Institution
University of Stuttgart
Education•Stuttgart, Germany•
About: University of Stuttgart is a education organization based out in Stuttgart, Germany. It is known for research contribution in the topics: Laser & Finite element method. The organization has 27715 authors who have published 56370 publications receiving 1363382 citations. The organization is also known as: Universität Stuttgart.
Papers published on a yearly basis
Papers
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TL;DR: In this article, the dominant recombination mechanism in ZnO/CdS/Cu(In,Ga)Se 2 heterojunction devices is reviewed and the role of Cd and Cu diffusion during junction formation and air-annealing of the completed device.
244 citations
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Max Planck Society1, École Normale Supérieure2, University of Coimbra3, University of Aveiro4, Yale University5, University of Stuttgart6, Ludwig Maximilian University of Munich7, University of Fribourg8, ETH Zurich9, National Tsing Hua University10, Instituto Politécnico Nacional11, Princeton University12, Paul Scherrer Institute13
TL;DR: The deuteron is too small, too The radius of the proton has remained a point of debate ever since the spectroscopy of muonic hydrogen indicated a large discrepancy from the previously accepted value.
Abstract: The deuteron is the simplest compound nucleus, composed of one proton and one neutron. Deuteron properties such as the root-mean-square charge radius r d and the polarizability serve as important benchmarks for understanding the nuclear forces and structure. Muonic deuterium μd is the exotic atom formed by a deuteron and a negative muon μ – . We measured three 2S-2P transitions in μd and obtain r d = 2.12562 ( 78 ) fm, which is 2.7 times more accurate but 7.5σ smaller than the CODATA-2010 value r d = 2.1424 ( 21 ) fm. The μd value is also 3.5σ smaller than the r d value from electronic deuterium spectroscopy. The smaller r d , when combined with the electronic isotope shift, yields a “small” proton radius r p , similar to the one from muonic hydrogen, amplifying the proton radius puzzle.
244 citations
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TL;DR: The authors' bounds provide a general class of constraints for nonequilibrium systems and show that the parabolic bound is also valid for three paradigmatic examples of driven diffusive systems for which the generating function can be calculated using the additivity principle.
Abstract: For current fluctuations in nonequilibrium steady states of Markovian processes, we derive four different universal bounds valid beyond the Gaussian regime. Different variants of these bounds apply to either the entropy change or any individual current, e.g., the rate of substrate consumption in a chemical reaction or the electron current in an electronic device. The bounds vary with respect to their degree of universality and tightness. A universal parabolic bound on the generating function of an arbitrary current depends solely on the average entropy production. A second, stronger bound requires knowledge both of the thermodynamic forces that drive the system and of the topology of the network of states. These two bounds are conjectures based on extensive numerics. An exponential bound that depends only on the average entropy production and the average number of transitions per time is rigorously proved. This bound has no obvious relation to the parabolic bound but it is typically tighter further away from equilibrium. An asymptotic bound that depends on the specific transition rates and becomes tight for large fluctuations is also derived. This bound allows for the prediction of the asymptotic growth of the generating function. Even though our results are restricted to networks with a finite number of states, we show that the parabolic bound is also valid for three paradigmatic examples of driven diffusive systems for which the generating function can be calculated using the additivity principle. Our bounds provide a general class of constraints for nonequilibrium systems.
243 citations
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28 Sep 2002TL;DR: The analytical model allows the evaluation at runtime, even on devices with restricted resources, and thus enables mobile nodes to dynamically adapt their diffusion strategies depending on the local node density.
Abstract: Choosing appropriate information dissemination strategies is crucial in mobile ad hoc networks (MANET) due to the frequent topology changes Flooding-based approaches like diffusion have a strong similarity with epidemic spreading of diseases Applying epidemiological models to information diffusion allows the evaluation of such strategies depending on the MANET characteristics, eg the node density In order to choose appropriate strategies at run time, the model should be easily evaluatedIn this paper, an epidemic model is developed for a simple information diffusion algorithm based on simulation results We analytically investigate the impact of node density on information diffusion The analytical model allows the evaluation at runtime, even on devices with restricted resources, and thus enables mobile nodes to dynamically adapt their diffusion strategies depending on the local node density
243 citations
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TL;DR: Protection against Fas-induced apoptosis in a FLIP-independent manner converted a proapoptotic Fas signal into an inflammatory NFκB-related response.
Abstract: Fas (APO-1/CD95) is the prototypic death receptor, and the molecular mechanisms of Fas-induced apoptosis are comparably well understood. Here, we show that Fas activates NFκB via a pathway involving RIP, FADD, and caspase-8. Remarkably, the enzymatic activity of the latter was dispensable for Fas-induced NFκB signaling pointing to a scaffolding-related function of caspase-8 in nonapoptotic Fas signaling. NFκB was activated by overexpressed FLIPL and FLIPS in a cell type–specific manner. However, in the context of Fas signaling both isoforms blocked FasL-induced NFκB activation. Moreover, down-regulation of both endogenous FLIP isoforms or of endogenous FLIPL alone was sufficient to enhance FasL-induced expression of the NFκB target gene IL8. As NFκB signaling is inhibited during apoptosis, FasL-induced NFκB activation was most prominent in cells that were protected by Bcl2 expression or caspase inhibitors and expressed no or minute amounts of FLIP. Thus, protection against Fas-induced apoptosis in a FLIP-independent manner converted a proapoptotic Fas signal into an inflammatory NFκB-related response.
243 citations
Authors
Showing all 28043 results
Name | H-index | Papers | Citations |
---|---|---|---|
Yi Chen | 217 | 4342 | 293080 |
Robert J. Lefkowitz | 214 | 860 | 147995 |
Michael Kramer | 167 | 1713 | 127224 |
Andrew G. Clark | 140 | 823 | 123333 |
Stephen D. Walter | 112 | 513 | 57012 |
Fedor Jelezko | 103 | 413 | 42616 |
Ulrich Gösele | 102 | 603 | 46223 |
Dirk Helbing | 101 | 642 | 56810 |
Ioan Pop | 101 | 1370 | 47540 |
Niyazi Serdar Sariciftci | 99 | 591 | 54055 |
Matthias Komm | 99 | 832 | 43275 |
Hans-Joachim Werner | 98 | 317 | 48508 |
Richard R. Ernst | 96 | 352 | 53100 |
Xiaoming Sun | 96 | 382 | 47153 |
Feng Chen | 95 | 2138 | 53881 |