@article{BanksNishiyamaHasebeetal.2011,
  author    = {Banks, Jo Ann and Nishiyama, Tomoaki and Hasebe, Mitsuyasu and Bowman, John L. and Gribskov, Michael and dePamphilis, Claude and Albert, Victor A. and Aono, Naoki and Aoyama, Tsuyoshi and Ambrose, Barbara A. and Ashton, Neil W. and Axtell, Michael J. and Barker, Elizabeth and Barker, Michael S. and Bennetzen, Jeffrey L. and Bonawitz, Nicholas D. and Chapple, Clint and Cheng, Chaoyang and Correa, Luiz Gustavo Guedes and Dacre, Michael and DeBarry, Jeremy and Dreyer, Ingo and Elias, Marek and Engstrom, Eric M. and Estelle, Mark and Feng, Liang and Finet, Cedric and Floyd, Sandra K. and Frommer, Wolf B. and Fujita, Tomomichi and Gramzow, Lydia and Gutensohn, Michael and Harholt, Jesper and Hattori, Mitsuru and Heyl, Alexander and Hirai, Tadayoshi and Hiwatashi, Yuji and Ishikawa, Masaki and Iwata, Mineko and Karol, Kenneth G. and Koehler, Barbara and Kolukisaoglu, Uener and Kubo, Minoru and Kurata, Tetsuya and Lalonde, Sylvie and Li, Kejie and Li, Ying and Litt, Amy and Lyons, Eric and Manning, Gerard and Maruyama, Takeshi and Michael, Todd P. and Mikami, Koji and Miyazaki, Saori and Morinaga, Shin-ichi and Murata, Takashi and M{\"u}ller-R{\"o}ber, Bernd and Nelson, David R. and Obara, Mari and Oguri, Yasuko and Olmstead, Richard G. and Onodera, Naoko and Petersen, Bent Larsen and Pils, Birgit and Prigge, Michael and Rensing, Stefan A. and Mauricio Riano-Pachon, Diego and Roberts, Alison W. and Sato, Yoshikatsu and Scheller, Henrik Vibe and Schulz, Burkhard and Schulz, Christian and Shakirov, Eugene V. and Shibagaki, Nakako and Shinohara, Naoki and Shippen, Dorothy E. and Sorensen, Iben and Sotooka, Ryo and Sugimoto, Nagisa and Sugita, Mamoru and Sumikawa, Naomi and Tanurdzic, Milos and Theissen, Guenter and Ulvskov, Peter and Wakazuki, Sachiko and Weng, Jing-Ke and Willats, William W. G. T. and Wipf, Daniel and Wolf, Paul G. and Yang, Lixing and Zimmer, Andreas D. and Zhu, Qihui and Mitros, Therese and Hellsten, Uffe and Loque, Dominique and Otillar, Robert and Salamov, Asaf and Schmutz, Jeremy and Shapiro, Harris and Lindquist, Erika and Lucas, Susan and Rokhsar, Daniel and Grigoriev, Igor V.},
  title     = {The selaginella genome identifies genetic changes associated with the evolution of vascular plants},
  series = {Science},
  volume    = {332},
  journal   = {Science},
  number    = {6032},
  publisher = {American Assoc. for the Advancement of Science},
  address   = {Washington},
  issn      = {0036-8075},
  doi       = {10.1126/science.1203810},
  pages     = {960 -- 963},
  year      = {2011},
  abstract  = {Vascular plants appeared similar to 410 million years ago, then diverged into several lineages of which only two survive: the euphyllophytes (ferns and seed plants) and the lycophytes. We report here the genome sequence of the lycophyte Selaginella moellendorffii (Selaginella), the first nonseed vascular plant genome reported. By comparing gene content in evolutionarily diverse taxa, we found that the transition from a gametophyte- to a sporophyte-dominated life cycle required far fewer new genes than the transition from a nonseed vascular to a flowering plant, whereas secondary metabolic genes expanded extensively and in parallel in the lycophyte and angiosperm lineages. Selaginella differs in posttranscriptional gene regulation, including small RNA regulation of repetitive elements, an absence of the trans-acting small interfering RNA pathway, and extensive RNA editing of organellar genes.},
  language  = {en}
}
@article{RichterSchulzSubkowskietal.2016,
  author    = {Richter, Marina Juliane and Schulz, Alexander and Subkowski, Thomas and B{\"o}ker, Alexander},
  title     = {Adsorption and rheological behavior of an amphiphilic protein at oil/water interfaces},
  series = {Journal of colloid and interface science},
  volume    = {479},
  journal   = {Journal of colloid and interface science},
  publisher = {Elsevier},
  address   = {San Diego},
  issn      = {0021-9797},
  doi       = {10.1016/j.jcis.2016.06.062},
  pages     = {199 -- 206},
  year      = {2016},
  abstract  = {Hydrophobins are highly surface active proteins which self-assemble at hydrophilic-hydrophobic interfaces into amphipathic membranes. We investigate hydrophobin self-assembly at oil/water interfaces to deepen the understanding of protein behavior in order to improve our biomimetic synthesis. Therefore, we carried out pendant drop measurements of hydrophobin stabilized oil/water systems determining the time-dependent IFT and the dilatational rheology with additional adaptation to the Serrien protein model. We show that the class I hydrophobin H*Protein B adsorbs at an oil/water interface where it forms a densely-packed interfacial protein layer, which dissipates energy during droplet oscillation. Furthermore, the interfacial protein layer exhibits shear thinning behavior. (C) 2016 Elsevier Inc. All rights reserved.},
  language  = {en}
}
@misc{GorskiJungLietal.2020,
  author    = {Gorski, Mathias and Jung, Bettina and Li, Yong and Matias-Garcia, Pamela R. and Wuttke, Matthias and Coassin, Stefan and Thio, Chris H. L. and Kleber, Marcus E. and Winkler, Thomas W. and Wanner, Veronika and Chai, Jin-Fang and Chu, Audrey Y. and Cocca, Massimiliano and Feitosa, Mary F. and Ghasemi, Sahar and Hoppmann, Anselm and Horn, Katrin and Li, Man and Nutile, Teresa and Scholz, Markus and Sieber, Karsten B. and Teumer, Alexander and Tin, Adrienne and Wang, Judy and Tayo, Bamidele O. and Ahluwalia, Tarunveer S. and Almgren, Peter and Bakker, Stephan J. L. and Banas, Bernhard and Bansal, Nisha and Biggs, Mary L. and Boerwinkle, Eric and B{\"o}ttinger, Erwin and Brenner, Hermann and Carroll, Robert J. and Chalmers, John and Chee, Miao-Li and Chee, Miao-Ling and Cheng, Ching-Yu and Coresh, Josef and de Borst, Martin H. and Degenhardt, Frauke and Eckardt, Kai-Uwe and Endlich, Karlhans and Franke, Andre and Freitag-Wolf, Sandra and Gampawar, Piyush and Gansevoort, Ron T. and Ghanbari, Mohsen and Gieger, Christian and Hamet, Pavel and Ho, Kevin and Hofer, Edith and Holleczek, Bernd and Foo, Valencia Hui Xian and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Josyula, Navya Shilpa and Kahonen, Mika and Khor, Chiea-Chuen and Koenig, Wolfgang and Kramer, Holly and Kraemer, Bernhard K. and Kuehnel, Brigitte and Lange, Leslie A. and Lehtimaki, Terho and Lieb, Wolfgang and Loos, Ruth J. F. and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Milaneschi, Yuri and Mishra, Pashupati P. and Mononen, Nina and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and O'Donoghue, Michelle L. and Orho-Melander, Marju and Pendergrass, Sarah A. and Penninx, Brenda W. J. H. and Preuss, Michael H. and Psaty, Bruce M. and Raffield, Laura M. and Raitakari, Olli T. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Rosenkranz, Alexander R. and Rossing, Peter and Rotter, Jerome and Sabanayagam, Charumathi and Schmidt, Helena and Schmidt, Reinhold and Schoettker, Ben and Schulz, Christina-Alexandra and Sedaghat, Sanaz and Shaffer, Christian M. and Strauch, Konstantin and Szymczak, Silke and Taylor, Kent D. and Tremblay, Johanne and Chaker, Layal and van der Harst, Pim and van der Most, Peter J. and Verweij, Niek and Voelker, Uwe and Waldenberger, Melanie and Wallentin, Lars and Waterworth, Dawn M. and White, Harvey D. and Wilson, James G. and Wong, Tien-Yin and Woodward, Mark and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Yan and Snieder, Harold and Wanner, Christoph and Boger, Carsten A. and Kottgen, Anna and Kronenberg, Florian and Pattaro, Cristian and Heid, Iris M.},
  title     = {Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline},
  series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Reihe der Digital Engineering Fakult{\"a}t},
  journal   = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Reihe der Digital Engineering Fakult{\"a}t},
  number    = {19},
  doi       = {10.25932/publishup-56537},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-565379},
  pages     = {14},
  year      = {2020},
  abstract  = {Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25\% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95\% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.},
  language  = {en}
}
@article{GorskiJungLietal.2020,
  author    = {Gorski, Mathias and Jung, Bettina and Li, Yong and Matias-Garcia, Pamela R. and Wuttke, Matthias and Coassin, Stefan and Thio, Chris H. L. and Kleber, Marcus E. and Winkler, Thomas W. and Wanner, Veronika and Chai, Jin-Fang and Chu, Audrey Y. and Cocca, Massimiliano and Feitosa, Mary F. and Ghasemi, Sahar and Hoppmann, Anselm and Horn, Katrin and Li, Man and Nutile, Teresa and Scholz, Markus and Sieber, Karsten B. and Teumer, Alexander and Tin, Adrienne and Wang, Judy and Tayo, Bamidele O. and Ahluwalia, Tarunveer S. and Almgren, Peter and Bakker, Stephan J. L. and Banas, Bernhard and Bansal, Nisha and Biggs, Mary L. and Boerwinkle, Eric and B{\"o}ttinger, Erwin and Brenner, Hermann and Carroll, Robert J. and Chalmers, John and Chee, Miao-Li and Chee, Miao-Ling and Cheng, Ching-Yu and Coresh, Josef and de Borst, Martin H. and Degenhardt, Frauke and Eckardt, Kai-Uwe and Endlich, Karlhans and Franke, Andre and Freitag-Wolf, Sandra and Gampawar, Piyush and Gansevoort, Ron T. and Ghanbari, Mohsen and Gieger, Christian and Hamet, Pavel and Ho, Kevin and Hofer, Edith and Holleczek, Bernd and Foo, Valencia Hui Xian and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Josyula, Navya Shilpa and Kahonen, Mika and Khor, Chiea-Chuen and Koenig, Wolfgang and Kramer, Holly and Kraemer, Bernhard K. and Kuehnel, Brigitte and Lange, Leslie A. and Lehtimaki, Terho and Lieb, Wolfgang and Loos, Ruth J. F. and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Milaneschi, Yuri and Mishra, Pashupati P. and Mononen, Nina and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and O'Donoghue, Michelle L. and Orho-Melander, Marju and Pendergrass, Sarah A. and Penninx, Brenda W. J. H. and Preuss, Michael H. and Psaty, Bruce M. and Raffield, Laura M. and Raitakari, Olli T. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Rosenkranz, Alexander R. and Rossing, Peter and Rotter, Jerome and Sabanayagam, Charumathi and Schmidt, Helena and Schmidt, Reinhold and Schoettker, Ben and Schulz, Christina-Alexandra and Sedaghat, Sanaz and Shaffer, Christian M. and Strauch, Konstantin and Szymczak, Silke and Taylor, Kent D. and Tremblay, Johanne and Chaker, Layal and van der Harst, Pim and van der Most, Peter J. and Verweij, Niek and Voelker, Uwe and Waldenberger, Melanie and Wallentin, Lars and Waterworth, Dawn M. and White, Harvey D. and Wilson, James G. and Wong, Tien-Yin and Woodward, Mark and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Yan and Snieder, Harold and Wanner, Christoph and Boger, Carsten A. and Kottgen, Anna and Kronenberg, Florian and Pattaro, Cristian and Heid, Iris M.},
  title     = {Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline},
  series = {Kidney international : official journal of the International Society of Nephrology},
  volume    = {99},
  journal   = {Kidney international : official journal of the International Society of Nephrology},
  number    = {4},
  publisher = {Elsevier},
  address   = {New York},
  organization    = {Lifelines Cohort Study<br /> Regeneron Genetics Ctr},
  issn      = {0085-2538},
  doi       = {10.1016/j.kint.2020.09.030},
  pages     = {926 -- 939},
  year      = {2020},
  abstract  = {Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25\% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95\% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.},
  language  = {en}
}
@article{SchulzErleGraefetal.2009,
  author    = {Schulz, Irene and Erle, Alexander and Gr{\"a}f, Ralph and Krueger, Anne and Lohmeier, Heiner and Putzler, Sascha and Samereier, Matthias and Weidenthaler, Sebastian},
  title     = {Identification and cell cycle-dependent localization of nine novel, genuine centrosomal components in Dictyostelium discoideum},
  issn      = {0886-1544},
  doi       = {10.1002/Cm.20384},
  year      = {2009},
  abstract  = {The centrosome is the main microtubule-organizing center and constitutes the largest protein complex in a eukaryotic cell. The Dictyostelium centrosome is an established model for acentriolar centrosomes and it consists of a layered core structure Surrounded by a so-called corona, which harbors microtubule nucleation complexes. We have identified 34 new centrosomal candidate proteins through mass spectrometrical analysis of the proteome of isolated Dictyostelium centrosomes. Here we present a characterization of 12 centrosomal candidate proteins all featuring coiled coil regions and low expression levels, which are the most common attributes of centrosomal proteins. We used GFP fusion proteins to localize the candidate proteins in whole cells and on microtubule-free, isolated centrosomes. Thus we were able to identify nine new genuine centrosomal proteins including a putative orthologue of Cep192, an interaction partner of polo-like kinase 4 in human centriole biogenesis. In this respect, centrosomal localization of the only polo-like kinase in Dictyostelium, Pik, is also shown in this work. Using confocal deconvolution microscopy, four components, CP39, CP55, CP75, and CP91 could be clearly assigned to the so far almost uncharacterized centrosomal core structure, while CP148 and Cep192 localized to a zone between that of corona marker and core proteins. Finally, CP103 and CP248 were constituents of the corona. In contrast, NE81 was localized at the nuclear envelope and three others, an orthologue of the spindle checkpoint component Mad1, the novel Cenp68, and the centrosomal CP248 were observed at the centromeres, which are clustered and linked to the centrosome throughout the entire cell cycle. Cell Motil. Cytoskeleton 66: 915-928, 2009.},
  language  = {en}
}
@article{SchulzErleGraefetal.2009,
  author    = {Schulz, Irene and Erle, Alexander and Gr{\"a}f, Ralph and Krueger, Anne and Putzler, Sascha and Samereier, Matthias and Weidenthaler, Sebastian},
  title     = {Cell cycle-dependent localization of novel centrosomal and centromeric proteins in Dictyostelium},
  issn      = {0171-9335},
  doi       = {10.1016/S0171-9335(09)00023-5},
  year      = {2009},
  language  = {en}
}
@article{RoggenbuckGoihlHanacketal.2017,
  author    = {Roggenbuck, Dirk and Goihl, Alexander and Hanack, Katja and Holzloehner, Pamela and Hentschel, Christian and Veiczi, Miklos and Schierack, Peter and Reinhold, Dirk and Schulz, Hans-Ulrich},
  title     = {Serological diagnosis and prognosis of severe acute pancreatitis by analysis of serum glycoprotein 2},
  series = {Clinical chemistry and laboratory medicine : journal of the Forum of the European Societies of Clinical Chemistry - the European Branch of the International Federation of Clinical Chemistry and Laboratory Medicine},
  volume    = {55},
  journal   = {Clinical chemistry and laboratory medicine : journal of the Forum of the European Societies of Clinical Chemistry - the European Branch of the International Federation of Clinical Chemistry and Laboratory Medicine},
  publisher = {De Gruyter},
  address   = {Berlin},
  issn      = {1434-6621},
  doi       = {10.1515/cclm-2016-0797},
  pages     = {854 -- 864},
  year      = {2017},
  abstract  = {To better understand emerging adults' perceptions of family interactions and value transmission to the next generation, we examined Hmong American emerging adults' reflections on their parents' parenting. Participants discussed what parenting practices they would do differently and others they hoped to emulate with their future adolescent children. Thirty Hmong American emerging adults (18-25 years; M = 21.2 years; 50\% female) participated in interviews that focused retrospectively on the parent-adolescent relationship. Results revealed that emerging adults wanted to parent differently in three ways: less pressure about education, fewer restrictions, and more open communication. Emerging adults imagined being a similar parent in four ways: promoting education, promoting life values, giving guidance, and offering love and support. The findings highlight parenting practices that Hmong American emerging adults plan on transmitting (and not transmitting) to their own children, offering a glimpse into the type of parents the emerging adults may become.},
  language  = {en}
}
@article{SwidsinskiLoeningBauckeSchulzetal.2016,
  author    = {Swidsinski, Alexander and Loening-Baucke, Vera and Schulz, Stefan and Manowsky, Julia and Verstraelen, Hans and Swidsinski, Sonja},
  title     = {Functional anatomy of the colonic bioreactor: Impact of antibiotics and Saccharomyces boulardii on bacterial composition in human fecal cylinders},
  series = {Systematic and Applied Microbiology},
  volume    = {39},
  journal   = {Systematic and Applied Microbiology},
  publisher = {Nature Publ. Group},
  address   = {Jena},
  issn      = {0723-2020},
  doi       = {10.1016/j.syapm.2015.11.002},
  pages     = {67 -- 75},
  year      = {2016},
  abstract  = {Sections of fecal cylinders were analyzed using fluorescence in situ hybridization targeting 180 bacterial groups. Samples were collected from three groups of women (N = 20 each) treated for bacterial vaginosis with ciprofloxacin + metronidazole. Group A only received the combined antibiotic regimen, whereas the A/Sb group received concomitant Saccharomyces boulardii CNCM I-745 treatment, and the A.Sb group received S. boulardii prophylaxis following the 14-day antibiotic course. The number of stool cylinders analyzed was 188 out of 228 in group A, 170 out of 228 in group A/Sb, and 172 out of 216 in group Ash. The colonic biomass was organized into a separate mucus layer with no bacteria, a 10-30 mu m broad unstirred transitional layer enriched with bacteria, and a patchy fermentative area that mixed digestive leftovers with bacteria. The antibiotics suppressed bacteria mainly in the fermentative area, whereas abundant bacterial clades retreated to the transitional mucus and survived. As a result, the total concentration of bacteria decreased only by one order. These effects were lasting, since the overall recovery of the microbial mass, bacterial diversity and concentrations were still below pre-antibiotic values 4 months after the end of antibiotic treatment. Sb-prophylaxis markedly reduced antibiotic effects and improved the recovery rates. Since the colon is a sophisticated bioreactor, the study indicated that the spatial anatomy of its biomass was crucial for its function. (C) 2015 The Authors. Published by Elsevier GmbH. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).},
  language  = {en}
}
@article{GrinbergHellElMellahetal.2017,
  author    = {Grinberg, Victoria and Hell, Natalie and El Mellah, Ileyk and Neilsen, Joseph and Sander, Andreas Alexander Christoph and Leutenegger, Maurice and F{\"u}rst, Felix and Huenemoerder, David P. and Kretschmar, Peter and Kuehnel, Matthias and Martinez-Nunez, Silvia and Niu, Shu and Pottschmidt, Katja and Schulz, Norbert S. and Wilms, Joern and Nowak, Michael A.},
  title     = {The clumpy absorber in the high-mass X-ray binary Vela X-1},
  series = {Astronomy and astrophysics : an international weekly journal},
  volume    = {608},
  journal   = {Astronomy and astrophysics : an international weekly journal},
  publisher = {EDP Sciences},
  address   = {Les Ulis},
  issn      = {1432-0746},
  doi       = {10.1051/0004-6361/201731843},
  pages     = {18},
  year      = {2017},
  abstract  = {Bright and eclipsing, the high-mass X-ray binary Vela X-1 offers a unique opportunity to study accretion onto a neutron star from clumpy winds of O/B stars and to disentangle the complex accretion geometry of these systems. In Chandra-HETGS spectroscopy at orbital phase similar to 0.25, when our line of sight towards the source does not pass through the large-scale accretion structure such as the accretion wake, we observe changes in overall spectral shape on timescales of a few kiloseconds. This spectral variability is, at least in part, caused by changes in overall absorption and we show that such strongly variable absorption cannot be caused by unperturbed clumpy winds of O/B stars. We detect line features from high and low ionization species of silicon, magnesium, and neon whose strengths and presence depend on the overall level of absorption. These features imply a co-existence of cool and hot gas phases in the system, which we interpret as a highly variable, structured accretion flow close to the compact object such as has been recently seen in simulations of wind accretion in high-mass X-ray binaries.},
  language  = {en}
}
@phdthesis{Schulz2016,
  author    = {Schulz, Alexander},
  title     = {Untersuchung der Wechselwirkung synoptisch-skaliger mit orographisch bedingten Prozessen in der arktischen Grenzschicht {\"u}ber Spitzbergen},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-400058},
  school      = {Universit{\"a}t Potsdam},
  pages     = {vi, 194},
  year      = {2016},
  abstract  = {In der vorliegenden Arbeit wird die planetare Grenzschicht in Ny-{\AA}lesund, Spitzbergen, sowohl bez{\"u}glich kleinskaliger („mikrometeorologischer") Effekte als auch in ihrer Kopplung mit der Synoptik untersucht. Dazu werden verschiedene Beobachtungsdaten aus der S{\"a}ule und in Bodenn{\"a}he zusammengezogen und bewertet. Die so gewonnenen Datens{\"a}tze werden dann zur Validierung eines nicht-hydrostatischen, regionalen Klimamodells genutzt. Weiterhin werden orographisch bedingte Einfl{\"u}sse, die Untergrundbeschaffenheit und die lokale Heterogenit{\"a}t der Unterlage untersucht. Hierzu werden meteorologische Gr{\"o}ßen, wie die Variabilit{\"a}t der Temperatur und insbesondere die j{\"a}hrliche Windverteilung in Bodenn{\"a}he untersucht und es erfolgt ein Vergleich von in-situ gemessenen turbulenten Fl{\"u}ssen von den Eddy-Kovarianz-Messkomplexen bei Ny-{\AA}lesund und im Bayelva-Tal unter demselben Aspekt. Es zeigt sich, dass der Eddy-Kovarianz-Messkomplex im Bayelva-Tal sehr stark durch eine orographisch bedingte Kanalisierung der Str{\"o}mung beeinflusst ist und sich nicht f{\"u}r Vergleiche mit regionalen Klimamodellen mit horizontalen Aufl{\"o}sungen von <1km eignet. Die hohe Bodenfeuchte im Bayelva-Tal f{\"u}hrt zudem zu einem deutlich kleineren Bowen-Verh{\"a}ltnis, als es f{\"u}r diese Region zu erwarten ist. Der Eddy-Kovarianz-Messkomplex bei Ny-{\AA}lesund erweist sich hingegen als geeigneter f{\"u}r solche Modellvergleiche, aufgrund der typischen, k{\"u}stennahen Windverteilung und des repr{\"a}sentativen Footprints. Letzteres wird durch die Bestimmung der Footprint-Klimatologie des Jahres 2013 mit einem aktuellen Footprint-Modell erarbeitet. Weiterhin wird die Auswirkung von (Anti-) Zyklonen {\"u}ber den Archipel auf die zeitliche Variabilit{\"a}t der lokalen Grenzschichteigenschaften untersucht und bewertet. Dazu wird ein Zyklonen-Detektions-Algorithmus auf ERA-Interim-Reanalysedatens{\"a}tze angewendet, wodurch die H{\"a}ufigkeit von nahezu ideal konzentrischen Hoch- und die Tiefdruckgebieten f{\"u}r drei Jahre bestimmt wird. Aus dieser Verteilung werden insgesamt drei interessante Zeitr{\"a}ume zu verschiedenen Jahreszeiten ausgew{\"a}hlt und im Rahmen von Prozessstudien die lokalen bodennahen meteorologischen Messungen, der turbulente Austausch an der Oberfl{\"a}che und die Grenzschichtdynamik in der S{\"a}ule untersucht. Die zeitliche Variabilit{\"a}t der dynamischen Grenzschichtstabilit{\"a}t in der S{\"a}ule wird anhand von zeitlich hoch aufgel{\"o}sten vertikalen Profilen der Bulk-Richardson-Zahl aus Kompositprofilen aus Fernerkundungsinstrumenten (Radiometer, Wind-LIDAR) sowie Mastdaten (BSRN-Mast) untersucht und die Grenzschichth{\"o}he ermittelt. Aus diesen Analysen ergibt sich eine deutliche Abh{\"a}ngigkeit der thermischen Stabilit{\"a}t beim Durchzug von Fronten, eine damit einhergehende erhebliche Abh{\"a}ngigkeit der Grenzschichtdynamik und der Grenzschichth{\"o}he sowie des turbulenten Austauschs von der zeitlichen Variabilit{\"a}t der Windgeschwindigkeit in der S{\"a}ule. Auf Grundlage der Standortanalysen und Prozessstudien erfolgt ein Vergleich der bodennahen Messungen und den Beobachtungen aus der S{\"a}ule, sowohl von den genannten Fernerkundungsinstrumenten als auch von In-situ-Messungen (Radiosonden) f{\"u}r den Zeitraum einer Radiosondierungskampagne mit dem nicht-hydrostatischen, regionalen Klimamodel WRF (ARW). Auf Grundlage der Fragestellung, inwieweit aktuelle Schemata die Grenzschichtcharakteristika in orographisch stark gegliedertem Gel{\"a}nde in der Arktis reproduzieren k{\"o}nnen, werden zwei Grenzschichtparametrisierungsschemata mit verschiedenen Ordnungen der Schließung validiert. Hierzu wird die zeitliche Variabilit{\"a}t der Temperatur, der Feuchte und des Windfeldes in der S{\"a}ule bis 2000m in den Simulationen mit den Beobachtungsdaten vergleichen. Es wird gezeigt, dass durch Modifikation der Initialwertfelder eine sehr gute {\"U}bereinstimmung zwischen den Simulationen und den Beobachtungen bereits bei einer horizontalen Aufl{\"o}sung von 1km erreicht werden kann und die Wahl des Grenzschichtschemas nur untergeordneten Einfluss hat. Hieraus werden Ans{\"a}tze der Weiterentwicklung der Parametrisierungen, aber auch Empfehlungen bez{\"u}glich der Initialwertfelder, wie der Landmaske und der Orographie, vorgeschlagen.},
  language  = {de}
}
@misc{BeckmannBeckerKadowetal.2019,
  author    = {Beckmann, Nadine and Becker, Katrin Anne and Kadow, Stephanie and Schumacher, Fabian and Kramer, Melanie and K{\"u}hn, Claudine and Schulz-Schaeffer, Walter J. and Edwards, Michael J. and Kleuser, Burkhard and Gulbins, Erich and Carpinteiro, Alexander},
  title     = {Acid sphingomyelinase deficiency ameliorates Farber disease},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {1087},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-44128},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-441282},
  pages     = {20},
  year      = {2019},
  abstract  = {Farber disease is a rare lysosomal storage disorder resulting from acid ceramidase deficiency and subsequent ceramide accumulation. No treatments for Farber disease are clinically available, and affected patients have a severely shortened lifespan. We have recently reported a novel acid ceramidase deficiency model that mirrors the human disease closely. Acid sphingomyelinase is the enzyme that generates ceramide upstream of acid ceramidase in the lysosomes. Using our acid ceramidase deficiency model, we tested if acid sphingomyelinase could be a potential novel therapeutic target for the treatment of Farber disease. A number of functional acid sphingomyelinase inhibitors are clinically available and have been used for decades to treat major depression. Using these as a therapeutic for Farber disease, thus, has the potential to improve central nervous symptoms of the disease as well, something all other treatment options for Farber disease can't achieve so far. As a proof-of-concept study, we first cross-bred acid ceramidase deficient mice with acid sphingomyelinase deficient mice in order to prevent ceramide accumulation. Double-deficient mice had reduced ceramide accumulation, fewer disease manifestations, and prolonged survival. We next targeted acid sphingomyelinase pharmacologically, to test if these findings would translate to a setting with clinical applicability. Surprisingly, the treatment of acid ceramidase deficient mice with the acid sphingomyelinase inhibitor amitriptyline was toxic to acid ceramidase deficient mice and killed them within a few days of treatment. In conclusion, our study provides the first proof-of-concept that acid sphingomyelinase could be a potential new therapeutic target for Farber disease to reduce disease manifestations and prolong survival. However, we also identified previously unknown toxicity of the functional acid sphingomyelinase inhibitor amitriptyline in the context of Farber disease, strongly cautioning against the use of this substance class for Farber disease patients},
  language  = {en}
}
@article{BeckmannKadowSchumacheretal.2018,
  author    = {Beckmann, Nadine and Kadow, Stephanie and Schumacher, Fabian and Goethert, Joachim R. and Kesper, Stefanie and Draeger, Annette and Schulz-Schaeffer, Walter J. and Wang, Jiang and Becker, Jan U. and Kramer, Melanie and Kuehn, Claudine and Kleuser, Burkhard and Becker, Katrin Anne and Gulbins, Erich and Carpinteiro, Alexander},
  title     = {Pathological manifestations of Farber disease in a new mouse model},
  series = {Biological chemistry},
  volume    = {399},
  journal   = {Biological chemistry},
  number    = {10},
  publisher = {De Gruyter},
  address   = {Berlin},
  issn      = {1431-6730},
  doi       = {10.1515/hsz-2018-0170},
  pages     = {1183 -- 1202},
  year      = {2018},
  abstract  = {Farber disease (FD) is a rare lysosomal storage disorder resulting from acid ceramidase deficiency and subsequent ceramide accumulation. No treatments are clinically available and affected patients have a severely shortened lifespan. Due to the low incidence, the pathogenesis of FD is still poorly understood. Here, we report a novel acid ceramidase mutant mouse model that enables the study of pathogenic mechanisms of FD and ceramide accumulation. Asah1(tmEx1) mice were generated by deletion of the acid ceramidase signal peptide sequence. The effects on lysosomal targeting and activity of the enzyme were assessed. Ceramide and sphingomyelin levels were quantified by liquid chromatography tandem-mass spectrometry (LC-MS/MS) and disease manifestations in several organ systems were analyzed by histology and biochemistry. We show that deletion of the signal peptide sequence disrupts lysosomal targeting and enzyme activity, resulting in ceramide and sphingomyelin accumulation. The affected mice fail to thrive and die early. Histiocytic infiltrations were observed in many tissues, as well as lung inflammation, liver fibrosis, muscular disease manifestations and mild kidney injury. Our new mouse model mirrors human FD and thus offers further insights into the pathogenesis of this disease. In the future, it may also facilitate the development of urgently needed therapies.},
  language  = {en}
}
@article{BeckmannBeckerKadowetal.2019,
  author    = {Beckmann, Nadine and Becker, Katrin Anne and Kadow, Stephanie and Schumacher, Fabian and Kramer, Melanie and Kuehn, Claudine and Schulz-Schaeffer, Walter J. and Edwards, Michael J. and Kleuser, Burkhard and Gulbins, Erich and Carpinteiro, Alexander},
  title     = {Acid Sphingomyelinase Deficiency Ameliorates Farber Disease},
  series = {International journal of molecular sciences},
  volume    = {20},
  journal   = {International journal of molecular sciences},
  number    = {24},
  publisher = {MDPI},
  address   = {Basel},
  issn      = {1422-0067},
  doi       = {10.3390/ijms20246253},
  pages     = {18},
  year      = {2019},
  abstract  = {Farber disease is a rare lysosomal storage disorder resulting from acid ceramidase deficiency and subsequent ceramide accumulation. No treatments for Farber disease are clinically available, and affected patients have a severely shortened lifespan. We have recently reported a novel acid ceramidase deficiency model that mirrors the human disease closely. Acid sphingomyelinase is the enzyme that generates ceramide upstream of acid ceramidase in the lysosomes. Using our acid ceramidase deficiency model, we tested if acid sphingomyelinase could be a potential novel therapeutic target for the treatment of Farber disease. A number of functional acid sphingomyelinase inhibitors are clinically available and have been used for decades to treat major depression. Using these as a therapeutic for Farber disease, thus, has the potential to improve central nervous symptoms of the disease as well, something all other treatment options for Farber disease can't achieve so far. As a proof-of-concept study, we first cross-bred acid ceramidase deficient mice with acid sphingomyelinase deficient mice in order to prevent ceramide accumulation. Double-deficient mice had reduced ceramide accumulation, fewer disease manifestations, and prolonged survival. We next targeted acid sphingomyelinase pharmacologically, to test if these findings would translate to a setting with clinical applicability. Surprisingly, the treatment of acid ceramidase deficient mice with the acid sphingomyelinase inhibitor amitriptyline was toxic to acid ceramidase deficient mice and killed them within a few days of treatment. In conclusion, our study provides the first proof-of-concept that acid sphingomyelinase could be a potential new therapeutic target for Farber disease to reduce disease manifestations and prolong survival. However, we also identified previously unknown toxicity of the functional acid sphingomyelinase inhibitor amitriptyline in the context of Farber disease, strongly cautioning against the use of this substance class for Farber disease patients.},
  language  = {en}
}
@book{RanaMohapatraSidorovaetal.2022,
  author    = {Rana, Kaushik and Mohapatra, Durga Prasad and Sidorova, Julia and Lundberg, Lars and Sk{\"o}ld, Lars and Lopes Grim, Lu{\´i}s Fernando and Sampaio Gradvohl, Andr{\´e} Leon and Cremerius, Jonas and Siegert, Simon and Weltzien, Anton von and Baldi, Annika and Klessascheck, Finn and Kalancha, Svitlana and Lichtenstein, Tom and Shaabani, Nuhad and Meinel, Christoph and Friedrich, Tobias and Lenzner, Pascal and Schumann, David and Wiese, Ingmar and Sarna, Nicole and Wiese, Lena and Tashkandi, Araek Sami and van der Walt, Est{\´e}e and Eloff, Jan H. P. and Schmidt, Christopher and H{\"u}gle, Johannes and Horschig, Siegfried and Uflacker, Matthias and Najafi, Pejman and Sapegin, Andrey and Cheng, Feng and Stojanovic, Dragan and Stojnev Ilić, Aleksandra and Djordjevic, Igor and Stojanovic, Natalija and Predic, Bratislav and Gonz{\´a}lez-Jim{\´e}nez, Mario and de Lara, Juan and Mischkewitz, Sven and Kainz, Bernhard and van Hoorn, Andr{\´e} and Ferme, Vincenzo and Schulz, Henning and Knigge, Marlene and Hecht, Sonja and Prifti, Loina and Krcmar, Helmut and Fabian, Benjamin and Ermakova, Tatiana and Kelkel, Stefan and Baumann, Annika and Morgenstern, Laura and Plauth, Max and Eberhard, Felix and Wolff, Felix and Polze, Andreas and Cech, Tim and Danz, Noel and Noack, Nele Sina and Pirl, Lukas and Beilharz, Jossekin Jakob and De Oliveira, Roberto C. L. and Soares, F{\´a}bio Mendes and Juiz, Carlos and Bermejo, Belen and M{\"u}hle, Alexander and Gr{\"u}ner, Andreas and Saxena, Vageesh and Gayvoronskaya, Tatiana and Weyand, Christopher and Krause, Mirko and Frank, Markus and Bischoff, Sebastian and Behrens, Freya and R{\"u}ckin, Julius and Ziegler, Adrian and Vogel, Thomas and Tran, Chinh and Moser, Irene and Grunske, Lars and Sz{\´a}rnyas, G{\´a}bor and Marton, J{\´o}zsef and Maginecz, J{\´a}nos and Varr{\´o}, D{\´a}niel and Antal, J{\´a}nos Benjamin},
  title     = {HPI Future SOC Lab - Proceedings 2018},
  number    = {151},
  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      = {978-3-86956-547-7},
  issn      = {1613-5652},
  doi       = {10.25932/publishup-56371},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-563712},
  publisher      = {Universit{\"a}t Potsdam},
  pages     = {x, 277},
  year      = {2022},
  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 2018. Selected projects have presented their results on April 17th and November 14th 2017 at the Future SOC Lab Day events.},
  language  = {en}
}
@article{PadashAghionSchulzetal.2022,
  author    = {Padash, Amin and Aghion, Erez and Schulz, Alexander and Barkai, Eli and Chechkin, Aleksei V. and Metzler, Ralf and Kantz, Holger},
  title     = {Local equilibrium properties of ultraslow diffusion in the Sinai model},
  series = {New journal of physics},
  volume    = {24},
  journal   = {New journal of physics},
  number    = {7},
  publisher = {IOP Publishing},
  address   = {Bristol},
  issn      = {1367-2630},
  doi       = {10.1088/1367-2630/ac7df8},
  pages     = {14},
  year      = {2022},
  abstract  = {We perform numerical studies of a thermally driven, overdamped particle in a random quenched force field, known as the Sinai model. We compare the unbounded motion on an infinite 1-dimensional domain to the motion in bounded domains with reflecting boundaries and show that the unbounded motion is at every time close to the equilibrium state of a finite system of growing size. This is due to time scale separation: inside wells of the random potential, there is relatively fast equilibration, while the motion across major potential barriers is ultraslow. Quantities studied by us are the time dependent mean squared displacement, the time dependent mean energy of an ensemble of particles, and the time dependent entropy of the probability distribution. Using a very fast numerical algorithm, we can explore times up top 10(17) steps and thereby also study finite-time crossover phenomena.},
  language  = {en}
}
@article{WuttkeLiLietal.2019,
  author    = {Wuttke, Matthias and Li, Yong and Li, Man and Sieber, Karsten B. and Feitosa, Mary F. and Gorski, Mathias and Tin, Adrienne and Wang, Lihua and Chu, Audrey Y. and Hoppmann, Anselm and Kirsten, Holger and Giri, Ayush and Chai, Jin-Fang and Sveinbjornsson, Gardar and Tayo, Bamidele O. and Nutile, Teresa and Fuchsberger, Christian and Marten, Jonathan and Cocca, Massimiliano and Ghasemi, Sahar and Xu, Yizhe and Horn, Katrin and Noce, Damia and Van der Most, Peter J. and Sedaghat, Sanaz and Yu, Zhi and Akiyama, Masato and Afaq, Saima and Ahluwalia, Tarunveer Singh and Almgren, Peter and Amin, Najaf and Arnlov, Johan and Bakker, Stephan J. L. and Bansal, Nisha and Baptista, Daniela and Bergmann, Sven and Biggs, Mary L. and Biino, Ginevra and Boehnke, Michael and Boerwinkle, Eric and Boissel, Mathilde and B{\"o}ttinger, Erwin and Boutin, Thibaud S. and Brenner, Hermann and Brumat, Marco and Burkhardt, Ralph and Butterworth, Adam S. and Campana, Eric and Campbell, Archie and Campbell, Harry and Canouil, Mickael and Carroll, Robert J. and Catamo, Eulalia and Chambers, John C. and Chee, Miao-Ling and Chee, Miao-Li and Chen, Xu and Cheng, Ching-Yu and Cheng, Yurong and Christensen, Kaare and Cifkova, Renata and Ciullo, Marina and Concas, Maria Pina and Cook, James P. and Coresh, Josef and Corre, Tanguy and Sala, Cinzia Felicita and Cusi, Daniele and Danesh, John and Daw, E. Warwick and De Borst, Martin H. and De Grandi, Alessandro and De Mutsert, Renee and De Vries, Aiko P. J. and Degenhardt, Frauke and Delgado, Graciela and Demirkan, Ayse and Di Angelantonio, Emanuele and Dittrich, Katalin and Divers, Jasmin and Dorajoo, Rajkumar and Eckardt, Kai-Uwe and Ehret, Georg and Elliott, Paul and Endlich, Karlhans and Evans, Michele K. and Felix, Janine F. and Foo, Valencia Hui Xian and Franco, Oscar H. and Franke, Andre and Freedman, Barry I. and Freitag-Wolf, Sandra and Friedlander, Yechiel and Froguel, Philippe and Gansevoort, Ron T. and Gao, He and Gasparini, Paolo and Gaziano, J. Michael and Giedraitis, Vilmantas and Gieger, Christian and Girotto, Giorgia and Giulianini, Franco and Gogele, Martin and Gordon, Scott D. and Gudbjartsson, Daniel F. and Gudnason, Vilmundur and Haller, Toomas and Hamet, Pavel and Harris, Tamara B. and Hartman, Catharina A. and Hayward, Caroline and Hellwege, Jacklyn N. and Heng, Chew-Kiat and Hicks, Andrew A. and Hofer, Edith and Huang, Wei and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Indridason, Olafur S. and Ingelsson, Erik and Ising, Marcus and Jaddoe, Vincent W. V. and Jakobsdottir, Johanna and Jonas, Jost B. and Joshi, Peter K. and Josyula, Navya Shilpa and Jung, Bettina and Kahonen, Mika and Kamatani, Yoichiro and Kammerer, Candace M. and Kanai, Masahiro and Kastarinen, Mika and Kerr, Shona M. and Khor, Chiea-Chuen and Kiess, Wieland and Kleber, Marcus E. and Koenig, Wolfgang and Kooner, Jaspal S. and Korner, Antje and Kovacs, Peter and Kraja, Aldi T. and Krajcoviechova, Alena and Kramer, Holly and Kramer, Bernhard K. and Kronenberg, Florian and Kubo, Michiaki and Kuhnel, Brigitte and Kuokkanen, Mikko and Kuusisto, Johanna and La Bianca, Martina and Laakso, Markku and Lange, Leslie A. and Langefeld, Carl D. and Lee, Jeannette Jen-Mai and Lehne, Benjamin and Lehtimaki, Terho and Lieb, Wolfgang and Lim, Su-Chi and Lind, Lars and Lindgren, Cecilia M. and Liu, Jun and Liu, Jianjun and Loeffler, Markus and Loos, Ruth J. F. and Lucae, Susanne and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Magi, Reedik and Magnusson, Patrik K. E. and Mahajan, Anubha and Martin, Nicholas G. and Martins, Jade and Marz, Winfried and Mascalzoni, Deborah and Matsuda, Koichi and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Metspalu, Andres and Mikaelsdottir, Evgenia K. and Milaneschi, Yuri and Miliku, Kozeta and Mishra, Pashupati P. and Program, V. A. Million Veteran and Mohlke, Karen L. and Mononen, Nina and Montgomery, Grant W. and Mook-Kanamori, Dennis O. and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nalls, Mike A. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and Noordam, Raymond and Olafsson, Isleifur and Oldehinkel, Albertine J. and Orho-Melander, Marju and Ouwehand, Willem H. and Padmanabhan, Sandosh and Palmer, Nicholette D. and Palsson, Runolfur and Penninx, Brenda W. J. H. and Perls, Thomas and Perola, Markus and Pirastu, Mario and Pirastu, Nicola and Pistis, Giorgio and Podgornaia, Anna I. and Polasek, Ozren and Ponte, Belen and Porteous, David J. and Poulain, Tanja and Pramstaller, Peter P. and Preuss, Michael H. and Prins, Bram P. and Province, Michael A. and Rabelink, Ton J. and Raffield, Laura M. and Raitakari, Olli T. and Reilly, Dermot F. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Ridker, Paul M. and Rivadeneira, Fernando and Rizzi, Federica and Roberts, David J. and Robino, Antonietta and Rossing, Peter and Rudan, Igor and Rueedi, Rico and Ruggiero, Daniela and Ryan, Kathleen A. and Saba, Yasaman and Sabanayagam, Charumathi and Salomaa, Veikko and Salvi, Erika and Saum, Kai-Uwe and Schmidt, Helena and Schmidt, Reinhold and Ben Schottker, and Schulz, Christina-Alexandra and Schupf, Nicole and Shaffer, Christian M. and Shi, Yuan and Smith, Albert V. and Smith, Blair H. and Soranzo, Nicole and Spracklen, Cassandra N. and Strauch, Konstantin and Stringham, Heather M. and Stumvoll, Michael and Svensson, Per O. and Szymczak, Silke and Tai, E-Shyong and Tajuddin, Salman M. and Tan, Nicholas Y. Q. and Taylor, Kent D. and Teren, Andrej and Tham, Yih-Chung and Thiery, Joachim and Thio, Chris H. L. and Thomsen, Hauke and Thorleifsson, Gudmar and Toniolo, Daniela and Tonjes, Anke and Tremblay, Johanne and Tzoulaki, Ioanna and Uitterlinden, Andre G. and Vaccargiu, Simona and Van Dam, Rob M. and Van der Harst, Pim and Van Duijn, Cornelia M. and Edward, Digna R. Velez and Verweij, Niek and Vogelezang, Suzanne and Volker, Uwe and Vollenweider, Peter and Waeber, Gerard and Waldenberger, Melanie and Wallentin, Lars and Wang, Ya Xing and Wang, Chaolong and Waterworth, Dawn M. and Bin Wei, Wen and White, Harvey and Whitfield, John B. and Wild, Sarah H. and Wilson, James F. and Wojczynski, Mary K. and Wong, Charlene and Wong, Tien-Yin and Xu, Liang and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Weihua and Zonderman, Alan B. and Rotter, Jerome I. and Bochud, Murielle and Psaty, Bruce M. and Vitart, Veronique and Wilson, James G. and Dehghan, Abbas and Parsa, Afshin and Chasman, Daniel I. and Ho, Kevin and Morris, Andrew P. and Devuyst, Olivier and Akilesh, Shreeram and Pendergrass, Sarah A. and Sim, Xueling and Boger, Carsten A. and Okada, Yukinori and Edwards, Todd L. and Snieder, Harold and Stefansson, Kari and Hung, Adriana M. and Heid, Iris M. and Scholz, Markus and Teumer, Alexander and Kottgen, Anna and Pattaro, Cristian},
  title     = {A catalog of genetic loci associated with kidney function from analyses of a million individuals},
  series = {Nature genetics},
  volume    = {51},
  journal   = {Nature genetics},
  number    = {6},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {Lifelines COHort Study},
  issn      = {1061-4036},
  doi       = {10.1038/s41588-019-0407-x},
  pages     = {957 -- +},
  year      = {2019},
  abstract  = {Chronic kidney disease (CKD) is responsible for a public health burden with multi-systemic complications. Through transancestry meta-analysis of genome-wide association studies of estimated glomerular filtration rate (eGFR) and independent replication (n = 1,046,070), we identified 264 associated loci (166 new). Of these,147 were likely to be relevant for kidney function on the basis of associations with the alternative kidney function marker blood urea nitrogen (n = 416,178). Pathway and enrichment analyses, including mouse models with renal phenotypes, support the kidney as the main target organ. A genetic risk score for lower eGFR was associated with clinically diagnosed CKD in 452,264 independent individuals. Colocalization analyses of associations with eGFR among 783,978 European-ancestry individuals and gene expression across 46 human tissues, including tubulo-interstitial and glomerular kidney compartments, identified 17 genes differentially expressed in kidney. Fine-mapping highlighted missense driver variants in 11 genes and kidney-specific regulatory variants. These results provide a comprehensive priority list of molecular targets for translational research.},
  language  = {en}
}