The University of Freiburg , sometimes referred to with its full title, the Albert Ludwig University of Freiburg, is a public research university located in Freiburg im Breisgau, Baden-Württemberg, Germany.The university was founded in 1457 by the Habsburg dynasty as the second university in Austrian-Habsburg territory after the University of Vienna. Today, Freiburg is the fifth-oldest university in Germany, with a long tradition of teaching the humanities, social science and natural science. The university is made up of 11 faculties and attracts students from across Germany as well as from over 120 other countries. Foreign students constitute about 16% of total student numbers.Named as one of elite universities of Germany by academics, political representatives and the media, the University of Freiburg stands amongst Europe's top research and teaching institutions. With its long-standing reputation of excellence, the university looks both to the past, to maintain its historic academic and cultural heritage, and to the future, developing new methods and opportunities to meet the needs of a changing world. The University of Freiburg has been home to some of the greatest minds of the Western tradition, including such eminent figures as Martin Heidegger, Hannah Arendt, Rudolf Carnap, David Daube, Johann Eck, Hans-Georg Gadamer, Friedrich Hayek, Edmund Husserl, Friedrich Meinecke, and Max Weber. In addition, 19 Nobel laureates are affiliated with the University of Freiburg and 15 academics have been honored with the highest German research prize, the Gottfried Wilhelm Leibniz Prize, while working at the University of Freiburg. Wikipedia.
Kineticor, University of Hawaii at Manoa and Albert Ludwigs University of Freiburg | Date: 2016-07-28
The systems, methods, and devices described herein generally relate to achieving accurate and robust motion correction by detecting and accounting for false movements in motion correction systems used in conjunction with medical imaging and/or therapeutic systems. In other words, in some embodiments of the systems, methods, and devices described herein can be configured to detect false movements for motion correction during a medical imaging scan and/or therapeutic procedure, and thereby ensure that such false movements are not accounted for in the motion correction process. Upon detection of false movements, the imaging or therapeutic system can be configured to transiently suppress and/or subsequently repeat acquisitions.
Agency: European Commission | Branch: H2020 | Program: SGA-RIA | Phase: FETFLAGSHIP | Award Amount: 89.00M | Year: 2016
This project is the second in the series of EC-financed parts of the Graphene Flagship. The Graphene Flagship is a 10 year research and innovation endeavour with a total project cost of 1,000,000,000 euros, funded jointly by the European Commission and member states and associated countries. The first part of the Flagship was a 30-month Collaborative Project, Coordination and Support Action (CP-CSA) under the 7th framework program (2013-2016), while this and the following parts are implemented as Core Projects under the Horizon 2020 framework. The mission of the Graphene Flagship is to take graphene and related layered materials from a state of raw potential to a point where they can revolutionise multiple industries. This will bring a new dimension to future technology a faster, thinner, stronger, flexible, and broadband revolution. Our program will put Europe firmly at the heart of the process, with a manifold return on the EU investment, both in terms of technological innovation and economic growth. To realise this vision, we have brought together a larger European consortium with about 150 partners in 23 countries. The partners represent academia, research institutes and industries, which work closely together in 15 technical work packages and five supporting work packages covering the entire value chain from materials to components and systems. As time progresses, the centre of gravity of the Flagship moves towards applications, which is reflected in the increasing importance of the higher - system - levels of the value chain. In this first core project the main focus is on components and initial system level tasks. The first core project is divided into 4 divisions, which in turn comprise 3 to 5 work packages on related topics. A fifth, external division acts as a link to the parts of the Flagship that are funded by the member states and associated countries, or by other funding sources. This creates a collaborative framework for the entire Flagship.
Reiter G.,Albert Ludwigs University of Freiburg
Chemical Society Reviews | Year: 2014
Mono-lamellar single crystals in thin films provide suitable model systems for studying crystallisation of long chain polymers, making distinct differences with respect to small molecules visible. Due to the high viscosity of polymeric melts, transport toward the growth front is slow and the corresponding crystal growth can suitably be followed in time. Besides being able to investigate generic processes in controlling crystal morphology like epitaxial growth or growth front instabilities, thin film studies reveal unique features of polymer crystallisation. In particular, it is possible to observe a logarithmic spatio-temporal evolution of the lamellar crystal thickness, caused by continuous rearrangements leading to regions of differing degrees of meta-stability within polymer single crystals. As a consequence of the kinetically determined lamellar thickness and the corresponding variations in melting temperature, polymer crystals allow for self-seeding, i.e., crystals can be re-grown from a melt which contains a few thermodynamically stable remnants of pre-existing crystals acting as seeds. Hence, when a single crystal is molten, all remnants have a unique orientation and thus also the crystals re-grown from these seeds. The logarithmic time-dependence of the variation in crystal thickness is reflected in a number of seeds decreasing exponentially with increasing seeding temperature. Despite their molecular complexity and some unique features, polymers proved to be valuable systems for detailed studies of crystal growth, allowing testing of theoretical concepts of morphology development. This journal is © the Partner Organisations 2014.
Fritz G.,Albert Ludwigs University of Freiburg
Trends in Biochemical Sciences | Year: 2011
The receptor for advanced glycation end products (RAGE) is a central signaling molecule in the innate immune system and is involved in the onset and sustainment of the inflammatory response. RAGE belongs to a class of pattern recognition receptors that recognize common features rather than a specific ligand. Recent structural information on the extracellular portion (ectodomain) of RAGE shed new light on this unusual ability. X-ray crystallographic, NMR and biochemical data suggest that ligand binding is driven largely by electrostatic interactions between the positively charged surface of the ectodomain and negatively charged ligands. In this article, I propose a putative mechanism of RAGE ligand recognition of receptor activation. © 2011 Elsevier Ltd.
Brabletz T.,Albert Ludwigs University of Freiburg
Nature Reviews Cancer | Year: 2012
Why are many metastases differentiated? Invading and disseminating carcinoma cells can undergo an epithelialg-mesenchymal transition (EMT), which is associated with a gain of stem cell-like behaviour. Therefore, EMT has been linked to the cancer stem cell concept. However, it is a matter of debate how subsequent mesenchymalg-epithelial transition (MET) fits into the metastatic process and whether a MET is essential. In this Opinion article, I propose two principle types of metastatic progression: phenotypic plasticity involving transient EMTg-MET processes and intrinsic genetic alterations keeping cells in an EMT and stemness state. This simplified classification integrates clinically relevant aspects of dormancy, metastatic tropism and therapy resistance, and implies perspectives on treatment strategies against metastasis. © 2012 Macmillan Publishers Limited. All rights reserved.
Manz B.,Albert Ludwigs University of Freiburg
Nature communications | Year: 2012
Infection of mammals by avian influenza viruses requires adaptive mutations to achieve high-level replication in the new host. However, the basic mechanism underlying this adaptation process is still unknown. Here we show that avian polymerases, lacking the human signature PB2-E627K, are incapable of generating usable complementary RNA templates in cultured human cells and therefore require adaptation. Characterization of the highly pathogenic human H5N1 isolate A/Thailand/1(KAN-1)/2004 that retained the avian PB2-E627 reveals that the defect in RNA replication is only partially compensated by mutations in the polymerase. Instead, mutations in the nuclear export protein are required for efficient polymerase activity. We demonstrate that adaptive mutations in nuclear export proteins of several human isolates enhance the polymerase activity of avian polymerases in human cultured cells. In conclusion, when crossing the species barrier, avian influenza viruses acquire adaptive mutations in nuclear export protein to escape restricted viral genome replication in mammalian cells.
Haller O.,Albert Ludwigs University of Freiburg
Cell Host and Microbe | Year: 2013
Human MxA (MX1) protein is an interferon-induced restriction factor for a diverse range of viruses, whereas the related MxB (MX2) protein was thought to lack such activity. Three recent papers, including one in this issue of Cell Host & Microbe, show that MxB inhibits human immunodeficiency virus type 1 (HIV-1) infection. © 2013 Elsevier Inc.
Niemeyer C.M.,Albert Ludwigs University of Freiburg
Nature genetics | Year: 2010
CBL encodes a member of the Cbl family of proteins, which functions as an E3 ubiquitin ligase. We describe a dominant developmental disorder resulting from germline missense CBL mutations, which is characterized by impaired growth, developmental delay, cryptorchidism and a predisposition to juvenile myelomonocytic leukemia (JMML). Some individuals experienced spontaneous regression of their JMML but developed vasculitis later in life. Importantly, JMML specimens from affected children show loss of the normal CBL allele through acquired isodisomy. Consistent with these genetic data, the common p.371Y>H altered Cbl protein induces cytokine-independent growth and constitutive phosphorylation of ERK, AKT and S6 only in hematopoietic cells in which normal Cbl expression is reduced by RNA interference. We conclude that germline CBL mutations have developmental, tumorigenic and functional consequences that resemble disorders that are caused by hyperactive Ras/Raf/MEK/ERK signaling and include neurofibromatosis type 1, Noonan syndrome, Costello syndrome, cardiofaciocutaneous syndrome and Legius syndrome.
Leonhardt F.,Albert Ludwigs University of Freiburg
Blood | Year: 2013
Acute graft-versus-host disease (GvHD) is a complex process involving endothelial damage and neovascularization. Better understanding of the pathophysiology of neovascularization during GvHD could help to target this process while leaving T-cell function intact. Under ischemic conditions, neovascularization is regulated by different micro RNAs (miRs), which potentially play a role in inflamed hypoxic GvHD target organs. We observed strong neovascularization in the murine inflamed intestinal tract (IT) during GvHD. Positron emission tomography imaging demonstrated abundant αvβ3 integrin expression within intestinal neovascularization areas. To interfere with neovascularization, we targeted αv integrin-expressing endothelial cells, which blocked their accumulation in the IT and reduced GvHD severity independent of immune reconstitution and graft-versus-tumor effects. Additionally, enhanced neovascularization and αv integrin expression correlated with GvHD severity in humans. Expression analysis of miRs in the inflamed IT of mice developing GvHD identified miR-100 as significantly downregulated. Inactivation of miR-100 enhanced GvHD indicating a protective role for miR-100 via blocking inflammatory neovascularization. Our data from the mouse model and patients indicate that inflammatory neovascularization is a central event during intestinal GvHD that can be inhibited by targeting αv integrin. We identify negative regulation of GvHD-related neovascularization by miR-100, which indicates common pathomechanistic features of GvHD and ischemia.
Aberg J.,Albert Ludwigs University of Freiburg
Physical Review Letters | Year: 2014
Because of conservation of energy we cannot directly turn a quantum system with a definite energy into a superposition of different energies. However, if we have access to an additional resource in terms of a system with a high degree of coherence, as for standard models of laser light, we can overcome this limitation. The question is to what extent coherence gets degraded when utilized. Here it is shown that coherence can be turned into a catalyst, meaning that we can use it repeatedly without ever diminishing its power to enable coherent operations. This finding stands in contrast to the degradation of other quantum resources and has direct consequences for quantum thermodynamics, as it shows that latent energy that may be locked into superpositions of energy eigenstates can be released catalytically. © 2014 American Physical Society.