@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{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{HorikoshiYaghootkarMookKanamorietal.2013,
  author    = {Horikoshi, Momoko and Yaghootkar, Hanieh and Mook-Kanamori, Dennis O. and Sovio, Ulla and Taal, H. Rob and Hennig, Branwen J. and Bradfield, Jonathan P. and St Pourcain, Beate and Evans, David M. and Charoen, Pimphen and Kaakinen, Marika and Cousminer, Diana L. and Lehtimaki, Terho and Kreiner-Moller, Eskil and Warrington, Nicole M. and Bustamante, Mariona and Feenstra, Bjarke and Berry, Diane J. and Thiering, Elisabeth and Pfab, Thiemo and Barton, Sheila J. and Shields, Beverley M. and Kerkhof, Marjan and van Leeuwen, Elisabeth M. and Fulford, Anthony J. and Kutalik, Zoltan and Zhao, Jing Hua and den Hoed, Marcel and Mahajan, Anubha and Lindi, Virpi and Goh, Liang-Kee and Hottenga, Jouke-Jan and Wu, Ying and Raitakari, Olli T. and Harder, Marie N. and Meirhaeghe, Aline and Ntalla, Ioanna and Salem, Rany M. and Jameson, Karen A. and Zhou, Kaixin and Monies, Dorota M. and Lagou, Vasiliki and Kirin, Mirna and Heikkinen, Jani and Adair, Linda S. and Alkuraya, Fowzan S. and Al-Odaib, Ali and Amouyel, Philippe and Andersson, Ehm Astrid and Bennett, Amanda J. and Blakemore, Alexandra I. F. and Buxton, Jessica L. and Dallongeville, Jean and Das, Shikta and de Geus, Eco J. C. and Estivill, Xavier and Flexeder, Claudia and Froguel, Philippe and Geller, Frank and Godfrey, Keith M. and Gottrand, Frederic and Groves, Christopher J. and Hansen, Torben and Hirschhorn, Joel N. and Hofman, Albert and Hollegaard, Mads V. and Hougaard, David M. and Hyppoenen, Elina and Inskip, Hazel M. and Isaacs, Aaron and Jorgensen, Torben and Kanaka-Gantenbein, Christina and Kemp, John P. and Kiess, Wieland and Kilpelainen, Tuomas O. and Klopp, Norman and Knight, Bridget A. and Kuzawa, Christopher W. and McMahon, George and Newnham, John P. and Niinikoski, Harri and Oostra, Ben A. and Pedersen, Louise and Postma, Dirkje S. and Ring, Susan M. and Rivadeneira, Fernando and Robertson, Neil R. and Sebert, Sylvain and Simell, Olli and Slowinski, Torsten and Tiesler, Carla M. T. and Toenjes, Anke and Vaag, Allan and Viikari, Jorma S. and Vink, Jacqueline M. and Vissing, Nadja Hawwa and Wareham, Nicholas J. and Willemsen, Gonneke and Witte, Daniel R. and Zhang, Haitao and Zhao, Jianhua and Wilson, James F. and Stumvoll, Michael and Prentice, Andrew M. and Meyer, Brian F. and Pearson, Ewan R. and Boreham, Colin A. G. and Cooper, Cyrus and Gillman, Matthew W. and Dedoussis, George V. and Moreno, Luis A. and Pedersen, Oluf and Saarinen, Maiju and Mohlke, Karen L. and Boomsma, Dorret I. and Saw, Seang-Mei and Lakka, Timo A. and Koerner, Antje and Loos, Ruth J. F. and Ong, Ken K. and Vollenweider, Peter and van Duijn, Cornelia M. and Koppelman, Gerard H. and Hattersley, Andrew T. and Holloway, John W. and Hocher, Berthold and Heinrich, Joachim and Power, Chris and Melbye, Mads and Guxens, Monica and Pennell, Craig E. and Bonnelykke, Klaus and Bisgaard, Hans and Eriksson, Johan G. and Widen, Elisabeth and Hakonarson, Hakon and Uitterlinden, Andre G. and Pouta, Anneli and Lawlor, Debbie A. and Smith, George Davey and Frayling, Timothy M. and McCarthy, Mark I. and Grant, Struan F. A. and Jaddoe, Vincent W. V. and Jarvelin, Marjo-Riitta and Timpson, Nicholas J. and Prokopenko, Inga and Freathy, Rachel M.},
  title     = {New loci associated with birth weight identify genetic links between intrauterine growth and adult height and metabolism},
  series = {Nature genetics},
  volume    = {45},
  journal   = {Nature genetics},
  number    = {1},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {MAGIC, Early Growth Genetics EGG},
  issn      = {1061-4036},
  doi       = {10.1038/ng.2477},
  pages     = {76 -- U115},
  year      = {2013},
  abstract  = {Birth weight within the normal range is associated with a variety of adult-onset diseases, but the mechanisms behind these associations are poorly understood(1). Previous genome-wide association studies of birth weight identified a variant in the ADCY5 gene associated both with birth weight and type 2 diabetes and a second variant, near CCNL1, with no obvious link to adult traits(2). In an expanded genome-wide association metaanalysis and follow-up study of birth weight (of up to 69,308 individuals of European descent from 43 studies), we have now extended the number of loci associated at genome-wide significance to 7, accounting for a similar proportion of variance as maternal smoking. Five of the loci are known to be associated with other phenotypes: ADCY5 and CDKAL1 with type 2 diabetes, ADRB1 with adult blood pressure and HMGA2 and LCORL with adult height. Our findings highlight genetic links between fetal growth and postnatal growth and metabolism.},
  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{vanderValkKreinerMollerKooijmanetal.2015,
  author    = {van der Valk, Ralf J. P. and Kreiner-Moller, Eskil and Kooijman, Marjolein N. and Guxens, Monica and Stergiakouli, Evangelia and Saaf, Annika and Bradfield, Jonathan P. and Geller, Frank and Hayes, M. Geoffrey and Cousminer, Diana L. and Koerner, Antje and Thiering, Elisabeth and Curtin, John A. and Myhre, Ronny and Huikari, Ville and Joro, Raimo and Kerkhof, Marjan and Warrington, Nicole M. and Pitkanen, Niina and Ntalla, Ioanna and Horikoshi, Momoko and Veijola, Riitta and Freathy, Rachel M. and Teo, Yik-Ying and Barton, Sheila J. and Evans, David M. and Kemp, John P. and St Pourcain, Beate and Ring, Susan M. and Smith, George Davey and Bergstrom, Anna and Kull, Inger and Hakonarson, Hakon and Mentch, Frank D. and Bisgaard, Hans and Chawes, Bo Lund Krogsgaard and Stokholm, Jakob and Waage, Johannes and Eriksen, Patrick and Sevelsted, Astrid and Melbye, Mads and van Duijn, Cornelia M. and Medina-Gomez, Carolina and Hofman, Albert and de Jongste, Johan C. and Taal, H. Rob and Uitterlinden, Andre G. and Armstrong, Loren L. and Eriksson, Johan and Palotie, Aarno and Bustamante, Mariona and Estivill, Xavier and Gonzalez, Juan R. and Llop, Sabrina and Kiess, Wieland and Mahajan, Anubha and Flexeder, Claudia and Tiesler, Carla M. T. and Murray, Clare S. and Simpson, Angela and Magnus, Per and Sengpiel, Verena and Hartikainen, Anna-Liisa and Keinanen-Kiukaanniemi, Sirkka and Lewin, Alexandra and Alves, Alexessander Da Silva Couto and Blakemore, Alexandra I. F. and Buxton, Jessica L. and Kaakinen, Marika and Rodriguez, Alina and Sebert, Sylvain and Vaarasmaki, Marja and Lakka, Timo and Lindi, Virpi and Gehring, Ulrike and Postma, Dirkje S. and Ang, Wei and Newnham, John P. and Lyytikainen, Leo-Pekka and Pahkala, Katja and Raitakari, Olli T. and Panoutsopoulou, Kalliope and Zeggini, Eleftheria and Boomsma, Dorret I. and Groen-Blokhuis, Maria and Ilonen, Jorma and Franke, Lude and Hirschhorn, Joel N. and Pers, Tune H. and Liang, Liming and Huang, Jinyan and Hocher, Berthold and Knip, Mikael and Saw, Seang-Mei and Holloway, John W. and Melen, Erik and Grant, Struan F. A. and Feenstra, Bjarke and Lowe, William L. and Widen, Elisabeth and Sergeyev, Elena and Grallert, Harald and Custovic, Adnan and Jacobsson, Bo and Jarvelin, Marjo-Riitta and Atalay, Mustafa and Koppelman, Gerard H. and Pennell, Craig E. and Niinikoski, Harri and Dedoussis, George V. and Mccarthy, Mark I. and Frayling, Timothy M. and Sunyer, Jordi and Timpson, Nicholas J. and Rivadeneira, Fernando and Bonnelykke, Klaus and Jaddoe, Vincent W. V.},
  title     = {A novel common variant in DCST2 is associated with length in early life and height in adulthood},
  series = {Human molecular genetics},
  volume    = {24},
  journal   = {Human molecular genetics},
  number    = {4},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  organization    = {Early Genetics Lifecourse, Genetic Invest ANthropometric, Early Growth Genetics EGG},
  issn      = {0964-6906},
  doi       = {10.1093/hmg/ddu510},
  pages     = {1155 -- 1168},
  year      = {2015},
  abstract  = {Common genetic variants have been identified for adult height, but not much is known about the genetics of skeletal growth in early life. To identify common genetic variants that influence fetal skeletal growth, we meta-analyzed 22 genome-wide association studies (Stage 1; N = 28 459). We identified seven independent top single nucleotide polymorphisms (SNPs) (P < 1 x 10(-6)) for birth length, of which three were novel and four were in or near loci known to be associated with adult height (LCORL, PTCH1, GPR126 and HMGA2). The three novel SNPs were followed-up in nine replication studies (Stage 2; N = 11 995), with rs905938 in DC-STAMP domain containing 2 (DCST2) genome-wide significantly associated with birth length in a joint analysis (Stages 1 + 2; beta = 0.046, SE = 0.008, P = 2.46 x 10(-8), explained variance = 0.05\%). Rs905938 was also associated with infant length (N = 28 228; P = 5.54 x 10(-4)) and adult height (N = 127 513; P = 1.45 x 10(-5)). DCST2 is a DC-STAMP-like protein family member and DC-STAMP is an osteoclast cell-fusion regulator. Polygenic scores based on 180 SNPs previously associated with human adult stature explained 0.13\% of variance in birth length. The same SNPs explained 2.95\% of the variance of infant length. Of the 180 known adult height loci, 11 were genome-wide significantly associated with infant length (SF3B4, LCORL, SPAG17, C6orf173, PTCH1, GDF5, ZNFX1, HHIP, ACAN, HLA locus and HMGA2). This study highlights that common variation in DCST2 influences variation in early growth and adult height.},
  language  = {en}
}
@article{ChipmanFerrierBrenaetal.2014,
  author    = {Chipman, Ariel D. and Ferrier, David E. K. and Brena, Carlo and Qu, Jiaxin and Hughes, Daniel S. T. and Schroeder, Reinhard and Torres-Oliva, Montserrat and Znassi, Nadia and Jiang, Huaiyang and Almeida, Francisca C. and Alonso, Claudio R. and Apostolou, Zivkos and Aqrawi, Peshtewani and Arthur, Wallace and Barna, Jennifer C. J. and Blankenburg, Kerstin P. and Brites, Daniela and Capella-Gutierrez, Salvador and Coyle, Marcus and Dearden, Peter K. and Du Pasquier, Louis and Duncan, Elizabeth J. and Ebert, Dieter and Eibner, Cornelius and Erikson, Galina and Evans, Peter D. and Extavour, Cassandra G. and Francisco, Liezl and Gabaldon, Toni and Gillis, William J. and Goodwin-Horn, Elizabeth A. and Green, Jack E. and Griffiths-Jones, Sam and Grimmelikhuijzen, Cornelis J. P. and Gubbala, Sai and Guigo, Roderic and Han, Yi and Hauser, Frank and Havlak, Paul and Hayden, Luke and Helbing, Sophie and Holder, Michael and Hui, Jerome H. L. and Hunn, Julia P. and Hunnekuhl, Vera S. and Jackson, LaRonda and Javaid, Mehwish and Jhangiani, Shalini N. and Jiggins, Francis M. and Jones, Tamsin E. and Kaiser, Tobias S. and Kalra, Divya and Kenny, Nathan J. and Korchina, Viktoriya and Kovar, Christie L. and Kraus, F. Bernhard and Lapraz, Francois and Lee, Sandra L. and Lv, Jie and Mandapat, Christigale and Manning, Gerard and Mariotti, Marco and Mata, Robert and Mathew, Tittu and Neumann, Tobias and Newsham, Irene and Ngo, Dinh N. and Ninova, Maria and Okwuonu, Geoffrey and Ongeri, Fiona and Palmer, William J. and Patil, Shobha and Patraquim, Pedro and Pham, Christopher and Pu, Ling-Ling and Putman, Nicholas H. and Rabouille, Catherine and Ramos, Olivia Mendivil and Rhodes, Adelaide C. and Robertson, Helen E. and Robertson, Hugh M. and Ronshaugen, Matthew and Rozas, Julio and Saada, Nehad and Sanchez-Gracia, Alejandro and Scherer, Steven E. and Schurko, Andrew M. and Siggens, Kenneth W. and Simmons, DeNard and Stief, Anna and Stolle, Eckart and Telford, Maximilian J. and Tessmar-Raible, Kristin and Thornton, Rebecca and van der Zee, Maurijn and von Haeseler, Arndt and Williams, James M. and Willis, Judith H. and Wu, Yuanqing and Zou, Xiaoyan and Lawson, Daniel and Muzny, Donna M. and Worley, Kim C. and Gibbs, Richard A. and Akam, Michael and Richards, Stephen},
  title     = {The first myriapod genome sequence reveals conservative arthropod gene content and genome organisation in the centipede Strigamia maritima},
  series = {PLoS biology},
  volume    = {12},
  journal   = {PLoS biology},
  number    = {11},
  publisher = {PLoS},
  address   = {San Fransisco},
  issn      = {1545-7885},
  doi       = {10.1371/journal.pbio.1002005},
  pages     = {24},
  year      = {2014},
  abstract  = {Myriapods (e. g., centipedes and millipedes) display a simple homonomous body plan relative to other arthropods. All members of the class are terrestrial, but they attained terrestriality independently of insects. Myriapoda is the only arthropod class not represented by a sequenced genome. We present an analysis of the genome of the centipede Strigamia maritima. It retains a compact genome that has undergone less gene loss and shuffling than previously sequenced arthropods, and many orthologues of genes conserved from the bilaterian ancestor that have been lost in insects. Our analysis locates many genes in conserved macro-synteny contexts, and many small-scale examples of gene clustering. We describe several examples where S. maritima shows different solutions from insects to similar problems. The insect olfactory receptor gene family is absent from S. maritima, and olfaction in air is likely effected by expansion of other receptor gene families. For some genes S. maritima has evolved paralogues to generate coding sequence diversity, where insects use alternate splicing. This is most striking for the Dscam gene, which in Drosophila generates more than 100,000 alternate splice forms, but in S. maritima is encoded by over 100 paralogues. We see an intriguing linkage between the absence of any known photosensory proteins in a blind organism and the additional absence of canonical circadian clock genes. The phylogenetic position of myriapods allows us to identify where in arthropod phylogeny several particular molecular mechanisms and traits emerged. For example, we conclude that juvenile hormone signalling evolved with the emergence of the exoskeleton in the arthropods and that RR-1 containing cuticle proteins evolved in the lineage leading to Mandibulata. We also identify when various gene expansions and losses occurred. The genome of S. maritima offers us a unique glimpse into the ancestral arthropod genome, while also displaying many adaptations to its specific life history.},
  language  = {en}
}
@article{CorcoranNicholsPabloetal.2015,
  author    = {Corcoran, Michael F. and Nichols, Joy S. and Pablo, Herbert and Shenar, Tomer and Pollock, Andy M. T. and Waldron, Wayne L. and Moffat, Anthony F. J. and Richardson, Noel D. and Russell, Christopher M. P. and Hamaguchi, Kenji and Huenemoerder, David P. and Oskinova, Lida and Hamann, Wolf-Rainer and Naze, Yael and Ignace, Richard and Evans, Nancy Remage and Lomax, Jamie R. and Hoffman, Jennifer L. and Gayley, Kenneth and Owocki, Stanley P. and Leutenegger, Maurice and Gull, Theodore R. and Hole, Karen Tabetha and Lauer, Jennifer and Iping, Rosina C.},
  title     = {A coordinated X-Ray and optical campaign of the nearest massive eclipsing binary, delta ORIONIS Aa. I. Overview of thr X-Ray spectrum},
  series = {The astrophysical journal : an international review of spectroscopy and astronomical physics},
  volume    = {809},
  journal   = {The astrophysical journal : an international review of spectroscopy and astronomical physics},
  number    = {2},
  publisher = {IOP Publ. Ltd.},
  address   = {Bristol},
  issn      = {0004-637X},
  doi       = {10.1088/0004-637X/809/2/132},
  pages     = {15},
  year      = {2015},
  abstract  = {We present an overview of four deep phase-constrained Chandra HETGS X-ray observations of delta Ori A. Delta Ori A is actually a triple system that includes the nearest massive eclipsing spectroscopic binary, delta Ori Aa, the only such object that can be observed with little phase-smearing with the Chandra gratings. Since the fainter star, delta Ori Aa2, has a much lower X-ray luminosity than the brighter primary (delta Ori Aa1), delta Ori Aa provides a unique system with which to test the spatial distribution of the X-ray emitting gas around delta Ori Aa1 via occultation by the photosphere of, and wind cavity around, the X-ray dark secondary. Here we discuss the X-ray spectrum and X-ray line profiles for the combined observation, having an exposure time of nearly 500 ks and covering nearly the entire binary orbit. The companion papers discuss the X-ray variability seen in the Chandra spectra, present new space-based photometry and ground-based radial velocities obtained simultaneously with the X-ray data to better constrain the system parameters, and model the effects of X-rays on the optical and UV spectra. We find that the X-ray emission is dominated by embedded wind shock emission from star Aa1, with little contribution from the tertiary star Ab or the shocked gas produced by the collision of the wind of Aa1 against the surface of Aa2. We find a similar temperature distribution to previous X-ray spectrum analyses. We also show that the line half-widths are about 0.3-0.5 times the terminal velocity of the wind of star Aa1. We find a strong anti-correlation between line widths and the line excitation energy, which suggests that longer-wavelength, lower-temperature lines form farther out in the wind. Our analysis also indicates that the ratio of the intensities of the strong and weak lines of Fe XVII and Ne X are inconsistent with model predictions, which may be an effect of resonance scattering.},
  language  = {en}
}
@article{NazeBroosOskinovaetal.2011,
  author    = {Naze, Y. and Broos, Patrick S. and Oskinova, Lida and Townsley, L. K. and Cohen, David H. and Corcoran, M. F. and Evans, N. R. and Gagne, M. and Moffat, Anthony F. J. and Pittard, J. M. and Rauw, G. and Ud-Doula, A. and Walborn, N. R.},
  title     = {GLOBAL X-RAY PROPERTIES OF THE O AND B STARS IN CARINA},
  series = {ASTROPHYSICAL JOURNAL SUPPLEMENT SERIES},
  volume    = {194},
  journal   = {ASTROPHYSICAL JOURNAL SUPPLEMENT SERIES},
  number    = {1},
  publisher = {IOP PUBLISHING LTD},
  address   = {BRISTOL},
  issn      = {0067-0049},
  doi       = {10.1088/0067-0049/194/1/7},
  pages     = {20},
  year      = {2011},
  abstract  = {The key empirical property of the X-ray emission from O stars is a strong correlation between the bolometric and X-ray luminosities. In the framework of the Chandra Carina Complex Project, 129 O and B stars have been detected as X-ray sources; 78 of those, all with spectral type earlier than B3, have enough counts for at least a rough X-ray spectral characterization. This leads to an estimate of the L-X-L-BOL ratio for an exceptional number of 60 O stars belonging to the same region and triples the number of Carina massive stars studied spectroscopically in X-rays. The derived log(L-X/L-BOL) is -7.26 for single objects, with a dispersion of only 0.21 dex. Using the properties of hot massive stars listed in the literature, we compare the X-ray luminosities of different types of objects. In the case of O stars, the L-X-L-BOL ratios are similar for bright and faint objects, as well as for stars of different luminosity classes or spectral types. Binaries appear only slightly harder and slightly more luminous in X-rays than single objects; the differences are not formally significant (at the 1\% level), except for the L-X-L-BOL ratio in the medium (1.0-2.5 keV) energy band. Weak-wind objects have similar X-ray luminosities but they display slightly softer spectra compared with "normal" O stars with the same bolometric luminosity. Discarding three overluminous objects, we find a very shallow trend of harder emission in brighter objects. The properties of the few B stars bright enough to yield some spectral information appear to be different overall (constant X-ray luminosities, harder spectra), hinting that another mechanism for producing X-rays, besides wind shocks, might be at work. However, it must be stressed that the earliest and X-ray brightest among these few detected objects are similar to the latest O stars, suggesting a possibly smooth transition between the two processes.},
  language  = {en}
}