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Energy-dispersive X-ray reflectivity and GID for real-time growth studies of pentacene thin films
(2007)
We use energy-dispersive X-ray reflectivity and grazing incidence diffraction (GID) to follow the growth of the crystalline organic semiconductor pentacene on silicon oxide in-situ and in real-time. The technique allows for monitoring Bragg reflections and measuring X-ray growth oscillations with a time resolution of 1 min in a wide q-range in reciprocal space extending over 0.25-0.80 angstrom(-1), i.e. sampling a large number of Fourier components simultaneously. A quantitative analysis of growth oscillations at several q-points yields the evolution of the surface roughness, showing a marked transition from layer-by-layer growth to strong roughening after four monolayers of pentacene have been deposited. (c) 2006 Elsevier B.V. All rights reserved.
This paper proposes a new independent component analysis (ICA) method which is able to unmix overcomplete mixtures of sparce or structured signals like speech, music or images. Furthermore, the method is designed to be robust against outliers, which is a favorable feature for ICA algorithms since most of them are extremely sensitive to outliers. Our approach is based on a simple outlier index. However, instead of robustifying an existing algorithm by some outlier rejection technique we show how this index can be used directly to solve the ICA problem for super-Gaussian sources. The resulting inlier-based ICA (IBICA) is outlier-robust by construction and can be used for standard ICA as well as for overcomplete ICA (i.e. more source signals than observed signals). (c) 2005 Wiley Periodicals, Inc
Usually, noise is considered to be destructive. We present a new method that constructively injects noise to assess the reliability and the grouping structure of empirical ICA component estimates. Our method can be viewed as a Monte-Carlo-style approximation of the curvature of some performance measure at the solution. Simulations show that the true root-mean-squared angle distances between the real sources and the source estimates can be approximated well by our method. In a toy experiment, we see that we are also able to reveal the underlying grouping structure of the extracted ICA components. Furthermore, an experiment with fetal ECG data demonstrates that our approach is useful for exploratory data analysis of real-world data. (C) 2003 Elsevier B.V. All rights reserved
The Cassini-Huygens Cosmic Dust Analyzer (CDA) is intended to provide direct observations of dust grains with masses between 10(-19) and 10(-9) kg in interplanetary space and in the jovian and saturnian systems, to investigate their physical, chemical and dynamical properties as functions of the distances to the Sun, to Jupiter and to Saturn and its satellites and rings, to study their interaction with the saturnian rings, satellites and magnetosphere. Chemical composition of interplanetary meteoroids will be compared with asteroidal and cometary dust, as well as with Saturn dust, ejecta from rings and satellites. Ring and satellites phenomena which might be effects of meteoroid impacts will be compared with the interplanetary dust environment. Electrical charges of particulate matter in the magnetosphere and its consequences will be studied, e.g. the effects of the ambient plasma and the magnetic held on the trajectories of dust particles as well as fragmentation of particles due to electrostatic disruption. The investigation will be performed with an instrument that measures the mass, composition, electric charge, speed, and flight direction of individual dust particles. It is a highly reliable and versatile instrument with a mass sensitivity 106 times higher than that of the Pioneer 10 and I I dust detectors which measured dust in the saturnian system. The Cosmic Dust Analyzer has significant inheritance from former space instrumentation developed for the VEGA, Giotto, Galileo, and Ulysses missions. It will reliably measure impacts from as low as I impact per month up to 104 impacts per second. The instrument weighs 17 kg and consumes 12 W, the integrated time-of-flight mass spectrometer has a mass resolution of up to 50. The nominal data transmission rate is 524 bits/s and varies between 50 and 4192 bps
Reduced expression of the Indy ("I am Not Dead, Yet") gene in lower organisms promotes longevity in a manner akin to caloric restriction. Deletion of the mammalian homolog of Indy (mIndy, Slc13a5) encoding for a plasma membrane-associated citrate transporter expressed highly in the liver, protects mice from high-fat diet-induced and aging-induced obesity and hepatic fat accumulation through a mechanism resembling caloric restriction. We studied a possible role of mIndy in human hepatic fat metabolism. In obese, insulin-resistant patients with nonalcoholic fatty liver disease, hepatic mIndy expression was increased and mIndy expression was also independently associated with hepatic steatosis. In nonhuman primates, a 2-year high-fat, high-sucrose diet increased hepatic mIndy expression. Liver microarray analysis showed that high mIndy expression was associated with pathways involved in hepatic lipid metabolism and immunological processes. Interleukin-6 (IL-6) was identified as a regulator of mIndy by binding to its cognate receptor. Studies in human primary hepatocytes confirmed that IL-6 markedly induced mIndy transcription through the IL-6 receptor and activation of the transcription factor signal transducer and activator of transcription 3, and a putative start site of the human mIndy promoter was determined. Activation of the IL-6-signal transducer and activator of transcription 3 pathway stimulated mIndy expression, enhanced cytoplasmic citrate influx, and augmented hepatic lipogenesis in vivo. In contrast, deletion of mIndy completely prevented the stimulating effect of IL-6 on citrate uptake and reduced hepatic lipogenesis. These data show that mIndy is increased in liver of obese humans and nonhuman primates with NALFD. Moreover, our data identify mIndy as a target gene of IL-6 and determine novel functions of IL-6 through mINDY. Conclusion: Targeting human mINDY may have therapeutic potential in obese patients with nonalcoholic fatty liver disease. German Clinical Trials Register: DRKS00005450.
Background & purpose: Recent studies suggested a role of prostaglandin E-2 (PGE(2)) in the expression of the chemokine IL-8 by monocytes. The function of EP4 receptor for TNF alpha-induced IL-8 expression was studied in monocytic cell lines. Experimental approach: IL-8 mRNA and protein induction as well as IL-8 promoter activity and transcription factor activation were assessed in monocytic cell lines, primary blood mononuclear cells (PBMC) and transgenic HEK293 cells expressing the EP4 receptor. Key results: In monocytic cell lines THP-1, MonoMac and U937 PGE(2) had only a marginal impact on IL-8 induction but strongly enhanced TNFa-induced IL-8 mRNA and protein synthesis. Similarly, in PBMC IL-8 mRNA induction was larger by simultaneous stimulation with TNF alpha and PGE(2) than by either stimulus alone. The EP4 receptor subtype was the most abundant EP receptor in all three cell lines and in PBMC. Stimulation of THP-1 cells with an EP4 specific agonist enhanced TNF alpha-induced IL-8 mRNA and protein formation to the same extent as PGE(2). In HEK293 cells expressing EP4, but not in wild type HEK293 cells lacking EP4, PGE(2) enhanced TNFainduced IL-8 protein and mRNA synthesis. In THP-1 cells, the enhancement of TNF alpha-mediated IL-8 mRNA induction by PGE(2) was mimicked by a PICA-activator. Furthermore in these cells PGE(2) induced expression of transcription factor C/EBPS, enhanced NF-KB activation by TNFa and inhibited TNF alpha-mediated AP-1 activation. PGE(2) and TNF alpha synergistically activated transcription factor CREB, induced C/EBPS expression and enhanced the activity of an IL-8 promoter fragment containing-223 bp upstream of the transcription start site. Conclusions and implications: These findings suggest that a combined stimulation of TNF alpha and PGE(2)/EP4 signal chains in monocytic cells leads to maximal IL-8 promoter activity, as well as IL-8 mRNA and protein induction, by activating the PICA/CREB/C/EB1313 as well as NF-kappa B signal chains.