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Munich, Germany

Ludwig Maximilian University of Munich is a public research university located in Munich, Germany.The University of Munich is among Germany's oldest universities. Originally established in Ingolstadt in 1472 by Duke Ludwig IX of Bavaria-Landshut, the university was moved in 1800 to Landshut by King Maximilian I of Bavaria when Ingolstadt was threatened by the French, before being relocated to its present-day location in Munich in 1826 by King Ludwig I of Bavaria. In 1802, the university was officially named Ludwig-Maximilians-Universität by King Maximilian I of Bavaria in his as well as the university's original founder's honour.The University of Munich has, particularly since the 19th century, been considered as one of Germany's as well as one of Europe's most prestigious universities; with 34 Nobel laureates associated with the university, it ranks 13th worldwide by number of Nobel laureates. Among these were Wilhelm Röntgen, Max Planck, Werner Heisenberg, Otto Hahn and Thomas Mann. Pope Benedict XVI was also a student and professor at the university. The LMU has recently been conferred the title of "elite university" under the German Universities Excellence Initiative.LMU is currently the second-largest university in Germany in terms of student population; in the winter semester of 2013/2014, the university had a total of 50,542 matriculated students. Of these, 8,719 were freshmen while international students totalled 7,403 or almost 15% of the student population. As for operating budget, the university records in 2013 a total of 571.3 million Euros in funding without the university hospital; with the university hospital, the university has a total funding amounting to approximately 1.5 billion Euros. Wikipedia.


Hermeking H.,Ludwig Maximilians University of Munich
Nature Reviews Cancer | Year: 2012

In recent years, microRNAs (miRNAs) have been identified as mediators of tumour suppression and stress responses exerted by the p53 tumour suppressor. p53-regulated miRNAs contribute to tumour suppression by controlling the expression of central components of multiple processes, including cell cycle progression, epithelialg-mesenchymal transition, stemness, metabolism, cell survival and angiogenesis. The expression and activity of p53 itself is also under the control of miRNAs. Finally, genetic and epigenetic alterations identified in the p53g-miRNA network indicate that these pathways are important for the initiation and progression of tumours. In the future, knowledge about the p53g-miRNA network may be able to be exploited for diagnostic and therapeutic approaches in cancer prevention and treatment. © 2012 Macmillan Publishers Limited. All rights reserved. Source


Soehnlein O.,Ludwig Maximilians University of Munich
Circulation Research | Year: 2012

Because of their rare detection in atherosclerotic lesions, the involvement of neutrophils in the pathophysiology of atherosclerosis has been largely denied. However, over the past couple of years, studies have provided convincing evidence for the presence of neutrophils in atherosclerotic plaques and further revealed the causal contribution of neutrophils during various stages of atherosclerosis. This review describes mechanisms underlying hyperlipidemia-mediated neutrophilia and how neutrophils may enter atherosclerotic lesions. It also highlights possible mechanisms of neutrophil-driven atherogenesis and plaque destabilization. Knowledge of the contribution of neutrophils to atherosclerosis will allow for exploration of new avenues in the treatment of atherogenesis and atherothrombosis. © 2012 American Heart Association, Inc. Source


Wagner E.,Ludwig Maximilians University of Munich
Accounts of Chemical Research | Year: 2012

Synthetic small interfering RNA (siRNA) presents an exciting novel medical opportunity. Although researchers agree that siRNA could have a great therapeutic impact, the required extracellular and intracellular delivery of these molecules into the disease-associated target cells presents the primary roadblock for the broader translation of these molecules into medicines. Thus, the design of adequate delivery technologies has utmost importance. Viruses are natural masterpieces of nucleic acid delivery and present chemists and drug delivery experts with a template for the design of artificial carriers for synthetic nucleic acids such as siRNA. They have been developed into gene vectors and have provided convincing successes in gene therapy. Optimized by biological evolution, viruses are programmed to be dynamic and bioresponsive as they enter living cells, and they carry out their functions in a precisely defined sequence. However, because they are synthesized within living cells and with naturally available nucleotides and amino acids, the chemistry of viruses is limited. With the use of diverse synthetic molecules and macromolecules, chemists can provide delivery solutions beyond the scope of the natural evolution of viruses.This Account describes the design and synthesis of "synthetic siRNA viruses." These structures contain elements that mimic the delivery functions of viral particles and surface domains that shield against undesired biological interactions and enable specific host cell receptor binding through the presentation of multiple targeting ligands. For example, cationic polymers can reversibly package one or more siRNA molecules into nanoparticle cores to protect them against a degradative bioenvironment. After internalization by receptor-mediated endocytosis into the acidifying endosomes of cells, synthetic siRNA can escape from these vesicles through the activation of membrane-disruption domains as viruses do and reach the cytoplasm, the location of RNA interference.This multistep task presents an attractive challenge for chemists. Similar to the design of prodrugs, the functional domains of these systems have to be activated in a dynamic mode, triggered by conformational changes or bond cleavages in the relevant microenvironment such as the acidic endosome or disulfide-reducing cytoplasm. These chemical analogues of viral domains are often synthetically simpler and more easily accessible molecules than viral proteins. Their precise assembly into multifunctional macromolecular and supramolecular structures is facilitated by improved analytical techniques, precise orthogonal conjugation chemistries, and sequence-defined polymer syntheses. The chemical evolution of microdomains using chemical libraries and macromolecular and supramolecular evolution could provide key strategies for optimizing siRNA carriers to selected medical indications. © 2011 American Chemical Society. Source


Hermeking H.,Ludwig Maximilians University of Munich
Cell Death and Differentiation | Year: 2010

Recently, the transcription factor encoded by tumor suppressor gene p53 was shown to regulate the expression of microRNAs. The most significant induction by p53 was observed for the microRNAs miR-34a and miR-34b/c, which turned out to be direct p53 target genes. Ectopic miR-34 expression induces apoptosis, cell-cycle arrest or senescence. In many tumor types the promoters of the miR-34a and the miR-34b/c genes are subject to inactivation by CpG methylation. MiR-34a resides on 1p36 and is commonly deleted in neuroblastomas. Furthermore, the loss of miR-34 expression has been linked to resistance against apoptosis induced by p53 activating agents used in chemotherapy. In this review, the evidence for a role of miR-34a and miR-34b/c in the apoptotic response of normal and tumor cells is surveyed. © 2010 Macmillan Publishers Limited All rights reserved. Source


Mascher T.,Ludwig Maximilians University of Munich
Current Opinion in Microbiology | Year: 2013

Extracytoplasmic function σ factors (ECFs) represent a fundamental and widely distributed principle of bacterial signal transduction that connects the perception of a stimulus (input) with the induction of an appropriate set of genes (output). In recent years, comparative genomics analyses have not only allowed a systematic and functional classification of ECFs but also indicated the presence of numerous novel and widely conserved mechanisms of ECF-dependent signaling. Some of these novel systems have been experimentally characterized and uncovered unique features not previously observed. These studies demonstrate that ECF-dependent signaling is much more versatile and diverse than has been appreciated before. They also indicate that the majority of mechanisms that regulate ECF activity still remain to be discovered and characterized. © 2013 Elsevier Ltd. Source

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