Monday Afternoon Science Seminar (MASS): MASS is an interdisciplinary platform to spread the message of science. In up to 30 minutes selected speakers will talk about their research interest and their latest exciting results. The seminars will be presented in English and will be introduced for non-professionals, professionals and others. To warm up our afternoons, we will begin with online science talks of our HMU staff.
14.11.2022, 17:00 h, Room 417 Schiffbauergasse
Professor Paul Baird from the University of Melbourne, Australia, visiting Professorial Fellow at the Institut für Humangenetik, Universität Regensburg
Abstract: Multiple sources of big data, particularly in the area of genetics have allowed identification of multiple genes and key gene networks involved in disease. To gain a more holistic view of disease causation and its progression requires that we also consider data from other sources including environmental risk factors and demographics. Analysis of these large quantities of data necessitates the use of advanced bioinformatics, machine learning and artificial intelligence. I will provide examples from eye diseases as to how these advances will help in our understanding of disease to personalize treatment approaches for the patient.
28.11.2022, 17:00 h, Room 417 Schiffbauergasse
Professor Tilman Grune, director of German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany will talk about ‘Oxidative Damage, Proteolysis and Cell Function’
Abstract: Changes in the redox state are inevitably associated with protein oxidation. Severe oxidation is often leading to irreversible protein modification. Most of these proteins cannot be repaired and need to be degraded in order to maintain cellular homeostasis.
The proteasomal system (UPS) is the dominating system responsible for the degradation of such oxidatively modified proteins. In contrast to the normal protein turnover, such proteins are degraded in an ATP- and ubiquitin-independent matter. Lately, it was demonstrated that the autophagy-lysosomal system (ALS) contributes to the clearance of oxidized proteins, too.
Often chronic oxidative stress and aging are accompanied by a decline of the UPS and ALS. In a set of studies we could clearly demonstrate that the activity of the core 20S proteasome as well as the autophagosomal flux is declining during senescence in various postmitotic cell types. This is accompanied by the accumulation of oxidized, cross-linked proteins, often referred to as the aging pigment ‘lipofuscin’. Lipofuscin in turn has a number of metabolism-modulating effects, often enhancing the aging process itself or disturbing cellular function.
It is, therefore, of utmost interest to prevent the accumulation of oxidized proteins. The most promising aspect here is the stimulation of the proteolytic systems, which is possible as well for the UPS as for the ALS, in order to restore cellular function.
23.01.2023, 17:00 h, Room 417 Schiffbauergasse
Professor Claudia Grünauer-Kloevekorn from the Martin Luther University Halle, Germany will talk about ‘CTG18.1 repeat expansion and the reduction of TCF4 gene expression in corneal endothelial cells of German patients with Fuchs dystrophy’
Abstract: Fuchs’endothelial corneal dystrophy (FECD) is an age-related bilateral disorder affecting the cornea’s internal endo-thelial cell monolayer. This progressive disorder is the most frequent indication for corneal transplantation in the USA and affects nearly 4% of its population over the age of40 years. Microscopic collagenous excrescences of the endothelial basement membrane, so called guttae, are FECD’s clinical hallmark. Its disease course is marked by the growing density of guttae and gradual thickening of Descemet’s membrane, the basement membrane of the corneal endothelium. The endothelium’s loss of cell density, the loss of normal hexagonal cell patterns, and the deficient fluid pumping function are typical of premature senescence of the corneal endothelial layer in FECD patients.