@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{BeaumontWarringtonCavadinoetal.2018,
  author    = {Beaumont, Robin N. and Warrington, Nicole M. and Cavadino, Alana and Tyrrell, Jessica and Nodzenski, Michael and Horikoshi, Momoko and Geller, Frank and Myhre, Ronny and Richmond, Rebecca C. and Paternoster, Lavinia and Bradfield, Jonathan P. and Kreiner-Moller, Eskil and Huikari, Ville and Metrustry, Sarah and Lunetta, Kathryn L. and Painter, Jodie N. and Hottenga, Jouke-Jan and Allard, Catherine and Barton, Sheila J. and Espinosa, Ana and Marsh, Julie A. and Potter, Catherine and Zhang, Ge and Ang, Wei and Berry, Diane J. and Bouchard, Luigi and Das, Shikta and Hakonarson, Hakon and Heikkinen, Jani and Helgeland, Oyvind and Hocher, Berthold and Hofman, Albert and Inskip, Hazel M. and Jones, Samuel E. and Kogevinas, Manolis and Lind, Penelope A. and Marullo, Letizia and Medland, Sarah E. and Murray, Anna and Murray, Jeffrey C. and Njolstad, Pal R. and Nohr, Ellen A. and Reichetzeder, Christoph and Ring, Susan M. and Ruth, Katherine S. and Santa-Marina, Loreto and Scholtens, Denise M. and Sebert, Sylvain and Sengpiel, Verena and Tuke, Marcus A. and Vaudel, Marc and Weedon, Michael N. and Willemsen, Gonneke and Wood, Andrew R. and Yaghootkar, Hanieh and Muglia, Louis J. and Bartels, Meike and Relton, Caroline L. and Pennell, Craig E. and Chatzi, Leda and Estivill, Xavier and Holloway, John W. and Boomsma, Dorret I. and Montgomery, Grant W. and Murabito, Joanne M. and Spector, Tim D. and Power, Christine and Jarvelin, Marjo-Ritta and Bisgaard, Hans and Grant, Struan F. A. and Sorensen, Thorkild I. A. and Jaddoe, Vincent W. and Jacobsson, Bo and Melbye, Mads and McCarthy, Mark I. and Hattersley, Andrew T. and Hayes, M. Geoffrey and Frayling, Timothy M. and Hivert, Marie-France and Felix, Janine F. and Hypponen, Elina and Lowe, William L. and Evans, David M. and Lawlor, Debbie A. and Feenstra, Bjarke and Freathy, Rachel M.},
  title     = {Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics},
  series = {Human molecular genetics},
  volume    = {27},
  journal   = {Human molecular genetics},
  number    = {4},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  organization    = {Early Growth Genetics EGG},
  issn      = {0964-6906},
  doi       = {10.1093/hmg/ddx429},
  pages     = {742 -- 756},
  year      = {2018},
  abstract  = {Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P< 5 x 10(-8). In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.},
  language  = {en}
}
@misc{BeaumontWarringtonCavadinoetal.2017,
  author    = {Beaumont, Robin N. and Warrington, Nicole M. and Cavadino, Alana and Tyrrell, Jessica and Nodzenski, Michael and Horikoshi, Momoko and Geller, Frank and Myhre, Ronny and Richmond, Rebecca C. and Paternoster, Lavinia and Bradfield, Jonathan P. and Kreiner-M{\o}ller, Eskil and Huikari, Ville and Metrustry, Sarah and Lunetta, Kathryn L. and Painter, Jodie N. and Hottenga, Jouke-Jan and Allard, Catherine and Barton, Sheila J. and Espinosa, Ana and Marsh, Julie A. and Potter, Catherine and Zhang, Ge and Ang, Wei and Berry, Diane J. and Bouchard, Luigi and Das, Shikta and Hakonarson, Hakon and Heikkinen, Jani and Helgeland, {\O}yvind and Hocher, Berthold and Hofman, Albert and Inskip, Hazel M. and Jones, Samuel E. and Kogevinas, Manolis and Lind, Penelope A. and Marullo, Letizia and Medland, Sarah E. and Murray, Anna and Murray, Jeffrey C. and Nj{\o}lstad, Pa ̊l R. and Nohr, Ellen A. and Reichetzeder, Christoph and Ring, Susan M. and Ruth, Katherine S. and Santa-Marina, Loreto and Scholtens, Denise M. and Sebert, Sylvain and Sengpiel, Verena and Tuke, Marcus A. and Vaudel, Marc and Weedon, Michael N. and Willemsen, Gonneke and Wood, Andrew R. and Yaghootkar, Hanieh and Muglia, Louis J. and Bartels, Meike and Relton, Caroline L. and Pennell, Craig E. and Chatzi, Leda and Estivill, Xavier and Holloway, John W. and Boomsma, Dorret I. and Montgomery, Grant W. and Murabito, Joanne M. and Spector, Tim D. and Power, Christine and Ja ̈rvelin, Marjo-Ritta and Bisgaard, Hans and Grant, Struan F.A. and S{\o}rensen, Thorkild I.A. and Jaddoe, Vincent W. and Jacobsson, Bo and Melbye, Mads and McCarthy, Mark I. and Hattersley, Andrew T. and Hayes, M. Geoffrey and Frayling, Timothy M. and Hivert, Marie-France and Felix, Janine F. and Hyppo ̈nen, Elina and Lowe, William L. , Jr and Evans, David M. and Lawlor, Debbie A. and Feenstra, Bjarke and Freathy, Rachel M.},
  title     = {Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {628},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-42310},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-423100},
  pages     = {15},
  year      = {2017},
  abstract  = {Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P < 5 {\^A} 10 {\`A}8 . In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.},
  language  = {en}
}
@article{ChipmanFerrierBrenaetal.2014,
  author    = {Chipman, Ariel D. and Ferrier, David E. K. and Brena, Carlo and Qu, Jiaxin and Hughes, Daniel S. T. and Schroeder, Reinhard and Torres-Oliva, Montserrat and Znassi, Nadia and Jiang, Huaiyang and Almeida, Francisca C. and Alonso, Claudio R. and Apostolou, Zivkos and Aqrawi, Peshtewani and Arthur, Wallace and Barna, Jennifer C. J. and Blankenburg, Kerstin P. and Brites, Daniela and Capella-Gutierrez, Salvador and Coyle, Marcus and Dearden, Peter K. and Du Pasquier, Louis and Duncan, Elizabeth J. and Ebert, Dieter and Eibner, Cornelius and Erikson, Galina and Evans, Peter D. and Extavour, Cassandra G. and Francisco, Liezl and Gabaldon, Toni and Gillis, William J. and Goodwin-Horn, Elizabeth A. and Green, Jack E. and Griffiths-Jones, Sam and Grimmelikhuijzen, Cornelis J. P. and Gubbala, Sai and Guigo, Roderic and Han, Yi and Hauser, Frank and Havlak, Paul and Hayden, Luke and Helbing, Sophie and Holder, Michael and Hui, Jerome H. L. and Hunn, Julia P. and Hunnekuhl, Vera S. and Jackson, LaRonda and Javaid, Mehwish and Jhangiani, Shalini N. and Jiggins, Francis M. and Jones, Tamsin E. and Kaiser, Tobias S. and Kalra, Divya and Kenny, Nathan J. and Korchina, Viktoriya and Kovar, Christie L. and Kraus, F. Bernhard and Lapraz, Francois and Lee, Sandra L. and Lv, Jie and Mandapat, Christigale and Manning, Gerard and Mariotti, Marco and Mata, Robert and Mathew, Tittu and Neumann, Tobias and Newsham, Irene and Ngo, Dinh N. and Ninova, Maria and Okwuonu, Geoffrey and Ongeri, Fiona and Palmer, William J. and Patil, Shobha and Patraquim, Pedro and Pham, Christopher and Pu, Ling-Ling and Putman, Nicholas H. and Rabouille, Catherine and Ramos, Olivia Mendivil and Rhodes, Adelaide C. and Robertson, Helen E. and Robertson, Hugh M. and Ronshaugen, Matthew and Rozas, Julio and Saada, Nehad and Sanchez-Gracia, Alejandro and Scherer, Steven E. and Schurko, Andrew M. and Siggens, Kenneth W. and Simmons, DeNard and Stief, Anna and Stolle, Eckart and Telford, Maximilian J. and Tessmar-Raible, Kristin and Thornton, Rebecca and van der Zee, Maurijn and von Haeseler, Arndt and Williams, James M. and Willis, Judith H. and Wu, Yuanqing and Zou, Xiaoyan and Lawson, Daniel and Muzny, Donna M. and Worley, Kim C. and Gibbs, Richard A. and Akam, Michael and Richards, Stephen},
  title     = {The first myriapod genome sequence reveals conservative arthropod gene content and genome organisation in the centipede Strigamia maritima},
  series = {PLoS biology},
  volume    = {12},
  journal   = {PLoS biology},
  number    = {11},
  publisher = {PLoS},
  address   = {San Fransisco},
  issn      = {1545-7885},
  doi       = {10.1371/journal.pbio.1002005},
  pages     = {24},
  year      = {2014},
  abstract  = {Myriapods (e. g., centipedes and millipedes) display a simple homonomous body plan relative to other arthropods. All members of the class are terrestrial, but they attained terrestriality independently of insects. Myriapoda is the only arthropod class not represented by a sequenced genome. We present an analysis of the genome of the centipede Strigamia maritima. It retains a compact genome that has undergone less gene loss and shuffling than previously sequenced arthropods, and many orthologues of genes conserved from the bilaterian ancestor that have been lost in insects. Our analysis locates many genes in conserved macro-synteny contexts, and many small-scale examples of gene clustering. We describe several examples where S. maritima shows different solutions from insects to similar problems. The insect olfactory receptor gene family is absent from S. maritima, and olfaction in air is likely effected by expansion of other receptor gene families. For some genes S. maritima has evolved paralogues to generate coding sequence diversity, where insects use alternate splicing. This is most striking for the Dscam gene, which in Drosophila generates more than 100,000 alternate splice forms, but in S. maritima is encoded by over 100 paralogues. We see an intriguing linkage between the absence of any known photosensory proteins in a blind organism and the additional absence of canonical circadian clock genes. The phylogenetic position of myriapods allows us to identify where in arthropod phylogeny several particular molecular mechanisms and traits emerged. For example, we conclude that juvenile hormone signalling evolved with the emergence of the exoskeleton in the arthropods and that RR-1 containing cuticle proteins evolved in the lineage leading to Mandibulata. We also identify when various gene expansions and losses occurred. The genome of S. maritima offers us a unique glimpse into the ancestral arthropod genome, while also displaying many adaptations to its specific life history.},
  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{JonesArridgeCoatesetal.2009,
  author    = {Jones, Geraint H. and Arridge, Christopher S. and Coates, Andrew J. and Lewis, Gethyn R. and Kanani, Sheila and Wellbrock, Anne and Young, David T. and Crary, Frank J. and Tokar, Robert L. and Wilson, R. J. and Hill, Thomas W. and Johnson, Robert E. and Mitchell, Donald G. and Schmidt, J{\"u}rgen and Kempf, Sascha and Beckmann, Uwe and Russell, Christopher T. and Jia, Y. D. and Dougherty, Michele K. and Waite, J. Hunter and Magee, Brian A.},
  title     = {Fine jet structure of electrically charged grains in Enceladus' plume},
  issn      = {0094-8276},
  doi       = {10.1029/2009gl038284},
  year      = {2009},
  abstract  = {By traversing the plume erupting from high southern latitudes on Saturn's moon Enceladus, Cassini orbiter instruments can directly sample the material therein. Cassini Plasma Spectrometer, CAPS, data show that a major plume component comprises previously-undetected particles of nanometer scales and larger that bridge the mass gap between previously observed gaseous species and solid icy grains. This population is electrically charged both negative and positive, indicating that subsurface triboelectric charging, i.e., contact electrification of condensed plume material may occur through mutual collisions within vents. The electric field of Saturn's magnetosphere controls the jets' morphologies, separating particles according to mass and charge. Fine-scale structuring of these particles' spatial distribution correlates with discrete plume jets' sources, and reveals locations of other possible active regions. The observed plume population likely forms a major component of high velocity nanometer particle streams detected outside Saturn's magnetosphere.},
  language  = {en}
}
@article{ChristopherAshwoodBittremieuxDeutschetal.2020,
  author    = {Christopher Ashwood, Wout Bittremieux and Bittremieux, Wout and Deutsch, Eric W. and Doncheva, Nadezhda T. and Dorfer, Viktoria and Gabriels, Ralf and Gorshkov, Vladimir and Gupta, Surya and Jones, Andrew R. and K{\"a}ll, Lukas and Kopczynski, Dominik and Lane, Lydie and Lautenbacher, Ludwig and Legeay, Marc and Locard-Paulet, Marie and Mesuere, Bart and Sachsenberg, Timo and Salz, Renee and Samaras, Patroklos and Schiebenhoefer, Henning and Schmidt, Tobias and Schw{\"a}mmle, Veit and Soggiu, Alessio and Uszkoreit, Julian and Van Den Bossche, Tim and Van Puyvelde, Bart and Van Strien, Joeri and Verschaffelt, Pieter and Webel, Henry and Willems, Sander and Perez-Riverolab, Yasset and Netz, Eugen and Pfeuffer, Julianus},
  title     = {Proceedings of the EuBIC-MS 2020 Developers' Meeting},
  series = {EuPA Open Proteomics},
  volume    = {24},
  journal   = {EuPA Open Proteomics},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {2212-9685},
  doi       = {10.1016/j.euprot.2020.11.001},
  pages     = {1 -- 6},
  year      = {2020},
  abstract  = {The 2020 European Bioinformatics Community for Mass Spectrometry (EuBIC-MS) Developers' meeting was held from January 13th to January 17th 2020 in Nyborg, Denmark. Among the participants were scientists as well as developers working in the field of computational mass spectrometry (MS) and proteomics. The 4-day program was split between introductory keynote lectures and parallel hackathon sessions. During the latter, the participants developed bioinformatics tools and resources addressing outstanding needs in the community. The hackathons allowed less experienced participants to learn from more advanced computational MS experts, and to actively contribute to highly relevant research projects. We successfully produced several new tools that will be useful to the proteomics community by improving data analysis as well as facilitating future research. All keynote recordings are available on https://doi.org/10.5281/zenodo.3890181.},
  language  = {en}
}