Institution
Karlsruhe Institute of Technology
Education•Karlsruhe, Germany•
About: Karlsruhe Institute of Technology is a education organization based out in Karlsruhe, Germany. It is known for research contribution in the topics: Computer science & Catalysis. The organization has 37946 authors who have published 82138 publications receiving 2197068 citations. The organization is also known as: KIT & University of Karlsruhe.
Papers published on a yearly basis
Papers
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TL;DR: This method discriminates the specimen-related scattered background from signal fluorescence, thereby removing out-of-focus light and optimizing the contrast of in-focus structures, and provides rapid control of the illumination pattern, exceptional imaging quality and high imaging speeds.
Abstract: The combination of digital scanned laser light sheet microscopy and incoherent structured illumination allows intrinsic removal of scattered background fluorescence from the desired fluorescent signal. This provides substantial advantages for imaging nontransparent organisms and allowed reconstruction of a fly digital embryo from a developing Drosophila embryo.
529 citations
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01 Nov 2016TL;DR: In this article, the authors survey recent trends in practical algorithms for balanced graph partitioning, point to applications, and discuss future research directions, and present a survey of the most popular algorithms.
Abstract: We survey recent trends in practical algorithms for balanced graph partitioning, point to applications and discuss future research directions.
529 citations
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Cardiff University1, University of Alberta2, University Centre in Svalbard3, University of Oslo4, University of Zurich5, Karlsruhe Institute of Technology6, Norwegian Meteorological Institute7, University of Tsukuba8, University of Sussex9, University of Edinburgh10, University of Helsinki11, ETH Zurich12
TL;DR: In this article, the authors present a review of the changing state of European permafrost within a spatial zone that includes the continuous high latitude arctic permfrost of Svalbard and the discontinuous high altitude mountain permaffrost of Iceland, Fennoscandia and the Alps.
529 citations
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TL;DR: This paper proposes a tentative list of information that could be included in published descriptions of tissue electrophysiology models, and used to support interpretation and evaluation of simulation results, to discuss challenges and open questions.
Abstract: Models of cardiac tissue electrophysiology are an important component of the Cardiac Physiome Project, which is an international effort to build biophysically based multi-scale mathematical models of the heart. Models of tissue electrophysiology can provide a bridge between electrophysiological cell models at smaller scales, and tissue mechanics, metabolism and blood flow at larger scales. This paper is a critical review of cardiac tissue electrophysiology models, focussing on the micro-structure of cardiac tissue, generic behaviours of action potential propagation, different models of cardiac tissue electrophysiology, the choice of parameter values and tissue geometry, emergent properties in tissue models, numerical techniques and computational issues. We propose a tentative list of information that could be included in published descriptions of tissue electrophysiology models, and used to support interpretation and evaluation of simulation results. We conclude with a discussion of challenges and open questions.
529 citations
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TL;DR: It is shown that the mitochondria are removed through autophagy system and that changes in mitochondrial network occur in atrophying muscles, indicating that disruption of the mitochondrial network is an essential amplificatory loop of the muscular atrophy programme.
Abstract: Mitochondria are crucial organelles in the production of energy and in the control of signalling cascades. A machinery of pro-fusion and fission proteins regulates their morphology and subcellular localization. In muscle this results in an orderly pattern of intermyofibrillar and subsarcolemmal mitochondria. Muscular atrophy is a genetically controlled process involving the activation of the autophagy-lysosome and the ubiquitin–proteasome systems. Whether and how the mitochondria are involved in muscular atrophy is unknown. Here, we show that the mitochondria are removed through autophagy system and that changes in mitochondrial network occur in atrophying muscles. Expression of the fission machinery is per se sufficient to cause muscle wasting in adult animals, by triggering organelle dysfunction and AMPK activation. Conversely, inhibition of the mitochondrial fission inhibits muscle loss during fasting and after FoxO3 overexpression. Mitochondrial-dependent muscle atrophy requires AMPK activation as inhibition of AMPK restores muscle size in myofibres with altered mitochondria. Thus, disruption of the mitochondrial network is an essential amplificatory loop of the muscular atrophy programme.
528 citations
Authors
Showing all 38468 results
Name | H-index | Papers | Citations |
---|---|---|---|
Hyun-Chul Kim | 176 | 4076 | 183227 |
Yury Gogotsi | 171 | 956 | 144520 |
Marc Weber | 167 | 2716 | 153502 |
Chad A. Mirkin | 164 | 1078 | 134254 |
J. S. Lange | 160 | 2083 | 145919 |
Hannes Jung | 159 | 2069 | 125069 |
Wolfgang Wagner | 156 | 2342 | 123391 |
Vivek Sharma | 150 | 3030 | 136228 |
Teresa Lenz | 150 | 1718 | 114725 |
Andreas Pfeiffer | 149 | 1756 | 131080 |
Daniel Bloch | 145 | 1819 | 119556 |
Th. Müller | 144 | 1798 | 125843 |
Martin Erdmann | 144 | 1562 | 100470 |
Tim Adye | 143 | 1898 | 109010 |
Daniela Bortoletto | 143 | 1883 | 108433 |