Institution
University of Kiel
Education•Kiel, Germany•
About: University of Kiel is a education organization based out in Kiel, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 27816 authors who have published 57114 publications receiving 2061802 citations. The organization is also known as: Christian Albrechts University & Christian-Albrechts-Universität zu Kiel.
Papers published on a yearly basis
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TL;DR: It is demonstrated that ADAM10 is involved in the constitutive cleavage of CX3CL1 and thereby may regulate the recruitment of monocytic cells to CX2CL1-expressing cell layers and prevent de-adhesion of bound THP-1 cells.
669 citations
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TL;DR: A mechanistic model to explain the activity of Fer-1 was developed, which guided the development of ferrostatins with improved properties, and that lipid peroxidation mediates diverse disease phenotypes are suggested.
Abstract: Ferrostatin-1 (Fer-1) inhibits ferroptosis, a form of regulated, oxidative, nonapoptotic cell death. We found that Fer-1 inhibited cell death in cellular models of Huntington’s disease (HD), periventricular leukomalacia (PVL), and kidney dysfunction; Fer-1 inhibited lipid peroxidation, but not mitochondrial reactive oxygen species formation or lysosomal membrane permeability. We developed a mechanistic model to explain the activity of Fer-1, which guided the development of ferrostatins with improved properties. These studies suggest numerous therapeutic uses for ferrostatins, and that lipid peroxidation mediates diverse disease phenotypes.
668 citations
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TL;DR: In this article, a chemo-thermo-dynamic subduction zone model was proposed to solve for slab dehydration during subduction, and the authors investigated how changes in the incoming plate's hydration and thermal structure may effect the efficiency of sub-arc water release from sediments, crust, and serpentinized mantle.
668 citations
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TL;DR: The research concept and methodological framework presented here for discussion have initially been applied in different case studies and shall be developed further to provide a useful tool for the quantification and spatial modelling of multiple ecosystem services in different landscapes.
Abstract: Landscapes differ in their capacities to provide ecosystem goods and services, which are the benefits humans obtain from nature. Structures and functions of ecosystems needed to sustain the provision of ecosystem services are altered by various human activities. In this paper, a concept for the assessment of multiple ecosystem services is proposed as a basis for discussion and further development of a respective evaluation instrument. Using quantitative and qualitative assessment data in combination with land cover and land use information originated from remote sensing and GIS, impacts of human activities can be evaluated. The results reveal typical patterns of different ecosystems‘ capacities to provide ecosystem services. The proposed approach thus delivers useful integrative information for environmental management and landscape planning, aiming at a sustainable use of services provided by nature. The research concept and methodological framework presented here for discussion have initially been applied in different case studies and shall be developed further to provide a useful tool for the quantification and spatial modelling of multiple ecosystem services in different landscapes. An exemplary application of the approach dealing with food provision in the Halle-Leipzig region in Germany is presented. It shows typical patterns of ecosystem service distribution around urban areas. As the approach is new and still rather general, there is great potential for improvement, especially with regard to a data-based quantification of the numerous hypotheses, which were formulated as base for the assessment. Moreover, the integration of more detailed landscape information on different scales will be needed in future in order to take the heterogeneous distribution of landscape properties and values into account. Therefore, the purpose of this paper is to foster critical discussions on the methodological development presented here.
667 citations
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Wellcome Trust Centre for Human Genetics1, Imperial College London2, University of Oulu3, Agency for Science, Technology and Research4, National Institutes of Health5, King's College London6, Ealing Hospital7, National University of Singapore8, University of Turin9, University Medical Center Groningen10, University of Tartu11, University of Bristol12, University College London13, University of Eastern Finland14, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico15, University of Kiel16, Leiden University Medical Center17, Dresden University of Technology18, University of Düsseldorf19, University of Surrey20, Erasmus University Rotterdam21, Max Healthcare22, Technische Universität München23, University of Naples Federico II24, Science for Life Laboratory25, Wellcome Trust Sanger Institute26, University of Ulm27, Ludwig Maximilian University of Munich28, University of Kelaniya29, Institute of Cancer Research30, King Abdulaziz University31, Queen Mary University of London32, Massachusetts Institute of Technology33, Health Protection Agency34, Churchill Hospital35, University of Oxford36, Imperial College Healthcare37
TL;DR: In this article, the authors used epigenome-wide association to show that body mass index (BMI), a key measure of adiposity, is associated with widespread changes in DNA methylation.
Abstract: Approximately 1.5 billion people worldwide are overweight or affected by obesity, and are at risk of developing type 2 diabetes, cardiovascular disease and related metabolic and inflammatory disturbances1,2. Although the mechanisms linking adiposity to associated clinical conditions are poorly understood, recent studies suggest that adiposity may influence DNA methylation3,4,5,6, a key regulator of gene expression and molecular phenotype7. Here we use epigenome-wide association to show that body mass index (BMI; a key measure of adiposity) is associated with widespread changes in DNA methylation (187 genetic loci with P < 1 × 10−7, range P = 9.2 × 10−8 to 6.0 × 10−46; n = 10,261 samples). Genetic association analyses demonstrate that the alterations in DNA methylation are predominantly the consequence of adiposity, rather than the cause. We find that methylation loci are enriched for functional genomic features in multiple tissues (P < 0.05), and show that sentinel methylation markers identify gene expression signatures at 38 loci (P < 9.0 × 10−6, range P = 5.5 × 10−6 to 6.1 × 10−35, n = 1,785 samples). The methylation loci identify genes involved in lipid and lipoprotein metabolism, substrate transport and inflammatory pathways. Finally, we show that the disturbances in DNA methylation predict future development of type 2 diabetes (relative risk per 1 standard deviation increase in methylation risk score: 2.3 (2.07–2.56); P = 1.1 × 10−54). Our results provide new insights into the biologic pathways influenced by adiposity, and may enable development of new strategies for prediction and prevention of type 2 diabetes and other adverse clinical consequences of obesity.
667 citations
Authors
Showing all 28103 results
Name | H-index | Papers | Citations |
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Stefan Schreiber | 178 | 1233 | 138528 |
Jun Wang | 166 | 1093 | 141621 |
William J. Sandborn | 162 | 1317 | 108564 |
Jens Nielsen | 149 | 1752 | 104005 |
Tak W. Mak | 148 | 807 | 94871 |
Annette Peters | 138 | 1114 | 101640 |
Severine Vermeire | 134 | 1086 | 76352 |
Peter M. Rothwell | 134 | 779 | 67382 |
Dusan Bruncko | 132 | 1042 | 84709 |
Gideon Bella | 129 | 1301 | 87905 |
Dirk Schadendorf | 127 | 1017 | 105777 |
Neal L. Benowitz | 126 | 792 | 60658 |
Thomas Schwarz | 123 | 701 | 54560 |
Meletios A. Dimopoulos | 122 | 1371 | 71871 |
Christian Weber | 122 | 776 | 53842 |