@article{HudsonNewboldContuetal.2014,
  author    = {Hudson, Lawrence N. and Newbold, Tim and Contu, Sara and Hill, Samantha L. L. and Lysenko, Igor and De Palma, Adriana and Phillips, Helen R. P. and Senior, Rebecca A. and Bennett, Dominic J. and Booth, Hollie and Choimes, Argyrios and Correia, David L. P. and Day, Julie and Echeverria-Londono, Susy and Garon, Morgan and Harrison, Michelle L. K. and Ingram, Daniel J. and Jung, Martin and Kemp, Victoria and Kirkpatrick, Lucinda and Martin, Callum D. and Pan, Yuan and White, Hannah J. and Aben, Job and Abrahamczyk, Stefan and Adum, Gilbert B. and Aguilar-Barquero, Virginia and Aizen, Marcelo and Ancrenaz, Marc and Arbelaez-Cortes, Enrique and Armbrecht, Inge and Azhar, Badrul and Azpiroz, Adrian B. and Baeten, Lander and B{\´a}ldi, Andr{\´a}s and Banks, John E. and Barlow, Jos and Bat{\´a}ry, P{\´e}ter and Bates, Adam J. and Bayne, Erin M. and Beja, Pedro and Berg, Ake and Berry, Nicholas J. and Bicknell, Jake E. and Bihn, Jochen H. and B{\"o}hning-Gaese, Katrin and Boekhout, Teun and Boutin, Celine and Bouyer, Jeremy and Brearley, Francis Q. and Brito, Isabel and Brunet, J{\"o}rg and Buczkowski, Grzegorz and Buscardo, Erika and Cabra-Garcia, Jimmy and Calvino-Cancela, Maria and Cameron, Sydney A. and Cancello, Eliana M. and Carrijo, Tiago F. and Carvalho, Anelena L. and Castro, Helena and Castro-Luna, Alejandro A. and Cerda, Rolando and Cerezo, Alexis and Chauvat, Matthieu and Clarke, Frank M. and Cleary, Daniel F. R. and Connop, Stuart P. and D'Aniello, Biagio and da Silva, Pedro Giovani and Darvill, Ben and Dauber, Jens and Dejean, Alain and Diek{\"o}tter, Tim and Dominguez-Haydar, Yamileth and Dormann, Carsten F. and Dumont, Bertrand and Dures, Simon G. and Dynesius, Mats and Edenius, Lars and Elek, Zolt{\´a}n and Entling, Martin H. and Farwig, Nina and Fayle, Tom M. and Felicioli, Antonio and Felton, Annika M. and Ficetola, Gentile F. and Filgueiras, Bruno K. C. and Fonte, Steve J. and Fraser, Lauchlan H. and Fukuda, Daisuke and Furlani, Dario and Ganzhorn, J{\"o}rg U. and Garden, Jenni G. and Gheler-Costa, Carla and Giordani, Paolo and Giordano, Simonetta and Gottschalk, Marco S. and Goulson, Dave and Gove, Aaron D. and Grogan, James and Hanley, Mick E. and Hanson, Thor and Hashim, Nor R. and Hawes, Joseph E. and H{\´e}bert, Christian and Helden, Alvin J. and Henden, John-Andr{\´e} and Hern{\´a}ndez, Lionel and Herzog, Felix and Higuera-Diaz, Diego and Hilje, Branko and Horgan, Finbarr G. and Horv{\´a}th, Roland and Hylander, Kristoffer and Horv{\´a}th, Roland and Isaacs-Cubides, Paola and Ishitani, Mashiro and Jacobs, Carmen T. and Jaramillo, Victor J. and Jauker, Birgit and Jonsell, Matts and Jung, Thomas S. and Kapoor, Vena and Kati, Vassiliki and Katovai, Eric and Kessler, Michael and Knop, Eva and Kolb, Annette and K{\"o}r{\"o}si, {\`A}d{\´a}m and Lachat, Thibault and Lantschner, Victoria and Le F{\´e}on, Violette and LeBuhn, Gretchen and L{\´e}gar{\´e}, Jean-Philippe and Letcher, Susan G. and Littlewood, Nick A. and L{\´o}pez-Quintero, Carlos A. and Louhaichi, Mounir and L{\"o}vei, Gabor L. and Lucas-Borja, Manuel Esteban and Luja, Victor H. and Maeto, Kaoru and Magura, Tibor and Mallari, Neil Aldrin and Marin-Spiotta, Erika and Marhall, E. J. P. and Mart{\´i}nez, Eliana and Mayfield, Margaret M. and Mikusinski, Gregorz and Milder, Jeffery C. and Miller, James R. and Morales, Carolina L. and Muchane, Mary N. and Muchane, Muchai and Naidoo, Robin and Nakamura, Akihiro and Naoe, Shoji and Nates-Parra, Guiomar and Navarerete Gutierrez, Dario A. and Neuschulz, Eike L. and Noreika, Norbertas and Norfolk, Olivia and Noriega, Jorge Ari and N{\"o}ske, Nicole M. and O'Dea, Niall and Oduro, William and Ofori-Boateng, Caleb and Oke, Chris O. and Osgathorpe, Lynne M. and Paritsis, Juan and Parrah, Alejandro and Pelegrin, Nicol{\´a}s and Peres, Carlos A. and Persson, Anna S. and Petanidou, Theodora and Phalan, Ben and Philips, T. Keith and Poveda, Katja and Power, Eileen F. and Presley, Steven J. and Proen{\c{c}}a, V{\^a}nia and Quaranta, Marino and Quintero, Carolina and Redpath-Downing, Nicola A. and Reid, J. Leighton and Reis, Yana T. and Ribeiro, Danilo B. and Richardson, Barbara A. and Richardson, Michael J. and Robles, Carolina A. and R{\"o}mbke, J{\"o}rg and Romero-Duque, Luz Piedad and Rosselli, Loreta and Rossiter, Stephen J. and Roulston, T'ai H. and Rousseau, Laurent and Sadler, Jonathan P. and S{\´a}fi{\´a}n, Szbolcs and Salda{\~n}a-V{\´a}squez, Romeo A. and Samneg{\aa}rd, Ulrika and Sch{\"u}epp, Christof and Schweiger, Oliver and Sedlock, Jodi L. and Shahabuddin, Ghazala and Sheil, Douglas and Silva, Fernando A. B. and Slade, Eleanor and Smith-Pardo, Allan H. and Sodhi, Navjot S. and Somarriba, Eduardo J. and Sosa, Ram{\´o}n A. and Stout, Jane C. and Struebig, Matthew J. and Sung, Yik-Hei and Threlfall, Caragh G. and Tonietto, Rebecca and T{\´o}thm{\´e}r{\´e}sz, B{\´e}la and Tscharntke, Teja and Turner, Edgar C. and Tylianakis, Jason M. and Vanbergen, Adam J. and Vassilev, Kiril and Verboven, Hans A. F. and Vergara, Carlos H. and Vergara, Pablo M. and Verhulst, Jort and Walker, Tony R. and Wang, Yanping and Watling, James I. and Wells, Konstans and Williams, Christopher D. and Willig, Michael R. and Woinarski, John C. Z. and Wolf, Jan H. D. and Woodcock, Ben A. and Yu, Douglas W. and Zailsev, Andreys and Collen, Ben and Ewers, Rob M. and Mace, Georgina M. and Purves, Drew W. and Scharlemann, J{\"o}rn P. W. and Pervis, Andy},
  title     = {The PREDICTS database: a global database of how local terrestrial biodiversity responds to human impacts},
  series = {Ecology and Evolution},
  volume    = {4},
  journal   = {Ecology and Evolution},
  number    = {24},
  doi       = {10.1002/ece3.1303},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-114425},
  pages     = {4701 - 4735},
  year      = {2014},
  abstract  = {Biodiversity continues to decline in the face of increasing anthropogenic pressures such as habitat destruction, exploitation, pollution and introduction of alien species. Existing global databases of species' threat status or population time series are dominated by charismatic species. The collation of datasets with broad taxonomic and biogeographic extents, and that support computation of a range of biodiversity indicators, is necessary to enable better understanding of historical declines and to project - and avert - future declines. We describe and assess a new database of more than 1.6 million samples from 78 countries representing over 28,000 species, collated from existing spatial comparisons of local-scale biodiversity exposed to different intensities and types of anthropogenic pressures, from terrestrial sites around the world. The database contains measurements taken in 208 (of 814) ecoregions, 13 (of 14) biomes, 25 (of 35) biodiversity hotspots and 16 (of 17) megadiverse countries. The database contains more than 1\% of the total number of all species described, and more than 1\% of the described species within many taxonomic groups - including flowering plants, gymnosperms, birds, mammals, reptiles, amphibians, beetles, lepidopterans and hymenopterans. The dataset, which is still being added to, is therefore already considerably larger and more representative than those used by previous quantitative models of biodiversity trends and responses. The database is being assembled as part of the PREDICTS project (Projecting Responses of Ecological Diversity In Changing Terrestrial Systems - ). We make site-level summary data available alongside this article. The full database will be publicly available in 2015.},
  language  = {en}
}
@article{AllertFoersterSvenssonetal.2018,
  author    = {Allert, Stefanie and F{\"o}rster, Toni M. and Svensson, Carl-Magnus and Richardson, Jonathan P. and Pawlik, Tony and Hebecker, Betty and Rudolphi, Sven and Juraschitz, Marc and Schaller, Martin and Blagojevic, Mariana and Morschh{\"a}user, Joachim and Figge, Marc Thilo and Jacobsen, Ilse D. and Naglik, Julian R. and Kasper, Lydia and Mogavero, Selene and Hube, Bernhard},
  title     = {\(Candida\) \(albicans\)-Induced Epithelial Damage Mediates Translocation through Intestinal Barriers},
  series = {mBio},
  volume    = {9},
  journal   = {mBio},
  number    = {3},
  doi       = {10.1128/mBio.00915-18},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-221084},
  pages     = {1-20},
  year      = {2018},
  abstract  = {Life-threatening systemic infections often occur due to the translocation of pathogens across the gut barrier and into the bloodstream. While the microbial and host mechanisms permitting bacterial gut translocation are well characterized, these mechanisms are still unclear for fungal pathogens such as Candida albicans, a leading cause of nosocomial fungal bloodstream infections. In this study, we dissected the cellular mechanisms of translocation of C. albicans across intestinal epithelia in vitro and identified fungal genes associated with this process. We show that fungal translocation is a dynamic process initiated by invasion and followed by cellular damage and loss of epithelial integrity. A screen of >2,000 C. albicans deletion mutants identified genes required for cellular damage of and translocation across enterocytes. Correlation analysis suggests that hypha formation, barrier damage above a minimum threshold level, and a decreased epithelial integrity are required for efficient fungal translocation. Translocation occurs predominantly via a transcellular route, which is associated with fungus-induced necrotic epithelial damage, but not apoptotic cell death. The cytolytic peptide toxin of C. albicans, candidalysin, was found to be essential for damage of enterocytes and was a key factor in subsequent fungal translocation, suggesting that transcellular translocation of C. albicans through intestinal layers is mediated by candidalysin. However, fungal invasion and low-level translocation can also occur via non-transcellular routes in a candidalysin-independent manner. This is the first study showing translocation of a human-pathogenic fungus across the intestinal barrier being mediated by a peptide toxin. IMPORTANCE Candida albicans, usually a harmless fungus colonizing human mucosae, can cause lethal bloodstream infections when it manages to translocate across the intestinal epithelium. This can result from antibiotic treatment, immune dysfunction, or intestinal damage (e.g., during surgery). However, fungal processes may also contribute. In this study, we investigated the translocation process of C. albicans using in vitro cell culture models. Translocation occurs as a stepwise process starting with invasion, followed by epithelial damage and loss of epithelial integrity. The ability to secrete candidalysin, a peptide toxin deriving from the hyphal protein Ece1, is key: C. albicans hyphae, secreting candidalysin, take advantage of a necrotic weakened epithelium to translocate through the intestinal layer.},
  language  = {en}
}
@article{WestburyTurroGreeneetal.2015,
  author    = {Westbury, Sarah K and Turro, Ernest and Greene, Daniel and Lentaigne, Claire and Kelly, Anne M and Bariana, Tadbir K and Simeoni, Ilenia and Pillois, Xavier and Attwood, Antony and Austin, Steve and Jansen, Sjoert BG and Bakchoul, Tamam and Crisp-Hihn, Abi and Erber, Wendy N and Favier, R{\´e}mi and Foad, Nicola and Gattens, Michael and Jolley, Jennifer D and Liesner, Ri and Meacham, Stuart and Millar, Carolyn M and Nurden, Alan T and Peerlinck, Kathelijne and Perry, David J and Poudel, Pawan and Schulman, Sol and Schulze, Harald and Stephens, Jonathan C and Furie, Bruce and Robinson, Peter N and van Geet, Chris and Rendon, Augusto and Gomez, Keith and Laffan, Michael A and Lambert, Michele P and Nurden, Paquita and Ouwehand, Willem H and Richardson, Sylvia and Mumford, Andrew D and Freson, Kathleen},
  title     = {Human phenotype ontology annotation and cluster analysis to unravel genetic defects in 707 cases with unexplained bleeding and platelet disorders},
  series = {Genome Medicine},
  volume    = {7},
  journal   = {Genome Medicine},
  number    = {36},
  doi       = {10.1186/s13073-015-0151-5},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-143329},
  year      = {2015},
  abstract  = {Background: Heritable bleeding and platelet disorders (BPD) are heterogeneous and frequently have an unknown genetic basis. The BRIDGE-BPD study aims to discover new causal genes for BPD by high throughput sequencing using cluster analyses based on improved and standardised deep, multi-system phenotyping of cases. Methods: We report a new approach in which the clinical and laboratory characteristics of BPD cases are annotated with adapted Human Phenotype Ontology (HPO) terms. Cluster analyses are then used to characterise groups of cases with similar HPO terms and variants in the same genes. Results: We show that 60\% of index cases with heritable BPD enrolled at 10 European or US centres were annotated with HPO terms indicating abnormalities in organ systems other than blood or blood-forming tissues, particularly the nervous system. Cases within pedigrees clustered closely together on the bases of their HPO-coded phenotypes, as did cases sharing several clinically suspected syndromic disorders. Cases subsequently found to harbour variants in ACTN1 also clustered closely, even though diagnosis of this recently described disorder was not possible using only the clinical and laboratory data available to the enrolling clinician. Conclusions: These findings validate our novel HPO-based phenotype clustering methodology for known BPD, thus providing a new discovery tool for BPD of unknown genetic basis. This approach will also be relevant for other rare diseases with significant genetic heterogeneity.},
  language  = {en}
}