Institution
University of Cologne
Education•Cologne, Germany•
About: University of Cologne is a education organization based out in Cologne, Germany. It is known for research contribution in the topics: Population & Gene. The organization has 32050 authors who have published 66350 publications receiving 2210092 citations. The organization is also known as: Universität zu Köln & Universitatis Coloniensis.
Topics: Population, Gene, Transplantation, Medicine, Cancer
Papers published on a yearly basis
Papers
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Hannover Medical School1, University of Cologne2, University Hospital Heidelberg3, University of Düsseldorf4, Sapienza University of Rome5, VU University Medical Center6, University of Zurich7, National Institutes of Health8, Katholieke Universiteit Leuven9, Leibniz Association10, Dresden University of Technology11
TL;DR: An abbreviated version of the risk assessment strategy proposed by the current European PH guidelines provides accurate mortality estimates in patients with PAH and proved valid at follow-up and in major PAH subgroups.
Abstract: The 2015 European pulmonary hypertension (PH) guidelines propose a risk stratification strategy for patients with pulmonary arterial hypertension (PAH). Low-, intermediate- and high-risk strata are defined by estimated 1-year mortality risks of 10%, respectively. This risk assessment strategy awaits validation. We analysed data from patients with newly diagnosed PAH enrolled into COMPERA (Comparative, Prospective Registry of Newly Initiated Therapies for Pulmonary Hypertension), a European-based PH registry. An abbreviated version of the risk assessment strategy proposed by the European PH guidelines was applied, using the following variables: World Health Organization functional class, 6-min walking distance, brain natriuretic peptide or its N-terminal fragment, right atrial pressure, cardiac index and mixed venous oxygen saturation. Data from 1588 patients were analysed. Mortality rates were significantly different between the three risk strata (p An abbreviated version of the risk assessment strategy proposed by the current European PH guidelines provides accurate mortality estimates in patients with PAH.
465 citations
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TL;DR: Two new immune regulators are defined through analysis of corresponding Arabidopsis loss-of-function insertion mutants, and it is found that SA antagonizes initiation of cell death and stunting of growth in nudt7 mutants.
Abstract: Arabidopsis thaliana ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) controls defense activation and programmed cell death conditioned by intracellular Toll-related immune receptors that recognize specific pathogen effectors. EDS1 is also needed for basal resistance to invasive pathogens by restricting the progression of disease. In both responses, EDS1, assisted by its interacting partner, PHYTOALEXIN-DEFICIENT4 (PAD4), regulates accumulation of the phenolic defense molecule salicylic acid (SA) and other as yet unidentified signal intermediates. An Arabidopsis whole genome microarray experiment was designed to identify genes whose expression depends on EDS1 and PAD4, irrespective of local SA accumulation, and potential candidates of an SA-independent branch of EDS1 defense were found. We define two new immune regulators through analysis of corresponding Arabidopsis loss-of-function insertion mutants. FLAVIN-DEPENDENT MONOOXYGENASE1 (FMO1) positively regulates the EDS1 pathway, and one member (NUDT7) of a family of cytosolic Nudix hydrolases exerts negative control of EDS1 signaling. Analysis of fmo1 and nudt7 mutants alone or in combination with sid2-1, a mutation that severely depletes pathogen-induced SA production, points to SA-independent functions of FMO1 and NUDT7 in EDS1-conditioned disease resistance and cell death. We find instead that SA antagonizes initiation of cell death and stunting of growth in nudt7 mutants.
464 citations
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TL;DR: In this paper, a graphene monolayer has been prepared on an Ir(111) single crystal via pyrolytic cleavage of ethylene (C2H4), and the resulting superstructure has been examined with scanning tunneling microscopy (STM) and low energy electron diffraction.
Abstract: A graphene monolayer has been prepared on an Ir(111) single crystal via pyrolytic cleavage of ethylene (C2H4). The resulting superstructure has been examined with scanning tunneling microscopy (STM) and low energy electron diffraction. It has been identified as a well aligned, incommensurate (9.32?9.32) pattern, which is described as a moir?. This pattern shows three distinct regions resulting from different local configurations of the carbon adlayer with respect to the Ir-substrate. These regions are imaged differently by STM and differ strongly in their ability to bind metal deposits.
463 citations
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TL;DR: In this paper, it was shown that the irrelevance of momentum conservation found by Metzner and Vollhardt applies more generally than their Gaussian density of states and that on-site interactions are the only dynamical interactions in the limit of infinite dimension.
Abstract: The limit of infinite dimension of the Hubbard model was recently introduced by Metzner and Vollhardt as a new type of model with interesting implications. In the present paper the same limit is applied to a family of lattice fermion models with generalized kinetic and potential energies. A simple method is introduced for investigating the important issue of handling momentum conservation at the interaction vertices. It is shown that the irrelevance of momentum conservation found by Metzner and Vollhardt applies more generally than their Gaussian density of states. Interactions between particles on different sites are shown to simplify to their Hartree substitute. This leaves on-site interactions as the only dynamical interactions in the limit of infinite dimension.
463 citations
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TL;DR: It is demonstrated that PLS3 is important for axonogenesis through increasing the F-actin level and rescued the axon length and outgrowth defects associated with SMN down-regulation in motor neurons of SMA mouse embryos and in zebrafish.
Abstract: Homozygous deletion of the survival motor neuron 1 gene (SMN1) causes spinal muscular atrophy (SMA), the most frequent genetic cause of early childhood lethality. In rare instances, however, individuals are asymptomatic despite carrying the same SMN1 mutations as their affected siblings, thereby suggesting the influence of modifier genes. We discovered that unaffected SMN1-deleted females exhibit significantly higher expression of plastin 3 (PLS3) than their SMA-affected counterparts. We demonstrated that PLS3 is important for axonogenesis through increasing the F-actin level. Overexpression of PLS3 rescued the axon length and outgrowth defects associated with SMN down-regulation in motor neurons of SMA mouse embryos and in zebrafish. Our study suggests that defects in axonogenesis are the major cause of SMA, thereby opening new therapeutic options for SMA and similar neuromuscular diseases.
463 citations
Authors
Showing all 32558 results
Name | H-index | Papers | Citations |
---|---|---|---|
Julie E. Buring | 186 | 950 | 132967 |
Stuart H. Orkin | 186 | 715 | 112182 |
Cornelia M. van Duijn | 183 | 1030 | 146009 |
Dorret I. Boomsma | 176 | 1507 | 136353 |
Frederick W. Alt | 171 | 577 | 95573 |
Donald E. Ingber | 164 | 610 | 100682 |
Klaus Müllen | 164 | 2125 | 140748 |
Klaus Rajewsky | 154 | 504 | 88793 |
Frederik Barkhof | 154 | 1449 | 104982 |
Stefanie Dimmeler | 147 | 574 | 81658 |
Detlef Weigel | 142 | 516 | 84670 |
Hidde L. Ploegh | 135 | 674 | 67437 |
Luca Valenziano | 130 | 437 | 94728 |
Peter Walter | 126 | 841 | 71580 |
Peter G. Martin | 125 | 553 | 97257 |