University of Würzburg

About: University of Würzburg is a education organization based out in Wurzburg, Bayern, Germany. It is known for research contribution in the topics: Population & Gene. The organization has 31437 authors who have published 62203 publications receiving 2337033 citations. The organization is also known as: Julius-Maximilians-Universität Würzburg & Würzburg University.

Building a new conceptual framework for receptor heteromers

Abstract: Receptor heteromers constitute a new area of research that is reshaping our thinking about biochemistry, cell biology, pharmacology and drug discovery. In this commentary, we recommend clear definitions that should facilitate both information exchange and research on this growing class of transmembrane signal transduction units and their complex properties. We also consider research questions underlying the proposed nomenclature, with recommendations for receptor heteromer identification in native tissues and their use as targets for drug development.

Boson Sampling with 20 Input Photons and a 60-Mode Interferometer in a 10^{14}-Dimensional Hilbert Space.

Abstract: Quantum computing experiments are moving into a new realm of increasing size and complexity, with the short-term goal of demonstrating an advantage over classical computers. Boson sampling is a promising platform for such a goal; however, the number of detected single photons is up to five so far, limiting these small-scale implementations to a proof-of-principle stage. Here, we develop solid-state sources of highly efficient, pure, and indistinguishable single photons and 3D integration of ultralow-loss optical circuits. We perform experiments with 20 pure single photons fed into a 60-mode interferometer. In the output, we detect up to 14 photons and sample over Hilbert spaces with a size up to 3.7×10^{14}, over 10 orders of magnitude larger than all previous experiments, which for the first time enters into a genuine sampling regime where it becomes impossible to exhaust all possible output combinations. The results are validated against distinguishable samplers and uniform samplers with a confidence level of 99.9%.

Morphology control of fluorescent nanoaggregates by co-self-assembly of wedge- and dumbbell-shaped amphiphilic perylene bisimides.

Abstract: Wedge- and dumbbell-shaped amphiphilic perylene bisimides PBI 1−4 were synthesized. The wedge-shaped PBI 1 and PBI 2 and dumbbell-shaped PBI 4 self-assemble into micelles, and rod aggregates in aqueous solution, respectively. Interestingly, the co-self-assembly of wedge-shaped PBI 1 with dumbbell-shaped PBI 3 generates hollow vesicles with bilayer structures because of the curvature changes during the self-assembly process. The bilayer vesicles could be stabilized by in situ photopolymerization.

Smad3 Null Mice Develop Airspace Enlargement and Are Resistant to TGF-β-Mediated Pulmonary Fibrosis

Abstract: Transforming growth factor-β1 plays a key role in the pathogenesis of pulmonary fibrosis, mediating extracellular matrix (ECM) gene expression through a series of intracellular signaling molecules, including Smad2 and Smad3 We show that Smad3 null mice (knockout (KO)) develop progressive age-related increases in the size of alveolar spaces, associated with high spontaneous presence of matrix metalloproteinases (MMP-9 and MMP-12) in the lung Moreover, transient overexpression of active TGF-β1 in lungs, using adenoviral vector-mediated gene transfer, resulted in progressive pulmonary fibrosis in wild-type mice, whereas no fibrosis was seen in the lungs of Smad3 KO mice up to 28 days Significantly higher levels of matrix components (procollagen 3A1, connective tissue growth factor) and antiproteinases (plasminogen activator inhibitor-1, tissue inhibitor of metalloproteinase-1) were detected in wild-type lungs 4 days after TGF-β1 administration, while no such changes were seen in KO lungs These data suggest a pivotal role of the Smad3 pathway in ECM metabolism Basal activity of the pathway is required to maintain alveolar integrity and ECM homeostasis, but excessive signaling through the pathway results in fibrosis characterized by inhibited degradation and enhanced ECM deposition The Smad3 pathway is involved in pathogenic mechanisms mediating tissue destruction (lack of repair) and fibrogenesis (excessive repair)