The European Union's digital assertiveness

The European institutions and EU member states are pushing hard for closer digital integration. In view of the diverse challenges -from protecting critical infrastructure and safeguarding civil liberties to the creation of common markets- "positive integration", that is targeted EU regulatory action, is the way to tackle market failure within and beyond Europe. Draft regulations at the EU level are to take effect inside and outside the internal market: the Digital Single Market Strategy (DSM), the General Data Protection Regulation (GDPR) and the Directive on Network and Information Security (NIS). Digital integration is a precondition for establishing European standards and norms effectively, especially in international politics. (Autorenreferat

Die digitale Selbstbehauptung der EU

Institutionen und Mitgliedstaaten der EU treiben derzeit mit Hochdruck die digitale Integration voran. In Anbetracht der vielfältigen Herausforderungen - vom Schutz kritischer Infrastrukturen über die Wahrung persönlicher Freiheitsrechte bis zur Schaffung grenzübergreifender Märkte - ist die "positive Integration", also regulative Vorgaben durch die EU, der richtige Weg, um gegen Marktversagen im Binnenmarkt und darüber hinaus anzugehen. Auf EU-Ebene sollen Regulierungen geschaffen werden, die inner- und außereuropäische Wirkung entfalten. Vehikel dazu sind die Strategie für einen digitalen Binnenmarkt (DSM), die Datenschutzgrundverordnung (DSGVO) und die Richtlinie zur Gewährleistung einer gemeinsamen Netzwerk- und Informationssicherheit (NIS). Die digitale Integration ist Voraussetzung dafür, europäische Standards und Normen auch in der internationalen Politik effektiver durchzusetzen. (Autorenreferat

Differential roles of nitric oxide synthase isozymes in cardiotoxicity and mortality following chronic doxorubicin treatment in mice

The roles of individual nitric oxide synthases (NOS) in anthracycline-related cardiotoxicity are not completely understood. We investigated the effects of a chronic treatment with doxorubicin (DOX) on knockouts of the individual NOS isozymes and on transgenic mice with myocardial overexpression of eNOS. Fractional shortening (FS) was reduced in untreated homozygous nNOS and iNOS knockouts as well as in eNOS transgenics. DOX-induced FS decrease in wild-type mice was attenuated only in eNOS knockouts, which were found to overexpress nNOS. No worsening of contractility was observed in DOX-treated eNOS transgenics and iNOS knockouts. Although the surviving DOX-treated nNOS knockouts exhibited no further impairment in contractility, most (70%) animals died within 7 weeks after treatment onset. In comparison to untreated wild-type hearts, the nitric oxide (NO) level was lower in hearts from DOX-treated wild-type mice and in all three untreated knockouts. DOX treatment had no effect on NO in the knockouts. These data indicate differential roles of the individual NOS in DOX-induced cardiotoxicity. Protection against DOX effects conferred by eNOS deletion may be mediated by a compensatory overexpression of nNOS. NOS inhibition-based prevention of anthracycline-induced cardiotoxicity should be eNOS-selective, simultaneously avoiding inhibiting nNOS