Electric Vehicle Powertrain Integrated Charging

Batterieelektrische Fahrzeuge benötigen ein im Fahrzeug eingebautes Ladegerät, um die Energie aus dem Wechselstromnetz für die Gleichstrom- Batterie aufzubereiten. Integriertes Laden ist eine Methode der Integration von Ladefunktionalität in die Antriebsstrangkomponenten, welche während des Parkens außer Betrieb sind, mit dem Ziel, Kosten, Gewicht und Volumen des Ladegerät zu sparen. Das Laden ohne die Sicherheitsmaßnahme einer galvanischen Trennung im Ladegerät ist möglich mit zusätzlichen Maßnahmen gegen elektrischen Schlag, z.B. mit einer Fehlerstromerkennung und entsprechenden Trenneinrichtung. Im Stand der Technik wurden 33 integrierte Ladekonzepte gefunden und bezüglich Antriebsstrangnutzung, benötigte Komponenten, Drehmoment der elektrischen Maschine und Wirkungsgrad verglichen. Im Rahmen dieser Arbeit wird ein neues galvanisch getrenntes integriertes Ladekonzept beschrieben, mit dem Ziel, die Effizienz zu verbessern und gleichzeitig auftretendes Drehmoment in der Maschine zu vermeiden. Der Antriebsstrang wird als DC/DC-Wandler mit der elektrischen Maschine als Transformator im Stillstand genutzt. Berechnungen zeigen eine maximale Effizienz von 88%. Ansätze zur Verbesserung des Wirkungsgrads und zur Integration des Energieflusses im Bordnetz werden in dieser Arbeit vorgeschlagen und diskutiert. Allerdings muss der Rotorkäfig geöffnet werden, um ein Drehmoment während des Laden zu vermeiden. Dies stellt einen ähnlichen Aufwand dar wie die Darstellung eines separaten Ladegeräts. Somit ist dieses Konzept aus heutiger Sicht wegen niedriger Effizienz und hoher Kosten gegenüber einem separaten Ladegerät nicht konkurrenzfähig. Zwei Ladekonzepte ohne galvanische Trennung, die eine sechsphasige elektrische Maschine als in Serie geschaltete Hoch- und Tiefsetzsteller nutzen, werden im Rahmen der Arbeit vorgestellt und bezüglich der benötigten Komponenten, der Effizienz und des Drehmoments des Maschine ausgearbeitet. Die Antriebsstrangverluste werden für die Ladebedingungen mit Gleichströmen analysiert, basierend auf neuen Materialcharakterisierungen für die angewendete Belastung. Es wurden Wirkungsgrade bis zu 93% demonstriert und auch in theoretischen Berechnungen mit einer maximalen Abweichung von ±1% zum experimentellen Befund bestätigt. Zum Schutz gegen elektrischen Schlag bei nicht isolierten Ladekonzepten werden drei Konzepte für eine Fehlerstrommessung präsentiert und anhand von Messergebnissen analysiert. Siliziumkarbid-Inverter-Technologien zeigen in Kombination mit diesen Ladekonzepten Wirkungsgrade, die vergleichbar zu herkömmlichen separaten Ladegeräten sind, und weisen dabei deutlich geringere Kosten auf

Loss of Gap Junction Delta-2 (GJD2) gene orthologs leads to refractive error in zebrafish

Myopia is the most common developmental disorder of juvenile eyes, and it has become an increasing cause of severe visual impairment. The GJD2 locus has been consistently associated with myopia in multiple independent genome-wide association studies. However, despite the strong genetic evidence, little is known about the functional role of GJD2 in refractive error development. Here, we find that depletion of gjd2a (Cx35.5) or gjd2b (Cx35.1) orthologs in zebrafish, cause changes in the biometry and refractive status of the eye. Our immunohistological and scRNA sequencing studies show that Cx35.5 (gjd2a) is a retinal connexin and its depletion leads to hyperopia and electrophysiological changes in the retina. These findings support a role for Cx35.5 (gjd2a) in the regulation of ocular biometry. Cx35.1 (gjd2b) has previously been identified in the retina, however, we found an additional lenticular role. Lack of Cx35.1 (gjd2b) led to a nuclear cataract that triggered axial elongation. Our results provide functional evidence of a link between gjd2 and refractive error

Depletion of Arg/Abl2 improves endothelial cell adhesion and prevents vascular leak during inflammation

Endothelial barrier disruption and vascular leak importantly contribute to organ dysfunction and mortality during inflammatory conditions like sepsis and acute respiratory distress syndrome. We identified the kinase Arg/Abl2 as a mediator of endothelial barrier disruption, but the role of Arg in endothelial monolayer regulation and its relevance in vivo remain poorly understood. Here we show that depletion of Arg in endothelial cells results in the activation of both RhoA and Rac1, increased cell spreading and elongation, redistribution of integrin-dependent cell-matrix adhesions to the cell periphery, and improved adhesion to the extracellular matrix. We further show that Arg is activated in the endothelium during inflammation, both in murine lungs exposed to barrier-disruptive agents, and in pulmonary microvessels of septic patients. Importantly, Arg-depleted endothelial cells were less sensitive to barrier-disruptive agents. Despite the formation of F-actin stress fibers and myosin light chain phosphorylation, Arg depletion diminished adherens junction disruption and intercellular gap formation, by reducing the disassembly of cell-matrix adhesions and cell retraction. In vivo, genetic deletion of Arg diminished vascular leak in the skin and lungs, in the presence of a normal immune response. Together, our data indicate that Arg is a central and non-redundant regulator of endothelial barrier integrity, which contributes to cell retraction and gap formation by increasing the dynamics of adherens junctions and cell-matrix adhesions in a Rho GTPase-dependent fashion. Therapeutic inhibition of Arg may provide a suitable strategy for the treatment of a variety of clinical conditions characterized by vascular leak

Loss of Gap Junction Delta-2 (GJD2) gene orthologs leads to refractive error in zebrafish

Myopia is the most common developmental disorder of juvenile eyes, and it has become an increasing cause of severe visual impairment. The GJD2 locus has been consistently associated with myopia in multiple independent genome-wide association studies. However, despite the strong genetic evidence, little is known about the functional role of GJD2 in refractive error development. Here, we find that depletion of gjd2a (Cx35.5) or gjd2b (Cx35.1) orthologs in zebrafish, cause changes in the biometry and refractive status of the eye. Our immunohistological and scRNA sequencing studies show that Cx35.5 (gjd2a) is a retinal connexin and its depletion leads to hyperopia and electrophysiological changes in the retina. These findings support a role for Cx35.5 (gjd2a) in the regulation of ocular biometry. Cx35.1 (gjd2b) has previously been identified in the retina, however, we found an additional lenticular role. Lack of Cx35.1 (gjd2b) led to a nuclear cataract that triggered axial elongation. Our results provide functional evidence of a link between gjd2 and refractive error.</p

Depletion of Arg/Abl2 improves endothelial cell adhesion and prevents vascular leak during inflammation

Endothelial barrier disruption and vascular leak importantly contribute to organ dysfunction and mortality during inflammatory conditions like sepsis and acute respiratory distress syndrome. We identified the kinase Arg/Abl2 as a mediator of endothelial barrier disruption, but the role of Arg in endothelial monolayer regulation and its relevance in vivo remain poorly understood. Here we show that depletion of Arg in endothelial cells results in the activation of both RhoA and Rac1, increased cell spreading and elongation, redistribution of integrin-dependent cell-matrix adhesions to the cell periphery, and improved adhesion to the extracellular matrix. We further show that Arg is activated in the endothelium during inflammation, both in murine lungs exposed to barrier-disruptive agents, and in pulmonary microvessels of septic patients. Importantly, Arg-depleted endothelial cells were less sensitive to barrier-disruptive agents. Despite the formation of F-actin stress fibers and myosin light chain phosphorylation, Arg depletion diminished adherens junction disruption and intercellular gap formation, by reducing the disassembly of cell-matrix adhesions and cell retraction. In vivo, genetic deletion of Arg diminished vascular leak in the skin and lungs, in the presence of a normal immune response. Together, our data indicate that Arg is a central and non-redundant regulator of endothelial barrier integrity, which contributes to cell retraction and gap formation by increasing the dynamics of adherens junctions and cell-matrix adhesions in a Rho GTPase-dependent fashion. Therapeutic inhibition of Arg may provide a suitable strategy for the treatment of a variety of clinical conditions characterized by vascular leak