Institution
University of Marburg
Education•Marburg, Germany•
About: University of Marburg is a education organization based out in Marburg, Germany. It is known for research contribution in the topics: Population & Virus. The organization has 23195 authors who have published 42907 publications receiving 1506069 citations. The organization is also known as: Philipps University of Marburg & Philipps-Universität.
Topics: Population, Virus, Gene, Exciton, Photoluminescence
Papers published on a yearly basis
Papers
More filters
••
TL;DR: It is proposed that the term 'stress' should be restricted to conditions where an environmental demand exceeds the natural regulatory capacity of an organism, in particular situations that include unpredictability and uncontrollability.
1,126 citations
••
University of Manchester1, University of Barcelona2, University of Texas Health Science Center at San Antonio3, National Institutes of Health4, McGill University Health Centre5, Brigham and Women's Hospital6, Temple University7, Flinders University8, Royal Devon and Exeter Hospital9, University of Michigan10, University of the Republic11, NewYork–Presbyterian Hospital12, Central University of Venezuela13, University of Ferrara14, Paris Descartes University15, University of British Columbia16, University of Birmingham17, University of Marburg18
TL;DR: Blood eosinophils are recommended as a biomarker to support clinical decisions regarding the use of inhaled corticosteroids in chronic obstructive pulmonary disease patients, based on recent evidence from clinical trials.
Abstract: Precision medicine is a patient-specific approach that integrates all relevant clinical, genetic and biological information in order to optimise the therapeutic benefit relative to the possibility of side-effects for each individual. Recent clinical trials have shown that higher blood eosinophil counts are associated with a greater efficacy of inhaled corticosteroids (ICSs) in chronic obstructive pulmonary disease (COPD) patients. Blood eosinophil counts are a biomarker with potential to be used in clinical practice, to help target ICS treatment with more precision in COPD patients with a history of exacerbations despite appropriate bronchodilator treatment. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 pharmacological treatment algorithms, based on the ABCD assessment, can be applied relatively easily to treatment-naive individuals at initial presentation. However, their use is more problematic during follow-up in patients who are already on maintenance treatment. There is a need for a different system to guide COPD pharmacological management during follow-up. Recent large randomised controlled trials have provided important new information concerning the therapeutic effects of ICSs and long-acting bronchodilators on exacerbations. The new evidence regarding blood eosinophils and inhaled treatments, and the need to distinguish between initial and follow-up pharmacological management, led to changes in the GOLD pharmacological treatment recommendations. This article explains the evidence and rationale for the GOLD 2019 pharmacological treatment recommendations.
1,122 citations
••
Max Planck Society1, University of Marburg2, Broad Institute3, Trent University4, University of Toronto5, California State University, Long Beach6, University of British Columbia7, University of Georgia8, University of Louisville9, Utrecht University10, Saint Joseph's University11, Spanish National Research Council12, Cornell University13, CINVESTAV14, University of Kentucky15, Duke University16, University of Valencia17, Saint Louis University18, Bayer19, Exelixis20, Technische Universität München21
TL;DR: The discovery of the secreted protein gene clusters and the functional demonstration of their decisive role in the infection process illuminate previously unknown mechanisms of pathogenicity operating in biotrophic fungi.
Abstract: Ustilago maydis is a ubiquitous pathogen of maize and a well-established model organism for the study of plant-microbe interactions. This basidiomycete fungus does not use aggressive virulence strategies to kill its host. U. maydis belongs to the group of biotrophic parasites (the smuts) that depend on living tissue for proliferation and development. Here we report the genome sequence for a member of this economically important group of biotrophic fungi. The 20.5-million-base U. maydis genome assembly contains 6,902 predicted protein-encoding genes and lacks pathogenicity signatures found in the genomes of aggressive pathogenic fungi, for example a battery of cell-wall-degrading enzymes. However, we detected unexpected genomic features responsible for the pathogenicity of this organism. Specifically, we found 12 clusters of genes encoding small secreted proteins with unknown function. A significant fraction of these genes exists in small gene families. Expression analysis showed that most of the genes contained in these clusters are regulated together and induced in infected tissue. Deletion of individual clusters altered the virulence of U. maydis in five cases, ranging from a complete lack of symptoms to hypervirulence. Despite years of research into the mechanism of pathogenicity in U. maydis, no 'true' virulence factors had been previously identified. Thus, the discovery of the secreted protein gene clusters and the functional demonstration of their decisive role in the infection process illuminate previously unknown mechanisms of pathogenicity operating in biotrophic fungi. Genomic analysis is, similarly, likely to open up new avenues for the discovery of virulence determinants in other pathogens.
1,120 citations
••
1,118 citations
••
TL;DR: Loss-of-function mutations in a previously uncharacterized, predominantly neuronal P-type ATPase gene, ATP13A2, underlying an autosomal recessive form of early-onset parkinsonism with pyramidal degeneration and dementia are described.
Abstract: Neurodegenerative disorders such as Parkinson and Alzheimer disease cause motor and cognitive dysfunction and belong to a heterogeneous group of common and disabling disorders. Although the complex molecular pathophysiology of neurodegeneration is largely unknown, major advances have been achieved by elucidating the genetic defects underlying mendelian forms of these diseases. This has led to the discovery of common pathophysiological pathways such as enhanced oxidative stress, protein misfolding and aggregation and dysfunction of the ubiquitin-proteasome system. Here, we describe loss-of-function mutations in a previously uncharacterized, predominantly neuronal P-type ATPase gene, ATP13A2, underlying an autosomal recessive form of early-onset parkinsonism with pyramidal degeneration and dementia (PARK9, Kufor-Rakeb syndrome). Whereas the wild-type protein was located in the lysosome of transiently transfected cells, the unstable truncated mutants were retained in the endoplasmic reticulum and degraded by the proteasome. Our findings link a class of proteins with unknown function and substrate specificity to the protein networks implicated in neurodegeneration and parkinsonism.
1,112 citations
Authors
Showing all 23488 results
Name | H-index | Papers | Citations |
---|---|---|---|
John C. Morris | 183 | 1441 | 168413 |
Russel J. Reiter | 169 | 1646 | 121010 |
Martin J. Blaser | 147 | 820 | 104104 |
Christopher T. Walsh | 139 | 819 | 74314 |
Markus Cristinziani | 131 | 1140 | 84538 |
James C. Paulson | 126 | 443 | 52152 |
Markus F. Neurath | 124 | 934 | 62376 |
Nicholas W. Wood | 123 | 614 | 66270 |
Florian Lang | 116 | 1421 | 66496 |
Howard I. Maibach | 116 | 1821 | 60765 |
Thomas G. Ksiazek | 113 | 398 | 46108 |
Frank Glorius | 113 | 663 | 49305 |
Eberhard Ritz | 111 | 1109 | 61530 |
Manfred T. Reetz | 110 | 959 | 42941 |
Wolfgang H. Oertel | 110 | 653 | 51147 |