper and cardboard, plastics, bio waste, green cuttings, and many recyclables) as well as with a good level of citizens’ awareness, its performance has frequently been linked to an increase in the collection rates of recyclables. However, the establishment and operation of PAYT systems can require significant resource inputs from municipalities. In this paper, PAYT is analysed through a case study from the German County of Aschaffenburg, covering nearly 20 years of implementation across 32 municipalities with 173,000 inhabitants. Key performance indicators include temporal trends in the county’s recyclables collection rate, waste treatment fees for residents, and municipal waste management costs, benchmarked against German municipalities not implementing PAYT. We conclude that PAYT could make an important contribution towards material reuse and recycling objectives for the new circular economy

    Schistosomes Induce Regulatory Features in Human and Mouse CD1dhi B Cells: Inhibition of Allergic Inflammation by IL-10 and Regulatory T Cells

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    Chronic helminth infections, such as schistosomes, are negatively associated with allergic disorders. Here, using B cell IL-10-deficient mice, Schistosoma mansoni-mediated protection against experimental ovalbumin-induced allergic airway inflammation (AAI) was shown to be specifically dependent on IL-10-producing B cells. To study the organs involved, we transferred B cells from lungs, mesenteric lymph nodes or spleen of OVA-infected mice to recipient OVA-sensitized mice, and showed that both lung and splenic B cells reduced AAI, but only splenic B cells in an IL-10-dependent manner. Although splenic B cell protection was accompanied by elevated levels of pulmonary FoxP3+ regulatory T cells, in vivo ablation of FoxP3+ T cells only moderately restored AAI, indicating an important role for the direct suppressory effect of regulatory B cells. Splenic marginal zone CD1d+ B cells proved to be the responsible splenic B cell subset as they produced high levels of IL-10 and induced FoxP3+ T cells in vitro. Indeed, transfer of CD1d+ MZ-depleted splenic B cells from infected mice restored AAI. Markedly, we found a similarly elevated population of CD1dhi B cells in peripheral blood of Schistosoma haematobium-infected Gabonese children compared to uninfected children and these cells produced elevated levels of IL-10. Importantly, the number of IL-10-producing CD1dhi B cells was reduced after anti-schistosome treatment. This study points out that in both mice and men schistosomes have the capacity to drive the development of IL-10-producing regulatory CD1dhi B cells and furthermore, these are instrumental in reducing experimental allergic inflammation in mice

    What determines the ZEW indicator?

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    Die Verfasser untersuchen, welche Faktoren den Geschaeftsklimaindex des ZEW beeinflussen. Auf der Basis einer Umfrage unter Teilnehmern der Untersuchung sowie gestuetzt auf Granger-Kausalitaetstests werden drei Gruppen von Einflussfaktoren sichtbar gemacht: andere Geschaeftsklima-Indikatoren, Finanzvariablen und realwirtschaftliche Daten. Diese Faktoren werden in einem zweiten Schritt zu Prognosen des ZEW-Indikators verwendet. Es zeigt sich, dass ein einfaches Modell mit dem Auftragseingang im produzierenden Gewerbe in Deutschland, der Ertragsstruktur in Deutschland und dem Consumer-Confidence-Indikator aus den USA als unabhaengigen Variablen bessere Ergebnisse bringt als ein univariates Benchmark-Modell oder Prognosen fuer den ZEW-Indikator, wie sie von Nachrichtenagenturen veroeffentlicht werden. (ICEUebers)'This paper analyzes which factors are driving the ZEW Indicator of Economic Sentiment. Using the results of a poll among survey participants as well as Granger causality tests we identify three groups of influence factors: other sentiment indicators, financial variables and real economy data. In a second step these factors are used to estimate out-of-sample forecasts for the ZEW Indicator. We find that a simple model that includes German manufacturing order data, the German yield structure and the US Consumer Confidence indicator as explanatory variables is able to outperform a naive univariate benchmark model as well as the consensus forecast for the ZEW Indicator as published by news agencies.' (author's abstract)German title: Welche Groessen bestimmen den ZEW-Indikator?Available from ftp://ftp.zew.de/pub/zew-docs/dp/dp0348.pdf / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman

    Immunostimulatory RNA Blocks Suppression by Regulatory T Cells

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    The role of immune suppression by regulatory T (Treg) cells in the maintenance of immune homeostasis is well established. However, little is known about how Treg cell function is inhibited on viral infection to allow the development of a protective immune response. As viral RNA is a crucial mediator for activation of antiviral immunity, we examined the effects of immunostimulatory RNA and infection with RNA viruses on Treg cell function. We show that synthetic RNA oligonucleotides potently inhibit Treg cell-induced suppression in a sequence-dependent manner. This effect is entirely dependent on TLR7 activation of APCs and subsequent IL-6 production. In addition, stimulation with the RNA viruses encephalomyocarditis virus and Sendai virus that specifically activate the RNA-sensing helicases melanoma differentiation-associated gene 5 (MDA-5) and retinoic acid-inducible gene I (RIG-I) also blocks Treg cell function. Interestingly, this effect is seen even in the absence of APCs. Consistent with this, both Treg and T effector cells express RIG-I and MDA-5. Using MDA-5–deficient mice, we demonstrate that the loss of Treg cell function on infection with encephalomyocarditis virus is strictly dependent on MDA-5 expression by Treg cells. Thus, we show in this study for the first time that activation of a RIG-I–like helicase on Treg cells blocks their suppressive function. Regulatory T (Treg) cells play a central role in the suppression of immune reactions and in the prevention of autoimmune responses harmful to the host (1, 2). In particular, Treg cells suppress the activation of naive T effector (Teff) cells by inhibiting TCR-triggered proliferation and differentiation of these cells (3). In the early phase of microbial infection, the suppressive effect of Treg cells must, however, be overcome to enable the generation of an efficient immune response against invading pathogens (4–6). In recent years, it has been shown that several bacterial components can block the suppressive function of Treg cells. Two distinct mechanisms have so far been described: first, bacterial molecules, such as LPS or CpG DNA, can activate APCs to produce inflammatory cytokines that render Teff cells resistant to suppression by Treg cells (7). Alternatively, Treg cells themselves can be directly stimulated: targeting human Treg cells with CpG DNA or with the bacterial lipoprotein Pam3Cys-SK4 abrogates their suppressive function even in the absence of APCs (8–10). The direct action of bacterial components on Treg cells can, however, also have the opposite effect: activation of Treg cells by flagellin enhances their suppressive function (11). Whereas the effect of bacterial ligands on Treg cell suppression has been described, little is known about the regulation of Treg cell function upon viral infection. Although Treg cells are capable of suppressing antiviral immunity (12), most viral infections can be cleared through the induction of an efficient host immune response, demonstrating that Treg cell suppression can be overcome. Viruses are recognized by the innate immune system through host pattern-recognition receptors (13, 14), and several receptors recognizing molecular patterns present within viral RNA have recently been described. Single-stranded RNA from influenza virus initiates the secretion of type I IFN through activation of TLR7 within the endosome (15). In our laboratory, we found that synthetic short RNA oligonucleotides potently activate TLR7 in a sequence-dependent manner (16). Furthermore, we showed that modification of the RNA by phosphorothioate (PTO) linkage of the backbone enhances TLR7 stimulation (17). Viral RNA can also be recognized by cytosolic RNA sensors, the retinoic acid-inducible gene I (RIG-I)–like helicases (18). This family of structurally related proteins includes RIG-I, melanoma differentiation-associated gene 5 (MDA-5) and LGP2. Many RNA viruses, such as the measles virus, the rabies virus, the vesicular stomatitis virus, the Sendai virus, or the encephalomyocarditis virus (EMCV) induce type I IFN through these receptors (19–22). We have recently identified virally encoded 5â€Č-triphosphate RNA as the natural ligand for the RIG-I receptor (23), whereas MDA-5 recognizes the synthetic long double-stranded RNA polyinosinic-polycytidylic acid [poly (I:C)] on cytosolic delivery (22). Although the detection of viral RNA by pattern recognition receptors leads to strong immune activation, little is known about the effect of RNA ligands on Treg cell-induced immune suppression. We show in this study that RNA oligonucleotides block suppression by Treg cells in a sequence-specific and TLR7-dependent manner through inflammatory cytokines produced by APC. Infection with viruses known to stimulate the cytosolic RNA-sensing receptors RIG-I and MDA-5 blocked Treg cell function in a direct, APC-independent manner. Indeed, we show that Treg cells express RIG-I-like helicases, and activation of the MDA-5 receptor leads to an arrest of their suppressive function. Thus, suppression can be overcome both indirectly by RNA oligonucleotides activating TLR7 on APC and through direct activation of RIG-I–like helicases expressed by Treg cells
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