Fallstudie zum Führungssystem für Stammdatenqualität bei der Bayer CropScience AG

Zusammenfassung: Zur Konsolidierung der Systemlandschaft führte die Bayer CropScience AG eine globale Harmonisierung der Geschäftsprozesse mit Stammdatenkonsolidierung durch. Die dabei ermittelten Defizite in den Unternehmensprozessen konnten auf mangelnde Datenqualität zurückgeführt werden. Zur langfristigen Verbesserung der Prozesseffizienz wurden Geschäftsregeln definiert, die die Daten qualitativ bewerten und Verbesserungsmaßnahmen nach sich ziehen. Ein Kennzahlensystem dient der Auswertung der Regeln. Zur kontinuierlichen Überwachung der Datenqualität und Steuerung von Maßnahmen sind Aufgaben und Verantwortung definiert, zugewiesen und in den Zielsystemen der Mitarbeiter veranker

Competition between a toxic and a non-toxic Microcystis strain under constant and pulsed nitrogen and phosphorus supply

The toxicity of a harmful algal bloom is strongly determined by the relative abundance of non-toxic and toxic genotypes and might therefore be regulated by competition for growth-limiting resources. Here, we studied how the toxic Microcystis aeruginosa strain PCC 7806 and a non-toxic mutant compete for nitrogen and phosphorus under constant and pulsed nutrient supply. Our monoculture and competition experiments show that these closely related genotypes have distinct nutrient physiologies and that they differ in their ability to compete for nitrogen and phosphorus. The toxic wild type won the competition under nitrogen limitation, while the non-toxic mutant dominated under phosphorus limitation. Pulses of both nitrogen and phosphorus increased the dominance of the toxic genotype, which lead to an even faster competitive exclusion of the non-toxic genotype under nitrogen pulses and to coexistence of both genotypes under phosphorus pulses. Our findings indicate that the genotype level dynamics driven by resource competition can be an important factor in determining cyanobacterial bloom toxicity.Peer reviewe

Integration und Desintegration der Kulturen im europäischen Mittelalter

Das mittelalterliche Europa war keine christliche Einheitskultur, sondern geprägt von vielfältigen Prozessen des Kontakts und der Abgrenzung zwischen Kulturen, bei denen die drei monotheistischen Religionen Christentum, Judentum und Islam eine herausragende Rolle spielten. Seit 2005 erforscht das DFG-Schwerpunktprogramm "Integration und Desintegration der Kulturen im europäischen Mittelalter" die Geschichte Europas als Geschichte kultureller Differenzen. Der Band dokumentiert die Dynamiken und Erträge eines wissenschaftsorganisatorischen Experiments: Gegliedert in fächerübergreifende Arbeitsgruppen, erforschten 24 Einzelprojekte aus 14 Disziplinen Integrations- und Desintegrationsprozesse von Skandinavien bis Ägypten, von der Iberischen Halbinsel bis zu den Steppen Zentralasiens in komparativem Zugriff; sie präsentieren ihre Ergebnisse nun in Beiträgen, die von mehreren Autorinnen und Autoren gemeinsam verfasst worden sind. Dabei werden Begriffe wie "Kultur" problematisiert und schon eingeführte Konzepte wie "Integration/Desintegration", "Inklusion/Exklusion", "Hybridisierung" und "Transfer" als Instrumente transkultureller Mediävistik auf den Prüfstand gestellt. Das Ende der Laufzeit des Schwerpunktprogramms gibt zugleich Anlass, methodisch-theoretische Einsichten der gemeinsamen Forschung wie auch praktische Erfahrungen bei der transdisziplinären Zusammenarbeit zu bilanzieren

Phase Responses to Light Pulses in Mice Lacking Functional per or cry Genes

The phase-resetting properties of the circadian system in mice with a functional deletion in mCry1, mCry2, mPer1, or mPer2 were studied in 2 experiments. In experiment 1, mCry1-/- and mCry2-/- mice as well as mPer1Brdm1 and mPer2Brdm1 mutant mice were exposed to 15-min light pulses during the 1st cycle following entrainment, either early (external time [ExT] 20) or late (ExT 4) in the subjective night. In experiment 2, a full PRC was measured for all these strains by exposure to light pulses of the same duration and intensity in free-running conditions in constant darkness. Directly after entrainment (experiment 1), mPer1Brdm1 animals did not show significant phase advances by a light pulse in the late subjective night (ExT 4), as in the study by Albrecht et al. In the same experiment, mPer2Brdm1 mice became arrhythmic too frequently to reliably measure their phase responses. Mice with a targeted gene disruption in mCry1 or mCry2 showed increased phase delays compared to wild type after exposure to a light pulse in the early subjective night (ExT 20). Otherwise, phase shifts were not significantly affected. In free run (experiment 2), all genotypes did show phase advances and phase delays. The mPer2Brdm1 mutant PRC was above the mPer1Brdm1 mutant and wild-type PRC (i.e., less delayed and more advanced) at most circadian phases. The mPer1Brdm1 mutant PRC was not distinguishable from the wildtype PRC. The mCry2-/- mice showed much smaller phase delays than did mCry1-/- mice in the subjective evening (delay phase). In general, mPer2Brdm1 mutant mice were more accelerated by light compared to mPer1Brdm1 and wildtype control mice, whereas mCry1-/- mice were more delayed by light than were mCry2-/- mice

Phase responses to light pulses in mice lacking functional per or cry genes

The phase-resetting properties of the circadian system in mice with a functional deletion in mCry1, mCry2, mPer1, or mPer2 were studied in 2 experiments. In experiment 1, mCry1(-/-) and mCry2(-/-) mice as well as mPer1(Brdm1) and mPer2(Brdm1) mutant mice were exposed to 15-min light pulses during the 1st cycle following entrainment, either early (external time [ExT] 20) or late (ExT 4) in the subjective night. In experiment 2, a full PRC was measured for all these strains by exposure to light pulses of the same duration and intensity in free-running conditions in constant darkness. Directly after entrainment (experiment 1), mPer1(Brdm1) animals did not show significant phase advances by a light pulse in the late subjective night (ExT 4), as in the study by Albrecht et al. In the same experiment, mPer2(Brdm1) mice became arrhythmic too frequently to reliably measure their phase responses. Mice with a targeted gene disruption in mCry1 or mCry2 showed increased phase delays compared to wild type after exposure to a light pulse in the early subjective night (ExT 20). Otherwise, phase shifts were not significantly affected. In free run (experiment 2), all genotypes did show phase advances and phase delays. The mPer2(Brdm1) mutant PRC was above the mPer1(Brdm1) mutant and wild-type PRC (i.e., less delayed and more advanced) at most circadian phases. The mPer1(Brdm1) mutant PRC was not distinguishable from the wildtype PRC. The mCry2(-/-) mice showed much smaller phase delays than did mCry1(-/-) mice in the subjective evening (delay phase). In general, mPer2(Brdm1) mutant mice were more accelerated by light compared to mPer1(Brdm1) and wildtype control mice, whereas mCry1(-/-) mice were more delayed by light than were mCry2(-/-) mice

Phase responses to light pulses in mice lacking functional per or cry genes

The phase-resetting properties of the circadian system in mice with a functional deletion in mCry1, mCry2, mPer1, or mPer2 were studied in 2 experiments. In experiment 1, mCry1-/- and mCry2-/- mice as well as mPer1Brdm1 and mPer2Brdm1 mutant mice were exposed to 15-min light pulses during the 1st cycle following entrainment, either early (external time [ExT] 20) or late (ExT 4) in the subjective night. In experiment 2, a full PRC was measured for all these strains by exposure to light pulses of the same duration and intensity in free-running conditions in constant darkness. Directly after entrainment (experiment 1), mPer1 Brdm1 animals did not show significant phase advances by a light pulse in the late subjective night (ExT 4), as in the study by Albrecht et al. In the same experiment, mPer2Brdm1 mice became arrhythmic too frequently to reliably measure their phase responses. Mice with a targeted gene disruption in mCry1 or mCry2 showed increased phase delays compared to wild type after exposure to a light pulse in the early subjective night (ExT 20). Otherwise, phase shifts were not significantly affected. In free run (experiment 2), all genotypes did show phase advances and phase delays. The mPer2 Brdm1 mutant PRC was above the mPer1Brdm1 mutant and wild-type PRC (i.e., less delayed and more advanced) at most circadian phases. The mPer1Brdm1 mutant PRC was not distinguishable from the wild-type PRC. The mCry2-/- mice showed much smaller phase delays than did mCry1-/- mice in the subjective evening (delay phase). In general, mPer2Brdm1 mutant mice were more accelerated by light compared to mPer1Brdm1 and wild-type control mice, whereas mCry1-/- mice were more delayed by light than were mCry2-/- mice