Institution
Saarland University
Education•Saarbrücken, Germany•
About: Saarland University is a education organization based out in Saarbrücken, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 19555 authors who have published 39678 publications receiving 1109295 citations. The organization is also known as: University of the Saarland & Universität des Saarlandes.
Topics: Population, Transplantation, Nanocrystalline material, Grain boundary, Endoplasmic reticulum
Papers published on a yearly basis
Papers
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31 Jul 2005
3,259 citations
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11 May 2004TL;DR: By proving that this scheme implements a coarse-to-fine warping strategy, this work gives a theoretical foundation for warping which has been used on a mainly experimental basis so far and demonstrates its excellent robustness under noise.
Abstract: We study an energy functional for computing optical flow that combines three assumptions: a brightness constancy assumption, a gradient constancy assumption, and a discontinuity-preserving spatio-temporal smoothness constraint. In order to allow for large displacements, linearisations in the two data terms are strictly avoided. We present a consistent numerical scheme based on two nested fixed point iterations. By proving that this scheme implements a coarse-to-fine warping strategy, we give a theoretical foundation for warping which has been used on a mainly experimental basis so far. Our evaluation demonstrates that the novel method gives significantly smaller angular errors than previous techniques for optical flow estimation. We show that it is fairly insensitive to parameter variations, and we demonstrate its excellent robustness under noise.
2,902 citations
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TL;DR: What is known about reprogramming in mammals and how it might relate to developmental potency and imprinting are discussed, including whether or not methylation is involved in the control of gene expression during normal development.
Abstract: DNA methylation is a major epigenetic modification of the genome that regulates crucial aspects of its function. Genomic methylation patterns in somatic differentiated cells are generally stable and heritable. However, in mammals there are at least two developmental periods-in germ cells and in preimplantation embryos-in which methylation patterns are reprogrammed genome wide, generating cells with a broad developmental potential. Epigenetic reprogramming in germ cells is critical for imprinting; reprogramming in early embryos also affects imprinting. Reprogramming is likely to have a crucial role in establishing nuclear totipotency in normal development and in cloned animals, and in the erasure of acquired epigenetic information. A role of reprogramming in stem cell differentiation is also envisaged. DNA methylation is one of the best-studied epigenetic modifications of DNA in all unicellular and multicellular organisms. In mammals and other vertebrates, methylation occurs predominantly at the symmetrical dinucleotide CpG (1-4). Symmetrical methylation and the discovery of a DNA methyltransferase that prefers a hemimethylated substrate, Dnmt1 (4), suggested a mechanism by which specific patterns of methylation in the genome could be maintained. Patterns imposed on the genome at defined developmental time points in precursor cells could be maintained by Dnmt1, and would lead to predetermined programs of gene expression during development in descendants of the precursor cells (5, 6). This provided a means to explain how patterns of differentiation could be maintained by populations of cells. In addition, specific demethylation events in differentiated tissues could then lead to further changes in gene expression as needed. Neat and convincing as this model is, it is still largely unsubstantiated. While effects of methylation on expression of specific genes, particularly imprinted ones (7) and some retrotransposons (8), have been demonstrated in vivo, it is still unclear whether or not methylation is involved in the control of gene expression during normal development (9-13). Although enzymes have been identified that can methylate DNA de novo (Dnmt3a and Dnmt3b) (14), it is unknown how specific patterns of methylation are established in the genome. Mechanisms for active demethylation have been suggested, but no enzymes have been identified that carry out this function in vivo (15-17). Genomewide alterations in methylation-brought about, for example, by knockouts of the methylase genes-result in embryo lethality or developmental defects, but the basis for abnormal development still remains to be discovered (7, 14). What is clear, however, is that in mammals there are developmental periods of genomewide reprogramming of methylation patterns in vivo. Typically, a substantial part of the genome is demethylated, and after some time remethylated, in a cell- or tissue-specific pattern. The developmental dynamics of these reprogramming events, as well as some of the enzymatic mechanisms involved and the biological purposes, are beginning to be understood. Here we look at what is known about reprogramming in mammals and discuss how it might relate to developmental potency and imprinting.
2,796 citations
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Icahn School of Medicine at Mount Sinai1, Carnegie Mellon University2, Harvard University3, University of Toronto4, Wellcome Trust Sanger Institute5, University of Pittsburgh6, Nagoya University7, University of Freiburg8, King's College London9, Vanderbilt University10, King Abdulaziz University11, University of Santiago de Compostela12, University of Utah13, Duke University14, Memorial University of Newfoundland15, Trinity College, Dublin16, University of Pennsylvania17, University of Illinois at Chicago18, Boston Children's Hospital19, Columbia University20, German Cancer Research Center21, University College London22, Kaiser Permanente23, Broad Institute24, Cardiff University25, Complutense University of Madrid26, Newcastle University27, Baylor College of Medicine28, University of California, San Francisco29, RWTH Aachen University30, National Health Service31, McMaster University32, Saarland University33, Karolinska Institutet34, National Institutes of Health35, University of Helsinki36, Emory University37
TL;DR: Using exome sequencing, it is shown that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate of < 0.05, plus a set of 107 genes strongly enriched for those likely to affect risk (FDR < 0.30).
Abstract: The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) < 0.05, plus a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR < 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur de novo loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic formation, transcriptional regulation and chromatin-remodelling pathways. These include voltage-gated ion channels regulating the propagation of action potentials, pacemaking and excitability-transcription coupling, as well as histone-modifying enzymes and chromatin remodellers-most prominently those that mediate post-translational lysine methylation/demethylation modifications of histones.
2,228 citations
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TL;DR: The study of imprinting provides new insights into epigenetic gene modification during development, and is thought to influence the transfer of nutrients to the fetus and the newborn from the mother.
Abstract: Genomic imprinting affects several dozen mammalian genes and results in the expression of those genes from only one of the two parental chromosomes. This is brought about by epigenetic instructions--imprints--that are laid down in the parental germ cells. Imprinting is a particularly important genetic mechanism in mammals, and is thought to influence the transfer of nutrients to the fetus and the newborn from the mother. Consistent with this view is the fact that imprinted genes tend to affect growth in the womb and behaviour after birth. Aberrant imprinting disturbs development and is the cause of various disease syndromes. The study of imprinting also provides new insights into epigenetic gene modification during development.
2,212 citations
Authors
Showing all 19735 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Schmitt | 134 | 2007 | 114667 |
Bernt Schiele | 130 | 568 | 70032 |
Peter Walter | 126 | 841 | 71580 |
David Zurakowski | 117 | 1168 | 55806 |
Kurt Binder | 114 | 1248 | 65308 |
Franz Hofmann | 113 | 471 | 49938 |
Bernd Nilius | 112 | 496 | 44812 |
Hans-Peter Seidel | 112 | 1213 | 51080 |
Stefan Zeuzem | 108 | 1027 | 50529 |
Rolf Müller | 104 | 905 | 50027 |
Samuel Klein | 101 | 363 | 46578 |
Michael Bauer | 100 | 1052 | 56841 |
Ulman Lindenberger | 100 | 554 | 41956 |
Thomas Brox | 99 | 329 | 94431 |
Elisabeth Kremmer | 99 | 413 | 34720 |