@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}
}
@unpublished{AcharyaActisAghajanietal.2013,
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O. and Saggion, A. and Safiakian, V. and Saito, K. and Saito, T. and Saito, Y. and Sakaki, N. and Sakonaka, R. and Salini, A. and Sanchez, F. and Sanchez-Conde, M. and Sandoval, A. and Sandaker, H. and Sant'Ambrogio, E. and Santangelo, A. and Santos, E. M. and Sanuy, A. and Sapozhnikov, L. and Sarkar, S. and Sartore, N. and Sasaki, H. and Satalecka, K. and Sawada, M. and Scalzotto, V. and Scapin, V. and Scarcioffolo, M. and Schafer, J. and Schanz, T. and Schlenstedt, S. and Schlickeiser, R. and Schmidt, T. and Schmoll, J. and Schovanek, P. and Schroedter, M. and Schultz, C. and Schultze, J. and Schulz, A. and Schure, K. and Schwab, T. and Schwanke, U. and Schwarz, J. and Schwarzburg, S. and Schweizer, T. and Schwemmer, S. and Segreto, A. and Seiradakis, J. -H. and Sembroski, G. H. and Seweryn, K. and Sharma, M. and Shayduk, M. and Shellard, R. C. and Shi, J. and Shibata, T. and Shibuya, A. and Shum, E. and Sidoli, L. and Sidz, M. and Sieiro, J. and Sikora, M. and Silk, J. and Sillanpaa, A. and Singh, B. B. and Sitarek, J. and Skole, C. and Smareglia, R. and Smith, A. and Smith, D. and Smith, J. and Smith, N. and Sobczynska, D. and Sol, H. and Sottile, G. and Sowinski, M. and Spanier, F. and Spiga, D. and Spyrou, S. and Stamatescu, V. and Stamerra, A. and Starling, R. and Stawarz, L. and Steenkamp, R. and Stegmann, Christian and Steiner, S. and Stergioulas, N. and Sternberger, R. and Sterzel, M. and Stinzing, F. and Stodulski, M. and Straumann, U. and Strazzeri, E. and Stringhetti, L. and Suarez, A. and Suchenek, M. and Sugawara, R. and Sulanke, K. -H. and Sun, S. and Supanitsky, A. D. and Suric, T. and Sutcliffe, P. and Sykes, J. and Szanecki, M. and Szepieniec, T. and Szostek, A. and Tagliaferri, G. and Tajima, H. and Takahashi, H. and Takahashi, K. and Takalo, L. and Takami, H. and Talbot, C. and Tammi, J. and Tanaka, M. and Tanaka, S. and Tasan, J. and Tavani, M. and Tavernet, J. -P. and Tejedor, L. A. and Telezhinsky, Igor O. and Temnikov, P. and Tenzer, C. and Terada, Y. and Terrier, R. and Teshima, M. and Testa, V. and Tezier, D. and Thuermann, D. and Tibaldo, L. and Tibolla, O. and Tiengo, A. and Tluczykont, M. and Todero Peixoto, C. J. and Tokanai, F. and Tokarz, M. and Toma, K. and Torii, K. and Tornikoski, M. and Torres, D. F. and Torres, M. and Tosti, G. and Totani, T. and Toussenel, C. and Tovmassian, G. and Travnicek, P. and Trifoglio, M. and Troyano, I. and Tsinganos, K. and Ueno, H. and Umehara, K. and Upadhya, S. S. and Usher, T. and Uslenghi, M. and Valdes-Galicia, J. F. and Vallania, P. and Vallejo, G. and van Driel, W. and van Eldik, C. and Vandenbrouke, J. and Vanderwalt, J. and Vankov, H. and Vasileiadis, G. and Vassiliev, V. and Veberic, D. and Vegas, I. and Vercellone, S. and Vergani, S. and Veyssiere, C. and Vialle, J. P. and Viana, A. and Videla, M. and Vincent, P. and Vincent, S. and Vink, J. and Vlahakis, N. and Vlahos, L. and Vogler, P. and Vollhardt, A. and von Gunten, H. P. and Vorobiov, S. and Vuerli, C. and Waegebaert, V. and Wagner, R. and Wagner, R. G. and Wagner, S. and Wakely, S. P. and Walter, R. and Walther, T. and Warda, K. and Warwick, R. and Wawer, P. and Wawrzaszek, R. and Webb, N. and Wegner, P. and Weinstein, A. and Weitzel, Q. and Welsing, R. and Werner, M. and Wetteskind, H. and White, R. and Wierzcholska, A. and Wiesand, S. and Wilkinson, M. and Williams, D. A. and Willingale, R. and Winiarski, K. and Wischnewski, R. and Wisniewski, L. and Wood, M. and Woernlein, A. and Xiong, Q. and Yadav, K. K. and Yamamoto, H. and Yamamoto, T. and Yamazaki, R. and Yanagita, S. and Yebras, J. M. and Yelos, D. and Yoshida, A. and Yoshida, T. and Yoshikoshi, T. and Zabalza, V. and Zacharias, M. and Zajczyk, A. and Zanin, R. and Zdziarski, A. and Zech, Alraune and Zhao, A. and Zhou, X. and Zietara, K. and Ziolkowski, J. and Ziolkowski, P. and Zitelli, V. and Zurbach, C. and Zychowski, P.},
  title     = {Introducing the CTA concept},
  series = {Astroparticle physics},
  volume    = {43},
  journal   = {Astroparticle physics},
  number    = {2},
  publisher = {Elsevier},
  address   = {Amsterdam},
  organization    = {CTA Consortium},
  issn      = {0927-6505},
  doi       = {10.1016/j.astropartphys.2013.01.007},
  pages     = {3 -- 18},
  year      = {2013},
  abstract  = {The Cherenkov Telescope Array (CTA) is a new observatory for very high-energy (VHE) gamma rays. CTA has ambitions science goals, for which it is necessary to achieve full-sky coverage, to improve the sensitivity by about an order of magnitude, to span about four decades of energy, from a few tens of GeV to above 100 TeV with enhanced angular and energy resolutions over existing VHE gamma-ray observatories. An international collaboration has formed with more than 1000 members from 27 countries in Europe, Asia, Africa and North and South America. In 2010 the CTA Consortium completed a Design Study and started a three-year Preparatory Phase which leads to production readiness of CTA in 2014. In this paper we introduce the science goals and the concept of CTA, and provide an overview of the project.},
  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{DeLombaerdeVerheyenPerringetal.2018,
  author    = {De Lombaerde, Emiel and Verheyen, Kris and Perring, Michael P. and Bernhardt-Roemermann, Markus and Van Calster, Hans and Brunet, Jorg and Chudomelova, Marketa and Decocq, Guillaume and Diekmann, Martin and Durak, Tomasz and Hedl, Radim and Heinken, Thilo and Hommel, Patrick and Jaroszewicz, Bogdan and Kopecky, Martin and Lenoir, Jonathan and Macek, Martin and M{\´a}liš, František and Mitchell, Fraser J. G. and Naaf, Tobias and Newman, Miles and Petř{\´i}k, Petr and Reczyńska, Kamila and Schmidt, Wolfgang and Swierkosz, Krzysztof and Vild, Ondrej and Wulf, Monika and Baetena, Lander},
  title     = {Responses of competitive understorey species to spatial environmental gradients inaccurately explain temporal changes},
  series = {Basic and applied ecology : Journal of the Gesellschaft f{\"u}r {\"O}kologie},
  volume    = {30},
  journal   = {Basic and applied ecology : Journal of the Gesellschaft f{\"u}r {\"O}kologie},
  publisher = {Elsevier GMBH},
  address   = {M{\"u}nchen},
  issn      = {1439-1791},
  doi       = {10.1016/j.baae.2018.05.013},
  pages     = {52 -- 64},
  year      = {2018},
  abstract  = {Understorey plant communities play a key role in the functioning of forest ecosystems. Under favourable environmental conditions, competitive understorey species may develop high abundances and influence important ecosystem processes such as tree regeneration. Thus, understanding and predicting the response of competitive understorey species as a function of changing environmental conditions is important for forest managers. In the absence of sufficient temporal data to quantify actual vegetation changes, space-for-time (SFT) substitution is often used, i.e. studies that use environmental gradients across space to infer vegetation responses to environmental change over time. Here we assess the validity of such SFT approaches and analysed 36 resurvey studies from ancient forests with low levels of recent disturbances across temperate Europe to assess how six competitive understorey plant species respond to gradients of overstorey cover, soil conditions, atmospheric N deposition and climatic conditions over space and time. The combination of historical and contemporary surveys allows (i) to test if observed contemporary patterns across space are consistent at the time of the historical survey, and, crucially, (ii) to assess whether changes in abundance over time given recorded environmental change match expectations from patterns recorded along environmental gradients in space. We found consistent spatial relationships at the two periods: local variation in soil variables and overstorey cover were the best predictors of individual species' cover while interregional variation in coarse-scale variables, i.e. N deposition and climate, was less important. However, we found that our SFT approach could not accurately explain the large variation in abundance changes over time. We thus recommend to be cautious when using SFT substitution to infer species responses to temporal changes.},
  language  = {en}
}
@article{PerringBernhardtRoemermannBaetenetal.2018,
  author    = {Perring, Michael P. and Bernhardt-Roemermann, Markus and Baeten, Lander and Midolo, Gabriele and Blondeel, Haben and Depauw, Leen and Landuyt, Dries and Maes, Sybryn L. and De Lombaerde, Emiel and Caron, Maria Mercedes and Vellend, Mark and Brunet, Joerg and Chudomelova, Marketa and Decocq, Guillaume and Diekmann, Martin and Dirnboeck, Thomas and Doerfler, Inken and Durak, Tomasz and De Frenne, Pieter and Gilliam, Frank S. and Hedl, Radim and Heinken, Thilo and Hommel, Patrick and Jaroszewicz, Bogdan and Kirby, Keith J. and Kopecky, Martin and Lenoir, Jonathan and Li, Daijiang and Malis, Frantisek and Mitchell, Fraser J. G. and Naaf, Tobias and Newman, Miles and Petrik, Petr and Reczynska, Kamila and Schmidt, Wolfgang and Standovar, Tibor and Swierkosz, Krzysztof and Van Calster, Hans and Vild, Ondrej and Wagner, Eva Rosa and Wulf, Monika and Verheyen, Kris},
  title     = {Global environmental change effects on plant community composition trajectories depend upon management legacies},
  series = {Global change biology},
  volume    = {24},
  journal   = {Global change biology},
  number    = {4},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {1354-1013},
  doi       = {10.1111/gcb.14030},
  pages     = {1722 -- 1740},
  year      = {2018},
  abstract  = {The contemporary state of functional traits and species richness in plant communities depends on legacy effects of past disturbances. Whether temporal responses of community properties to current environmental changes are altered by such legacies is, however, unknown. We expect global environmental changes to interact with land-use legacies given different community trajectories initiated by prior management, and subsequent responses to altered resources and conditions. We tested this expectation for species richness and functional traits using 1814 survey-resurvey plot pairs of understorey communities from 40 European temperate forest datasets, syntheses of management transitions since the year 1800, and a trait database. We also examined how plant community indicators of resources and conditions changed in response to management legacies and environmental change. Community trajectories were clearly influenced by interactions between management legacies from over 200 years ago and environmental change. Importantly, higher rates of nitrogen deposition led to increased species richness and plant height in forests managed less intensively in 1800 (i.e., high forests), and to decreases in forests with a more intensive historical management in 1800 (i.e., coppiced forests). There was evidence that these declines in community variables in formerly coppiced forests were ameliorated by increased rates of temperature change between surveys. Responses were generally apparent regardless of sites' contemporary management classifications, although sometimes the management transition itself, rather than historic or contemporary management types, better explained understorey responses. Main effects of environmental change were rare, although higher rates of precipitation change increased plant height, accompanied by increases in fertility indicator values. Analysis of indicator values suggested the importance of directly characterising resources and conditions to better understand legacy and environmental change effects. Accounting for legacies of past disturbance can reconcile contradictory literature results and appears crucial to anticipating future responses to global environmental change.},
  language  = {en}
}
@article{LauchtSkowronekBeckeretal.2008,
  author    = {Laucht, Manfred and Skowronek, Markus H. and Becker, Katja and Schulze, Thomas G. and Schmidt, Martin H. and Esser, G{\"u}nter and Rietschel, Marcella},
  title     = {Environmental risk factors and attention-deficit : hyperactivity discorder symptoms ; reply},
  issn      = {0003-990X},
  year      = {2008},
  language  = {en}
}
@article{LauchtSkowronekBeckeretal.2007,
  author    = {Laucht, Manfred and Skowronek, Markus H. and Becker, Katja and Schmidt, Martin H. and Esser, G{\"u}nter and Rietschel, Marcella and Schulze, Thomas G.},
  title     = {Interacting effects of the dopamine transporter gene and psychosocial adversity on attention-deficit/ hyperactivity disorder symptoms among 15-year-olds from high-risk community sample},
  issn      = {0003-990X},
  year      = {2007},
  abstract  = {Context: Recent evidence suggests that gene X environment interactions could explain the inconsistent findings of association studies relating the dopamine transporter (DAT1) gene with attention-deficit/hyperactivity disorder (ADHD). 1bjective: To examine whether psychosocial adversity moderated the effect of genetic variation in DAT1 on ADHD symptoms in. adolescents from a high-risk community sample. Design: Prospective cohort study. Setting: Data were taken from the Mannheim Study of Children at Risk, an ongoing longitudinal study of the long-term outcomes of early risk factors followed up from birth on. Participants: Three hundred five adolescents (146 boys, 159 girls) participated in a follow-up assessment at age 15 years. Main Outcome Measures: Measures of ADHD symptoms according to DSM-IV were obtained using standardized structural interviews with adolescents and their parents. Psychosocial adversity was determined according to an "enriched" family adversity index as proposed by Rutter and Quinton. DNA was genotyped for the common DAT1 40-base pair (bp) variable number of tandem repeats (VNTR) polymorphism in the 3' untranslated region; 3 previously described single nucleotide polymorphisms in exon 15, intron 9, and exon 9; and a novel 30-bp VNTR polymorphism in intron 8. Results: Adolescents homozygous for the 10-repeat allele of the 40-bp VNTR polymorphism who grew up in greater psychosocial adversity exhibited significantly more inattention and hyperactivity-impulsivity than adolescents with other genotypes or who lived in less adverse family conditions (significant interaction, P=.013-017). This gene X environment interaction was also observed in individuals homozygous for the 6-repeat allele of the 30-bp VNTR polymorphism and the haplotype comprising both markers. Conclusions: These findings provide initial evidence that environmental risks as described by the Rutter Family Adversity Index moderate the impact of the DAT1 gene on ADHD symptoms, suggesting a DAT1 effect only in those individuals exposed to psychosocial adversity.},
  language  = {en}
}
@article{BernhardtRoemermannBaetenCravenetal.2015,
  author    = {Bernhardt-R{\"o}mermann, Markus and Baeten, Lander and Craven, Dylan and De Frenne, Pieter and Hedl, Radim and Lenoir, Jonathan and Bert, Didier and Brunet, Jorg and Chudomelova, Marketa and Decocq, Guillaume and Dierschke, Hartmut and Dirnboeck, Thomas and D{\"o}rfler, Inken and Heinken, Thilo and Hermy, Martin and Hommel, Patrick and Jaroszewicz, Bogdan and Keczynski, Andrzej and Kelly, Daniel L. and Kirby, Keith J. and Kopecky, Martin and Macek, Martin and Malis, Frantisek and Mirtl, Michael and Mitchell, Fraser J. G. and Naaf, Tobias and Newman, Miles and Peterken, George and Petrik, Petr and Schmidt, Wolfgang and Standovar, Tibor and Toth, Zoltan and Van Calster, Hans and Verstraeten, Gorik and Vladovic, Jozef and Vild, Ondrej and Wulf, Monika and Verheyen, Kris},
  title     = {Drivers of temporal changes in temperate forest plant diversity vary across spatial scales},
  series = {Global change biology},
  volume    = {21},
  journal   = {Global change biology},
  number    = {10},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {1354-1013},
  doi       = {10.1111/gcb.12993},
  pages     = {3726 -- 3737},
  year      = {2015},
  abstract  = {Global biodiversity is affected by numerous environmental drivers. Yet, the extent to which global environmental changes contribute to changes in local diversity is poorly understood. We investigated biodiversity changes in a meta-analysis of 39 resurvey studies in European temperate forests (3988 vegetation records in total, 17-75years between the two surveys) by assessing the importance of (i) coarse-resolution (i.e., among sites) vs. fine-resolution (i.e., within sites) environmental differences and (ii) changing environmental conditions between surveys. Our results clarify the mechanisms underlying the direction and magnitude of local-scale biodiversity changes. While not detecting any net local diversity loss, we observed considerable among-site variation, partly explained by temporal changes in light availability (a local driver) and density of large herbivores (a regional driver). Furthermore, strong evidence was found that presurvey levels of nitrogen deposition determined subsequent diversity changes. We conclude that models forecasting future biodiversity changes should consider coarse-resolution environmental changes, account for differences in baseline environmental conditions and for local changes in fine-resolution environmental conditions.},
  language  = {en}
}
@article{Schmidt2011,
  author    = {Schmidt, Markus G.},
  title     = {Reform of the United Nations Human Rights Programs},
  series = {Die Vereinten Nationen vor globalen Herausforderungen : Referate der Potsdamer UNO-Konferenzen 2000-2008},
  journal   = {Die Vereinten Nationen vor globalen Herausforderungen : Referate der Potsdamer UNO-Konferenzen 2000-2008},
  publisher = {Universit{\"a}tsverlag Potsdam},
  address   = {Potsdam},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-60964},
  pages     = {81 -- 93},
  year      = {2011},
  abstract  = {Inhalt: - Kurzzusammenfassung - I. Introduction - II. Current challenges to the United Nations Human Rights Programme - III. The Secretary General's Reform report "In larger Freedom" and its impact for the human rights programme - IV. The High Commissioner's Plan of Action of May 2005 - V. Negotiations on the establishment of the Human Rights Council and first Council activities - VI. Reform of the treaty body system and debates over the creation of a unified standing treaty body},
  language  = {en}
}
@book{BummelFuesGareisetal.2006,
  author    = {Bummel, Andreas and Fues, Thomas and Gareis, Sven Bernhard and Griep, Ekkehard and Leininger, Julia and Paroz, Jean-Fran{\c{c}}ois and Schmidt, Markus G. and Weiß, Norman},
  title     = {Ein Jahr nach dem UN-Weltgipfel 2005 : eine Bilanz der Reformbem{\"u}hungen ; 8. Potsdamer UNO-Konferenz vom 23. bis 24. Juni 2006},
  series = {Potsdamer UNO-Konferenzen},
  journal   = {Potsdamer UNO-Konferenzen},
  number    = {7},
  publisher = {Universit{\"a}tsverlag Potsdam},
  address   = {Potsdam},
  isbn      = {978-3-939469-43-8},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-66966},
  publisher      = {Universit{\"a}t Potsdam},
  pages     = {122},
  year      = {2006},
  abstract  = {Das Heft dokumentiert die siebte Konferenz des Forschungskreises Vereinte Nationen, die am 23. und 24. Juni 2006 an der Universit{\"a}t Potsdam stattfand. Unter dem Titel „Ein Jahr nach dem UN-Weltgipfel 2005 - Eine Bilanz der Reformbem{\"u}hungen " widmete sich die Konferenz wichtigen strukturellen Fragen und nahm einzelne T{\"a}tigkeitsfelder der Weltorganisation in den Blick. Die aus unterschiedlichen Disziplinen und aus Wissenschaft und Praxis kommenden Referentinnen und Referenten ziehen in den Referaten eine kritische Bilanz und untersuchen, was den Erkl{\"a}rungen des feierlichen Weltgipfels vom September 2005 an konkreten Reformschritten gefolgt ist. In f{\"u}r die „Potsdamer UNO-Konferenzen" typischer Weise wird allen Interessierten die M{\"o}glichkeit gegeben, wichtige Aspekte der aktuellen Diskussion kennenzulernen, welche vor allem die Reform der UN-Hauptorgane, Reformen im Entwicklungssystem der Vereinten Nationen und im Bereich der {\"U}berwachung von Menschenrechtsvertr{\"a}gen betreffen sowie Fragen der Friedenssicherung und die Beteiligung von Zivilgesellschaft und Parlamentariern. Außerdem w{\"u}rdigt die Brosch{\"u}re schweizerische Reforminitiativen in den UN und dokumentiert die aktuelle Diskussion {\"u}ber die deutschsprachige UN-Forschung.},
  language  = {de}
}
@article{PesterSchmidtRuppeletal.2015,
  author    = {Pester, Christian W. and Schmidt, Kristin and Ruppel, Markus and Schoberth, Heiko G. and B{\"o}ker, Alexander},
  title     = {Electric-Field-Induced Order-Order Transition from Hexagonally Perforated Lamellae to Lamellae},
  series = {Macromolecules : a publication of the American Chemical Society},
  volume    = {48},
  journal   = {Macromolecules : a publication of the American Chemical Society},
  number    = {17},
  publisher = {American Chemical Society},
  address   = {Washington},
  issn      = {0024-9297},
  doi       = {10.1021/acs.macromol.5b01336},
  pages     = {6206 -- 6213},
  year      = {2015},
  abstract  = {Block copolymers form a variety of microphase morphologies due to their ability to phase separate. The hexagonally perforated lamellar (HPL) morphology represents an unusually long-lived, nonequilibrium transient structure between lamellar and cylindrical phases. We present a detailed study of a concentrated, HPL-forming poly(styrene-b-isoprene) diblock copolymer solution in toluene in the presence of an electric field. We will show that this phase is readily aligned by a moderate electric field and provide experimental evidence for an electric-field-induced order order transition toward the lamellar phase under sufficiently strong fields. This process is shown to be fully reversible as lamellar perforations reconnect immediately upon secession of the external stimulus, recovering highly aligned perforated lamellae.},
  language  = {en}
}
@article{Schmidt2006,
  author    = {Schmidt, Markus G.},
  title     = {Reform of the United Nations Human Rights Programme - current challenges and trends},
  series = {Ein Jahr nach dem UN-Weltgipfel 2005 , eine Bilanz der Reformbem{\"u}hungen},
  volume    = {2006},
  journal   = {Ein Jahr nach dem UN-Weltgipfel 2005 , eine Bilanz der Reformbem{\"u}hungen},
  number    = {7},
  publisher = {Universit{\"a}tsverlag Potsdam},
  address   = {Potsdam},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-101694},
  pages     = {45 -- 59},
  year      = {2006},
  abstract  = {I. Introduction II. Current challenges to the United Nations Human Rights Programme III. The Secretary General's Reform report "In larger Freedom" andits impact for the human rights programme IV. The High Commissioner's Plan of Action of May 2005 V. Negotiations on the establishment of the Human Rights Counciland first Council activities VI. Reform of the treaty body system and debates over the creationof a unified standing treaty body},
  language  = {de}
}