@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}
}
@misc{GorskiJungLietal.2020,
  author    = {Gorski, Mathias and Jung, Bettina and Li, Yong and Matias-Garcia, Pamela R. and Wuttke, Matthias and Coassin, Stefan and Thio, Chris H. L. and Kleber, Marcus E. and Winkler, Thomas W. and Wanner, Veronika and Chai, Jin-Fang and Chu, Audrey Y. and Cocca, Massimiliano and Feitosa, Mary F. and Ghasemi, Sahar and Hoppmann, Anselm and Horn, Katrin and Li, Man and Nutile, Teresa and Scholz, Markus and Sieber, Karsten B. and Teumer, Alexander and Tin, Adrienne and Wang, Judy and Tayo, Bamidele O. and Ahluwalia, Tarunveer S. and Almgren, Peter and Bakker, Stephan J. L. and Banas, Bernhard and Bansal, Nisha and Biggs, Mary L. and Boerwinkle, Eric and B{\"o}ttinger, Erwin and Brenner, Hermann and Carroll, Robert J. and Chalmers, John and Chee, Miao-Li and Chee, Miao-Ling and Cheng, Ching-Yu and Coresh, Josef and de Borst, Martin H. and Degenhardt, Frauke and Eckardt, Kai-Uwe and Endlich, Karlhans and Franke, Andre and Freitag-Wolf, Sandra and Gampawar, Piyush and Gansevoort, Ron T. and Ghanbari, Mohsen and Gieger, Christian and Hamet, Pavel and Ho, Kevin and Hofer, Edith and Holleczek, Bernd and Foo, Valencia Hui Xian and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Josyula, Navya Shilpa and Kahonen, Mika and Khor, Chiea-Chuen and Koenig, Wolfgang and Kramer, Holly and Kraemer, Bernhard K. and Kuehnel, Brigitte and Lange, Leslie A. and Lehtimaki, Terho and Lieb, Wolfgang and Loos, Ruth J. F. and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Milaneschi, Yuri and Mishra, Pashupati P. and Mononen, Nina and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and O'Donoghue, Michelle L. and Orho-Melander, Marju and Pendergrass, Sarah A. and Penninx, Brenda W. J. H. and Preuss, Michael H. and Psaty, Bruce M. and Raffield, Laura M. and Raitakari, Olli T. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Rosenkranz, Alexander R. and Rossing, Peter and Rotter, Jerome and Sabanayagam, Charumathi and Schmidt, Helena and Schmidt, Reinhold and Schoettker, Ben and Schulz, Christina-Alexandra and Sedaghat, Sanaz and Shaffer, Christian M. and Strauch, Konstantin and Szymczak, Silke and Taylor, Kent D. and Tremblay, Johanne and Chaker, Layal and van der Harst, Pim and van der Most, Peter J. and Verweij, Niek and Voelker, Uwe and Waldenberger, Melanie and Wallentin, Lars and Waterworth, Dawn M. and White, Harvey D. and Wilson, James G. and Wong, Tien-Yin and Woodward, Mark and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Yan and Snieder, Harold and Wanner, Christoph and Boger, Carsten A. and Kottgen, Anna and Kronenberg, Florian and Pattaro, Cristian and Heid, Iris M.},
  title     = {Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline},
  series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Reihe der Digital Engineering Fakult{\"a}t},
  journal   = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Reihe der Digital Engineering Fakult{\"a}t},
  number    = {19},
  doi       = {10.25932/publishup-56537},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-565379},
  pages     = {14},
  year      = {2020},
  abstract  = {Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25\% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95\% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.},
  language  = {en}
}
@article{GorskiJungLietal.2020,
  author    = {Gorski, Mathias and Jung, Bettina and Li, Yong and Matias-Garcia, Pamela R. and Wuttke, Matthias and Coassin, Stefan and Thio, Chris H. L. and Kleber, Marcus E. and Winkler, Thomas W. and Wanner, Veronika and Chai, Jin-Fang and Chu, Audrey Y. and Cocca, Massimiliano and Feitosa, Mary F. and Ghasemi, Sahar and Hoppmann, Anselm and Horn, Katrin and Li, Man and Nutile, Teresa and Scholz, Markus and Sieber, Karsten B. and Teumer, Alexander and Tin, Adrienne and Wang, Judy and Tayo, Bamidele O. and Ahluwalia, Tarunveer S. and Almgren, Peter and Bakker, Stephan J. L. and Banas, Bernhard and Bansal, Nisha and Biggs, Mary L. and Boerwinkle, Eric and B{\"o}ttinger, Erwin and Brenner, Hermann and Carroll, Robert J. and Chalmers, John and Chee, Miao-Li and Chee, Miao-Ling and Cheng, Ching-Yu and Coresh, Josef and de Borst, Martin H. and Degenhardt, Frauke and Eckardt, Kai-Uwe and Endlich, Karlhans and Franke, Andre and Freitag-Wolf, Sandra and Gampawar, Piyush and Gansevoort, Ron T. and Ghanbari, Mohsen and Gieger, Christian and Hamet, Pavel and Ho, Kevin and Hofer, Edith and Holleczek, Bernd and Foo, Valencia Hui Xian and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Josyula, Navya Shilpa and Kahonen, Mika and Khor, Chiea-Chuen and Koenig, Wolfgang and Kramer, Holly and Kraemer, Bernhard K. and Kuehnel, Brigitte and Lange, Leslie A. and Lehtimaki, Terho and Lieb, Wolfgang and Loos, Ruth J. F. and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Milaneschi, Yuri and Mishra, Pashupati P. and Mononen, Nina and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and O'Donoghue, Michelle L. and Orho-Melander, Marju and Pendergrass, Sarah A. and Penninx, Brenda W. J. H. and Preuss, Michael H. and Psaty, Bruce M. and Raffield, Laura M. and Raitakari, Olli T. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Rosenkranz, Alexander R. and Rossing, Peter and Rotter, Jerome and Sabanayagam, Charumathi and Schmidt, Helena and Schmidt, Reinhold and Schoettker, Ben and Schulz, Christina-Alexandra and Sedaghat, Sanaz and Shaffer, Christian M. and Strauch, Konstantin and Szymczak, Silke and Taylor, Kent D. and Tremblay, Johanne and Chaker, Layal and van der Harst, Pim and van der Most, Peter J. and Verweij, Niek and Voelker, Uwe and Waldenberger, Melanie and Wallentin, Lars and Waterworth, Dawn M. and White, Harvey D. and Wilson, James G. and Wong, Tien-Yin and Woodward, Mark and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Yan and Snieder, Harold and Wanner, Christoph and Boger, Carsten A. and Kottgen, Anna and Kronenberg, Florian and Pattaro, Cristian and Heid, Iris M.},
  title     = {Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline},
  series = {Kidney international : official journal of the International Society of Nephrology},
  volume    = {99},
  journal   = {Kidney international : official journal of the International Society of Nephrology},
  number    = {4},
  publisher = {Elsevier},
  address   = {New York},
  organization    = {Lifelines Cohort Study<br /> Regeneron Genetics Ctr},
  issn      = {0085-2538},
  doi       = {10.1016/j.kint.2020.09.030},
  pages     = {926 -- 939},
  year      = {2020},
  abstract  = {Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25\% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95\% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.},
  language  = {en}
}
@article{AbeysekaraArcherBenbowetal.2018,
  author    = {Abeysekara, A. U. and Archer, A. and Benbow, Wystan and Bird, Ralph and Brose, Robert and Buchovecky, M. and Buckley, J. H. and Bugaev, V. and Chromey, A. J. and Connolly, M. P. and Cui, Wei and Daniel, M. K. and Falcone, A. and Feng, Qi and Finley, John P. and Fortson, L. and Furniss, Amy and Huetten, M. and Hanna, David and Hervet, O. and Holder, J. and Hughes, G. and Humensky, T. B. and Johnson, Caitlin A. and Kaaret, Philip and Kar, P. and Kertzman, M. and Kieda, David and Krause, M. and Krennrich, F. and Kumar, S. and Lang, M. J. and Lin, T. T. Y. and McArthur, S. and Moriarty, P. and Mukherjee, Reshmi and Ong, R. A. and Otte, Adam Nepomuk and Park, Nahee and Petrashyk, A. and Pohl, Martin and Pueschel, Elisa and Quinn, J. and Ragan, K. and Reynolds, P. T. and Richards, Gregory T. and Roache, E. and Rulten, C. and Sadeh, I. and Santander, Marcos and Sembroski, G. H. and Shahinyan, Karlen and Sushch, I. and Tyler, J. and Wakely, S. P. and Weinstein, A. and Wells, R. M. and Wilcox, P. and Wilhelm, Alina and Williams, D. A. and Williamson, T. J. and Zitzer, B. and Abdollahi, S. and Ajello, Marco and Baldini, Luca and Barbiellini, G. and Bastieri, Denis and Bellazzini, Ronaldo and Berenji, B. and Bissaldi, Elisabetta and Blandford, R. D. and Bonino, R. and Bottacini, E. and Brandt, Terri J. and Bruel, P. and Buehler, R. and Cameron, R. A. and Caputo, R. and Caraveo, P. A. and Castro, D. and Cavazzuti, E. and Charles, Eric and Chiaro, G. and Ciprini, S. and Cohen-Tanugi, Johann and Costantin, D. and Cutini, S. and de Palma, F. and Di Lalla, N. and Di Mauro, M. and Di Venere, L. and Dominguez, A. and Favuzzi, C. and Fegan, S. J. and Franckowiak, Anna and Fukazawa, Yasushi and Funk, Stefan and Fusco, Piergiorgio and Gargano, Fabio and Gasparrini, Dario and Giglietto, Nicola and Giordano, F. and Giroletti, Marcello and Green, D. and Grenier, I. A. and Guillemot, L. and Guiriec, Sylvain and Hays, Elizabeth and Hewitt, John W. and Horan, D. and Johannesson, G. and Kensei, S. and Kuss, M. and Larsson, Stefan and Latronico, L. and Lemoine-Goumard, Marianne and Li, J. and Longo, Francesco and Loparco, Francesco and Lovellette, M. N. and Lubrano, Pasquale and Magill, Jeffrey D. and Maldera, Simone and Mazziotta, Mario Nicola and McEnery, J. E. and Michelson, P. F. and Mitthumsiri, W. and Mizuno, Tsunefumi and Monzani, Maria Elena and Morselli, Aldo and Moskalenko, Igor V. and Negro, M. and Nuss, E. and Ojha, R. and Omodei, Nicola and Orienti, M. and Orlando, E. and Palatiello, M. and Paliya, Vaidehi S. and Paneque, D. and Perkins, Jeremy S. and Persic, M. and Pesce-Rollins, Melissa and Petrosian, Vahe' and Piron, F. and Porter, Troy A. and Principe, G. and Raino, S. and Rando, Riccardo and Rani, B. and Razzano, Massimilano and Razzaque, Soebur and Reimer, A. and Reimer, Olaf and Reposeur, T. and Sgro, C. and Siskind, E. J. and Spandre, Gloria and Spinelli, P. and Suson, D. J. and Tajima, Hiroyasu and Thayer, J. B. and Thompson, David J. and Torres, Diego F. and Tosti, Gino and Troja, Eleonora and Valverde, J. and Vianello, Giacomo and Vogel, M. and Wood, K. and Yassine, M. and Alfaro, R. and Alvarez, C. and Alvarez, J. D. and Arceo, R. and Arteaga-Velazquez, J. C. and Rojas, D. Avila and Ayala Solares, H. A. and Becerril, A. and Belmont-Moreno, E. and BenZvi, S. Y. and Bernal, A. and Braun, J. and Brisbois, C. and Caballero-Mora, K. S. and Capistran, T. and Carraminana, A. and Casanova, Sabrina and Castillo, M. and Cotti, U. and Cotzomi, J. and Coutino de Leon, S. and De Leon, C. and De la Fuente, E. and Dichiara, S. and Dingus, B. L. and DuVernois, M. A. and Diaz-Velez, J. C. and Engel, K. and Enriquez-Rivera, O. and Fiorino, D. W. and Fleischhack, H. and Fraija, N. and Garcia-Gonzalez, J. A. and Garfias, F. and Gonzalez Munoz, A. and Gonzalez, M. M. and Goodman, J. A. and Hampel-Arias, Z. and Harding, J. P. and Hernandez, S. and Hernandez-Almada, A. and Hona, B. and Hueyotl-Zahuantitla, F. and Hui, C. M. and Huntemeyer, P. and Iriarte, A. and Jardin-Blicq, A. and Joshi, V. and Kaufmann, S. and Lara, A. and Lauer, R. J. and Lee, W. H. and Lennarz, D. and Leon Vargas, H. and Linnemann, J. T. and Longinotti, A. L. and Luis-Raya, G. and Luna-Garcia, R. and Lopez-Coto, R. and Malone, K. and Marinelli, S. S. and Martinez, O. and Martinez-Castellanos, I. and Martinez-Castro, J. and Martinez-Huerta, H. and Matthews, J. A. and Miranda-Romagnoli, P. and Moreno, E. and Mostafa, M. and Nayerhoda, A. and Nellen, L. and Newbold, M. and Nisa, M. U. and Noriega-Papaqui, R. and Pelayo, R. and Pretz, J. and Perez-Perez, E. G. and Ren, Z. and Rho, C. D. and Riviere, C. and Rosa-Gonzalez, D. and Rosenberg, M. and Ruiz-Velasco, E. and Salazar, H. and Greus, F. Salesa and Sandoval, A. and Schneider, M. and Arroyo, M. Seglar and Sinnis, G. and Smith, A. J. and Springer, R. W. and Surajbali, P. and Taboada, Ignacio and Tibolla, O. and Tollefson, K. and Torres, I. and Ukwatta, Tilan N. and Villasenor, L. and Weisgarber, T. and Westerhoff, Stefan and Wisher, I. G. and Wood, J. and Yapici, Tolga and Yodh, G. and Zepeda, A. and Zhou, H.},
  title     = {VERITAS and Fermi-LAT Observations of TeV Gamma-Ray Sources Discovered by HAWC in the 2HWC Catalog},
  series = {The astrophysical journal : an international review of spectroscopy and astronomical physics},
  volume    = {866},
  journal   = {The astrophysical journal : an international review of spectroscopy and astronomical physics},
  number    = {1},
  publisher = {IOP Publ. Ltd.},
  address   = {Bristol},
  organization    = {VERITAS Collaboration Fermi-LAT Collaboration HAWC Collaboration},
  issn      = {0004-637X},
  doi       = {10.3847/1538-4357/aade4e},
  pages     = {18},
  year      = {2018},
  abstract  = {The High Altitude Water Cherenkov (HAWC) collaboration recently published their 2HWC catalog, listing 39 very high energy (VHE; >100 GeV) gamma-ray sources based on 507 days of observation. Among these, 19 sources are not associated with previously known teraelectronvolt (TeV) gamma-ray sources. We have studied 14 of these sources without known counterparts with VERITAS and Fermi-LAT. VERITAS detected weak gamma-ray emission in the 1 TeV-30 TeV band in the region of DA 495, a pulsar wind nebula coinciding with 2HWC J1953+294, confirming the discovery of the source by HAWC. We did not find any counterpart for the selected 14 new HAWC sources from our analysis of Fermi-LAT data for energies higher than 10 GeV. During the search, we detected gigaelectronvolt (GeV) gamma-ray emission coincident with a known TeV pulsar wind nebula, SNR G54.1+0.3 (VER J1930+188), and a 2HWC source, 2HWC J1930+188. The fluxes for isolated, steady sources in the 2HWC catalog are generally in good agreement with those measured by imaging atmospheric Cherenkov telescopes. However, the VERITAS fluxes for SNR G54.1+0.3, DA 495, and TeV J2032+4130 are lower than those measured by HAWC, and several new HAWC sources are not detected by VERITAS. This is likely due to a change in spectral shape, source extension, or the influence of diffuse emission in the source region.},
  language  = {en}
}
@article{ArchambaultArlenAuneetal.2014,
  author    = {Archambault, S. and Arlen, T. and Aune, T. and Beilicke, M. and Benbow, W. and Bird, R. and Boettcher, Markus and Bouvier, A. and Buckley, J. H. and Bugaev, V. and Ciupik, L. and Collins-Hughes, E. and Connolly, M. P. and Cui, W. and Dickherber, R. and Dumm, J. and Errando, M. and Falcone, A. and Federici, Simone and Feng, Q. and Finley, J. P. and Fortson, L. and Furniss, A. and Galante, N. and Gall, D. and Garson, A. III. and Gillanders, G. H. and Griffin, S. and Grube, J. and Gusbar, C. and Gyuk, G. and Hanna, D. and Holder, J. and Hughes, G. and Kaaret, P. and Kertzman, M. and Khassen, Y. and Kieda, D. and Krawczynski, H. and Lamerato, A. and Lang, M. J. and Li, K. and Madhavan, A. S. and Maier, G. and Majumdar, P. and McArthur, S. and McCann, A. and Millis, J. and Moriarty, P. and Mukherjee, R. and Nieto, D. and Ong, R. A. and Orr, M. and Otte, A. N. and Park, N. and Perkins, J. S. and Pohl, Martin and Popkow, A. and Prokoph, H. and Quinn, J. and Ragan, K. and Reynolds, P. T. and Richards, G. T. and Roache, E. and Roustazadeh, P. and Saxon, D. B. and Sembroski, G. H. and Senturk, G. D. and Skole, C. and Staszak, D. and Telezhinsky, Igor O. and Tesic, G. and Theiling, M. and Varlotta, A. and Vassiliev, V. V. and Vincent, S. and Wakely, S. P. and Weinstein, A. and Welsing, R. and Williams, D. A. and Zitzer, B.},
  title     = {Test of models of the cosmic infrared background with multiwavelength observations of the blazar 1ES 1218+30.4 IN 2009},
  series = {The astrophysical journal : an international review of spectroscopy and astronomical physics},
  volume    = {788},
  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/788/2/158},
  pages     = {9},
  year      = {2014},
  abstract  = {We present the results of a multi-wavelength campaign targeting the blazar 1ES 1218+30.4 with observations with the 1.3 m McGraw-Hill optical telescope, the Rossi X-ray Timing Explorer (RXTE), the Fermi Gamma-Ray Space Telescope, and the Very Energetic Radiation Imaging Telescope Array System (VERITAS). The RXTE and VERITAS observations were spread over a 13 day period and revealed clear evidence for flux variability, and a strong X-ray and gamma-ray flare on 2009 February 26 (MJD 54888). The campaign delivered a well-sampled broadband energy spectrum with simultaneous RXTE and VERITAS very high energy (VHE, > 100 GeV) observations, as well as contemporaneous optical and Fermi observations. The 1ES 1218+30.4 broadband energy spectrum-the first with simultaneous X-ray and VHE gamma-ray energy spectra-is of particular interest as the source is located at a high cosmological redshift for a VHE source (z = 0.182), leading to strong absorption of VHE gamma rays by photons from the optical/infrared extragalactic background light (EBL) via gamma VHE +gamma EBL -> e(+) e(-)pair-creation processes. We model the data with a one-zone synchrotron self-Compton (SSC) emission model and with the extragalactic absorption predicted by several recent EBL models. We find that the observations are consistent with the SSC scenario and all the EBL models considered in this work. We discuss observational and theoretical avenues to improve on the EBL constraints.},
  language  = {en}
}
@article{AldorettaStLouisRichardsonetal.2016,
  author    = {Aldoretta, E. J. and St-Louis, N. and Richardson, N. D. and Moffat, Anthony F. J. and Eversberg, T. and Hill, G. M. and Shenar, Tomer and Artigau, E. and Gauza, B. and Knapen, J. H. and Kubat, Jiř{\´i} and Kubatova, Brankica and Maltais-Tariant, R. and Munoz, M. and Pablo, H. and Ramiaramanantsoa, T. and Richard-Laferriere, A. and Sablowski, D. P. and Simon-Diaz, S. and St-Jean, L. and Bolduan, F. and Dias, F. M. and Dubreuil, P. and Fuchs, D. and Garrel, T. and Grutzeck, G. and Hunger, T. and Kuesters, D. and Langenbrink, M. and Leadbeater, R. and Li, D. and Lopez, A. and Mauclaire, B. and Moldenhawer, T. and Potter, M. and dos Santos, E. M. and Schanne, L. and Schmidt, J. and Sieske, H. and Strachan, J. and Stinner, E. and Stinner, P. and Stober, B. and Strandbaek, K. and Syder, T. and Verilhac, D. and Waldschlaeger, U. and Weiss, D. and Wendt, A.},
  title     = {An extensive spectroscopic time series of three Wolf-Rayet stars - I. The lifetime of large-scale structures in the wind of WR 134},
  series = {Monthly notices of the Royal Astronomical Society},
  volume    = {460},
  journal   = {Monthly notices of the Royal Astronomical Society},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {0035-8711},
  doi       = {10.1093/mnras/stw1188},
  pages     = {3407 -- 3417},
  year      = {2016},
  abstract  = {During the summer of 2013, a 4-month spectroscopic campaign took place to observe the variabilities in three Wolf-Rayet stars. The spectroscopic data have been analysed for WR 134 (WN6b), to better understand its behaviour and long-term periodicity, which we interpret as arising from corotating interaction regions (CIRs) in the wind. By analysing the variability of the He ii lambda 5411 emission line, the previously identified period was refined to P = 2.255 +/- 0.008 (s.d.) d. The coherency time of the variability, which we associate with the lifetime of the CIRs in the wind, was deduced to be 40 +/- 6 d, or similar to 18 cycles, by cross-correlating the variability patterns as a function of time. When comparing the phased observational grey-scale difference images with theoretical grey-scales previously calculated from models including CIRs in an optically thin stellar wind, we find that two CIRs were likely present. A separation in longitude of Delta I center dot a parts per thousand integral 90A degrees was determined between the two CIRs and we suggest that the different maximum velocities that they reach indicate that they emerge from different latitudes. We have also been able to detect observational signatures of the CIRs in other spectral lines (C iv lambda lambda 5802,5812 and He i lambda 5876). Furthermore, a DAC was found to be present simultaneously with the CIR signatures detected in the He i lambda 5876 emission line which is consistent with the proposed geometry of the large-scale structures in the wind. Small-scale structures also show a presence in the wind, simultaneously with the larger scale structures, showing that they do in fact co-exist.},
  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{VanHoutTachmazidouBackmanetal.2020,
  author    = {Van Hout, Cristopher V. and Tachmazidou, Ioanna and Backman, Joshua D. and Hoffman, Joshua D. and Liu, Daren and Pandey, Ashutosh K. and Gonzaga-Jauregui, Claudia and Khalid, Shareef and Ye, Bin and Banerjee, Nilanjana and Li, Alexander H. and O'Dushlaine, Colm and Marcketta, Anthony and Staples, Jeffrey and Schurmann, Claudia and Hawes, Alicia and Maxwell, Evan and Barnard, Leland and Lopez, Alexander and Penn, John and Habegger, Lukas and Blumenfeld, Andrew L. and Bai, Xiaodong and O'Keeffe, Sean and Yadav, Ashish and Praveen, Kavita and Jones, Marcus and Salerno, William J. and Chung, Wendy K. and Surakka, Ida and Willer, Cristen J. and Hveem, Kristian and Leader, Joseph B. and Carey, David J. and Ledbetter, David H. and Cardon, Lon and Yancopoulos, George D. and Economides, Aris and Coppola, Giovanni and Shuldiner, Alan R. and Balasubramanian, Suganthi and Cantor, Michael and Nelson, Matthew R. and Whittaker, John and Reid, Jeffrey G. and Marchini, Jonathan and Overton, John D. and Scott, Robert A. and Abecasis, Goncalo R. and Yerges-Armstrong, Laura M. and Baras, Aris},
  title     = {Exome sequencing and characterization of 49,960 individuals in the UK Biobank},
  series = {Nature : the international weekly journal of science},
  volume    = {586},
  journal   = {Nature : the international weekly journal of science},
  number    = {7831},
  publisher = {Macmillan Publishers Limited},
  address   = {London},
  organization    = {Regeneron Genetics Ctr},
  issn      = {0028-0836},
  doi       = {10.1038/s41586-020-2853-0},
  pages     = {749 -- 756},
  year      = {2020},
  abstract  = {The UK Biobank is a prospective study of 502,543 individuals, combining extensive phenotypic and genotypic data with streamlined access for researchers around the world(1). Here we describe the release of exome-sequence data for the first 49,960 study participants, revealing approximately 4 million coding variants (of which around 98.6\% have a frequency of less than 1\%). The data include 198,269 autosomal predicted loss-of-function (LOF) variants, a more than 14-fold increase compared to the imputed sequence. Nearly all genes (more than 97\%) had at least one carrier with a LOF variant, and most genes (more than 69\%) had at least ten carriers with a LOF variant. We illustrate the power of characterizing LOF variants in this population through association analyses across 1,730 phenotypes. In addition to replicating established associations, we found novel LOF variants with large effects on disease traits, includingPIEZO1on varicose veins,COL6A1on corneal resistance,MEPEon bone density, andIQGAP2andGMPRon blood cell traits. We further demonstrate the value of exome sequencing by surveying the prevalence of pathogenic variants of clinical importance, and show that 2\% of this population has a medically actionable variant. Furthermore, we characterize the penetrance of cancer in carriers of pathogenicBRCA1andBRCA2variants. Exome sequences from the first 49,960 participants highlight the promise of genome sequencing in large population-based studies and are now accessible to the scientific community. <br /> Exome sequences from the first 49,960 participants in the UK Biobank highlight the promise of genome sequencing in large population-based studies and are now accessible to the scientific community.},
  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{LevermannWinkelmannNowickietal.2014,
  author    = {Levermann, Anders and Winkelmann, Ricarda and Nowicki, S. and Fastook, J. L. and Frieler, Katja and Greve, R. and Hellmer, H. H. and Martin, M. A. and Meinshausen, Malte and Mengel, Matthias and Payne, A. J. and Pollard, D. and Sato, T. and Timmermann, R. and Wang, Wei Li and Bindschadler, Robert A.},
  title     = {Projecting antarctic ice discharge using response functions from SeaRISE ice-sheet models},
  series = {Earth system dynamics},
  volume    = {5},
  journal   = {Earth system dynamics},
  number    = {2},
  publisher = {Copernicus},
  address   = {G{\"o}ttingen},
  issn      = {2190-4979},
  doi       = {10.5194/esd-5-271-2014},
  pages     = {271 -- 293},
  year      = {2014},
  abstract  = {The largest uncertainty in projections of future sea-level change results from the potentially changing dynamical ice discharge from Antarctica. Basal ice-shelf melting induced by a warming ocean has been identified as a major cause for additional ice flow across the grounding line. Here we attempt to estimate the uncertainty range of future ice discharge from Antarctica by combining uncertainty in the climatic forcing, the oceanic response and the ice-sheet model response. The uncertainty in the global mean temperature increase is obtained from historically constrained emulations with the MAGICC-6.0 (Model for the Assessment of Greenhouse gas Induced Climate Change) model. The oceanic forcing is derived from scaling of the subsurface with the atmospheric warming from 19 comprehensive climate models of the Coupled Model Intercomparison Project (CMIP-5) and two ocean models from the EU-project Ice2Sea. The dynamic ice-sheet response is derived from linear response functions for basal ice-shelf melting for four different Antarctic drainage regions using experiments from the Sea-level Response to Ice Sheet Evolution (SeaRISE) intercomparison project with five different Antarctic ice-sheet models. The resulting uncertainty range for the historic Antarctic contribution to global sea-level rise from 1992 to 2011 agrees with the observed contribution for this period if we use the three ice-sheet models with an explicit representation of ice-shelf dynamics and account for the time-delayed warming of the oceanic subsurface compared to the surface air temperature. The median of the additional ice loss for the 21st century is computed to 0.07 m (66\% range: 0.02-0.14 m; 90\% range: 0.0-0.23 m) of global sea-level equivalent for the low-emission RCP-2.6 (Representative Concentration Pathway) scenario and 0.09 m (66\% range: 0.04-0.21 m; 90\% range: 0.01-0.37 m) for the strongest RCP-8.5. Assuming no time delay between the atmospheric warming and the oceanic subsurface, these values increase to 0.09 m (66\% range: 0.04-0.17 m; 90\% range: 0.02-0.25 m) for RCP-2.6 and 0.15 m (66\% range: 0.07-0.28 m; 90\% range: 0.04-0.43 m) for RCP-8.5. All probability distributions are highly skewed towards high values. The applied ice-sheet models are coarse resolution with limitations in the representation of grounding-line motion. Within the constraints of the applied methods, the uncertainty induced from different ice-sheet models is smaller than that induced by the external forcing to the ice sheets.},
  language  = {en}
}
@misc{ArnisonBibbBierbaumetal.2013,
  author    = {Arnison, Paul G. and Bibb, Mervyn J. and Bierbaum, Gabriele and Bowers, Albert A. and Bugni, Tim S. and Bulaj, Grzegorz and Camarero, Julio A. and Campopiano, Dominic J. and Challis, Gregory L. and Clardy, Jon and Cotter, Paul D. and Craik, David J. and Dawson, Michael and Dittmann-Th{\"u}nemann, Elke and Donadio, Stefano and Dorrestein, Pieter C. and Entian, Karl-Dieter and Fischbach, Michael A. and Garavelli, John S. and Goeransson, Ulf and Gruber, Christian W. and Haft, Daniel H. and Hemscheidt, Thomas K. and Hertweck, Christian and Hill, Colin and Horswill, Alexander R. and Jaspars, Marcel and Kelly, Wendy L. and Klinman, Judith P. and Kuipers, Oscar P. and Link, A. James and Liu, Wen and Marahiel, Mohamed A. and Mitchell, Douglas A. and Moll, Gert N. and Moore, Bradley S. and Mueller, Rolf and Nair, Satish K. and Nes, Ingolf F. and Norris, Gillian E. and Olivera, Baldomero M. and Onaka, Hiroyasu and Patchett, Mark L. and Piel, J{\"o}rn and Reaney, Martin J. T. and Rebuffat, Sylvie and Ross, R. Paul and Sahl, Hans-Georg and Schmidt, Eric W. and Selsted, Michael E. and Severinov, Konstantin and Shen, Ben and Sivonen, Kaarina and Smith, Leif and Stein, Torsten and Suessmuth, Roderich D. and Tagg, John R. and Tang, Gong-Li and Truman, Andrew W. and Vederas, John C. and Walsh, Christopher T. and Walton, Jonathan D. and Wenzel, Silke C. and Willey, Joanne M. and van der Donk, Wilfred A.},
  title     = {Ribosomally synthesized and post-translationally modified peptide natural products overview and recommendations for a universal nomenclature},
  series = {Natural product reports : a journal of current developments in bio-organic chemistry},
  volume    = {30},
  journal   = {Natural product reports : a journal of current developments in bio-organic chemistry},
  number    = {1},
  publisher = {Royal Society of Chemistry},
  address   = {Cambridge},
  issn      = {0265-0568},
  doi       = {10.1039/c2np20085f},
  pages     = {108 -- 160},
  year      = {2013},
  abstract  = {This review presents recommended nomenclature for the biosynthesis of ribosomally synthesized and post-translationally modified peptides (RiPPs), a rapidly growing class of natural products. The current knowledge regarding the biosynthesis of the >20 distinct compound classes is also reviewed, and commonalities are discussed.},
  language  = {en}
}
@article{KronerWildeO'Brienetal.2005,
  author    = {Kroner, Alfred and Wilde, S. A. and O'Brien, Patrick J. and Li, J. H. and Passchier, C. W. and Walte, N. P. and Liu, Dun Yi},
  title     = {Field relationships, geochemistry, zircon ages and evolution of a late Archaean to Palaeoproterozoic lower crustal section in the Hengshan Terrain of northern China},
  issn      = {1000-9515},
  year      = {2005},
  abstract  = {The Hengshan complex forms part of the central zone of the North China Craton and consists predominantly of ductilely-deformed late Archaean to Palaeoproterozoic high-grade, partly migmatitic, granitoid orthogneisses, intruded by mafic dykes of gabbroic composition. Many highly strained rocks were previously misinterpreted as supracrustal sequences and represent mylonitized granitoids and sheared dykes. Our single zircon dating documents magmatic granitoid emplacement ages between 2.52 Ga and 2.48 Ga, with rare occurrences of 2.7 Ga gneisses, possibly reflecting an older basement. A few granitic gneisses have emplacement ages between 2.35 and 2.1 Ga and show the same structural features as the older rocks, indicating that the main deformation occurred after similar to 2.1 Ga. Intrusion of gabbroic dykes occurred at similar to 1920 Ma, and all Hengshan rocks underwent granulite-facies metamorphism at 1.88-1.85 Ga, followed by retrogression, shearing and uplift. We interpret the Hengshan and adjacent Fuping granitoid gneisses as the lower, plutonic, part of a late Archaean to early Palaeoproterozoic Japan-type magmatic arc, with the upper, volcanic part represented by the nearby Wutai complex. Components of this arc may have evolved at a continental margin as indicated by the 2.7 Ga zircons. Major deformation and HP metamorphism occurred in the late Palaeoproterozoic during the Luliang orogeny when the Eastern and Western blocks of the North China Craton collided to form the Trans-North China orogen. Shear zones in the Hengshan are interpreted as major lower crustal discontinuities post-dating the peak of HP metamorphism, and we suggest that they formed during orogenic collapse and uplift of the Hengshan complex in the late Palaeoproterozoic (< 1.85 Ga)},
  language  = {en}
}
@article{O'BrienWalteLi2005,
  author    = {O'Brien, Patrick J. and Walte, N. P and Li, J. H.},
  title     = {The petrology of two distinct granulite types in the Hengshan Mts, China, and tectonic implications},
  issn      = {1367-9120},
  year      = {2005},
  abstract  = {The Archean to Proterozoic Hengshan Complex (North China Craton), comprises tonalitic and granodioritic gneisses with subordinate mafic lenses, pegmatites and granites. Amphibolite facies assemblages predominate, although granulite-facies relics are widespread, and greenschist-facies retrogression occurs in km-wide shear zones. Mafic lenses, locally abundant, occur as strongly deformed amphibolite (hornblende + plagioclase) boudins or sheets. In contrast to previously published models we find two series of mafic rocks with distinctly different granulite-facies evolutions. In the north of the complex, relict high-pressure mafic granulites are garnet + clinopyroxene-bearing rocks with a secondary development of orthopyroxene around both garnet (kelyphites) and clinopyroxene (coronas). South of the newly defined central, E-W-trending, Zhujiafang shear zone, numerous mafic boudins and less-deformed dykes exhibit a macroscopically visible magmatic texture with coronitic growth of metamorphic garnet (full of quartz inclusions) between the magmatic plagioclase and pyroxene domains. Additional orthopyroxene (after magmatic augite) and sodic rims to magmatic plagioclase clearly indicate medium-pressure granulite-facies metamorphism. These findings suggest tectonic juxtaposition in this area of three different structural levels of the same Proterozoic-imprinted crust: high-pressure granulite grade in the northern Hengshan, medium-pressure granulite grade in the southern Hengshan and amphibolite- to greenschist-facies grade in the Wutaishan to the SE. (c) 2004 Elsevier Ltd. All rights reserved},
  language  = {en}
}
@article{LiKroenerQianetal.2000,
  author    = {Li, J. H. and Kr{\"o}ner, Alfred and Qian, X. L. and O'Brien, Patrick J.},
  title     = {Tectonic evolution of an early Precambrian high-pressure granulite belt in the North China Craton},
  year      = {2000},
  language  = {en}
}
@article{LorenzMillerHochheimeretal.1995,
  author    = {Lorenz, Bernd and Miller, A. J. and Hochheimer, H. D. and H{\"o}nle, W. and Li, T. and Ruoff, A. L.},
  title     = {High pressure phase transition in tetramethylammonium tetra bromocuprate},
  year      = {1995},
  language  = {en}
}
@misc{BehmYoungWhittenetal.2017,
  author    = {Behm, David George and Young, James D. and Whitten, Joseph H. D. and Reid, Jonathan C. and Quigley, Patrick J. and Low, Jonathan and Li, Yimeng and Lima, Camila D. and Hodgson, Daniel D. and Chaouachi, Anis and Prieske, Olaf and Granacher, Urs},
  title     = {Effectiveness of Traditional Strength vs. Power Training on Muscle Strength, Power and Speed with Youth: A Systematic Review and Meta-Analysis},
  series = {Frontiers in physiology},
  volume    = {8},
  journal   = {Frontiers in physiology},
  publisher = {Frontiers Research Foundation},
  address   = {Lausanne},
  issn      = {1664-042X},
  doi       = {10.3389/fphys.2017.00423},
  pages     = {37},
  year      = {2017},
  abstract  = {Numerous national associations and multiple reviews have documented the safety and efficacy of strength training for children and adolescents. The literature highlights the significant training-induced increases in strength associated with youth strength training. However, the effectiveness of youth strength training programs to improve power measures is not as clear. This discrepancy may be related to training and testing specificity. Most prior youth strength training programs emphasized lower intensity resistance with relatively slow movements. Since power activities typically involve higher intensity, explosive-like contractions with higher angular velocities (e.g., plyometrics), there is a conflict between the training medium and testing measures. This meta-analysis compared strength (e.g., training with resistance or body mass) and power training programs (e.g., plyometric training) on proxies of muscle strength, power, and speed. A systematic literature search using a Boolean Search Strategy was conducted in the electronic databases PubMed, SPORT Discus, Web of Science, and Google Scholar and revealed 652 hits. After perusal of title, abstract, and full text, 107 studies were eligible for inclusion in this systematic review and meta-analysis. The meta-analysis showed small to moderate magnitude changes for training specificity with jump measures. In other words, power training was more effective than strength training for improving youth jump height. For sprint measures, strength training was more effective than power training with youth. Furthermore, strength training exhibited consistently large magnitude changes to lower body strength measures, which contrasted with the generally trivial, small and moderate magnitude training improvements of power training upon lower body strength, sprint and jump measures, respectively. Maturity related inadequacies in eccentric strength and balance might influence the lack of training specificity with the unilateral landings and propulsions associated with sprinting. Based on this meta-analysis, strength training should be incorporated prior to power training in order to establish an adequate foundation of strength for power training activities.},
  language  = {en}
}