Institution
University of Freiburg
Education•Freiburg, Baden-Württemberg, Germany•
About: University of Freiburg is a education organization based out in Freiburg, Baden-Württemberg, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 41992 authors who have published 77296 publications receiving 2896269 citations. The organization is also known as: alberto-ludoviciana & Albert-Ludwigs-Universität Freiburg.
Topics: Population, Transplantation, Gene, Large Hadron Collider, Medicine
Papers published on a yearly basis
Papers
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TL;DR: The ATLAS trigger system as discussed by the authors selects events by rapidly identifying signatures of muon, electron, photon, tau lepton, jet, and B meson candidates, as well as using global event signatures, such as missing transverse energy.
Abstract: Proton-proton collisions at root s = 7 TeV and heavy ion collisions at root(NN)-N-s = 2.76 TeV were produced by the LHC and recorded using the ATLAS experiment's trigger system in 2010. The LHC is designed with a maximum bunch crossing rate of 40 MHz and the ATLAS trigger system is designed to record approximately 200 of these per second. The trigger system selects events by rapidly identifying signatures of muon, electron, photon, tau lepton, jet, and B meson candidates, as well as using global event signatures, such as missing transverse energy. An overview of the ATLAS trigger system, the evolution of the system during 2010 and the performance of the trigger system components and selections based on the 2010 collision data are shown. A brief outline of plans for the trigger system in 2011 is presented.
417 citations
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TL;DR: This article developed two instructional approaches to improve collaboration in computer-mediated settings by promoting people's capabilities to collaborate in a fruitful way and furthering their understanding of what characterizes good collaboration.
Abstract: Effective collaboration in computer-mediated settings among spatially distributed people is a precondition for success in many new learning and working contexts but it is hard to achieve. We have developed two instructional approaches to improve collaboration in such settings by promoting people's capabilities to collaborate in a fruitful way and furthering their understanding of what characterizes good collaboration. The rationale is that strategies necessary for a good and effective computer-mediated collaboration may be conveyed to people by exposing them to an elaborated worked-out collaboration example (observational learning) or by giving them the opportunity to learn from scripted collaborative problem-solving. An experimental study was conducted that compared learning from observing a worked-out collaboration example with the learning effects of scripted collaborative problem-solving, the effects of unscripted collaborative problem-solving, and a control condition without a learning phase. The exp...
417 citations
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TL;DR: Pathway and enrichment analyses, including mouse models with renal phenotypes, support the kidney as the main target organ and provide a comprehensive priority list of molecular targets for translational research.
Abstract: Chronic kidney disease (CKD) is responsible for a public health burden with multi-systemic complications. Through trans-ancestry meta-analysis of genome-wide association studies of estimated glomerular filtration rate (eGFR) and independent replication (n = 1,046,070), we identified 264 associated loci (166 new). Of these, 147 were likely to be relevant for kidney function on the basis of associations with the alternative kidney function marker blood urea nitrogen (n = 416,178). Pathway and enrichment analyses, including mouse models with renal phenotypes, support the kidney as the main target organ. A genetic risk score for lower eGFR was associated with clinically diagnosed CKD in 452,264 independent individuals. Colocalization analyses of associations with eGFR among 783,978 European-ancestry individuals and gene expression across 46 human tissues, including tubulo-interstitial and glomerular kidney compartments, identified 17 genes differentially expressed in kidney. Fine-mapping highlighted missense driver variants in 11 genes and kidney-specific regulatory variants. These results provide a comprehensive priority list of molecular targets for translational research.
416 citations
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TL;DR: It is proposed that PIF3 acts transiently, and its major function is to mediate phytochrome-induced signaling during the developmental switch from skotomorphogenesis to photomorphogenesis and/or dark to light transitions.
Abstract: Light, in a quality- and quantity-dependent fashion, induces nuclear import of the plant photoreceptors phytochrome, promotes interaction of phytochrome A (phyA) and phyB with transcription factors including phytochrome interacting factor 3 (PIF3), and is thought to trigger a transcriptional cascade to regulate the expression of ∼2500 genes in Arabidopsis thaliana. Here, we show that controlled degradation of the transcription factor PIF3 is a major regulatory step in light signaling. We demonstrate that accumulation of PIF3 in the nucleus in dark requires constitutive photomorphogenesis 1 (COP1), a negative regulator of photomorphogenesis, and show that red (R) and far-red light (FR) induce rapid degradation of the PIF3 protein. This process is controlled by the concerted action of the R/FR absorbing phyA, phyB, and phyD photoreceptors, and it is not affected by COP1. Rapid light-induced degradation of PIF3 indicates that interaction of PIF3 with these phytochrome species is transient. In addition, we provide evidence that the poc1 mutant, a postulated PIF3 overexpressor that displays hypersensitivity to R but not to FR, lacks detectable amounts of the PIF3 protein. Thus, we propose that PIF3 acts transiently, and its major function is to mediate phytochrome-induced signaling during the developmental switch from skotomorphogenesis to photomorphogenesis and/or dark to light transitions.
416 citations
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TL;DR: Strategies for targeting peripheral immune cells to reduce CNS disease burden are assessed on the basis of observations of myeloid cells in the CNS parenchyma and at CNS–periphery interfaces.
Abstract: The CNS is protected by the immune system, including cells that reside directly within the CNS and help to ensure proper neural function, as well as cells that traffic into the CNS with disease. The CNS-resident immune system is comprised mainly of innate immune cells and operates under homeostatic conditions. These myeloid cells in the CNS parenchyma and at CNS-periphery interfaces are highly specialized but also extremely plastic cells that immediately react to any changes in CNS homeostasis and become reactive in the context of neurodegenerative disorders such as Alzheimer's disease or Parkinson's disease. However, when the blood-brain barrier is impaired during CNS diseases such as multiple sclerosis or altered with cerebral ischemia, peripheral adaptive and innate immune cells, including monocytes, neutrophils, T cells and B cells, can enter the CNS, where they execute distinct cell-mediated effects. On the basis of these observations, we assess strategies for targeting peripheral immune cells to reduce CNS disease burden.
415 citations
Authors
Showing all 42309 results
Name | H-index | Papers | Citations |
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Mark Hallett | 186 | 1170 | 123741 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Anders Björklund | 165 | 769 | 84268 |
Si Xie | 148 | 1575 | 120243 |
Kypros H. Nicolaides | 147 | 1302 | 87091 |
Peter J. Schwartz | 147 | 647 | 107695 |
Michael E. Phelps | 144 | 637 | 77797 |
Martin Erdmann | 144 | 1562 | 100470 |
Holger J. Schünemann | 141 | 810 | 113169 |
Maksym Titov | 139 | 1573 | 128335 |
Karl Jakobs | 138 | 1379 | 97670 |
Annette Peters | 138 | 1114 | 101640 |
Suman Bala Beri | 137 | 1608 | 104798 |
Bert Sakmann | 137 | 283 | 90979 |
Vipin Bhatnagar | 137 | 1756 | 104163 |