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5 results on '"Snorradottir, Steinunn"'

1. The sequences of 150,119 genomes in the UK Biobank

Author

Halldorsson, Bjarni V., Eggertsson, Hannes P., Moore, Kristjan H. S., Hauswedell, Hannes, Eiriksson, Ogmundur, Ulfarsson, Magnus O., Palsson, Gunnar, Hardarson, Marteinn T., Oddsson, Asmundur, Jensson, Brynjar O., Kristmundsdottir, Snaedis, Sigurpalsdottir, Brynja D., Stefansson, Olafur A., Beyter, Doruk, Holley, Guillaume, Tragante, Vinicius, Gylfason, Arnaldur, Olason, Pall I., Zink, Florian, Asgeirsdottir, Margret, Sverrisson, Sverrir T., Sigurdsson, Brynjar, Gudjonsson, Sigurjon A., Sigurdsson, Gunnar T., Halldorsson, Gisli H., Sveinbjornsson, Gardar, Norland, Kristjan, Styrkarsdottir, Unnur, Magnusdottir, Droplaug N., Snorradottir, Steinunn, Kristinsson, Kari, Sobech, Emilia, Jonsson, Helgi, Geirsson, Arni J., Olafsson, Isleifur, Jonsson, Palmi, Pedersen, Ole Birger, Erikstrup, Christian, Brunak, Søren, Ostrowski, Sisse Rye, Thorleifsson, Gudmar, Jonsson, Frosti, Melsted, Pall, Jonsdottir, Ingileif, Rafnar, Thorunn, Holm, Hilma, Stefansson, Hreinn, Saemundsdottir, Jona, Gudbjartsson, Daniel F., Magnusson, Olafur T., Masson, Gisli, Thorsteinsdottir, Unnur, Helgason, Agnar, Jonsson, Hakon, Sulem, Patrick, and Stefansson, Kari

Published
2022
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2. The population genomic legacy of the second plague pandemic

Author

Gopalakrishnan, Shyam, Ebenesersdottir, S. Sunna, Lundström, Inge K. C., Turner-Walker, Gordon, Moore, Kristjan H. S., Luisi, Pierre, Margaryan, Ashot, Martin, Michael D., Ellegaard, Martin Rene, Magnusson, Olafur P., Sigurosson, Asgeir, Snorradottir, Steinunn, Magnusdottir, Droplaug N., Laffoon, Jason E., van Dorp, Lucy, Liu, Xiaodong, Moltke, Ida, Avila-Arcos, Maria C., Schraiber, Joshua G., Rasmussen, Simon, Juan, David, Gelabert, Pere, de-Dios, Toni, Fotakis, Anna K., Iraeta-Orbegozo, Miren, Vågene, Åshild J., Denham, Sean Dexter, Christophersen, Axel, Stenøien, Hans K., Vieira, Filipe G., Liu, Shanlin, Günther, Torsten, Kivisild, Toomas, Moseng, Ole Georg, Skar, Birgitte, Cheung, Christina, Sandoval-Velasco, Marcela, Wales, Nathan, Schroeder, Hannes, Campos, Paula F., Guomundsdottir, Valdis B., Sicheritz-Ponten, Thomas, Peterson, Bent, Halgunset, Jostein, Gilbert, Edmund, Cavalleri, Gianpiero L., Hovig, Eivind, Kockum, Ingrid, Olsson, Tomas, Alfredsson, Lars, Hansen, Thomas F., Werge, Thomas, Willerslev, Eske, Balloux, Francois, Marques-Bonet, Tomas, Lalueza-Fox, Carles, Nielsen, Rasmus, Stefansson, Kari, Holgason, Agnar, Gilbert, M. Thomas P., Gopalakrishnan, Shyam, Ebenesersdottir, S. Sunna, Lundström, Inge K. C., Turner-Walker, Gordon, Moore, Kristjan H. S., Luisi, Pierre, Margaryan, Ashot, Martin, Michael D., Ellegaard, Martin Rene, Magnusson, Olafur P., Sigurosson, Asgeir, Snorradottir, Steinunn, Magnusdottir, Droplaug N., Laffoon, Jason E., van Dorp, Lucy, Liu, Xiaodong, Moltke, Ida, Avila-Arcos, Maria C., Schraiber, Joshua G., Rasmussen, Simon, Juan, David, Gelabert, Pere, de-Dios, Toni, Fotakis, Anna K., Iraeta-Orbegozo, Miren, Vågene, Åshild J., Denham, Sean Dexter, Christophersen, Axel, Stenøien, Hans K., Vieira, Filipe G., Liu, Shanlin, Günther, Torsten, Kivisild, Toomas, Moseng, Ole Georg, Skar, Birgitte, Cheung, Christina, Sandoval-Velasco, Marcela, Wales, Nathan, Schroeder, Hannes, Campos, Paula F., Guomundsdottir, Valdis B., Sicheritz-Ponten, Thomas, Peterson, Bent, Halgunset, Jostein, Gilbert, Edmund, Cavalleri, Gianpiero L., Hovig, Eivind, Kockum, Ingrid, Olsson, Tomas, Alfredsson, Lars, Hansen, Thomas F., Werge, Thomas, Willerslev, Eske, Balloux, Francois, Marques-Bonet, Tomas, Lalueza-Fox, Carles, Nielsen, Rasmus, Stefansson, Kari, Holgason, Agnar, and Gilbert, M. Thomas P.

Abstract

Human populations have been shaped by catastrophes that may have left long-lasting signatures in their genomes. One notable example is the second plague pandemic that entered Europe in ca. 1,347 CE and repeatedly returned for over 300 years, with typical village and town mortality estimated at 10%–40%.1 It is assumed that this high mortality affected the gene pools of these populations. First, local population crashes reduced genetic diversity. Second, a change in frequency is expected for sequence variants that may have affected survival or susceptibility to the etiologic agent (Yersinia pestis).2 Third, mass mortality might alter the local gene pools through its impact on subsequent migration patterns. We explored these factors using the Norwegian city of Trondheim as a model, by sequencing 54 genomes spanning three time periods: (1) prior to the plague striking Trondheim in 1,349 CE, (2) the 17th–19th century, and (3) the present. We find that the pandemic period shaped the gene pool by reducing long distance immigration, in particular from the British Isles, and inducing a bottleneck that reduced genetic diversity. Although we also observe an excess of large FST values at multiple loci in the genome, these are shaped by reference biases introduced by mapping our relatively low genome coverage degraded DNA to the reference genome. This implies that attempts to detect selection using ancient DNA (aDNA) datasets that vary by read length and depth of sequencing coverage may be particularly challenging until methods have been developed to account for the impact of differential reference bias on test statistics.

Published
2022
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3. The same sequence variant on 9p21 associates with myocardial infarction, abdominal aortic aneurysm and intracranial aneurysm

Author

Helgadottir, Anna, Thorleifsson, Gudmar, Magnusson, Kristinn P, Grétarsdottir, Solveig, Steinthorsdottir, Valgerdur, Manolescu, Andrei, Jones, Gregory T, Rinkel, Gabriel J E, Blankensteijn, Jan D, Ronkainen, Antti, Jääskeläinen, Juha E, Kyo, Yoshiki, Lenk, Guy M, Sakalihasan, Natzi, Kostulas, Konstantinos, Gottsäter, Anders, Flex, Andrea, Stefansson, Hreinn, Hansen, Torben, Andersen, Gitte, Weinsheimer, Shantel, Borch-Johnsen, Knut, Jørgensen, Torben, Shah, Svati H, Quyyumi, Arshed A, Granger, Christopher B, Reilly, Muredach P, Austin, Harland, Levey, Allan I, Vaccarino, Viola, Palsdottir, Ebba, Walters, G Bragi, Jonsdottir, Thorbjorg, Snorradottir, Steinunn, Magnusdottir, Dana, Gudmundsson, Gudmundur, Ferrell, Robert E, Sveinbjornsdottir, Sigurlaug, Hernesniemi, Juha, Niemelä, Mika, Limet, Raymond, Andersen, Karl, Sigurdsson, Gunnar, Benediktsson, Rafn, Verhoeven, Eric L G, Teijink, Joep A W, Grobbee, Diederick E, Rader, Daniel J, Collier, David A, Pedersen, Oluf, Pola, Roberto, Hillert, Jan, Lindblad, Bengt, Valdimarsson, Einar M, Magnadottir, Hulda B, Wijmenga, Cisca, Tromp, Gerard, Baas, Annette F, Ruigrok, Ynte M, van Rij, Andre M, Kuivaniemi, Helena, Powell, Janet T, Matthiasson, Stefan E, Gulcher, Jeffrey R, Thorgeirsson, Gudmundur, Kong, Augustine, Thorsteinsdottir, Unnur, Stefansson, Kari, Helgadottir, Anna, Thorleifsson, Gudmar, Magnusson, Kristinn P, Grétarsdottir, Solveig, Steinthorsdottir, Valgerdur, Manolescu, Andrei, Jones, Gregory T, Rinkel, Gabriel J E, Blankensteijn, Jan D, Ronkainen, Antti, Jääskeläinen, Juha E, Kyo, Yoshiki, Lenk, Guy M, Sakalihasan, Natzi, Kostulas, Konstantinos, Gottsäter, Anders, Flex, Andrea, Stefansson, Hreinn, Hansen, Torben, Andersen, Gitte, Weinsheimer, Shantel, Borch-Johnsen, Knut, Jørgensen, Torben, Shah, Svati H, Quyyumi, Arshed A, Granger, Christopher B, Reilly, Muredach P, Austin, Harland, Levey, Allan I, Vaccarino, Viola, Palsdottir, Ebba, Walters, G Bragi, Jonsdottir, Thorbjorg, Snorradottir, Steinunn, Magnusdottir, Dana, Gudmundsson, Gudmundur, Ferrell, Robert E, Sveinbjornsdottir, Sigurlaug, Hernesniemi, Juha, Niemelä, Mika, Limet, Raymond, Andersen, Karl, Sigurdsson, Gunnar, Benediktsson, Rafn, Verhoeven, Eric L G, Teijink, Joep A W, Grobbee, Diederick E, Rader, Daniel J, Collier, David A, Pedersen, Oluf, Pola, Roberto, Hillert, Jan, Lindblad, Bengt, Valdimarsson, Einar M, Magnadottir, Hulda B, Wijmenga, Cisca, Tromp, Gerard, Baas, Annette F, Ruigrok, Ynte M, van Rij, Andre M, Kuivaniemi, Helena, Powell, Janet T, Matthiasson, Stefan E, Gulcher, Jeffrey R, Thorgeirsson, Gudmundur, Kong, Augustine, Thorsteinsdottir, Unnur, and Stefansson, Kari

Abstract

Udgivelsesdato: 2008-Feb, Recently, two common sequence variants on 9p21, tagged by rs10757278-G and rs10811661-T, were reported to be associated with coronary artery disease (CAD) and type 2 diabetes (T2D), respectively. We proceeded to further investigate the contributions of these variants to arterial diseases and T2D. Here we report that rs10757278-G is associated with, in addition to CAD, abdominal aortic aneurysm (AAA; odds ratio (OR) = 1.31, P = 1.2 x 10(-12)) and intracranial aneurysm (OR = 1.29, P = 2.5 x 10(-6)), but not with T2D. This variant is the first to be described that affects the risk of AAA and intracranial aneurysm in many populations. The association of rs10811661-T to T2D replicates in our samples, but the variant does not associate with any of the five arterial diseases examined. These findings extend our insight into the role of the sequence variant tagged by rs10757278-G and show that it is not confined to atherosclerotic diseases.

Published
2008

4. A variant in CDKAL1 influences insulin response and risk of type 2 diabetes

Author

Steinthorsdottir, Valgerdur, Thorleifsson, Gudmar, Reynisdottir, Inga, Benediktsson, Rafn, Jonsdottir, Thorbjorg, Walters, G Bragi, Styrkarsdottir, Unnur, Gretarsdottir, Solveig, Emilsson, Valur, Ghosh, Shyamali, Baker, Adam, Snorradottir, Steinunn, Bjarnason, Hjordis, Ng, Maggie C Y, Hansen, Torben, Bagger, Yu, Wilensky, Robert L, Reilly, Muredach P, Adeyemo, Adebowale, Chen, Yuanxiu, Zhou, Jie, Gudnason, Vilmundur, Chen, Guanjie, Huang, Hanxia, Lashley, Kerrie, Doumatey, Ayo, So, Wing-Yee, Ma, Ronald C Y, Andersen, Gitte, Borch-Johnsen, Knut, Jorgensen, Torben, van Vliet-Ostaptchouk, Jana V, Hofker, Marten H, Wijmenga, Cisca, Christiansen, Claus, Rader, Daniel J, Rotimi, Charles, Gurney, Mark, Chan, Juliana C N, Pedersen, Oluf, Sigurdsson, Gunnar, Gulcher, Jeffrey R, Thorsteinsdottir, Unnur, Kong, Augustine, Stefansson, Kari, Steinthorsdottir, Valgerdur, Thorleifsson, Gudmar, Reynisdottir, Inga, Benediktsson, Rafn, Jonsdottir, Thorbjorg, Walters, G Bragi, Styrkarsdottir, Unnur, Gretarsdottir, Solveig, Emilsson, Valur, Ghosh, Shyamali, Baker, Adam, Snorradottir, Steinunn, Bjarnason, Hjordis, Ng, Maggie C Y, Hansen, Torben, Bagger, Yu, Wilensky, Robert L, Reilly, Muredach P, Adeyemo, Adebowale, Chen, Yuanxiu, Zhou, Jie, Gudnason, Vilmundur, Chen, Guanjie, Huang, Hanxia, Lashley, Kerrie, Doumatey, Ayo, So, Wing-Yee, Ma, Ronald C Y, Andersen, Gitte, Borch-Johnsen, Knut, Jorgensen, Torben, van Vliet-Ostaptchouk, Jana V, Hofker, Marten H, Wijmenga, Cisca, Christiansen, Claus, Rader, Daniel J, Rotimi, Charles, Gurney, Mark, Chan, Juliana C N, Pedersen, Oluf, Sigurdsson, Gunnar, Gulcher, Jeffrey R, Thorsteinsdottir, Unnur, Kong, Augustine, and Stefansson, Kari

Abstract

We conducted a genome-wide association study for type 2 diabetes (T2D) in Icelandic cases and controls, and we found that a previously described variant in the transcription factor 7-like 2 gene (TCF7L2) gene conferred the most significant risk. In addition to confirming two recently identified risk variants, we identified a variant in the CDKAL1 gene that was associated with T2D in individuals of European ancestry (allele-specific odds ratio (OR) = 1.20 (95% confidence interval, 1.13-1.27), P = 7.7 x 10(-9)) and individuals from Hong Kong of Han Chinese ancestry (OR = 1.25 (1.11-1.40), P = 0.00018). The genotype OR of this variant suggested that the effect was substantially stronger in homozygous carriers than in heterozygous carriers. The ORs for homozygotes were 1.50 (1.31-1.72) and 1.55 (1.23-1.95) in the European and Hong Kong groups, respectively. The insulin response for homozygotes was approximately 20% lower than for heterozygotes or noncarriers, suggesting that this variant confers risk of T2D through reduced insulin secretion.

Published
2007

5. A genome-wide scan reveals a maternal susceptibility locus for pre-eclampsia on chromosome 2p13.

Author

Arngrimsson, Reynir, Siguroardottir, Sigrun, Frigge, Michael L., Bjarnadottir, Ragnheiour I., Jonsson, Thorlakur, Stefansson, Hreinn, Baldursdottir, Asdis, Einarsdottir, Anna S., Palsson, Birgir, Snorradottir, Steinunn, Lachmeijer, A. M. A., Nicolae, Dan, Kong, Augustine, Bragason, Birkir Thor, Gulcher, Jeffrey R., Geirsson, Reynir Tomas, and Stefansson, Kari

Abstract

Pre-eclampsia is a common and serious disease and a major cause of maternal and infant mortality. Antenatal care systems world-wide screen for signs of the disease such as hypertension and proteinuria. Unlike most other human disorders it impacts two individuals, the mother and the child, both of whom can be severely affected. The pathophysiology of the disorder is incompletely understood, but familial clustering of the disease is apparent. Here we report the results of a genome-wide screen of Icelandic families representing 343 affected women. Including those patients with non-proteinuric pre-eclampsia (gestational hypertension), proteinuric pre-eclampsia and eclampsia, we detected a significant locus on 2p13 with a lod score of 4.70 (single point P < 3.49 x 10[sup -6]). This is the first reported locus for pre-eclampsia meeting the criteria for genome-wide significance. [ABSTRACT FROM AUTHOR]

Published
1999
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