@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{SunZhangXiaetal.2011,
  author    = {Sun, Zhuanlan and Zhang, Xiaoqing and Xia, Zhongfu and Qiu, Xunlin and Wirges, Werner and Gerhard, Reimund and Zeng, Changchun and Zhang, Chuck and Wang, Ben},
  title     = {Polarization and piezoelectricity in polymer films with artificial void structure},
  series = {Applied physics : A, Materials science \& processing},
  volume    = {105},
  journal   = {Applied physics : A, Materials science \& processing},
  number    = {1},
  publisher = {Springer},
  address   = {New York},
  issn      = {0947-8396},
  doi       = {10.1007/s00339-011-6481-2},
  pages     = {197 -- 205},
  year      = {2011},
  abstract  = {Laminated polymer-film systems with well-defined void structures were prepared from fluoroethylenepropylene (FEP) and polytetrafluoroethylene (PTFE) layers. First the PTFE films were patterned and then fusion-bonded with the FEP films. The laminates were subjected to either corona or contact charging in order to obtain the desired piezoelectricity. The build-up of the "macro-dipoles" in the laminated films was studied by recording the electric hysteresis loops. The resulting electro-mechanical properties were investigated by means of dielectric resonance spectroscopy (DRS) and direct measurements of the stress-strain relationship. Moreover, the thermal stability of the piezoelectric d (33) coefficient was investigated at elevated temperatures and via thermally stimulated discharge (TSD) current measurements in short circuit. For 150 mu m thick laminated films, consisting of one 25 mu m thick PTFE layer, two 12.5 mu m thick FEP layers, and a void of 100 mu m height, the critical voltage necessary for the build-up of the "macro-dipoles" in the inner voids was approximately 1400 V, which agrees with the value calculated from the Paschen Law. A quasi-static piezoelectric d (33) coefficient up to 300 pC/N was observed after corona charging. The mechanical properties of the film systems are highly anisotropic. At room temperature, the Young's moduli of the laminated film system are around 0.37 MPa in the thickness direction and 274 MPa in the lateral direction, respectively. Using these values, the theoretical shape anisotropy ratio of the void was calculated, which agrees well with experimental observation. Compared with films that do not exhibit structural regularity, the laminates showed improved thermal stability of the d (33) coefficients. The thermal stability of d (33) can be further improved by pre-aging. E.g., the reduction of the d (33) value in the sample pre-aged at 150A degrees C for 5 h was less than 5\% after annealing for 30 h at a temperature of 90A degrees C.},
  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}
}
@techreport{BrodeurMikolaCooketal.2024,
  type      = {Working Paper},
  author    = {Brodeur, Abel and Mikola, Derek and Cook, Nikolai and Brailey, Thomas and Briggs, Ryan and Gendre, Alexandra de and Dupraz, Yannick and Fiala, Lenka and Gabani, Jacopo and Gauriot, Romain and Haddad, Joanne and Lima, Goncalo and Ankel-Peters, J{\"o}rg and Dreber, Anna and Campbell, Douglas and Kattan, Lamis and Fages, Diego Marino and Mierisch, Fabian and Sun, Pu and Wright, Taylor and Connolly, Marie and Hoces de la Guardia, Fernando and Johannesson, Magnus and Miguel, Edward and Vilhuber, Lars and Abarca, Alejandro and Acharya, Mahesh and Adjisse, Sossou Simplice and Akhtar, Ahwaz and Lizardi, Eduardo Alberto Ramirez and Albrecht, Sabina and Andersen, Synve Nygaard and Andlib, Zubaria and Arrora, Falak and Ash, Thomas and Bacher, Etienne and Bachler, Sebastian and Bacon, F{\´e}lix and Bagues, Manuel and Balogh, Timea and Batmanov, Alisher and Barschkett, Mara and Basdil, B. Kaan and Dower, Jaromneda and Castek, Ondrej and Caviglia-Harris, Jill and Strand, Gabriella Chauca and Chen, Shi and Chzhen, Asya and Chung, Jong and Collins, Jason and Coppock, Alexander and Cordeau, Hugo and Couillard, Ben and Crechet, Jonathan and Crippa, Lorenzo and Cui, Jeanne and Czymara, Christian and Daarstad, Haley and Dao, Danh Chi and Dao, Dong and Schmandt, Marco David and Linde, Astrid de and Melo, Lucas De and Deer, Lachlan and Vera, Micole De and Dimitrova, Velichka and Dollbaum, Jan Fabian and Dollbaum, Jan Matti and Donnelly, Michael and Huynh, Luu Duc Toan and Dumbalska, Tsvetomira and Duncan, Jamie and Duong, Kiet Tuan and Duprey, Thibaut and Dworschak, Christoph and Ellingsrud, Sigmund and Elminejad, Ali and Eissa, Yasmine and Erhart, Andrea and Etingin-Frati, Giulian and Fatemi-Pour, Elaheh and Federice, Alexa and Feld, Jan and Fenig, Guidon and Firouzjaeiangalougah, Mojtaba and Fleisje, Erlend and Fortier-Chouinard, Alexandre and Engel, Julia Francesca and Fries, Tilman and Fortier, Reid and Fr{\´e}chet, Nadjim and Galipeau, Thomas and Gallegos, Sebasti{\´a}n and Gangji, Areez and Gao, Xiaoying and Garnache, Clo{\´e} and G{\´a}sp{\´a}r, Attila and Gavrilova, Evelina and Ghosh, Arijit and Gibney, Garreth and Gibson, Grant and Godager, Geir and Goff, Leonard and Gong, Da and Gonz{\´a}lez, Javier and Gretton, Jeremy and Griffa, Cristina and Grigoryeva, Idaliya and Grtting, Maja and Guntermann, Eric and Guo, Jiaqi and Gugushvili, Alexi and Habibnia, Hooman and H{\"a}ffner, Sonja and Hall, Jonathan D. and Hammar, Olle and Kordt, Amund Hanson and Hashimoto, Barry and Hartley, Jonathan S. and Hausladen, Carina I. and Havr{\´a}nek, Tom{\´a}š and Hazen, Jacob and He, Harry and Hepplewhite, Matthew and Herrera-Rodriguez, Mario and Heuer, Felix and Heyes, Anthony and Ho, Anson T. Y. and Holmes, Jonathan and Holzknecht, Armando and Hsu, Yu-Hsiang Dexter and Hu, Shiang-Hung and Huang, Yu-Shiuan and Huebener, Mathias and Huber, Christoph and Huynh, Kim P. and Irsova, Zuzana and Isler, Ozan and Jakobsson, Niklas and Frith, Michael James and Jananji, Rapha{\"e}l and Jayalath, Tharaka A. and Jetter, Michael and John, Jenny and Forshaw, Rachel Joy and Juan, Felipe and Kadriu, Valon and Karim, Sunny and Kelly, Edmund and Dang, Duy Khanh Hoang and Khushboo, Tazia and Kim, Jin and Kjellsson, Gustav and Kjelsrud, Anders and Kotsadam, Andreas and Korpershoek, Jori and Krashinsky, Lewis and Kundu, Suranjana and Kustov, Alexander and Lalayev, Nurlan and Langlois, Audr{\´e}e and Laufer, Jill and Lee-Whiting, Blake and Leibing, Andreas and Lenz, Gabriel and Levin, Joel and Li, Peng and Li, Tongzhe and Lin, Yuchen and Listo, Ariel and Liu, Dan and Lu, Xuewen and Lukmanova, Elvina and Luscombe, Alex and Lusher, Lester R. and Lyu, Ke and Ma, Hai and M{\"a}der, Nicolas and Makate, Clifton and Malmberg, Alice and Maitra, Adit and Mandas, Marco and Marcus, Jan and Margaryan, Shushanik and M{\´a}rk, Lili and Martignano, Andres and Marsh, Abigail and Masetto, Isabella and McCanny, Anthony and McManus, Emma and McWay, Ryan and Metson, Lennard and Kinge, Jonas Minet and Mishra, Sumit and Mohnen, Myra and M{\"o}ller, Jakob and Montambeault, Rosalie and Montpetit, S{\´e}bastien and Morin, Louis-Philippe and Morris, Todd and Moser, Scott and Motoki, Fabio and Muehlenbachs, Lucija and Musulan, Andreea and Musumeci, Marco and Nabin, Munirul and Nchare, Karim and Neubauer, Florian and Nguyen, Quan M. P. and Nguyen, Tuan and Nguyen-Tien, Viet and Niazi, Ali and Nikolaishvili, Giorgi and Nordstrom, Ardyn and N{\"u}, Patrick and Odermatt, Angela and Olson, Matt and ien, Henning and {\"O}lkers, Tim and Vert, Miquel Oliver i. and Oral, Emre and Oswald, Christian and Ousman, Ali and {\"O}zak, {\"O}mer and Pandey, Shubham and Pavlov, Alexandre and Pelli, Martino and Penheiro, Romeo and Park, RyuGyung and Martel, Eva P{\´e}rez and Petrovičov{\´a}, Tereza and Phan, Linh and Prettyman, Alexa and Proch{\´a}zka, Jakub and Putri, Aqila and Quandt, Julian and Qiu, Kangyu and Nguyen, Loan Quynh Thi and Rahman, Andaleeb and Rea, Carson H. and Reiremo, Adam and Ren{\´e}e, La{\"e}titia and Richardson, Joseph and Rivers, Nicholas and Rodrigues, Bruno and Roelofs, William and Roemer, Tobias and Rogeberg, Ole and Rose, Julian and Roskos-Ewoldsen, Andrew and Rosmer, Paul and Sabada, Barbara and Saberian, Soodeh and Salamanca, Nicolas and Sator, Georg and Sawyer, Antoine and Scates, Daniel and Schl{\"u}ter, Elmar and Sells, Cameron and Sen, Sharmi and Sethi, Ritika and Shcherbiak, Anna and Sogaolu, Moyosore and Soosalu, Matt and Srensen, Erik and Sovani, Manali and Spencer, Noah and Staubli, Stefan and Stans, Renske and Stewart, Anya and Stips, Felix and Stockley, Kieran and Strobel, Stephenson and Struby, Ethan and Tang, John and Tanrisever, Idil and Yang, Thomas Tao and Tastan, Ipek and Tatić, Dejan and Tatlow, Benjamin and Seuyong, F{\´e}raud Tchuisseu and Th{\´e}riault, R{\´e}mi and Thivierge, Vincent and Tian, Wenjie and Toma, Filip-Mihai and Totarelli, Maddalena and Tran, Van-Anh and Truong, Hung and Tsoy, Nikita and Tuzcuoglu, Kerem and Ubfal, Diego and Villalobos, Laura and Walterskirchen, Julian and Wang, Joseph Taoyi and Wattal, Vasudha and Webb, Matthew D. and Weber, Bryan and Weisser, Reinhard and Weng, Wei-Chien and Westheide, Christian and White, Kimberly and Winter, Jacob and Wochner, Timo and Woerman, Matt and Wong, Jared and Woodard, Ritchie and Wroński, Marcin and Yazbeck, Myra and Yang, Gustav Chung and Yap, Luther and Yassin, Kareman and Ye, Hao and Yoon, Jin Young and Yurris, Chris and Zahra, Tahreen and Zaneva, Mirela and Zayat, Aline and Zhang, Jonathan and Zhao, Ziwei and Yaolang, Zhong},
  title     = {Mass reproducibility and replicability},
  series = {I4R discussion paper series},
  journal   = {I4R discussion paper series},
  number    = {107},
  publisher = {Institute for Replication},
  address   = {Essen},
  issn      = {2752-1931},
  pages     = {250},
  year      = {2024},
  abstract  = {This study pushes our understanding of research reliability by reproducing and replicating claims from 110 papers in leading economic and political science journals. The analysis involves computational reproducibility checks and robustness assessments. It reveals several patterns. First, we uncover a high rate of fully computationally reproducible results (over 85\%). Second, excluding minor issues like missing packages or broken pathways, we uncover coding errors for about 25\% of studies, with some studies containing multiple errors. Third, we test the robustness of the results to 5,511 re-analyses. We find a robustness reproducibility of about 70\%. Robustness reproducibility rates are relatively higher for re-analyses that introduce new data and lower for re-analyses that change the sample or the definition of the dependent variable. Fourth, 52\% of re-analysis effect size estimates are smaller than the original published estimates and the average statistical significance of a re-analysis is 77\% of the original. Lastly, we rely on six teams of researchers working independently to answer eight additional research questions on the determinants of robustness reproducibility. Most teams find a negative relationship between replicators' experience and reproducibility, while finding no relationship between reproducibility and the provision of intermediate or even raw data combined with the necessary cleaning codes.},
  language  = {en}
}