Institution
University of Freiburg
Education•Freiburg, Baden-Württemberg, Germany•
About: University of Freiburg is a(n) education organization based out in Freiburg, Baden-Württemberg, Germany. It is known for research contribution in the topic(s): Population & Transplantation. The organization has 41992 authors who have published 77296 publication(s) receiving 2896269 citation(s). The organization is also known as: alberto-ludoviciana & Albert-Ludwigs-Universität Freiburg.
Topics: Population, Transplantation, Large Hadron Collider, Gene, Immune system
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05 Oct 2015
Abstract: There is large consent that successful training of deep networks requires many thousand annotated training samples. In this paper, we present a network and training strategy that relies on the strong use of data augmentation to use the available annotated samples more efficiently. The architecture consists of a contracting path to capture context and a symmetric expanding path that enables precise localization. We show that such a network can be trained end-to-end from very few images and outperforms the prior best method (a sliding-window convolutional network) on the ISBI challenge for segmentation of neuronal structures in electron microscopic stacks. Using the same network trained on transmitted light microscopy images (phase contrast and DIC) we won the ISBI cell tracking challenge 2015 in these categories by a large margin. Moreover, the network is fast. Segmentation of a 512x512 image takes less than a second on a recent GPU. The full implementation (based on Caffe) and the trained networks are available at http://lmb.informatik.uni-freiburg.de/people/ronneber/u-net .
28,273 citations
Posted Content•
TL;DR: It is shown that such a network can be trained end-to-end from very few images and outperforms the prior best method (a sliding-window convolutional network) on the ISBI challenge for segmentation of neuronal structures in electron microscopic stacks.
Abstract: There is large consent that successful training of deep networks requires many thousand annotated training samples. In this paper, we present a network and training strategy that relies on the strong use of data augmentation to use the available annotated samples more efficiently. The architecture consists of a contracting path to capture context and a symmetric expanding path that enables precise localization. We show that such a network can be trained end-to-end from very few images and outperforms the prior best method (a sliding-window convolutional network) on the ISBI challenge for segmentation of neuronal structures in electron microscopic stacks. Using the same network trained on transmitted light microscopy images (phase contrast and DIC) we won the ISBI cell tracking challenge 2015 in these categories by a large margin. Moreover, the network is fast. Segmentation of a 512x512 image takes less than a second on a recent GPU. The full implementation (based on Caffe) and the trained networks are available at this http URL .
19,534 citations
Abstract: A search for the Standard Model Higgs boson in proton–proton collisions with the ATLAS detector at the LHC is presented. The datasets used correspond to integrated luminosities of approximately 4.8 fb−1 collected at View the MathML source in 2011 and 5.8 fb−1 at View the MathML source in 2012. Individual searches in the channels H→ZZ(⁎)→4l, H→γγ and H→WW(⁎)→eνμν in the 8 TeV data are combined with previously published results of searches for H→ZZ(⁎), WW(⁎), View the MathML source and τ+τ− in the 7 TeV data and results from improved analyses of the H→ZZ(⁎)→4l and H→γγ channels in the 7 TeV data. Clear evidence for the production of a neutral boson with a measured mass of View the MathML source is presented. This observation, which has a significance of 5.9 standard deviations, corresponding to a background fluctuation probability of 1.7×10−9, is compatible with the production and decay of the Standard Model Higgs boson.
8,774 citations
TL;DR: In patients with acute coronary syndromes with scheduled percutaneous coronary intervention, prasugrel therapy was associated with significantly reduced rates of ischemic events, including stent thrombosis, but with an increased risk of major bleeding, including fatal bleeding.
Abstract: The primary efficacy end point occurred in 12.1% of patients receiving clopidogrel and 9.9% of patients receiving prasugrel (hazard ratio for prasugrel vs. clopidogrel, 0.81; 95% confidence interval [CI], 0.73 to 0.90; P<0.001). We also found significant reductions in the prasugrel group in the rates of myocardial infarction (9.7% for clopidogrel vs. 7.4% for prasugrel; P<0.001), urgent target-vessel revascularization (3.7% vs. 2.5%; P<0.001), and stent thrombosis (2.4% vs. 1.1%; P<0.001). Major bleeding was observed in 2.4% of patients receiving prasugrel and in 1.8% of patients receiving clopidogrel (hazard ratio, 1.32; 95% CI, 1.03 to 1.68; P = 0.03). Also greater in the prasugrel group was the rate of life-threatening bleeding (1.4% vs. 0.9%; P = 0.01), including nonfatal bleeding (1.1% vs. 0.9%; hazard ratio, 1.25; P = 0.23) and fatal bleeding (0.4% vs. 0.1%; P = 0.002). Conclusions In patients with acute coronary syndromes with scheduled percutaneous coronary intervention, prasugrel therapy was associated with significantly reduced rates of ischemic events, including stent thrombosis, but with an increased risk of major bleeding, including fatal bleeding. Overall mortality did not differ significantly between treatment groups. (ClinicalTrials.gov number, NCT00097591.)
5,561 citations
Abstract: In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes.
For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure flux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy.
Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation, it is imperative to target by gene knockout or RNA interference more than one autophagy-related protein. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways implying that not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular assays, we hope to encourage technical innovation in the field.
4,756 citations
Authors
Showing all 41992 results
Name | H-index | Papers | Citations |
---|---|---|---|
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 |