Albert Ludwigs University of Freiburg
Freiburg, Germany

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.

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Hahn Schickard Gesellschaft fuer angewandte Forschung e.V. and Albert Ludwigs University of Freiburg | Date: 2016-12-05

A fluidic module rotatable about a center of rotation includes a first compression chamber having a fluid inlet and a fluid outlet, a second compression chamber having a fluid inlet, a first fluid channel connected to the first chamber via the fluid inlet of the first chamber, and a second fluid channel connecting the fluid outlet of the first chamber to the fluid inlet of the second chamber. Due to rotation of the fluidic module a liquid may be centrifugally driven into the first chamber and the second fluid channel through the first fluid channel, and thereby a compressible medium may be entrapped and compressed within the second chamber. By lowering the rotary frequency and due to the resultant expansion of the compressible medium, liquid may be driven out of the second fluid channel into the first chamber, out of the first chamber into and through an outlet channel.

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.

Hoffmann-La Roche and Albert Ludwigs University of Freiburg | Date: 2015-06-18

The present invention pertains to the use of an Integrative pharmacokinetic/pharmacodynamic (PK/PD) ESA-EpoR mathematical model for calculating the binding behaviour of erythropoiesis stimulating agents (ESA). The invention provides methods for the determining of ESA binding sites in cells or patients suffering from anemia. Knowing the amount of ESA binding sites enables the clinical practitioner to optimize the dosage regimen during a treatment of anemia, in particular in patients suffering from a cancerous disease. Further provided are methods for screening ESAs which have a higher specificity for cells strongly expressing the EPO receptor such as colony forming units-erythroid (CFU-E) cells, and not to cells with a low level of EPO receptor cell surface expression, which is the case in cancer cells. Also provided is a computer implemented method, comprising the use of the mathematical model of the invention.

Albert Ludwigs University of Freiburg | Date: 2015-03-06

The present invention is inter alia concerned with a method of diagnosing Alzheimers disease in a patient, wherein said method is based on determining the amount of at least one premature mitochondrial protein. Further, the present invention relates to the use of such a protein as marker for Alzheimers disease. Accordingly, antibodies binding to such a preprotein may be used for diagnosing Alzheimers disease. The present invention is based on the finding that premature mitochondrial proteins accumulate in Alzheimers disease.

The present invention relates to a circuit arrangement and a method for reading a capacitive vibratory gyroscope with an at least primary mass and at least one secondary mass that is connected to the primary mass, wherein the primary mass is excited to a primary vibration during operation, and wherein the secondary mass is deflected out of a resting position in a direction that is transversal to the primary vibration when the vibratory gyroscope rotates around a sensitive axis. The circuit arrangement comprises a delta-sigma modulator with at least one control loop to perform a force feedback that resets the secondary mass into its resting state by applying a reset signal, wherein the reset signal forms a modulator output signal of the delta-sigma modulator, a correction unit that receives the modulator output signal and that is operated to generate a corrected modulator output signal that corresponds to an actually acting feedback force, a demodulator that is connected to the correction unit for demodulation of the corrected modulator output signal, and a filter arrangement to filter the demodulated signals and to output a rotary rate signal.

Prinz M.,Albert Ludwigs University of Freiburg | Priller J.,Charité - Medical University of Berlin
Nature Reviews Neuroscience | Year: 2014

Mononuclear phagocytic cells in the CNS used to be defined according to their anatomical location and surface marker expression. Recently, this concept has been challenged by the results of developmental and gene expression profiling studies that have used novel molecular biological tools to unravel the origin of microglia and to define their role as specialized tissue macrophages with long lifespans. Here, we describe how these results have redefined microglia and helped us to understand how different myeloid cell populations operate in the CNS based on their cell-specific gene expression signatures, distinct ontogeny and differential functions. Moreover, we describe the vulnerability of microglia to dysfunction and propose that myelomonocytic cells might be used in the treatment of neurological and psychiatric disorders that are characterized by primary or secondary 'microgliopathy'. © 2014 Macmillan Publishers Limited. All rights reserved.

Frotscher M.,Albert Ludwigs University of Freiburg
Trends in Neurosciences | Year: 2010

Reelin controls the migration of neurons and layer formation during brain development. However, recent studies have shown that disrupting Reelin function in the adult hippocampus induces repositioning of fully differentiated neurons, suggesting a stabilizing effect of Reelin on mature neuronal circuitry. Indeed, Reelin was recently found to stabilize the actin cytoskeleton by inducing cofilin phosphorylation. When unphosphorylated, cofilin acts as an actin-depolymerizing protein that promotes the disassembly of F-actin. Here, a novel hypothesis is proposed whereby decreased Reelin expression in the mature brain causes destabilization of neurons and their processes, leading to aberrant plasticity and aberrant wiring of brain circuitry. This has implications for brain disorders, such as epilepsy and schizophrenia, in which deficiencies in Reelin expression occur. © 2010 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.

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.

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.

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