Online ISSN:
3042-1772
Volume 1 , Issue 1, (2024)
Published:
29.08.2024.
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Issue 1 - 2024
Published: 29.08.2024.
Authors in this issue:
Abdelhameed Mohamed, Abhipsita De, Adam Sikora, Adrianna Skoneczna, Agnes Tessier, Albrecht Stroh, Aleksandra Andreyeva, Aleksandra Drašković, Aleksandra Korać, Aleksandra Yu Andreyeva, Aleksandra Cvoro, Aleksandra Jankovic, Aleksandra Korac, Aleksandra Ristić Fira, Aleksandra Stanković, Alena Pecinová, Alessandra Pecorelli, Alex Lyakhovich, Ana Popović Bijelić, Ana Ružanović, Ana Vesković, Ana Djordjevic, Ana Kijanović, Ana Ledo, Ana Ninić, Ana Penezic, Ana Teofilovic, Anastasia A Tkachuk, Anastasia Ioanna Papantonaki, Anastasiya Volkova, Andrea Vallese, Andrea Pozzer, Andreas Daiber, Andreas Vitsos, Aneta Wiesyk, Anna Giorak, Anna Guiotto, Anna V Goropashnaya, Anne-Françoise Rousseau, Anthony L. Moore, Arijan Valar, Arvand Haschemi, Azra Guzonjić, Barbara Ostanek, Bárbara S. Rocha, Barry Halliwell, Bato Korac, Bengu Cetinkaya, Biljana Srdić Galić, Biljana Srdic-Galic, Blanca Romero-Llopis, Blandine Poulet, Bojan Labachevski, Branislav Milovanović, Branka R Gavrilović, Bruna Rafaela Pereira Resende, Can Tunçay, Cândida Dias, Carlo Cervellati, Carlo Viscomi, Caroline Le Goff, Cátia F. Lourenço, Cátia Lourenço, Cemile Uslu, Chiranjit Panja, Christina Barda, Christopher Kremslehner, Dalila Laoudj-Chevinesse, Daniel C Moreira, Daniela Ardalic, Daniela Caporossi, Danijela Vojnovic Milutinovic, Danilo Cetic, Darko Davitkov, David Nußbaum, Dejan Stevanovic, Diana Mikhailova, Dimitra Ieronymaki, Dimitrios Katsiris, Dimitrios Vlachodimitropoulos, Dirk Cleppien, Dominika Mihalikova, Dragana Jovanović, Dragana Robajac, Dragica Zendelovska, Eda Kapan, Ekaterina S. Kladchenko, Elina S Chelebieva, Elisabeth Ponweiser, Elizabeth Hood, Emilija Atanasovska, Ena Šimunić, Erdi Sozen, Erika Fernandez-Vizarra, Etienne Cavalier, Etna Abad, Evica Dincić, Federico V Pallardó, Filip Janjić, Florian Gruber, Francesca Marcato, Francesco Galli, Fulvio Ursini, Gaelle Gendronneau, Georgios Gkikas, Georgios Parthymos, Giada Petringa, Giuseppe Valacchi, Giuseppe Poli, Goran Miljus, Guilherme Horta, Guillermo Puertas-Frias, Hagar Fadda, Hamada Elwan, Hansjörg Habisch, Hemdan Mahmoud, Henning Ubbens, Homer Black, Igor Mindukshev, Igor Golic, Iñigo Yoldi Bergua, Ioannis Sfiniadakis, Ionela Mariana Nagelreiter, Irina Iskortseva, Isidora Protic, Iva I. Podgorski, Iva Perović-Blagojević, Ivan Spasojević, Ivan Petrović, Ivana Simić, Ivana Kuntić, Jacek Zielonka, Janja Marc, Jaroslaw Ciesla, Jean-Olivier Defraigne, Jean-Paul Cheramy-Bien, Jelena Kotur Stevuljević, Jelena Kotur-Stevuljević, Jelena Francuski Andrić, Jelena Jevtic, Jelena P Gavrić, Jiayin Zheng, Jiří Neužil, João Gonçalves, João Laranjinha, Joël Pincemai, Johanne Anastassopoulou, Jonathan Maury, Jos Lelieveld, Joussef Hayek, Jovana Stevanovic, Jovana Kuveljić, Juan Sastre, Kelly L Drew, Kristina Spariosu, Kristýna Čunátová, Ksenija Vujacic-Mirski, Larin Deeb, Lazar Karić, Lea Strohm, Leonardo Nardi, Ljupka Gligorovska, Lorena Baquero, Lucija Dončević, Lukáš Alán, Maja Ajduković, Maja Bosković, Maja Vukobratovic, Maja Živković, Marek Vrbacký, María José Saucedo-Rodríguez, Maria Giakoumaki, Maria Kyriazi, Maria S Podolskaya, Maria Teresa Bayo Jimenez, Marie Vanišová, Marie Sophie Narzt, Marija Vasić, Marija Aleksic, Marija D. Milošević, Marija Petrushevska, Marija Popova-Labachevska, Marija Takić, Marijana Popović Hadžija, Marin Kuntić, Marko D Prokić, Marko Mirč, Marta Kaloper, Marta Roldán-Lázaro, Marta Sipko, Martina Marchetti-Deschmann, Masanta Suchismita, Matea Juric, Matthias Kohl, Matthias Oelze, Micael Hardy, Michael Schmeißer, Michaela Sochorová, Michail Christou Rallis, Michelangelo Mancuso, Milena Dimitrijević, Milena Cvijanović, Milena Radaković, Milica Mandic, Milica Kovačević Filipović, Milica Mamić, Milos Sunderic, Miloš Đorđević, Miloš Mitrović, Milos Vrataric, Minja Derikonjić, Mirjana Udicki, Miron Sopić, Mladen Paradžik, Mohamed Mohany, Natalija Samardzić, Nataša Tomašević Kolarov, Natasa Velickovic, Natasa Z Djordjevic, Natzi Sakalihasan, Nejla H Zupic, Nesrin Kartal Ozer, Nevena Đukić, Niki Chondrogianni, Ninoslav Mitic, Ognjen Radojicic, Olga L Gostyukhina, Olgica Nedic, Omar Hahad, Ondrej Kuda, Otilija Keta, Pablo Cirrone, Panagoula Pavlou, Petr Pecina, Phaedra Winstanley-Zarach, Pilar González-Cabo, Radmila Ristić, Raffaele Cerutti, Raheema Hassan Khan, Ratko Tomašević, Rita Noverques, Robert Belužić, Roman Maslanka, Ron Kohen, Roza Kucharczyk, Salim S. Al-Rejaie, Samuele Zoratto, Sandra Sobočanec, Sanja Erceg, Sanja Kovacevic, Sanja Milenkovic, Sanja Stojanovic, Sara Stojanovic, Sebastian Steven, Shaaban S. Elnesr, Slavica Ranković, Snežana Kovačević, Sophie Christelbach, Steffen Daub, Stephan Sudowe, Stevo Najman, Strahinja Đurić, Strahinja Djuric, Sven Danckwardt, Svetlana G Despotović, Sylwia Pilch, Tamara G Petrović, Tamara Lapeña, Tamara Zakic, Tanja Vukov, Tarun Pant, Tatiana B Sigacheva, Tatjana Ivković Kapicl, Tawfeeq Shekh-Ahmad, Thomas Berkemeier, Thomas Münzel, Tihomir Balog, Tijana B Radovanović, Tijana Vučić, Tobias Madl, Tomáš Mráček, Tomáš Čajka, Tristan Junglas, Tugce Demirel-Yalciner, Tuguldur Enkhbaatar, Ufuk Ersoy, Vadim B Fedorov, Valeria Cordone, Valeria Balmaceda, Vanja Pekovic-Vaughan, Vesna Ćeriman Krstić, Vesna Mandic Markovic, Vladana Petković, Vsevolod Belousov, Willem H Koppenol, Yara Shqair, Zana C Dolicanin, Zeljko Mikovic, Zeynep Ülker, Zorana Dobrijevic, Zorana Milosavljević, Zorka Drvendžija,
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Volume 1, Issue 1, 2024
- All Sections
- Opening lecture
- Plenary lectures
- Keynote lectures
- Selected oral presentations
- Short oral presentations
29.08.2024.
Professional paper
MITOCHONDRIAL TESTS THAT EXPOSE DISEASE CLUES AND LIFESTYLE EFFECTS
The impairment of mitochondrial respiration, observed in neurodegenerative and cardiovascular disease, diabetes, cancer, and migraine headaches, has emerged as a biomarker of mitochondrial dysfunctions. Chronic fatigue, depression, and other behavior/mood disorders are also associated with mitochondrial malfunctioning, but so is our lifestyle! Our lab offers tests for insight into mitochondrial fitness, linking not only diseases but also behaviors and modern lifestyles that lead to health damage. Firstly, we focused on 88 (relatively) healthy volunteers, of which 32% were taking some medication (such as for high blood pressure or mood disorders), however, they considered themselves fit and healthy. The blood was drawn 3h before PBMC (peripheral blood mononuclear cells) isolation, followed by an immediate Seahorse XF Cell Mito Stress Test (Agilent) on the SeahorseXF96e instrument (Agilent). Parameters of mitochondrial respiration were carefully examined. There was a significant difference between BHI (bioenergetic health index), reserve capacity, coupling efficiency, and proton leak, between people who took medication for chronic but manageable comorbidities and completely healthy individuals. Later, in another group we examined the alterations in NAD+ levels (by Q-NADMED Blood NAD+ assay kit, NADMED) and mitochondrial respiration parameters in a binge-drinking session (consuming 10 or more units of alcohol in less than three days). The decrease in NAD+ levels was positively correlated with the amount of alcohol consumed. Additionally, total NAD+ levels positively correlated with the BHI. In another experiment, supplementation with niacin for 20 days, did not increase NAD+ levels in (relatively) healthy individuals. Apart from mitochondrial respiration and NAD+ levels, we focus on optimizing tests for mtDNA count and mitochondrial potential. All of these tests not only explore disease but also serve to monitor behaviors that lead to health damage or improvements.
Ksenija Vujacic-Mirski, Stephan Sudowe
29.08.2024.
Professional paper
MITOCHONDRIAL TARGETING AS A MEANS OF OVERCOMING CANCER DRUG RESISTANCE
Our recent observations show that both resistant and stem-like cancer cells predominantly responsible for metastasis differ from chemotherapy-sensitive cells. We have shown bioinformatically and experimentally that mitochondria of such cells are much more prone to oxidative phosphorylation (OXPHOS) than radio- or chemotherapy-sensitive cancer cells from which they evolved during therapeutic interventions. Specifically, in triple-negative breast cancer models, we observed that such resistant cells exhibit higher mitochondrial membrane potential, higher OXPHOS and respiration, and increased resistance to oxidative stress, allowing them to survive chemo-radiotherapy. These findings of increased expression of OXPHOS-associated genes and proteins in chemoresistant cells and biopsies of relapsed tumors suggest an alternative druggable target. Our in vitro and in vivo (nude mice and Artemia salina) data suggest that certain antibiotics, inducers of mitochondrial dysfunction, create additive oxidative stress and can reduce the growth rate of tumors developed from resistant or stem-like cancer cells. Such repurposed drugs, selected from a chemical library, are also able to resensitize resistant tumors, allowing reuse of chemotherapeutic agents. In addition, their modification with a specific moiety (TPP) allows for increased delivery to mitochondria to reduce cytotoxic pressure on normal cells. Thus, research from our laboratory offers an alternative strategy for anticancer therapy of resistant tumors.
Cemile Uslu, Eda Kapan, Hagar Fadda, Raheema Hassan Khan, Yara Shqair, Zeynep Ülker, Can Tunçay, Etna Abad, Alex Lyakhovich
29.08.2024.
Professional paper
MIR-146A AND MIR-21 FROM PBMCS AND EXTRACELLULAR VESICLES IN GESTATIONAL DIABETES: A COMPARISON OF PAIRED SAMPLES FOR THE ANALYSIS OF POTENTIAL INDICATORS OF THE REDOX STATUS
Dysregulation of the redox system and the interconnected low-level inflammation (LLI) act as a driving force of damaging mechanisms in gestational diabetes mellitus (GDM) and are strongly related to severe obstetric and neonatal complications of hyperglycaemic pregnancies. Major disturbances in microRNA-based mechanism accompany (glyco)oxidative stress ((g)OS), for which reason we hypothesized that microRNAs may serve as sensors and/or effectors of (g)OS/LLI in GDM and we chose candidates for GDM biomarker analysis among known (g)OS/LLI-associated microRNAs. The aim of the study was to analyze the properties of miR-146a-5p and miR-21-5p as redox status indicators in GDM, as well as to compare two different biological samples as sources of potentially relevant GDM biomarkers. miR-146a-5p and miR-21-5p were quantified by real-time polymerase chain reaction in peripheral blood mononuclear cells of patients with GDM and normoglycaemic pregnant controls (n=40 each), as well as in paired samples of extracellular vesicles (EVs) extracted from serum. Correlation analysis was conducted for the expression levels of tested microRNAs and the activities of glutathione reductase (GR), total superoxide dismutase (SOD), catalase (CAT), concentration of serum thiol groups and the level of Nrf2 mRNA. In both samples, tested microRNAs were upregulated in GDM group, with a more pronounced increase in expression in EVs, compared to peripheral blood mononuclear cells (PBMCs) (1.81 vs. 1.52 fold for miR-146a-5p and 1.98 vs. 1.58 fold for miR-21-5p). There was a significant positive correlation between the expression of miR-21-5p from PBMCs and Nrf2 in both GDM patients and controls, as well as a positive correlation with the activity of total SOD in GDM patients. On the other hand, miR-146a-5p from EVs demonstrated negative correlation with Nrf2 expression and the activity of total SOD. These data demonstrate the potential of (g)OS/LLI-related microRNAs miR-146a-5p and miR-21-5p to serve as indicators of GDM and the associated (g)OS-related changes.
Ana Penezic, Jovana Stevanovic, Ognjen Radojicic, Ninoslav Mitic, Dragana Robajac, Milos Sunderic, Goran Miljus, Danilo Cetic, Milica Mandic, Daniela Ardalic, Vesna Mandic Markovic, Zeljko Mikovic, Olgica Nedic, Zorana Dobrijevic
29.08.2024.
Professional paper
FMP40 AMPYLASE REGULATES CELL SURVIVAL UPON OXIDATIVE STRESS BY CONTROLLING PRX1 AND TRX3 OXIDATION
AMPylation (adenylation) is one of the post-translational protein modifications (PTM) leading to the diversification of protein functions and activity. With our collaborators, we discovered that the SelO family members of humans, yeast, and E. coli have AMPylase activity. The yeast SelO – Fmp40 – was identified in the proteome of the inter-membrane space of mitochondria. We have shown that Fmp40 is involved in the response of cells to hydrogen peroxide (H2O2) and menadione treatment: cells lacking the Fmp40 AMPylase grow sensitivity upon H2O2 and menadione treatment. E. coli SelO AMPylates glutaredoxin GrxA and the s-glutathionylation level of proteins is reduced in bacterial and yeast cells lacking SelO1. The objective of the study is to reveal the biological functions of Fmp40 in mitochondrial redox regulation. The decreased survival of fmp40Δ cells, observed in survival tests, depends on the oxidation of Trx3 upon oxidative stress. In contrast, we verified that fmp40Δ cells are resistant upon exposure to high concentrations of the hydrogen peroxide - phenotype dependent on the presence of the Glutaredoxin Grx2, Thioredoxin Trx3, Peroxiredoxin Prx1, Oxidation Resistance Oxr1, and Apoptotic inducing factor Aif1 basing on qPCR analysis. We found multidimensional genetic interactions of FMP40 with other known redox genes upon low or high oxidative stress. We revealed that Fmp40 AMPylates Prx1, Trx3, and Grx2 in vitro and it has a matrix-localized echo form. We discovered that Fmp40 is critical for the efficient reduction of Prx1 upon high oxidative stress. Moreover, Grx2 is involved in the Prx1 reduction directly and at the level of Trx3 reduction in vivo. Fmp40 regulates its function on Trx3 protein, most probably through Threonine66 which is AMPylated in vivo. In addition, Fmp40 is necessary to maintain the balance of cellular redox buffers GSH and NADPH. Overall Fmp40 regulates redox gene expression for efficient ROS neutralization and signaling which eventually determines the fate of cell survival upon oxidative stress.
Financed by National Science Centre of Poland: 2018/31/B/NZ3/01117.
Masanta Suchismita, Aneta Wiesyk, Chiranjit Panja, Sylwia Pilch, Jaroslaw Ciesla, Marta Sipko, Abhipsita De, Tuguldur Enkhbaatar, Roman Maslanka, Adrianna Skoneczna, Roza Kucharczyk
29.08.2024.
Professional paper
FRIEND OR FOE: ASSOCIATION OF URIC ACID WITH OXIDATIVE STRESS IN CANINE HYPERADRENOCORTICISM
Canine hyperadrenocorticism (HAC) or Cushing’s syndrome is a multisystemic clinical condition caused by chronic exposure to elevated concentrations of glucocorticoids. It has been considered that oxidative stress is implicated in pathophysiology of HAC. The exact impact of uric acid (UA) on oxidative stress in hyperadrenocorticism remains unclear, given its ability to act as both an antioxidant and a pro-oxidant. In addition, increased UA levels are related to the development of hypertension, dyslipidemia, and type II diabetes in humans with HAC. For this purpose, we aimed to investigate the association of UA with the components of oxidative stress in dogs with HAC. This study included 12 dogs with newly diagnosed HAC and 12 healthy controls. The oxidative stress in serum samples was assessed by advanced oxidation protein product (AOPP) and thiobarbituric acid–reactive substances (TBARS), and antioxidative status by total antioxidant capacity (TAC), reduced glutathione (GSH) and paraoxonase-1 (PON-1). Uric acid was compared between two groups and correlated with oxidative stress parameters. The results showed that dogs with HAC exerted markedly higher level of UA compared to healthy controls (p<0.001). Additionally, higher levels of AOPP and TBARS (p=0.001; p =0.043) were observed in the HAC group, indicating oxidative damage compared to the controls. Among antioxidants, only GSH exhibited a difference between groups (p=0.001). Correlation analysis of UA revealed strong association with TBARS (r=0.615; p=0.037), which implies that UA is linked to an increase of oxidative stress in canine Cushing’s syndrome. The results of this study indicate a possible pro-oxidant role of UA in dogs with HAC.
Lazar Karić, Kristina Spariosu, Darko Davitkov, Filip Janjić, Jelena Francuski Andrić, Milica Kovačević Filipović, Milena Radaković
29.08.2024.
Professional paper
IS REDOX-HYPERACTIVITY IN EXTREMOPHILIC MICROALGAE LINKED TO THEIR INCREASED METABOLIC BURDEN?
The diverse uses of microalgae in ecological remediation, wastewater treatment, pharmaceutics, or food and biofuel production, have long kept these single-celled organisms in the spotlight. The focus of this study was on Chlamydomonas acidophila strain PM01, which thrives in acidic aquatic systems and is resistant to the presence of heavy metals in its environment. The redox metabolism of this microalga was assessed by its ability to reduce the EPR-active spin probe TEMPO (2,2,6,6-tetramethylpiperidine-1-oxyl), and compared to that of Chlorella sorokiniana strain CCAP 211/8K, a freshwater green microalga. The results showed that C. acidophila has a faster redox metabolic rate than C. sorokiniana, reducing 50% of TEMPO after 2.5, and 13 min, respectively. The addition of Mn2+ or Fe3+ to the culture medium of C. acidophila did not affect its reduction capacity, while it had a minor effect on C. sorokiniana. The faster rate in C. acidophila most likely represents the result of its adaptation to acidic environments. Namely, it has previously been suggested that acidophilic algae perform energy-demanding cellular processes in order to cope with the high pH gradient across the membrane. Moreover, the increased metabolic turnover requires an increased mitochondrial activity, resulting in a higher baseline production of superoxide and hydrogen-peroxide, subsequently compensated by an elevated baseline reduction capacity. Interestingly, the redox metabolic rate of C. sorokiniana was unaltered in suspensions that were kept in non-standard cultivation conditions (diurnal fluctuations of temperature and ambient lighting, absence of shaking) for five weeks. However, C. acidophila lost all of its reduction capacity in these conditions already after three days. These findings may be important when selecting the most appropriate microalgal strain for a specific application. Specifically, C. acidophila would likely be a good candidate for high-yield rapid production of endogenous products that are the result of its unique survival mechanism under extreme conditions.
Ana Vesković, Milena Dimitrijević, Snežana Kovačević, Ivan Spasojević, Ana Popović Bijelić
29.08.2024.
Professional paper
BODY SIZE, BODY SHAPE AND BREAST CANCER RISK – METABOLIC AND REDOX LINK
Variations in body size and shape might be linked to different biological processes that affect breast cancer risk. Еpidemiological studies have confirmed that obesity, which is characterized by increased overall adiposity and assessed using body mass index (BMI), has direct relationship with the risk of breast cancer among postmenopausal women, and opposite relationship with the risk among premenopausal women (“obesity paradox”). In addition to BMI, anthropometric descriptors of body shape, like waist and hip circumference and waist-to-hip ratio are directly associated with both pre- and postmenopausal breast cancer risk. Excess adipose tissue, adipose tissue dysfunction, and adipose tissue-to-breast cancer crosstalk have important role in the initiation and progression of breast cancer due to the altered production of proinflammatory and proangiogenic mediators, growth factors, adipokines, and sex hormones, dysregulated insulin signaling pathway, as well as mitochondrial dysfunction and oxidative stress. Fat distribution pattern exerts an effect beyond the effect of overall obesity in relation to breast cancer development because of more adverse systemic metabolic effects related to visceral adiposity. Body height and its components have direct association with postmenopausal breast cancer risk. Increased risk of breast cancer in taller persons is probably due to increased levels of insulin-like growth factor (IGF-1), which is one of the major determinants of height, plays an important role in regulating breast stem cell number, and can affect cancer growth. Adult-attained height also reflects different aspects of maturation, including genetic, nutritional, and environmental factors. Assessment of changes in body height, mass, and distribution of adipose tissue throughout life is another important aspect of understanding the complex processes of metabolic reprogramming of energy pathways in breast cancer pathophysiology. Use of anthropometric descriptors of body size and shape can provide insight into underlying biological mechanisms, which is essential for developing targeted prevention and treatment strategies.
This research was supported by the Science Fund of the Republic of Serbia, #7750238, Exploring new avenues in breast cancer research: Redox and metabolic reprogramming of cancer and associated adipose tissue - REFRAME.
Biljana Srdić Galić, Mirjana Udicki, Zorka Drvendžija, Tatjana Ivković Kapicl, Tamara Zakić, Aleksandra Janković, Aleksandra Korać, Bato Korać
29.08.2024.
Professional paper
DIFFERENTIAL SPATIAL DISTRIBUTION OF SYNTHETIC NANO- AND MICRO-PARTICLES EXPLAINS THE EFFECTS ON CARDIOVASCULAR FUNCTION – IMPLICATIONS FOR AIR POLLUTION HEALTH EFFECTS
Particulate matter (PM) air pollution presents a major environmental and public health challenge because of its non-uniform size distribution and chemical composition. Air quality regulations generally categorize particulate matter (PM) size into PM10, PM2.5, and ultrafine particles (UFPs) with aerodynamic diameters smaller than 10, 2.5, and 0.1 µm, respectively. We examined the differential impact of particle size per se on selected organ systems using a custom whole-body mouse exposure system using synthetic PM (SPM). The micrometer-sized SPM accumulated in the lungs as the primary entry organ, while ultrafine SPM showed less accumulation, implying a transition into circulation. Micro SPM-exposed mice exhibited inflammation and NADPH oxidase-derived oxidative stress in the lungs. Ultrafine SPM-exposed mice did not show oxidative stress in the lungs but rather at the brain, heart, and vasculature levels. Endothelial dysfunction and blood pressure increase were more pronounced in ultrafine SPM exposed mice, supported by increased endothelin-1 and decreased endothelial nitric oxide synthase expression, enhancing constriction and reducing vasodilation. To derive a preliminary estimate of the cardiovascular disease burden of UFPs in humans, we used new high-resolution exposure data at a global scale, and applied hazard ratios from an epidemiological cohort study. We derived a UFP-associated incidence of 419 (95% CI 78–712) thousand cardiovascular disease cases per year in the European Union and 5.6 (95% CI 1.1–9.3) million globally. This work provides novel insights into the different toxicological profiles of inhaled ultrafine particles and public health consequences of exposure, guiding future studies.
Marin Kuntic, Ivana Kuntic, Dirk Cleppien, Andrea Pozzer, David Nußbaum, Matthias Oelze, Tristan Junglas, Lea Strohm, Henning Ubbens, Steffen Daub, Maria Teresa Bayo Jimenez, Sven Danckwardt, Thomas Berkemeier, Omar Hahad, Matthias Kohl, Sebastian Steven, Albrecht Stroh, Jos Lelieveld, Thomas Münzel, Andreas Daiber
