@book{ZhangPlauthEberhardtetal.2020, author = {Zhang, Shuhao and Plauth, Max and Eberhardt, Felix and Polze, Andreas and Lehmann, Jens and Sejdiu, Gezim and Jabeen, Hajira and Servadei, Lorenzo and M{\"o}stl, Christian and B{\"a}r, Florian and Netzeband, Andr{\´e} and Schmidt, Rainer and Knigge, Marlene and Hecht, Sonja and Prifti, Loina and Krcmar, Helmut and Sapegin, Andrey and Jaeger, David and Cheng, Feng and Meinel, Christoph and Friedrich, Tobias and Rothenberger, Ralf and Sutton, Andrew M. and Sidorova, Julia A. and Lundberg, Lars and Rosander, Oliver and Sk{\"o}ld, Lars and Di Varano, Igor and van der Walt, Est{\´e}e and Eloff, Jan H. P. and Fabian, Benjamin and Baumann, Annika and Ermakova, Tatiana and Kelkel, Stefan and Choudhary, Yash and Cooray, Thilini and Rodr{\´i}guez, Jorge and Medina-P{\´e}rez, Miguel Angel and Trejo, Luis A. and Barrera-Animas, Ari Yair and Monroy-Borja, Ra{\´u}l and L{\´o}pez-Cuevas, Armando and Ram{\´i}rez-M{\´a}rquez, Jos{\´e} Emmanuel and Grohmann, Maria and Niederleithinger, Ernst and Podapati, Sasidhar and Schmidt, Christopher and Huegle, Johannes and de Oliveira, Roberto C. L. and Soares, F{\´a}bio Mendes and van Hoorn, Andr{\´e} and Neumer, Tamas and Willnecker, Felix and Wilhelm, Mathias and Kuster, Bernhard}, title = {HPI Future SOC Lab - Proceedings 2017}, number = {130}, editor = {Meinel, Christoph and Polze, Andreas and Beins, Karsten and Strotmann, Rolf and Seibold, Ulrich and R{\"o}dszus, Kurt and M{\"u}ller, J{\"u}rgen}, publisher = {Universit{\"a}tsverlag Potsdam}, address = {Potsdam}, isbn = {978-3-86956-475-3}, issn = {1613-5652}, doi = {10.25932/publishup-43310}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-433100}, publisher = {Universit{\"a}t Potsdam}, pages = {ix, 235}, year = {2020}, abstract = {The "HPI Future SOC Lab" is a cooperation of the Hasso Plattner Institute (HPI) and industry partners. Its mission is to enable and promote exchange and interaction between the research community and the industry partners. The HPI Future SOC Lab provides researchers with free of charge access to a complete infrastructure of state of the art hard and software. This infrastructure includes components, which might be too expensive for an ordinary research environment, such as servers with up to 64 cores and 2 TB main memory. The offerings address researchers particularly from but not limited to the areas of computer science and business information systems. Main areas of research include cloud computing, parallelization, and In-Memory technologies. This technical report presents results of research projects executed in 2017. Selected projects have presented their results on April 25th and November 15th 2017 at the Future SOC Lab Day events.}, language = {en} } @article{GubertPuntelLehmenetal.2016, author = {Gubert, Priscila and Puntel, Bruna and Lehmen, Tassia and Bornhorst, Julia and Avila, Daiana Silva and Aschner, Michael A. and Soares, Felix A. A.}, title = {Reversible reprotoxic effects of manganese through DAF-16 transcription factor activation and vitellogenin downregulation in Caenorhabditis elegans}, series = {Life sciences : molecular, cellular and functional basis of therapy}, volume = {151}, journal = {Life sciences : molecular, cellular and functional basis of therapy}, publisher = {Elsevier}, address = {Oxford}, issn = {0024-3205}, doi = {10.1016/j.lfs.2016.03.016}, pages = {218 -- 223}, year = {2016}, abstract = {Aims Vitellogenesis is the yolk production process which provides the essential nutrients for the developing embryos. Yolk is a lipoprotein particle that presents lipids and lipid-binding proteins, referred to as vitellogenins (VIT). The Caenorhabditis elegans nematode has six genes encoding VIT lipoproteins. Several pathways are known to regulate vitellogenesis, including the DAF-16 transcription factor. Some reports have shown that heavy metals, such as manganese (Mn), impair brood size in C. elegans; however the mechanisms associated with this effect have yet to be identified. Our aim was to evaluate Mn\&\#8242;s effects on C. elegans reproduction and better understand the pathways related to these effects. Main methods. Young adult larval stage worms were treated for 4 h with Mn in 85 mM NaCl and Escherichia coli OP50 medium. Key findings. Mn reduced egg-production and egg-laying during the first 24 h after the treatment, although the total number of progenies were indistinguishable from the control group levels. This delay may have occurred due to DAF-16 activation, which was noted only after the treatment and was not apparent 24 h later. Moreover, the expression, protein levels and green fluorescent protein (GFP) fluorescence associated with VIT were decreased soon after Mn treatment and recovered after 24 h. Significance Combined, these data suggest that the delay in egg-production is likely regulated by DAF-16 and followed by the inhibition of VIT transport activity. Further studies are needed to clarify the mechanisms associated with Mn-induced DAF-16 activation.}, language = {en} } @article{ChenDeWittBornhorstetal.2015, author = {Chen, Pan and DeWitt, Margaret R. and Bornhorst, Julia and Soares, Felix A. and Mukhopadhyay, Somshuvra and Bowman, Aaron B. and Aschner, Michael A.}, title = {Age- and manganese-dependent modulation of dopaminergic phenotypes in a}, series = {Metallomics : integrated biometal science}, volume = {7}, journal = {Metallomics : integrated biometal science}, number = {2}, publisher = {Royal Society of Chemistry}, address = {Cambridge}, issn = {1756-5901}, doi = {10.1039/c4mt00292j}, pages = {289 -- 298}, year = {2015}, language = {en} } @article{GubertPuntelLehmenetal.2018, author = {Gubert, Priscila and Puntel, Bruna and Lehmen, Tassia and Fessel, Joshua P. and Cheng, Pan and Bornhorst, Julia and Trindade, Lucas Siqueira and Avila, Daiana S. and Aschner, Michael and Soares, Felix A. A.}, title = {Metabolic effects of manganese in the nematode Caenorhabditis elegans through DAergic pathway and transcription factors activation}, series = {Neurotoxicology : the interdisciplinary journal of effects to toxic substances on the nervous system}, volume = {67}, journal = {Neurotoxicology : the interdisciplinary journal of effects to toxic substances on the nervous system}, publisher = {Elsevier}, address = {Amsterdam}, issn = {0161-813X}, doi = {10.1016/j.neuro.2018.04.008}, pages = {65 -- 72}, year = {2018}, abstract = {Manganese (Mn) is an essential trace element for physiological functions since it acts as an enzymatic co-factor. Nevertheless, overexposure to Mn has been associated with a pathologic condition called manganism. Furthermore, Mn has been reported to affect lipid metabolism by mechanisms which have yet to be established. Herein, we used the nematode Caenorhabditis elegans to examine Mn's effects on the dopaminergic (DAergic) system and determine which transcription factors that regulate with lipid metabolism are affected by it. Worms were exposed to Mn for four hours in the presence of bacteria and in a liquid medium (85 mM NaCl). Mn increased fat storage as evidenced both by Oil Red O accumulation and triglyceride levels. In addition, metabolic activity was reduced as a reflection of decreased oxygen consumption caused by Mn. Mn also affected feeding behavior as evidenced by decreased pharyngeal pumping rate. DAergic neurons viability were not altered by Mn, however the dopamine levels were significantly reduced following Mn exposure. Furthermore, the expression of sbp-1 transcription factor and let-363 protein kinase responsible for lipid accumulation control was increased and decreased, respectively, by Mn. Altogether, our data suggest that Mn increases the fat storage in C. elegans, secondary to DAergic system alterations, under the control of SBP-1 and LET-363 proteins.}, language = {en} } @article{RuszkiewiczdeMacedoMirandaVizueteetal.2019, author = {Ruszkiewicz, Joanna and de Macedo, Gabriel Teixeira and Miranda-Vizuete, Antonio and Bowman, Aaron B. and Bornhorst, Julia and Schwerdtle, Tanja and Antunes Soares, Felix A. and Aschner, Michael}, title = {Sex-Specific response of caenorhabditis elegans to Methylmercury Toxicity}, series = {Neurotoxicity Research}, volume = {35}, journal = {Neurotoxicity Research}, number = {1}, publisher = {Springer}, address = {New York}, issn = {1029-8428}, doi = {10.1007/s12640-018-9949-4}, pages = {208 -- 216}, year = {2019}, abstract = {Methylmercury (MeHg), an abundant environmental pollutant, has long been known to adversely affect neurodevelopment in both animals and humans. Several reports from epidemiological studies, as well as experimental data indicate sex-specific susceptibility to this neurotoxicant; however, the molecular bases of this process are still not clear. In the present study, we used Caenorhabditis elegans (C. elegans), to investigate sex differences in response to MeHg toxicity during development. Worms at different developmental stage (L1, L4, and adult) were treated with MeHg for 1h. Lethality assays revealed that male worms exhibited significantly higher resistance to MeHg than hermaphrodites, when at L4 stage or adults. However, the number of worms with degenerated neurons was unaffected by MeHg, both in males and hermaphrodites. Lower susceptibility of males was not related to changes in mercury (Hg) accumulation, which was analogous for both wild-type (wt) and male-rich him-8 strain. Total glutathione (GSH) levels decreased upon MeHg in him-8, but not in wt. Moreover, the sex-dependent response of the cytoplasmic thioredoxin system was observedmales exhibited significantly higher expression of thioredoxin TRX-1, and thioredoxin reductase TRXR-1 expression was downregulated upon MeHg treatment only in hermaphrodites. These outcomes indicate that the redox status is an important contributor to sex-specific sensitivity to MeHg in C. elegans.}, language = {en} }