Ultraschnelle Dynamik elektronischer Korrelationen in Dichalkogenid-Monolagen und van-der-Waals-Heterostrukturen

Die Untersuchung von Exzitonen in atomar dünnen Wolframdiselenidschichten und deren Dynamik bildet den wissenschaftlichen Kern dieser Arbeit. Mittels zeitaufgelöster Anrege-Multi-THz-Abtastspektroskopie kann ein umfassendes Bild der fundamentalen elektronischen Korrelationen erstellt werden, um so grundlegende Fragestellungen zu beantworten. Zum einen: Wie schnell bilden sich Exzitonen in einer Wolframdiselenid-Monolage aus ursprünglich ungebundenen Elektron-Loch-Paaren? Zum anderen: Wie lassen sich durch Heterostrukturierung die elektronischen Korrelationen, sprich die Exzitonen, in einer Wolframdiselenid-Monolage gezielt manipulieren? Dass sich die Methode der Anrege-Multi-THz-Abtast Spektroskopie auch auf weitere hochinteressante, atomar dünne Probensysteme anwenden lässt, zeigen die am Ende der Arbeit vorgestellten weiterführenden Experimente

Firewall Traversal in Mobile IPv6 Networks

Middleboxes, wie zum Beispiel Firewalls, sind ein wichtiger Aspekt für eine Großzahl moderner IP-Netzwerke. Heute IP-Netzwerke basieren überwiegend auf IPv4 Technologien, daher sind viele Firewalls und Network Address Translators (NATs) ursprünglich für diese Netzwerke entwickelt worden. Die Entwicklung von IPv6 Netzwerken findet zur Zeit statt. Da Mobile IPv6 ein relativ neuer Standard ist, unterstützen die meisten Firewalls die für IPv6 Netzwerke verfügbar sind, noch kein Mobile IPv6. Sofern Firewalls sich nicht der Details des Mobile IPv6 Protokolls bewusst sind, werden sie entweder Mobile IPv6 Kommunikation blockieren oder diesen sorgfältig handhaben. Dieses stellt einen der Haupthinderunggründe zum erfolgreichen Einsatz von Mobile IPv6 da.Diese Arbeit beschreibt die Probleme und Auswirkungen des Vorhandenseins von Middleboxes in Mobile IPv6 Umgebungen. Dazu wird zuerst erklärt welche Arten von Middleboxes es gibt, was genau eine Middlebox ist und wie eine solche Middlebox arbeiten und zweitens die Probleme identifiziert und die Auswirkungen des Vorhandenseins von Firewalls in Mobile IPv6 Umgebungen erklärt. Anschließend werden einige State-of-the-Art Middlebox Traversal Ansätze untersucht, die als mögliche Lösungen um die Mobile IPv6 Firewall Traversal Probleme zu bewältigen betrachtet werden können. Es wird detailiert erklärt wie diese Lösungen arbeiten und ihre Anwendbarkeit für Mobile IPv6 Firewall Traversal evaluiert.Als Hauptbeitrag bringt diese Arbeit zwei detailierte Lösungsansätze ein, welche das Mobile IPv6 Firewall Traversal Problem bewältigen können. Der erste Lösungsansatz, der NSIS basierte Mobile IPv6 Firewall Traversal, basiert auf dem Next Steps in Signaling (NSIS) Rahmenwerk und dem NAT/Firewall NSIS Signaling Layer Protocol (NAT/FW NSLP). Anschließend wird der zweite Lösungsansatz vorgestellt, der Mobile IPv6 Application Layer Gateway. Diese Arbeit erklärt detailiert, wie diese Lösungsansätze die Probleme und Auswirkungen des Vorhandenseins von Middleboxes in Mobile IPv6 Umgebungen bewältigen. Desweitern stellt diese Arbeit vor, wie die NSIS basierte Mobile IPv6 Firewall Traversal und die Mobile IPv6 Application Layer Gateway Proof-of-Concept Implementierungen, die im Rahmen dieser Arbeit entwicklet wurden, implementiert wurden. Abschließend werden die Proof-of-Concept Implementierungen sowie die beiden Lösungsansätze allgemein evaluiert und analysiert

A gene expression profile associated with relapse of cytogenetically normal acute myeloid leukemia is enriched for leukemia stem cell genes

Some 50 – 80% of patients with acute myeloid leukemia (AML) achieve a complete remission with contemporary chemotherapy protocols, yet the majority of them eventually relapse with resistant disease: some patients no longer respond to chemotherapy at disease recurrence; others accomplish second and even third remissions whose decreasing duration nevertheless indicates that the pool of residual leukemic cells, i.e. of cells that persisted during treatment with cytotoxic drugs, increases with every round of therapy [1]. Either of these clinical courses therefore refl ects an enhanced chemotherapy resistance of leukemic cells at relapse as compared to the cell population at diagnosis. Molecular changes enabling malignant cells to survive exposure to cytotoxic drugs may already have been present in a subset of the leukemic cell population at presentation, or may emerge during treatment [2,3], but in any case are thought to be selected as a consequence of drug therapy, and to play a major role in therapy resistance at relapse. Remarkably, however, even though various types of molecular alterations may be acquired at relapse, neither specifi c cytogenetic alterations nor functionally relevant point mutations as identifi ed by whole genome sequencing were associated with relapse in a recurrent manner [2,3]. Certain copy number variations and known AML associated point mutations were newly present at relapse in small proportions of patients (usually 10%), but the latter were lost in other patients, indicating that they are unlikely to represent drivers of therapy resistance at disease recurrence [4]. Th ese fi ndings could either indicate that chemotherapy resistance at relapse is acquired through a large variety of different mechanisms, or that molecular changes of other types than those mentioned above are of more general relevance in this context. Indeed, an earlier study has suggested that the expression of specifi c genes may change in a consistent manner between diagnosis and relapse of AML [5]. However, only a limited number of genes and mostly unpaired samples were probed in this investigation. Th erefore, in the present study, genes whose expression changed in a relapse-specifi c manner were sought in a set of paired AML samples and on a genome-wide scale. To limit the genetic heterogeneity of the study population, only samples from patients with cytogenetically normal (CN) AML were used.Letter to the Edito

Overexpression of primary microRNA 221/222 in acute myeloid leukemia

BACKGROUND: Acute myeloid leukemia (AML) is a hematopoietic malignancy with a dismal outcome in the majority of cases. A detailed understanding of the genetic alterations and gene expression changes that contribute to its pathogenesis is important to improve prognostication, disease monitoring, and therapy. In this context, leukemia-associated misexpression of microRNAs (miRNAs) has been studied, but no coherent picture has emerged yet, thus warranting further investigations. METHODS: The expression of 636 human miRNAs was compared between samples from 52 patients with AML and 13 healthy individuals by highly specific locked nucleic acid (LNA) based microarray technology. The levels of individual mature miRNAs and of primary miRNAs (pri-miRs) were determined by quantitative reverse transcriptase (qRT) PCR. Transfections and infections of human cell lines were performed using standard procedures. RESULTS: 64 miRNAs were significantly differentially expressed between AML and controls. Further studies on the clustered miRNAs 221 and 222, already known to act as oncogenes in other tumor types, revealed a deficiency of human myeloid cell lines to process vector derived precursor transcripts. Moreover, endogenous pri-miR-221/222 was overexpressed to a substantially higher extent than its mature products in most primary AML samples, indicating that its transcription was enhanced, but processing was rate limiting, in these cells. Comparison of samples from the times of diagnosis, remission, and relapse of AML demonstrated that pri-miR-221/222 levels faithfully reflected the stage of disease. CONCLUSIONS: Expression of some miRNAs is strongly regulated at the posttranscriptional level in AML. Pri-miR-221/222 represents a novel molecular marker and putative oncogene in this disease

Mapping of the dark exciton landscape in transition metal dichalcogenides

Transition metal dichalcogenides (TMDs) exhibit a remarkable exciton physics including bright and optically forbidden dark excitonic states. Here, we show how dark excitons can be experimentally revealed by probing the intraexcitonic 1s-2p transition. Distinguishing the optical response shortly after the excitation and after the exciton thermalization allows us to reveal the relative position of bright and dark excitons. We find both in theory and experiment a clear blueshift in the optical response demonstrating the transition of bright exciton populations into lower-lying dark excitonic states