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Recent developments in medical education have created increasing challenges for medical teachers which is why the majority of German medical schools already offer educational and instructional skills trainings for their teaching staff. However, to date no framework for educational core competencies for medical teachers exists that might serve as guidance for the qualification of the teaching faculty. Against the background of the discussion about competency based medical education and based upon the international literature, the GMA Committee for Faculty and Organizational Development in Teaching developed a model of core teaching competencies for medical teachers. This framework is designed not only to provide guidance with regard to individual qualification profiles but also to support further advancement of the content, training formats and evaluation of faculty development initiatives and thus, to establish uniform quality criteria for such initiatives in German-speaking medical schools. The model comprises a framework of six competency fields, subdivided into competency components and learning objectives. Additional examples of their use in medical teaching scenarios illustrate and clarify each specific teaching competency. The model has been designed for routine application in medical schools and is thought to be complemented consecutively by additional competencies for teachers with special duties and responsibilities in a future step.
Die Entwicklungen in der Medizinischen Ausbildung der letzten Jahre konfrontieren Lehrende zunehmend mit neuen didaktischen Herausforderungen. An zahlreichen Standorten im deutschsprachigen Raum werden bereits Qualifizierungsangebote für Lehrende angeboten, jedoch fehlt bisher ein Orientierungsrahmen für medizindidaktische Kompetenzen, der ein Qualifikationsprofil für Lehrende darstellt.
Vor dem Hintergrund der Diskussion um die Kompetenzorientierung des Medizinstudiums und auf Grundlage aktueller internationaler Literatur wurde durch den GMA Ausschuss für Personal- und Organisationsentwicklung in der Lehre ein Kernkompetenzmodell für Lehrende in der Medizin entwickelt. Das Modell soll nicht nur den Lehrenden Orientierung zu ihrem Qualifikationsprofil geben, sondern auch die inhaltliche Ausrichtung hochschuldidaktischer (Aus-) Weiter- und Fortbildungen sowie die Evaluation von Fakultätsentwicklungsprozessen erleichtern und nicht zuletzt einheitliche Kriterien für die Beurteilung der Lehrqualifikation in deutschsprachigen Raum definieren.
Das Modell besteht aus sechs Kompetenzfeldern, für die jeweils Teilkompetenzen definiert und Lernziele beschrieben wurden. Anwendungsbeispiele sollen die jeweiligen Kompetenzen verdeutlichen.
Das Modell ist für die praktische Anwendung konzipiert und soll in einem nächsten Schritt durch spezifische Kompetenzen für Lehrende mit besonderen Aufgaben ergänzt werden.
BACKGROUND: Human SAMHD1 is a triphosphohydrolase that restricts the replication of retroviruses, retroelements and DNA viruses in noncycling cells. While modes of action have been extensively described for human SAMHD1, only little is known about the regulation of SAMHD1 in the mouse. Here, we characterize the antiviral activity of murine SAMHD1 with the help of knockout mice to shed light on the regulation and the mechanism of the SAMHD1 restriction and to validate the SAMHD1 knockout mouse model for the use in future infectivity studies.
RESULTS: We found that endogenous mouse SAMHD1 restricts not only HIV-1 but also MLV reporter virus infection at the level of reverse transcription in primary myeloid cells. Similar to the human protein, the antiviral activity of murine SAMHD1 is regulated through phosphorylation at threonine 603 and is limited to nondividing cells. Comparing the susceptibility to infection with intracellular dNTP levels and SAMHD1 phosphorylation in different cell types shows that both functions are important determinants of the antiviral activity of murine SAMHD1. In contrast, we found the proposed RNase activity of SAMHD1 to be less important and could not detect any effect of mouse or human SAMHD1 on the level of incoming viral RNA.
CONCLUSION: Our findings show that SAMHD1 in the mouse blocks retroviral infection at the level of reverse transcription and is regulated through cell cycle-dependent phosphorylation. We show that the antiviral restriction mediated by murine SAMHD1 is mechanistically similar to what is known for the human protein, making the SAMHD1 knockout mouse model a valuable tool to characterize the influence of SAMHD1 on the replication of different viruses in vivo.