@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}
}