1,516 research outputs found

    Internet-Kreditplattformen ziehen immer mehr traditionelle Kreditnehmer an

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    Immer mehr Menschen nehmen Kredite nicht mehr bei einer Bank oder einem Finanzdienstleister auf, sondern leihen sich über das Internet Geld von anderen Privatpersonen. Sie nutzen dazu sogenannte Internet-Kreditplattformen, die als Alternative zu traditionellen Kreditmärkten zunehmende Bedeutung gewinnen. Eine Studie des DIW Berlin hat die demografischen Merkmale dieser Nutzer untersucht und mit der Gesamtheit der Kreditnehmer in Deutschland verglichen. Dabei zeigt sich, dass Männer den neuen Kreditmarkt überdurchschnittlich häufig nutzen: Bisher wurden 72 Prozent der Darlehen auf der größten deutschen Internet-Kreditplattform von Männern aufgenommen. Insgesamt unterscheiden sich die Nutzergruppen jedoch weniger stark als erwartet. Insbesondere die Altersverteilung hat sich derjenigen der traditionellen Kreditnehmer deutlich angenähert. Dies deutet darauf hin, dass traditionelle und neue Kreditgeber im Internet zunehmend die gleichen Kunden bedienen.Peer-to-peer lending, consumer credit, loan markets

    Eine Theorie der Medienumbrüche 1900/2000

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    Das vorliegende Buch ist ein Ergebnis der Arbeitsgruppe "Theorie der Medienumbrüche", die während der zweiten Förderphase des DFG-Forschungskollegs 615 "Medienumbrüche" von 2005-2009 arbeitete. In der Gruppe wurde der Begriff des Medienumbruchs ausgehend von Lektüren einschlägiger medientheoretischer Texte intensiv diskutiert und schließlich zu einem Modell fortentwickelt. Dieses Modell und seine Begriffe (Emergenzereignis, Rekognitionsniveau, Faszinationskerne etc.) werden im ersten Kapitel vorgestellt. Die Kapitel 2-7 widmen sich drei entscheidenden Faszinationskernen des Medien­umbruchs um 1900 und ihren Entsprechungen im Medienumbruch um 2000. In Kapitel 8 werden diese Darstellungen nochmals perspektiviert und angereichert mit einer dichten Analyse der Verarbeitung der Faszinationskerne im Feuilleton. Das Buch versteht sich als ein Diskussionsbeitrag zur medienhistoriographischen Methodik. Unser Ziel war es, einen Weg zu finden zwischen der sensiblen und dichten Beschreibung heterogener historischer Medienpraktiken und einer Begrifflichkeit, die Orientierung verschafft sowie Differenzen und Veränderungen hinreichend pointiert. Wir hoffen, mit unseren Begriffen die Umbrüche, die mit dem Auftreten neuer Medien verbunden werden, jenseits von Evolutionismus und Revolutionismus beschreiben zu können. Da alle Texte in intensiver Diskussion der Arbeitsgruppe entstanden sind, versteht sich das vorliegende Buch als gemeinsame Monographie von Nicola Glaubitz, Henning Groscurth, Katja Hoffmann, Jörgen Schäfer, Jens Schröter, Gregor Schwering und Jochen Venus. Das Buch spiegelt auch manche offene Frage wider, der manchmal kontroverse Prozess der konzeptuellen Arbeit zeigt sich auch in manchem offenen Ende und losen Faden. Das Buch zeigt aber auch, dass Teamwork kein leeres Wort sein muss. Es ist Zeugnis einer sehr produktiven und von Freundschaft geprägten Zeit

    Rho meson properties from combining QCD-based models

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    Aiming at the calculation of the properties of rho-mesons, non-perturbative QCD-based methods are discussed concerning their potentials as well as their short-comings. The latter are overcome by combining these techniques. The utilized methods are (i) the chiral constituent quark model deduced from the instanton vacuum model and large-N_c arguments, (ii) chiral perturbation theory unitarized by the inverse amplitude method and (iii) QCD sum rules. Advantages of the combination of these methods are especially the absence of un-physical quark-production thresholds and parameter-free results. Already in the chiral limit and in leading order in 1/N_c one obtains a reasonable result for the mass of the rho-meson, namely m_rho = 790 \pm 30 MeV. Using the KSFR relation the universality of the rho-meson coupling is recovered. The latter is found to be g = 6.0 \pm 0.3.Comment: 16 pages, 1 figure, Revtex

    Endothelial mineralocorticoid receptor activation mediates endothelial dysfunction in diet-induced obesity

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    Received 22 July 2012; revised 29 January 2013; accepted 4 March 2013Aims Aldosterone plays a crucial role in cardiovascular disease. ‘Systemic' inhibition of its mineralocorticoid receptor (MR) decreases atherosclerosis by reducing inflammation and oxidative stress. Obesity, an important cardiovascular risk factor, is an inflammatory disease associated with increased plasma aldosterone levels. We have investigated the role of the ‘endothelial' MR in obesity-induced endothelial dysfunction, the earliest stage in atherogenesis. Methods and results C57BL/6 mice were exposed to a normal chow diet (ND) or a high-fat diet (HFD) alone or in combination with the MR antagonist eplerenone (200 mg/kg/day) for 14 weeks. Diet-induced obesity impaired endothelium-dependent relaxation in response to acetylcholine, whereas eplerenone treatment of obese mice prevented this. Expression analyses in aortic endothelial cells isolated from these mice revealed that eplerenone attenuated expression of pro-oxidative NADPH oxidase (subunits p22phox, p40phox) and increased expression of antioxidative genes (glutathione peroxidase-1, superoxide dismutase-1 and -3) in obesity. Eplerenone did not affect obesity-induced upregulation of cyclooxygenase (COX)-1 or prostacyclin synthase. Endothelial-specific MR deletion prevented endothelial dysfunction in obese (exhibiting high ‘endogenous' aldosterone) and in ‘exogenous' aldosterone-infused lean mice. Pre-incubation of aortic rings from aldosterone-treated animals with the COX-inhibitor indomethacin restored endothelial function. Exogenous aldosterone administration induced endothelial expression of p22phox in the presence, but not in the absence of the endothelial MR. Conclusion Obesity-induced endothelial dysfunction depends on the ‘endothelial' MR and is mediated by an imbalance of oxidative stress-modulating mechanisms. Therefore, MR antagonists may represent an attractive therapeutic strategy in the increasing population of obese patients to decrease vascular dysfunction and subsequent atherosclerotic complication

    LSDV-Vectored SARS-CoV-2 S and N Vaccine Protects against Severe Clinical Disease in Hamsters

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    The SARS-CoV-2 pandemic demonstrated the need for potent and broad-spectrum vaccines. This study reports the development and testing of a lumpy skin disease virus (LSDV)-vectored vaccine against SARS-CoV-2, utilizing stabilized spike and conserved nucleocapsid proteins as antigens to develop robust immunogenicity. Construction of the vaccine (LSDV-SARS2-S,N) was confirmed by polymerase chain reaction (PCR) amplification and sequencing. In vitro characterization confirmed that cells infected with LSDV-SARS2-S,N expressed SARS-CoV-2 spike and nucleocapsid protein. In BALB/c mice, the vaccine elicited high magnitude IFN-γ ELISpot responses (spike: 2808 SFU/106 splenocytes) and neutralizing antibodies (ID50 = 6552). Testing in hamsters, which emulate human COVID-19 disease progression, showed the development of high titers of neutralizing antibodies against the Wuhan and Delta SARS-CoV-2 variants (Wuhan ID50 = 2905; Delta ID50 = 4648). Additionally, hamsters vaccinated with LSDV-SARS2-S,N displayed significantly less weight loss, lung damage, and reduced viral RNA copies following SARS-CoV-2 infection with the Delta variant as compared to controls, demonstrating protection against disease. These data demonstrate that LSDV-vectored vaccines display promise as an effective SARS-CoV-2 vaccine and as a potential vaccine platform for communicable diseases in humans and animals. Further efficacy testing and immune response analysis, particularly in non-human primates, are warranted

    SIRT1 decreases Lox-1-mediated foam cell formation in atherogenesis

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    Aims Endothelial activation, macrophage infiltration, and foam cell formation are pivotal steps in atherogenesis. Our aim in this study was to analyse the role of SIRT1, a class III deacetylase with important metabolic functions, in plaque macrophages and atherogenesis. Methods and results Using partial SIRT1 deletion in atherosclerotic mice, we demonstrate that SIRT1 protects against atherosclerosis by reducing macrophage foam cell formation. Peritoneal macrophages from heterozygous SIRT1 mice accumulate more oxidized low-density lipoprotein (oxLDL), thereby promoting foam cell formation. Bone marrow-restricted SIRT1 deletion confirmed that SIRT1 function in macrophages is sufficient to decrease atherogenesis. Moreover, we show that SIRT1 reduces the uptake of oxLDL by diminishing the expression of lectin-like oxLDL receptor-1 (Lox-1) via suppression of the NF-κB signalling pathway. Conclusion Our findings demonstrate protective effects of SIRT1 in atherogenesis and suggest pharmacological SIRT1 activation as a novel anti-atherosclerotic strategy by reducing macrophage foam cell formatio

    SIRT1 decreases Lox-1-mediated foam cell formation in atherogenesis

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    Aims Endothelial activation, macrophage infiltration, and foam cell formation are pivotal steps in atherogenesis. Our aim in this study was to analyse the role of SIRT1, a class III deacetylase with important metabolic functions, in plaque macrophages and atherogenesis. Methods and results Using partial SIRT1 deletion in atherosclerotic mice, we demonstrate that SIRT1 protects against atherosclerosis by reducing macrophage foam cell formation. Peritoneal macrophages from heterozygous SIRT1 mice accumulate more oxidized low-density lipoprotein (oxLDL), thereby promoting foam cell formation. Bone marrow-restricted SIRT1 deletion confirmed that SIRT1 function in macrophages is sufficient to decrease atherogenesis. Moreover, we show that SIRT1 reduces the uptake of oxLDL by diminishing the expression of lectin-like oxLDL receptor-1 (Lox-1) via suppression of the NF-kappaB signalling pathway. Conclusion Our findings demonstrate protective effects of SIRT1 in atherogenesis and suggest pharmacological SIRT1 activation as a novel anti-atherosclerotic strategy by reducing macrophage foam cell formation

    Dietary α-linolenic acid diminishes experimental atherogenesis and restricts T cell-driven inflammation

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    Aims Epidemiological studies report an inverse association between plant-derived dietary α-linolenic acid (ALA) and cardiovascular events. However, little is known about the mechanism of this protection. We assessed the cellular and molecular mechanisms of dietary ALA (flaxseed) on atherosclerosis in a mouse model. Methods and results Eight-week-old male apolipoprotein E knockout (ApoE−/−) mice were fed a 0.21 % (w/w) cholesterol diet for 16 weeks containing either a high ALA [7.3 % (w/w); n = 10] or low ALA content [0.03 % (w/w); n = 10]. Bioavailability, chain elongation, and fatty acid metabolism were measured by gas chromatography of tissue lysates and urine. Plaques were assessed using immunohistochemistry. T cell proliferation was investigated in primary murine CD3-positive lymphocytes. T cell differentiation and activation was assessed by expression analyses of interferon-γ, interleukin-4, and tumour necrosis factor α (TNFα) using quantitative PCR and ELISA. Dietary ALA increased aortic tissue levels of ALA as well as of the n−3 long chain fatty acids (LC n−3 FA) eicosapentaenoic acid, docosapentaenoic acid, and docosahexaenoic acid. The high ALA diet reduced plaque area by 50% and decreased plaque T cell content as well as expression of vascular cell adhesion molecule-1 and TNFα. Both dietary ALA and direct ALA exposure restricted T cell proliferation, differentiation, and inflammatory activity. Dietary ALA shifted prostaglandin and isoprostane formation towards 3-series compounds, potentially contributing to the atheroprotective effects of ALA. Conclusion Dietary ALA diminishes experimental atherogenesis and restricts T cell-driven inflammation, thus providing the proof-of-principle that plant-derived ALA may provide a valuable alternative to marine LC n−3 F
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