@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}
}
@article{WarringtonBeaumontHorikoshietal.2019,
  author    = {Warrington, Nicole and Beaumont, Robin and Horikoshi, Momoko and Day, Felix R. and Helgeland, {\O}yvind and Laurin, Charles and Bacelis, Jonas and Peng, Shouneng and Hao, Ke and Feenstra, Bjarke and Wood, Andrew R. and Mahajan, Anubha and Tyrrell, Jessica and Robertson, Neil R. and Rayner, N. William and Qiao, Zhen and Moen, Gunn-Helen and Vaudel, Marc and Marsit, Carmen and Chen, Jia and Nodzenski, Michael and Schnurr, Theresia M. and Zafarmand, Mohammad Hadi and Bradfield, Jonathan P. and Grarup, Niels and Kooijman, Marjolein N. and Li-Gao, Ruifang and Geller, Frank and Ahluwalia, Tarunveer Singh and Paternoster, Lavinia and Rueedi, Rico and Huikari, Ville and Hottenga, Jouke-Jan and Lyytik{\"a}inen, Leo-Pekka and Cavadino, Alana and Metrustry, Sarah and Cousminer, Diana L. and Wu, Ying and Thiering, Elisabeth Paula and Wang, Carol A. and Have, Christian Theil and Vilor-Tejedor, Natalia and Joshi, Peter K. and Painter, Jodie N. and Ntalla, Ioanna and Myhre, Ronny and Pitk{\"a}nen, Niina and van Leeuwen, Elisabeth M. and Joro, Raimo and Lagou, Vasiliki and Richmond, Rebecca C. and Espinosa, Ana and Barton, Sheila J. and Inskip, Hazel M. and Holloway, John W. and Santa-Marina, Loreto and Estivill, Xavier and Ang, Wei and Marsh, Julie A. and Reichetzeder, Christoph and Marullo, Letizia and Hocher, Berthold and Lunetta, Kathryn L. and Murabito, Joanne M. and Relton, Caroline L. and Kogevinas, Manolis and Chatzi, Leda and Allard, Catherine and Bouchard, Luigi and Hivert, Marie-France and Zhang, Ge and Muglia, Louis J. and Heikkinen, Jani and Morgen, Camilla S. and van Kampen, Antoine H. C. and van Schaik, Barbera D. C. and Mentch, Frank D. and Langenberg, Claudia and Scott, Robert A. and Zhao, Jing Hua and Hemani, Gibran and Ring, Susan M. and Bennett, Amanda J. and Gaulton, Kyle J. and Fernandez-Tajes, Juan and van Zuydam, Natalie R. and Medina-Gomez, Carolina and de Haan, Hugoline G. and Rosendaal, Frits R. and Kutalik, Zolt{\´a}n and Marques-Vidal, Pedro and Das, Shikta and Willemsen, Gonneke and Mbarek, Hamdi and M{\"u}ller-Nurasyid, Martina and Standl, Marie and Appel, Emil V. R. and Fonvig, Cilius Esmann and Trier, Caecilie and van Beijsterveldt, Catharina E. M. and Murcia, Mario and Bustamante, Mariona and Bon{\`a}s-Guarch, S{\´i}lvia and Hougaard, David M. and Mercader, Josep M. and Linneberg, Allan and Schraut, Katharina E. and Lind, Penelope A. and Medland, Sarah Elizabeth and Shields, Beverley M. and Knight, Bridget A. and Chai, Jin-Fang and Panoutsopoulou, Kalliope and Bartels, Meike and S{\´a}nchez, Friman and Stokholm, Jakob and Torrents, David and Vinding, Rebecca K. and Willems, Sara M. and Atalay, Mustafa and Chawes, Bo L. and Kovacs, Peter and Prokopenko, Inga and Tuke, Marcus A. and Yaghootkar, Hanieh and Ruth, Katherine S. and Jones, Samuel E. and Loh, Po-Ru and Murray, Anna and Weedon, Michael N. and T{\"o}njes, Anke and Stumvoll, Michael and Michaelsen, Kim Fleischer and Eloranta, Aino-Maija and Lakka, Timo A. and van Duijn, Cornelia M. and Kiess, Wieland and Koerner, Antje and Niinikoski, Harri and Pahkala, Katja and Raitakari, Olli T. and Jacobsson, Bo and Zeggini, Eleftheria and Dedoussis, George V. and Teo, Yik-Ying and Saw, Seang-Mei and Montgomery, Grant W. and Campbell, Harry and Wilson, James F. and Vrijkotte, Tanja G. M. and Vrijheid, Martine and de Geus, Eco J. C. N. and Hayes, M. Geoffrey and Kadarmideen, Haja N. and Holm, Jens-Christian and Beilin, Lawrence J. and Pennell, Craig E. and Heinrich, Joachim and Adair, Linda S. and Borja, Judith B. and Mohlke, Karen L. and Eriksson, Johan G. and Widen, Elisabeth E. and Hattersley, Andrew T. and Spector, Tim D. and Kaehoenen, Mika and Viikari, Jorma S. and Lehtimaeki, Terho and Boomsma, Dorret I. and Sebert, Sylvain and Vollenweider, Peter and Sorensen, Thorkild I. A. and Bisgaard, Hans and Bonnelykke, Klaus and Murray, Jeffrey C. and Melbye, Mads and Nohr, Ellen A. and Mook-Kanamori, Dennis O. and Rivadeneira, Fernando and Hofman, Albert and Felix, Janine F. and Jaddoe, Vincent W. V. and Hansen, Torben and Pisinger, Charlotta and Vaag, Allan A. and Pedersen, Oluf and Uitterlinden, Andre G. and Jarvelin, Marjo-Riitta and Power, Christine and Hypponen, Elina and Scholtens, Denise M. and Lowe, William L. and Smith, George Davey and Timpson, Nicholas J. and Morris, Andrew P. and Wareham, Nicholas J. and Hakonarson, Hakon and Grant, Struan F. A. and Frayling, Timothy M. and Lawlor, Debbie A. and Njolstad, Pal R. and Johansson, Stefan and Ong, Ken K. and McCarthy, Mark I. and Perry, John R. B. and Evans, David M. and Freathy, Rachel M.},
  title     = {Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors},
  series = {Nature genetics},
  volume    = {51},
  journal   = {Nature genetics},
  number    = {5},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {EGG Consortium},
  issn      = {1061-4036},
  pages     = {804 -- +},
  year      = {2019},
  abstract  = {Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.},
  language  = {en}
}
@article{MiddeldorpMahajanHorikoshietal.2019,
  author    = {Middeldorp, Christel M. and Mahajan, Anubha and Horikoshi, Momoko and Robertson, Neil R. and Beaumont, Robin N. and Bradfield, Jonathan P. and Bustamante, Mariona and Cousminer, Diana L. and Day, Felix R. and De Silva, N. Maneka and Guxens, Monica and Mook-Kanamori, Dennis O. and St Pourcain, Beate and Warrington, Nicole M. and Adair, Linda S. and Ahlqvist, Emma and Ahluwalia, Tarunveer Singh and Almgren, Peter and Ang, Wei and Atalay, Mustafa and Auvinen, Juha and Bartels, Meike and Beckmann, Jacques S. and Bilbao, Jose Ramon and Bond, Tom and Borja, Judith B. and Cavadino, Alana and Charoen, Pimphen and Chen, Zhanghua and Coin, Lachlan and Cooper, Cyrus and Curtin, John A. and Custovic, Adnan and Das, Shikta and Davies, Gareth E. and Dedoussis, George V. and Duijts, Liesbeth and Eastwood, Peter R. and Eliasen, Anders U. and Elliott, Paul and Eriksson, Johan G. and Estivill, Xavier and Fadista, Joao and Fedko, Iryna O. and Frayling, Timothy M. and Gaillard, Romy and Gauderman, W. James and Geller, Frank and Gilliland, Frank and Gilsanz, Vincente and Granell, Raquel and Grarup, Niels and Groop, Leif and Hadley, Dexter and Hakonarson, Hakon and Hansen, Torben and Hartman, Catharina A. and Hattersley, Andrew T. and Hayes, M. Geoffrey and Hebebrand, Johannes and Heinrich, Joachim and Helgeland, Oyvind and Henders, Anjali K. and Henderson, John and Henriksen, Tine B. and Hirschhorn, Joel N. and Hivert, Marie-France and Hocher, Berthold and Holloway, John W. and Holt, Patrick and Hottenga, Jouke-Jan and Hypponen, Elina and Iniguez, Carmen and Johansson, Stefan and Jugessur, Astanand and Kahonen, Mika and Kalkwarf, Heidi J. and Kaprio, Jaakko and Karhunen, Ville and Kemp, John P. and Kerkhof, Marjan and Koppelman, Gerard H. and Korner, Antje and Kotecha, Sailesh and Kreiner-Moller, Eskil and Kulohoma, Benard and Kumar, Ashish and Kutalik, Zoltan and Lahti, Jari and Lappe, Joan M. and Larsson, Henrik and Lehtimaki, Terho and Lewin, Alexandra M. and Li, Jin and Lichtenstein, Paul and Lindgren, Cecilia M. and Lindi, Virpi and Linneberg, Allan and Liu, Xueping and Liu, Jun and Lowe, William L. and Lundstrom, Sebastian and Lyytikainen, Leo-Pekka and Ma, Ronald C. W. and Mace, Aurelien and Magi, Reedik and Magnus, Per and Mamun, Abdullah A. and Mannikko, Minna and Martin, Nicholas G. and Mbarek, Hamdi and McCarthy, Nina S. and Medland, Sarah E. and Melbye, Mads and Melen, Erik and Mohlke, Karen L. and Monnereau, Claire and Morgen, Camilla S. and Morris, Andrew P. and Murray, Jeffrey C. and Myhre, Ronny and Najman, Jackob M. and Nivard, Michel G. and Nohr, Ellen A. and Nolte, Ilja M. and Ntalla, Ioanna and Oberfield, Sharon E. and Oken, Emily and Oldehinkel, Albertine J. and Pahkala, Katja and Palviainen, Teemu and Panoutsopoulou, Kalliope and Pedersen, Oluf and Pennell, Craig E. and Pershagen, Goran and Pitkanen, Niina and Plomin, Robert and Power, Christine and Prasad, Rashmi B. and Prokopenko, Inga and Pulkkinen, Lea and Raikkonen, Katri and Raitakari, Olli T. and Reynolds, Rebecca M. and Richmond, Rebecca C. and Rivadeneira, Fernando and Rodriguez, Alina and Rose, Richard J. and Salem, Rany and Santa-Marina, Loreto and Saw, Seang-Mei and Schnurr, Theresia M. and Scott, James G. and Selzam, Saskia and Shepherd, John A. and Simpson, Angela and Skotte, Line and Sleiman, Patrick M. A. and Snieder, Harold and Sorensen, Thorkild I. A. and Standl, Marie and Steegers, Eric A. P. and Strachan, David P. and Straker, Leon and Strandberg, Timo and Taylor, Michelle and Teo, Yik-Ying and Thiering, Elisabeth and Torrent, Maties and Tyrrell, Jessica and Uitterlinden, Andre G. and van Beijsterveldt, Toos and van der Most, Peter J. and van Duijn, Cornelia M. and Viikari, Jorma and Vilor-Tejedor, Natalia and Vogelezang, Suzanne and Vonk, Judith M. and Vrijkotte, Tanja G. M. and Vuoksimaa, Eero and Wang, Carol A. and Watkins, William J. and Wichmann, H-Erich and Willemsen, Gonneke and Williams, Gail M. and Wilson, James F. and Wray, Naomi R. and Xu, Shujing and Xu, Cheng-Jian and Yaghootkar, Hanieh and Yi, Lu and Zafarmand, Mohammad Hadi and Zeggini, Eleftheria and Zemel, Babette S. and Hinney, Anke and Lakka, Timo A. and Whitehouse, Andrew J. O. and Sunyer, Jordi and Widen, Elisabeth E. and Feenstra, Bjarke and Sebert, Sylvain and Jacobsson, Bo and Njolstad, Pal R. and Stoltenberg, Camilla and Smith, George Davey and Lawlor, Debbie A. and Paternoster, Lavinia and Timpson, Nicholas J. and Ong, Ken K. and Bisgaard, Hans and Bonnelykke, Klaus and Jaddoe, Vincent W. V. and Tiemeier, Henning and Jarvelin, Marjo-Riitta and Evans, David M. and Perry, John R. B. and Grant, Struan F. A. and Boomsma, Dorret I. and Freathy, Rachel M. and McCarthy, Mark I. and Felix, Janine F.},
  title     = {The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia},
  series = {European journal of epidemiology},
  volume    = {34},
  journal   = {European journal of epidemiology},
  number    = {3},
  publisher = {Springer},
  address   = {Dordrecht},
  organization    = {EArly Genetics Lifecourse EGG Consortium EGG Membership EAGLE Membership},
  issn      = {0393-2990},
  doi       = {10.1007/s10654-019-00502-9},
  pages     = {279 -- 300},
  year      = {2019},
  abstract  = {The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.},
  language  = {en}
}
@article{BeaumontWarringtonCavadinoetal.2018,
  author    = {Beaumont, Robin N. and Warrington, Nicole M. and Cavadino, Alana and Tyrrell, Jessica and Nodzenski, Michael and Horikoshi, Momoko and Geller, Frank and Myhre, Ronny and Richmond, Rebecca C. and Paternoster, Lavinia and Bradfield, Jonathan P. and Kreiner-Moller, Eskil and Huikari, Ville and Metrustry, Sarah and Lunetta, Kathryn L. and Painter, Jodie N. and Hottenga, Jouke-Jan and Allard, Catherine and Barton, Sheila J. and Espinosa, Ana and Marsh, Julie A. and Potter, Catherine and Zhang, Ge and Ang, Wei and Berry, Diane J. and Bouchard, Luigi and Das, Shikta and Hakonarson, Hakon and Heikkinen, Jani and Helgeland, Oyvind and Hocher, Berthold and Hofman, Albert and Inskip, Hazel M. and Jones, Samuel E. and Kogevinas, Manolis and Lind, Penelope A. and Marullo, Letizia and Medland, Sarah E. and Murray, Anna and Murray, Jeffrey C. and Njolstad, Pal R. and Nohr, Ellen A. and Reichetzeder, Christoph and Ring, Susan M. and Ruth, Katherine S. and Santa-Marina, Loreto and Scholtens, Denise M. and Sebert, Sylvain and Sengpiel, Verena and Tuke, Marcus A. and Vaudel, Marc and Weedon, Michael N. and Willemsen, Gonneke and Wood, Andrew R. and Yaghootkar, Hanieh and Muglia, Louis J. and Bartels, Meike and Relton, Caroline L. and Pennell, Craig E. and Chatzi, Leda and Estivill, Xavier and Holloway, John W. and Boomsma, Dorret I. and Montgomery, Grant W. and Murabito, Joanne M. and Spector, Tim D. and Power, Christine and Jarvelin, Marjo-Ritta and Bisgaard, Hans and Grant, Struan F. A. and Sorensen, Thorkild I. A. and Jaddoe, Vincent W. and Jacobsson, Bo and Melbye, Mads and McCarthy, Mark I. and Hattersley, Andrew T. and Hayes, M. Geoffrey and Frayling, Timothy M. and Hivert, Marie-France and Felix, Janine F. and Hypponen, Elina and Lowe, William L. and Evans, David M. and Lawlor, Debbie A. and Feenstra, Bjarke and Freathy, Rachel M.},
  title     = {Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics},
  series = {Human molecular genetics},
  volume    = {27},
  journal   = {Human molecular genetics},
  number    = {4},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  organization    = {Early Growth Genetics EGG},
  issn      = {0964-6906},
  doi       = {10.1093/hmg/ddx429},
  pages     = {742 -- 756},
  year      = {2018},
  abstract  = {Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P< 5 x 10(-8). In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.},
  language  = {en}
}
@misc{BeaumontWarringtonCavadinoetal.2017,
  author    = {Beaumont, Robin N. and Warrington, Nicole M. and Cavadino, Alana and Tyrrell, Jessica and Nodzenski, Michael and Horikoshi, Momoko and Geller, Frank and Myhre, Ronny and Richmond, Rebecca C. and Paternoster, Lavinia and Bradfield, Jonathan P. and Kreiner-M{\o}ller, Eskil and Huikari, Ville and Metrustry, Sarah and Lunetta, Kathryn L. and Painter, Jodie N. and Hottenga, Jouke-Jan and Allard, Catherine and Barton, Sheila J. and Espinosa, Ana and Marsh, Julie A. and Potter, Catherine and Zhang, Ge and Ang, Wei and Berry, Diane J. and Bouchard, Luigi and Das, Shikta and Hakonarson, Hakon and Heikkinen, Jani and Helgeland, {\O}yvind and Hocher, Berthold and Hofman, Albert and Inskip, Hazel M. and Jones, Samuel E. and Kogevinas, Manolis and Lind, Penelope A. and Marullo, Letizia and Medland, Sarah E. and Murray, Anna and Murray, Jeffrey C. and Nj{\o}lstad, Pa ̊l R. and Nohr, Ellen A. and Reichetzeder, Christoph and Ring, Susan M. and Ruth, Katherine S. and Santa-Marina, Loreto and Scholtens, Denise M. and Sebert, Sylvain and Sengpiel, Verena and Tuke, Marcus A. and Vaudel, Marc and Weedon, Michael N. and Willemsen, Gonneke and Wood, Andrew R. and Yaghootkar, Hanieh and Muglia, Louis J. and Bartels, Meike and Relton, Caroline L. and Pennell, Craig E. and Chatzi, Leda and Estivill, Xavier and Holloway, John W. and Boomsma, Dorret I. and Montgomery, Grant W. and Murabito, Joanne M. and Spector, Tim D. and Power, Christine and Ja ̈rvelin, Marjo-Ritta and Bisgaard, Hans and Grant, Struan F.A. and S{\o}rensen, Thorkild I.A. and Jaddoe, Vincent W. and Jacobsson, Bo and Melbye, Mads and McCarthy, Mark I. and Hattersley, Andrew T. and Hayes, M. Geoffrey and Frayling, Timothy M. and Hivert, Marie-France and Felix, Janine F. and Hyppo ̈nen, Elina and Lowe, William L. , Jr and Evans, David M. and Lawlor, Debbie A. and Feenstra, Bjarke and Freathy, Rachel M.},
  title     = {Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {628},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-42310},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-423100},
  pages     = {15},
  year      = {2017},
  abstract  = {Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P < 5 {\^A} 10 {\`A}8 . In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.},
  language  = {en}
}
@article{AartsAndersonAndersonetal.2015,
  author    = {Aarts, Alexander A. and Anderson, Joanna E. and Anderson, Christopher J. and Attridge, Peter R. and Attwood, Angela and Axt, Jordan and Babel, Molly and Bahnik, Stepan and Baranski, Erica and Barnett-Cowan, Michael and Bartmess, Elizabeth and Beer, Jennifer and Bell, Raoul and Bentley, Heather and Beyan, Leah and Binion, Grace and Borsboom, Denny and Bosch, Annick and Bosco, Frank A. and Bowman, Sara D. and Brandt, Mark J. and Braswell, Erin and Brohmer, Hilmar and Brown, Benjamin T. and Brown, Kristina and Bruening, Jovita and Calhoun-Sauls, Ann and Callahan, Shannon P. and Chagnon, Elizabeth and Chandler, Jesse and Chartier, Christopher R. and Cheung, Felix and Christopherson, Cody D. and Cillessen, Linda and Clay, Russ and Cleary, Hayley and Cloud, Mark D. and Cohn, Michael and Cohoon, Johanna and Columbus, Simon and Cordes, Andreas and Costantini, Giulio and Alvarez, Leslie D. Cramblet and Cremata, Ed and Crusius, Jan and DeCoster, Jamie and DeGaetano, Michelle A. and Della Penna, Nicolas and den Bezemer, Bobby and Deserno, Marie K. and Devitt, Olivia and Dewitte, Laura and Dobolyi, David G. and Dodson, Geneva T. and Donnellan, M. Brent and Donohue, Ryan and Dore, Rebecca A. and Dorrough, Angela and Dreber, Anna and Dugas, Michelle and Dunn, Elizabeth W. and Easey, Kayleigh and Eboigbe, Sylvia and Eggleston, Casey and Embley, Jo and Epskamp, Sacha and Errington, Timothy M. and Estel, Vivien and Farach, Frank J. and Feather, Jenelle and Fedor, Anna and Fernandez-Castilla, Belen and Fiedler, Susann and Field, James G. and Fitneva, Stanka A. and Flagan, Taru and Forest, Amanda L. and Forsell, Eskil and Foster, Joshua D. and Frank, Michael C. and Frazier, Rebecca S. and Fuchs, Heather and Gable, Philip and Galak, Jeff and Galliani, Elisa Maria and Gampa, Anup and Garcia, Sara and Gazarian, Douglas and Gilbert, Elizabeth and Giner-Sorolla, Roger and Gl{\"o}ckner, Andreas and G{\"o}llner, Lars and Goh, Jin X. and Goldberg, Rebecca and Goodbourn, Patrick T. and Gordon-McKeon, Shauna and Gorges, Bryan and Gorges, Jessie and Goss, Justin and Graham, Jesse and Grange, James A. and Gray, Jeremy and Hartgerink, Chris and Hartshorne, Joshua and Hasselman, Fred and Hayes, Timothy and Heikensten, Emma and Henninger, Felix and Hodsoll, John and Holubar, Taylor and Hoogendoorn, Gea and Humphries, Denise J. and Hung, Cathy O. -Y. and Immelman, Nathali and Irsik, Vanessa C. and Jahn, Georg and Jaekel, Frank and Jekel, Marc and Johannesson, Magnus and Johnson, Larissa G. and Johnson, David J. and Johnson, Kate M. and Johnston, William J. and Jonas, Kai and Joy-Gaba, Jennifer A. and Kappes, Heather Barry and Kelso, Kim and Kidwell, Mallory C. and Kim, Seung Kyung and Kirkhart, Matthew and Kleinberg, Bennett and Knezevic, Goran and Kolorz, Franziska Maria and Kossakowski, Jolanda J. and Krause, Robert Wilhelm and Krijnen, Job and Kuhlmann, Tim and Kunkels, Yoram K. and Kyc, Megan M. and Lai, Calvin K. and Laique, Aamir and Lakens, Daniel and Lane, Kristin A. and Lassetter, Bethany and Lazarevic, Ljiljana B. and LeBel, Etienne P. and Lee, Key Jung and Lee, Minha and Lemm, Kristi and Levitan, Carmel A. and Lewis, Melissa and Lin, Lin and Lin, Stephanie and Lippold, Matthias and Loureiro, Darren and Luteijn, Ilse and Mackinnon, Sean and Mainard, Heather N. and Marigold, Denise C. and Martin, Daniel P. and Martinez, Tylar and Masicampo, E. J. and Matacotta, Josh and Mathur, Maya and May, Michael and Mechin, Nicole and Mehta, Pranjal and Meixner, Johannes and Melinger, Alissa and Miller, Jeremy K. and Miller, Mallorie and Moore, Katherine and M{\"o}schl, Marcus and Motyl, Matt and M{\"u}ller, Stephanie M. and Munafo, Marcus and Neijenhuijs, Koen I. and Nervi, Taylor and Nicolas, Gandalf and Nilsonne, Gustav and Nosek, Brian A. and Nuijten, Michele B. and Olsson, Catherine and Osborne, Colleen and Ostkamp, Lutz and Pavel, Misha and Penton-Voak, Ian S. and Perna, Olivia and Pernet, Cyril and Perugini, Marco and Pipitone, R. Nathan and Pitts, Michael and Plessow, Franziska and Prenoveau, Jason M. and Rahal, Rima-Maria and Ratliff, Kate A. and Reinhard, David and Renkewitz, Frank and Ricker, Ashley A. and Rigney, Anastasia and Rivers, Andrew M. and Roebke, Mark and Rutchick, Abraham M. and Ryan, Robert S. and Sahin, Onur and Saide, Anondah and Sandstrom, Gillian M. and Santos, David and Saxe, Rebecca and Schlegelmilch, Rene and Schmidt, Kathleen and Scholz, Sabine and Seibel, Larissa and Selterman, Dylan Faulkner and Shaki, Samuel and Simpson, William B. and Sinclair, H. Colleen and Skorinko, Jeanine L. M. and Slowik, Agnieszka and Snyder, Joel S. and Soderberg, Courtney and Sonnleitner, Carina and Spencer, Nick and Spies, Jeffrey R. and Steegen, Sara and Stieger, Stefan and Strohminger, Nina and Sullivan, Gavin B. and Talhelm, Thomas and Tapia, Megan and te Dorsthorst, Anniek and Thomae, Manuela and Thomas, Sarah L. and Tio, Pia and Traets, Frits and Tsang, Steve and Tuerlinckx, Francis and Turchan, Paul and Valasek, Milan and Van Aert, Robbie and van Assen, Marcel and van Bork, Riet and van de Ven, Mathijs and van den Bergh, Don and van der Hulst, Marije and van Dooren, Roel and van Doorn, Johnny and van Renswoude, Daan R. and van Rijn, Hedderik and Vanpaemel, Wolf and Echeverria, Alejandro Vasquez and Vazquez, Melissa and Velez, Natalia and Vermue, Marieke and Verschoor, Mark and Vianello, Michelangelo and Voracek, Martin and Vuu, Gina and Wagenmakers, Eric-Jan and Weerdmeester, Joanneke and Welsh, Ashlee and Westgate, Erin C. and Wissink, Joeri and Wood, Michael and Woods, Andy and Wright, Emily and Wu, Sining and Zeelenberg, Marcel and Zuni, Kellylynn},
  title     = {Estimating the reproducibility of psychological science},
  series = {Science},
  volume    = {349},
  journal   = {Science},
  number    = {6251},
  publisher = {American Assoc. for the Advancement of Science},
  address   = {Washington},
  organization    = {Open Sci Collaboration},
  issn      = {1095-9203},
  doi       = {10.1126/science.aac4716},
  pages     = {8},
  year      = {2015},
  abstract  = {Reproducibility is a defining feature of science, but the extent to which it characterizes current research is unknown. We conducted replications of 100 experimental and correlational studies published in three psychology journals using high-powered designs and original materials when available. Replication effects were half the magnitude of original effects, representing a substantial decline. Ninety-seven percent of original studies had statistically significant results. Thirty-six percent of replications had statistically significant results; 47\% of original effect sizes were in the 95\% confidence interval of the replication effect size; 39\% of effects were subjectively rated to have replicated the original result; and if no bias in original results is assumed, combining original and replication results left 68\% with statistically significant effects. Correlational tests suggest that replication success was better predicted by the strength of original evidence than by characteristics of the original and replication teams.},
  language  = {en}
}
@article{LaveeImesonBorketal.1995,
  author    = {Lavee, Hanoch and Imeson, A. and Bork, Hans-Rudolf and Shoshani, M. and Kutiel, P. and Benyamin, Yves and Sarah, P.},
  title     = {Eco-geomorphic systems along a climatic gradient},
  year      = {1995},
  language  = {en}
}
@article{RenteriaSchmaalHibaretal.2017,
  author    = {Renteria, Miguel E. and Schmaal, L. and Hibar, D. P. and Couvy-Duchesne, B. and Strike, L. T. and Mills, N. T. and de Zubicaray, Greig. I. and McMahon, Katie. L. and Medland, Sarah E. and Gillespie, N. A. and Hatton, S. N. and Lagopoulos, J. and Veltman, D. J. and van der Wee, N. and van Erp, T. G. M. and Wittfeld, K. and Grabe, H. J. and Block, Andrea and Hegenscheid, K. and Voelzke, H. and Veer, I. M. and Walter, H. and Schnell, K. and Schramm, E. and Normann, C. and Schoepf, Dieter and Konrad, C. and Zurowski, B. and Godlewska, B. R. and Cowen, P. J. and Penninx, B. W. J. H. and Jahanshad, N. and Thompson, Paul M. and Wright, M. J. and Martin, N. G. and Christensen, H. and Hickie, I. B.},
  title     = {Subcortical brain structure and suicidal behaviour in major depressive disorder: a meta-analysis from the ENIGMA-MDD working group},
  series = {Translational Psychiatry},
  volume    = {7},
  journal   = {Translational Psychiatry},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {ENIGMA-Major Depressive Disorde},
  issn      = {2158-3188},
  doi       = {10.1038/tp.2017.84},
  pages     = {2301 -- 2320},
  year      = {2017},
  language  = {en}
}
@misc{UhligGehreKammereretal.2018,
  author    = {Uhlig, Katja and Gehre, Christian P. and Kammerer, Sarah and K{\"u}pper, Jan-Heiner and Coleman, Charles Dominic and P{\"u}schel, Gerhard Paul and Duschl, Claus},
  title     = {Real-time monitoring of oxygen consumption of hepatocytes in a microbioreactor},
  series = {Toxicology letters},
  volume    = {295},
  journal   = {Toxicology letters},
  publisher = {Elsevier},
  address   = {Clare},
  issn      = {0378-4274},
  doi       = {10.1016/j.toxlet.2018.06.652},
  pages     = {S115 -- S115},
  year      = {2018},
  language  = {en}
}
@misc{SachseBillaultBowenetal.2012,
  author    = {Sachse, Dirk and Billault, Isabelle and Bowen, Gabriel J. and Chikaraishi, Yoshito and Dawson, Todd E. and Feakins, Sarah J. and Freeman, Katherine H. and Magill, Clayton R. and McInerney, Francesca A. and van der Meer, Marcel T. J. and Polissar, Pratigya and Robins, Richard J. and Sachs, Julian P. and Schmidt, Hanns-Ludwig and Sessions, Alex L. and White, James W. C. and West, Jason B. and Kahmen, Ansgar},
  title     = {Molecular Paleohydrology interpreting the Hydrogen- Isotopic Composition of Lipid Biomarkers from Photosynthesizing Organisms},
  series = {Annual review of earth and planetary sciences},
  volume    = {40},
  journal   = {Annual review of earth and planetary sciences},
  number    = {1},
  editor    = {Jeanloz, R},
  publisher = {Annual Reviews},
  address   = {Palo Alto},
  isbn      = {978-0-8243-2040-9},
  issn      = {0084-6597},
  doi       = {10.1146/annurev-earth-042711-105535},
  pages     = {221 -- 249},
  year      = {2012},
  abstract  = {Hydrogen-isotopic abundances of lipid biomarkers are emerging as important proxies in the study of ancient environments and ecosystems. A decade ago, pioneering studies made use of new analytical methods and demonstrated that the hydrogen-isotopic composition of individual lipids from aquatic and terrestrial organisms can be related to the composition of their growth (i.e., environmental) water. Subsequently, compound-specific deuterium/hydrogen (D/H) ratios of sedimentary biomarkers have been increasingly used as paleohydrological proxies over a range of geological timescales. Isotopic fractionation observed between hydrogen in environmental water and hydrogen in lipids, however, is sensitive to biochemical, physiological, and environmental influences on the composition of hydrogen available for biosynthesis in cells. Here we review the factors and processes that are known to influence the hydrogen-isotopic compositions of lipids-especially n-alkanes-from photosynthesizing organisms, and we provide a framework for interpreting their D/H ratios from ancient sediments and identify future research opportunities.},
  language  = {en}
}
@article{WintleBekessyKeithetal.2011,
  author    = {Wintle, Brendan A. and Bekessy, Sarah A. and Keith, David A. and van Wilgen, Brian W. and Cabeza, Mar and Schr{\"o}der-Esselbach, Boris and Carvalho, Silvia B. and Falcucci, Alessandra and Maiorano, Luigi and Regan, Tracey J. and Rondinini, Carlo and Boitani, Luigi and Possingham, Hugh P.},
  title     = {Ecological-economic optimization of biodiversity conservation under climate change},
  series = {Nature climate change},
  volume    = {1},
  journal   = {Nature climate change},
  number    = {7},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {1758-678X},
  doi       = {10.1038/NCLIMATE1227},
  pages     = {355 -- 359},
  year      = {2011},
  abstract  = {Substantial investment in climate change research has led to dire predictions of the impacts and risks to biodiversity. The Intergovernmental Panel on Climate Change fourth assessment report(1) cites 28,586 studies demonstrating significant biological changes in terrestrial systems(2). Already high extinction rates, driven primarily by habitat loss, are predicted to increase under climate change(3-6). Yet there is little specific advice or precedent in the literature to guide climate adaptation investment for conserving biodiversity within realistic economic constraints(7). Here we present a systematic ecological and economic analysis of a climate adaptation problem in one of the world's most species-rich and threatened ecosystems: the South African fynbos. We discover a counterintuitive optimal investment strategy that switches twice between options as the available adaptation budget increases. We demonstrate that optimal investment is nonlinearly dependent on available resources, making the choice of how much to invest as important as determining where to invest and what actions to take. Our study emphasizes the importance of a sound analytical framework for prioritizing adaptation investments(4). Integrating ecological predictions in an economic decision framework will help support complex choices between adaptation options under severe uncertainty. Our prioritization method can be applied at any scale to minimize species loss and to evaluate the robustness of decisions to uncertainty about key assumptions.},
  language  = {en}
}
@article{HoffmannFeakinsBookhagenetal.2016,
  author    = {Hoffmann, Bernd and Feakins, Sarah J. and Bookhagen, Bodo and Olen, Stephanie M. and Adhikari, Danda P. and Mainali, Janardan and Sachse, Dirk},
  title     = {Climatic and geomorphic drivers of plant organic matter transport in the Arun River, E Nepal},
  series = {Earth \& planetary science letters},
  volume    = {452},
  journal   = {Earth \& planetary science letters},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0012-821X},
  doi       = {10.1016/j.epsl.2016.07.008},
  pages     = {104 -- 114},
  year      = {2016},
  language  = {en}
}
@misc{DoegeHoenzkeSchumacheretal.2016,
  author    = {Doege, N. and Hoenzke, S. and Schumacher, Fabian and Balzus, Benjamin and Colombo, Miriam and Hadam, S. and Rancan, F. and Blume-Peytavi, Ulrike and Schindler, A. and Ruehl, E. and Skov, P. and Church, Martin K. and Hedtrich, Sarah and Kleuser, Burkhard and Bodmeier, Roland and Vogt, A.},
  title     = {Ex vivo microdialysis used for the preclinical assessment of anti-inflammatory therapy},
  series = {Experimental dermatology : the official journal of the European Immunodermatology Society},
  volume    = {25},
  journal   = {Experimental dermatology : the official journal of the European Immunodermatology Society},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {0906-6705},
  pages     = {E32 -- E32},
  year      = {2016},
  language  = {en}
}
@article{RadchukReedTeplitskyetal.2019,
  author    = {Radchuk, Viktoriia and Reed, Thomas and Teplitsky, Celine and van de Pol, Martijn and Charmantier, Anne and Hassall, Christopher and Adamik, Peter and Adriaensen, Frank and Ahola, Markus P. and Arcese, Peter and Miguel Aviles, Jesus and Balbontin, Javier and Berg, Karl S. and Borras, Antoni and Burthe, Sarah and Clobert, Jean and Dehnhard, Nina and de Lope, Florentino and Dhondt, Andre A. and Dingemanse, Niels J. and Doi, Hideyuki and Eeva, Tapio and Fickel, J{\"o}rns and Filella, Iolanda and Fossoy, Frode and Goodenough, Anne E. and Hall, Stephen J. G. and Hansson, Bengt and Harris, Michael and Hasselquist, Dennis and Hickler, Thomas and Jasmin Radha, Jasmin and Kharouba, Heather and Gabriel Martinez, Juan and Mihoub, Jean-Baptiste and Mills, James A. and Molina-Morales, Mercedes and Moksnes, Arne and Ozgul, Arpat and Parejo, Deseada and Pilard, Philippe and Poisbleau, Maud and Rousset, Francois and R{\"o}del, Mark-Oliver and Scott, David and Carlos Senar, Juan and Stefanescu, Constanti and Stokke, Bard G. and Kusano, Tamotsu and Tarka, Maja and Tarwater, Corey E. and Thonicke, Kirsten and Thorley, Jack and Wilting, Andreas and Tryjanowski, Piotr and Merila, Juha and Sheldon, Ben C. and Moller, Anders Pape and Matthysen, Erik and Janzen, Fredric and Dobson, F. Stephen and Visser, Marcel E. and Beissinger, Steven R. and Courtiol, Alexandre and Kramer-Schadt, Stephanie},
  title     = {Adaptive responses of animals to climate change are most likely insufficient},
  series = {Nature Communications},
  volume    = {10},
  journal   = {Nature Communications},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {2041-1723},
  doi       = {10.1038/s41467-019-10924-4},
  pages     = {14},
  year      = {2019},
  abstract  = {Biological responses to climate change have been widely documented across taxa and regions, but it remains unclear whether species are maintaining a good match between phenotype and environment, i.e. whether observed trait changes are adaptive. Here we reviewed 10,090 abstracts and extracted data from 71 studies reported in 58 relevant publications, to assess quantitatively whether phenotypic trait changes associated with climate change are adaptive in animals. A meta-analysis focussing on birds, the taxon best represented in our dataset, suggests that global warming has not systematically affected morphological traits, but has advanced phenological traits. We demonstrate that these advances are adaptive for some species, but imperfect as evidenced by the observed consistent selection for earlier timing. Application of a theoretical model indicates that the evolutionary load imposed by incomplete adaptive responses to ongoing climate change may already be threatening the persistence of species.},
  language  = {en}
}
@article{GuerreroFickelBenhaiemetal.2020,
  author    = {Guerrero, Tania P. and Fickel, J{\"o}rns and Benhaiem, Sarah and Weyrich, Alexandra},
  title     = {Epigenomics and gene regulation in mammalian social systems},
  series = {Current zoology},
  volume    = {66},
  journal   = {Current zoology},
  number    = {3},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {1674-5507},
  doi       = {10.1093/cz/zoaa005},
  pages     = {307 -- 319},
  year      = {2020},
  abstract  = {Social epigenomics is a new field of research that studies how the social environment shapes the epigenome and how in turn the epigenome modulates behavior. We focus on describing known gene-environment interactions (GEIs) and epigenetic mechanisms in different mammalian social systems. To illustrate how epigenetic mechanisms integrate GEls, we highlight examples where epigenetic mechanisms are associated with social behaviors and with their maintenance through neuroendocrine, locomotor, and metabolic responses. We discuss future research trajectories and open questions for the emerging field of social epigenomics in nonmodel and naturally occurring social systems. Finally, we outline the technological advances that aid the study of epigenetic mechanisms in the establishment of GEIs and vice versa.},
  language  = {en}
}
@article{SteffenRoeckstromRichardsonetal.2018,
  author    = {Steffen, Will and R{\"o}ckstrom, Johan and Richardson, Katherine and Lenton, Timothy M. and Folke, Carl and Liverman, Diana and Summerhayes, Colin P. and Barnosky, Anthony D. and Cornell, Sarah E. and Crucifix, Michel and Donges, Jonathan and Fetzer, Ingo and Lade, Steven J. and Scheffer, Marten and Winkelmann, Ricarda and Schellnhuber, Hans Joachim},
  title     = {Trajectories of the Earth System in the Anthropocene},
  series = {Proceedings of the National Academy of Sciences of the United States of America},
  volume    = {115},
  journal   = {Proceedings of the National Academy of Sciences of the United States of America},
  number    = {33},
  publisher = {National Acad. of Sciences},
  address   = {Washington},
  issn      = {0027-8424},
  doi       = {10.1073/pnas.1810141115},
  pages     = {8252 -- 8259},
  year      = {2018},
  abstract  = {We explore the risk that self-reinforcing feedbacks could push the Earth System toward a planetary threshold that, if crossed, could prevent stabilization of the climate at intermediate temperature rises and cause continued warming on a "Hothouse Earth" pathway even as human emissions are reduced. Crossing the threshold would lead to a much higher global average temperature than any interglacial in the past 1.2 million years and to sea levels significantly higher than at any time in the Holocene. We examine the evidence that such a threshold might exist and where it might be. If the threshold is crossed, the resulting trajectory would likely cause serious disruptions to ecosystems, society, and economies. Collective human action is required to steer the Earth System away from a potential threshold and stabilize it in a habitable interglacial-like state. Such action entails stewardship of the entire Earth System-biosphere, climate, and societies-and could include decarbonization of the global economy, enhancement of biosphere carbon sinks, behavioral changes, technological innovations, new governance arrangements, and transformed social values.},
  language  = {en}
}
@article{TuckerBoehningGaeseFaganetal.2018,
  author    = {Tucker, Marlee A. and Boehning-Gaese, Katrin and Fagan, William F. and Fryxell, John M. and Van Moorter, Bram and Alberts, Susan C. and Ali, Abdullahi H. and Allen, Andrew M. and Attias, Nina and Avgar, Tal and Bartlam-Brooks, Hattie and Bayarbaatar, Buuveibaatar and Belant, Jerrold L. and Bertassoni, Alessandra and Beyer, Dean and Bidner, Laura and van Beest, Floris M. and Blake, Stephen and Blaum, Niels and Bracis, Chloe and Brown, Danielle and de Bruyn, P. J. Nico and Cagnacci, Francesca and Calabrese, Justin M. and Camilo-Alves, Constanca and Chamaille-Jammes, Simon and Chiaradia, Andre and Davidson, Sarah C. and Dennis, Todd and DeStefano, Stephen and Diefenbach, Duane and Douglas-Hamilton, Iain and Fennessy, Julian and Fichtel, Claudia and Fiedler, Wolfgang and Fischer, Christina and Fischhoff, Ilya and Fleming, Christen H. and Ford, Adam T. and Fritz, Susanne A. and Gehr, Benedikt and Goheen, Jacob R. and Gurarie, Eliezer and Hebblewhite, Mark and Heurich, Marco and Hewison, A. J. Mark and Hof, Christian and Hurme, Edward and Isbell, Lynne A. and Janssen, Rene and Jeltsch, Florian and Kaczensky, Petra and Kane, Adam and Kappeler, Peter M. and Kauffman, Matthew and Kays, Roland and Kimuyu, Duncan and Koch, Flavia and Kranstauber, Bart and LaPoint, Scott and Leimgruber, Peter and Linnell, John D. C. and Lopez-Lopez, Pascual and Markham, A. Catherine and Mattisson, Jenny and Medici, Emilia Patricia and Mellone, Ugo and Merrill, Evelyn and Mourao, Guilherme de Miranda and Morato, Ronaldo G. and Morellet, Nicolas and Morrison, Thomas A. and Diaz-Munoz, Samuel L. and Mysterud, Atle and Nandintsetseg, Dejid and Nathan, Ran and Niamir, Aidin and Odden, John and Oliveira-Santos, Luiz Gustavo R. and Olson, Kirk A. and Patterson, Bruce D. and de Paula, Rogerio Cunha and Pedrotti, Luca and Reineking, Bjorn and Rimmler, Martin and Rogers, Tracey L. and Rolandsen, Christer Moe and Rosenberry, Christopher S. and Rubenstein, Daniel I. and Safi, Kamran and Said, Sonia and Sapir, Nir and Sawyer, Hall and Schmidt, Niels Martin and Selva, Nuria and Sergiel, Agnieszka and Shiilegdamba, Enkhtuvshin and Silva, Joao Paulo and Singh, Navinder and Solberg, Erling J. and Spiegel, Orr and Strand, Olav and Sundaresan, Siva and Ullmann, Wiebke and Voigt, Ulrich and Wall, Jake and Wattles, David and Wikelski, Martin and Wilmers, Christopher C. and Wilson, John W. and Wittemyer, George and Zieba, Filip and Zwijacz-Kozica, Tomasz and Mueller, Thomas},
  title     = {Moving in the Anthropocene},
  series = {Science},
  volume    = {359},
  journal   = {Science},
  number    = {6374},
  publisher = {American Assoc. for the Advancement of Science},
  address   = {Washington},
  issn      = {0036-8075},
  doi       = {10.1126/science.aam9712},
  pages     = {466 -- 469},
  year      = {2018},
  abstract  = {Animal movement is fundamental for ecosystem functioning and species survival, yet the effects of the anthropogenic footprint on animal movements have not been estimated across species. Using a unique GPS-tracking database of 803 individuals across 57 species, we found that movements of mammals in areas with a comparatively high human footprint were on average one-half to one-third the extent of their movements in areas with a low human footprint. We attribute this reduction to behavioral changes of individual animals and to the exclusion of species with long-range movements from areas with higher human impact. Global loss of vagility alters a key ecological trait of animals that affects not only population persistence but also ecosystem processes such as predator-prey interactions, nutrient cycling, and disease transmission.},
  language  = {en}
}
@article{SmithDupontMcCarthyetal.2019,
  author    = {Smith, Sarah R. and Dupont, Chris L. and McCarthy, James K. and Broddrick, Jared T. and Obornik, Miroslav and Horak, Ales and F{\"u}ssy, Zolt{\´a}n and Cihlar, Jaromir and Kleessen, Sabrina and Zheng, Hong and McCrow, John P. and Hixson, Kim K. and Araujo, Wagner L. and Nunes-Nesi, Adriano and Fernie, Alisdair R. and Nikoloski, Zoran and Palsson, Bernhard O. and Allen, Andrew E.},
  title     = {Evolution and regulation of nitrogen flux through compartmentalized metabolic networks in a marine diatom},
  series = {Nature Communications},
  volume    = {10},
  journal   = {Nature Communications},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {2041-1723},
  doi       = {10.1038/s41467-019-12407-y},
  pages     = {14},
  year      = {2019},
  abstract  = {Diatoms outcompete other phytoplankton for nitrate, yet little is known about the mechanisms underpinning this ability. Genomes and genome-enabled studies have shown that diatoms possess unique features of nitrogen metabolism however, the implications for nutrient utilization and growth are poorly understood. Using a combination of transcriptomics, proteomics, metabolomics, fluxomics, and flux balance analysis to examine short-term shifts in nitrogen utilization in the model pennate diatom in Phaeodactylum tricornutum, we obtained a systems-level understanding of assimilation and intracellular distribution of nitrogen. Chloroplasts and mitochondria are energetically integrated at the critical intersection of carbon and nitrogen metabolism in diatoms. Pathways involved in this integration are organelle-localized GS-GOGAT cycles, aspartate and alanine systems for amino moiety exchange, and a split-organelle arginine biosynthesis pathway that clarifies the role of the diatom urea cycle. This unique configuration allows diatoms to efficiently adjust to changing nitrogen status, conferring an ecological advantage over other phytoplankton taxa.},
  language  = {en}
}
@article{SchaffenrothCasewellSchneideretal.2020,
  author    = {Schaffenroth, Veronika and Casewell, Sarah L. and Schneider, D. and Kilkenny, David and Geier, Stephan and Heber, Ulrich and Irrgang, Andreas and Przybilla, Norbert and Marsh, Thomas R. and Littlefair, Stuart P. and Dhillon, Vik S.},
  title     = {A quantitative in-depth analysis of the prototype sdB plus BD system SDSS J08205+0008 revisited in the Gaia era},
  series = {Monthly notices of the Royal Astronomical Society},
  volume    = {501},
  journal   = {Monthly notices of the Royal Astronomical Society},
  number    = {3},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {0035-8711},
  doi       = {10.1093/mnras/staa3661},
  pages     = {3847 -- 3870},
  year      = {2020},
  abstract  = {Subdwarf B stars are core-helium-burning stars located on the extreme horizontal branch (EHB). Extensive mass loss on the red giant branch is necessary to form them. It has been proposed that substellar companions could lead to the required mass loss when they are engulfed in the envelope of the red giant star. J08205+0008 was the first example of a hot subdwarf star with a close, substellar companion candidate to be found. Here, we perform an in-depth re-analysis of this important system with much higher quality data allowing additional analysis methods. From the higher resolution spectra obtained with ESO-VLT/XSHOOTER, we derive the chemical abundances of the hot subdwarf as well as its rotational velocity. Using the Gaia parallax and a fit to the spectral energy distribution in the secondary eclipse, tight constraints to the radius of the hot subdwarf are derived. From a long-term photometric campaign, we detected a significant period decrease of -3.2(8) x 10(-12) dd(-1). This can be explained by the non-synchronized hot subdwarf star being spun up by tidal interactions forcing it to become synchronized. From the rate of period decrease we could derive the synchronization time-scale to be 4 Myr, much smaller than the lifetime on EHB. By combining all different methods, we could constrain the hot subdwarf to a mass of 0.39-0.50 M-circle dot and a radius of R-sdB = 0.194 +/- 0.008 R-circle dot, and the companion to 0.061-0.071 M-circle dot with a radius of R-comp = 0.092 +/- 0.005 R-circle dot, below the hydrogen-burning limit. We therefore confirm that the companion is most likely a massive brown dwarf.},
  language  = {en}
}
@misc{FinchBrakerReindletal.2019,
  author    = {Finch, Nicolle L. and Braker, I. P. and Reindl, Nicole and Barstow, Martin A. and Casewell, Sarah L. and Burleigh, M. and Kupfer, Thomas and Kilkenny, D. and Geier, Stephan and Schaffenroth, Veronika and Bertolami Miller, Marcelo Miguel and Taubenberger, Stefan and Freudenthal, Joseph},
  title     = {Spectral Analysis of Binary Pre-white Dwarf Systems},
  series = {Radiative signatures from the cosmos},
  volume    = {519},
  journal   = {Radiative signatures from the cosmos},
  publisher = {Astronomical soc pacific},
  address   = {San Fransisco},
  isbn      = {978-1-58381-925-8},
  issn      = {1050-3390},
  pages     = {231 -- 238},
  year      = {2019},
  abstract  = {Short period double degenerate white dwarf (WD) binaries with periods of less than similar to 1 day are considered to be one of the likely progenitors of type Ia supernovae. These binaries have undergone a period of common envelope evolution. If the core ignites helium before the envelope is ejected, then a hot subdwarf remains prior to contracting into a WD. Here we present a comparison of two very rare systems that contain two hot subdwarfs in short period orbits. We provide a quantitative spectroscopic analysis of the systems using synthetic spectra from state-of-the-art non-LTE models to constrain the atmospheric parameters of the stars. We also use these models to determine the radial velocities, and thus calculate dynamical masses for the stars in each system.},
  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}
}