@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} } @article{ThomasCarvalhoHaileetal.2019, author = {Thomas, Jessica E. and Carvalho, Gary R. and Haile, James and Rawlence, Nicolas J. and Martin, Michael D. and Ho, Simon Y. W. and Sigfusson, Arnor P. and Josefsson, Vigfus A. and Frederiksen, Morten and Linnebjerg, Jannie F. and Castruita, Jose A. Samaniego and Niemann, Jonas and Sinding, Mikkel-Holger S. and Sandoval-Velasco, Marcela and Soares, Andre E. R. and Lacy, Robert and Barilaro, Christina and Best, Juila and Brandis, Dirk and Cavallo, Chiara and Elorza, Mikelo and Garrett, Kimball L. and Groot, Maaike and Johansson, Friederike and Lifjeld, Jan T. and Nilson, Goran and Serjeanston, Dale and Sweet, Paul and Fuller, Errol and Hufthammer, Anne Karin and Meldgaard, Morten and Fjeldsa, Jon and Shapiro, Beth and Hofreiter, Michael and Stewart, John R. and Gilbert, M. Thomas P. and Knapp, Michael}, title = {Demographic reconstruction from ancient DNA supports rapid extinction of the great auk}, series = {eLife}, volume = {8}, journal = {eLife}, publisher = {eLife Sciences Publications}, address = {Cambridge}, issn = {2050-084X}, doi = {10.7554/eLife.47509}, pages = {35}, year = {2019}, abstract = {The great auk was once abundant and distributed across the North Atlantic. It is now extinct, having been heavily exploited for its eggs, meat, and feathers. We investigated the impact of human hunting on its demise by integrating genetic data, GPS-based ocean current data, and analyses of population viability. We sequenced complete mitochondrial genomes of 41 individuals from across the species' geographic range and reconstructed population structure and population dynamics throughout the Holocene. Taken together, our data do not provide any evidence that great auks were at risk of extinction prior to the onset of intensive human hunting in the early 16th century. In addition, our population viability analyses reveal that even if the great auk had not been under threat by environmental change, human hunting alone could have been sufficient to cause its extinction. Our results emphasise the vulnerability of even abundant and widespread species to intense and localised exploitation.}, language = {en} } @article{ThomasCarvalhoHaileetal.2017, author = {Thomas, Jessica E. and Carvalho, Gary R. and Haile, James and Martin, Michael D. and Castruita, Jose A. Samaniego and Niemann, Jonas and Sinding, Mikkel-Holger S. and Sandoval-Velasco, Marcela and Rawlence, Nicolas J. and Fuller, Errol and Fjeldsa, Jon and Hofreiter, Michael and Stewart, John R. and Gilbert, M. Thomas P. and Knapp, Michael}, title = {An ‛Aukward' tale}, series = {Genes}, volume = {8}, journal = {Genes}, number = {6}, publisher = {MDPI}, address = {Basel}, issn = {2073-4425}, doi = {10.3390/genes8060164}, pages = {164}, year = {2017}, abstract = {One hundred and seventy-three years ago, the last two Great Auks, Pinguinus impennis, ever reliably seen were killed. Their internal organs can be found in the collections of the Natural History Museum of Denmark, but the location of their skins has remained a mystery. In 1999, Great Auk expert Errol Fuller proposed a list of five potential candidate skins in museums around the world. Here we take a palaeogenomic approach to test which—if any—of Fuller's candidate skins likely belong to either of the two birds. Using mitochondrial genomes from the five candidate birds (housed in museums in Bremen, Brussels, Kiel, Los Angeles, and Oldenburg) and the organs of the last two known individuals, we partially solve the mystery that has been on Great Auk scholars' minds for generations and make new suggestions as to the whereabouts of the still-missing skin from these two birds.}, language = {en} } @article{ZhengLuanSofianopoulouetal.2020, author = {Zheng, Ju-Sheng and Luan, Jian'an and Sofianopoulou, Eleni and Imamura, Fumiaki and Stewart, Isobel D. and Day, Felix R. and Pietzner, Maik and Wheeler, Eleanor and Lotta, Luca A. and Gundersen, Thomas E. and Amiano, Pilar and Ardanaz, Eva and Chirlaque, Maria-Dolores and Fagherazzi, Guy and Franks, Paul W. and Kaaks, Rudolf and Laouali, Nasser and Mancini, Francesca Romana and Nilsson, Peter M. and Onland-Moret, N. Charlotte and Olsen, Anja and Overvad, Kim and Panico, Salvatore and Palli, Domenico and Ricceri, Fulvio and Rolandsson, Olov and Spijkerman, Annemieke M. W. and Sanchez, Maria-Jose and Schulze, Matthias Bernd and Sala, Nuria and Sieri, Sabina and Tjonneland, Anne and Tumino, Rosario and van der Schouw, Yvonne T. and Weiderpass, Elisabete and Riboli, Elio and Danesh, John and Butterworth, Adam S. and Sharp, Stephen J. and Langenberg, Claudia and Forouhi, Nita G. and Wareham, Nicholas J.}, title = {Plasma vitamin C and type 2 diabetes}, series = {Diabetes care}, volume = {44}, journal = {Diabetes care}, number = {1}, publisher = {American Diabetes Association}, address = {Alexandria}, issn = {0149-5992}, doi = {10.2337/dc20-1328}, pages = {98 -- 106}, year = {2020}, abstract = {OBJECTIVE: Higher plasma vitamin C levels are associated with lower type 2 diabetes risk, but whether this association is causal is uncertain. To investigate this, we studied the association of genetically predicted plasma vitamin C with type 2 diabetes. RESEARCH DESIGN AND METHODS: We conducted genome-wide association studies of plasma vitamin C among 52,018 individuals of European ancestry to discover novel genetic variants. We performed Mendelian randomization analyses to estimate the association of genetically predicted differences in plasma vitamin C with type 2 diabetes in up to 80,983 case participants and 842,909 noncase participants. We compared this estimate with the observational association between plasma vitamin C and incident type 2 diabetes, including 8,133 case participants and 11,073 noncase participants. RESULTS: We identified 11 genomic regions associated with plasma vitamin C (P < 5 x 10(-8)), with the strongest signal at SLC23A1, and 10 novel genetic loci including SLC23A3, CHPT1, BCAS3, SNRPF, RER1, MAF, GSTA5, RGS14, AKT1, and FADS1. Plasma vitamin C was inversely associated with type 2 diabetes (hazard ratio per SD 0.88; 95\% CI 0.82, 0.94), but there was no association between genetically predicted plasma vitamin C (excluding FADS1 variant due to its apparent pleiotropic effect) and type 2 diabetes (1.03; 95\% CI 0.96, 1.10). CONCLUSIONS: These findings indicate discordance between biochemically measured and genetically predicted plasma vitamin C levels in the association with type 2 diabetes among European populations. The null Mendelian randomization findings provide no strong evidence to suggest the use of vitamin C supplementation for type 2 diabetes prevention.}, language = {en} }