@article{TaalStPourcainThieringetal.2012,
  author    = {Taal, H. Rob and St Pourcain, Beate and Thiering, Elisabeth and Das, Shikta and Mook-Kanamori, Dennis O. and Warrington, Nicole M. and Kaakinen, Marika and Kreiner-Moller, Eskil and Bradfield, Jonathan P. and Freathy, Rachel M. and Geller, Frank and Guxens, Monica and Cousminer, Diana L. and Kerkhof, Marjan and Timpson, Nicholas J. and Ikram, M. Arfan and Beilin, Lawrence J. and Bonnelykke, Klaus and Buxton, Jessica L. and Charoen, Pimphen and Chawes, Bo Lund Krogsgaard and Eriksson, Johan and Evans, David M. and Hofman, Albert and Kemp, John P. and Kim, Cecilia E. and Klopp, Norman and Lahti, Jari and Lye, Stephen J. and McMahon, George and Mentch, Frank D. and Mueller-Nurasyid, Martina and O'Reilly, Paul F. and Prokopenko, Inga and Rivadeneira, Fernando and Steegers, Eric A. P. and Sunyer, Jordi and Tiesler, Carla and Yaghootkar, Hanieh and Breteler, Monique M. B. and Debette, Stephanie and Fornage, Myriam and Gudnason, Vilmundur and Launer, Lenore J. and van der Lugt, Aad and Mosley, Thomas H. and Seshadri, Sudha and Smith, Albert V. and Vernooij, Meike W. and Blakemore, Alexandra I. F. and Chiavacci, Rosetta M. and Feenstra, Bjarke and Fernandez-Banet, Julio and Grant, Struan F. A. and Hartikainen, Anna-Liisa and van der Heijden, Albert J. and Iniguez, Carmen and Lathrop, Mark and McArdle, Wendy L. and Molgaard, Anne and Newnham, John P. and Palmer, Lyle J. and Palotie, Aarno and Pouta, Annneli and Ring, Susan M. and Sovio, Ulla and Standl, Marie and Uitterlinden, Andre G. and Wichmann, H-Erich and Vissing, Nadja Hawwa and DeCarli, Charles and van Duijn, Cornelia M. and McCarthy, Mark I. and Koppelman, Gerard H. and Estivill, Xavier and Hattersley, Andrew T. and Melbye, Mads and Bisgaard, Hans and Pennell, Craig E. and Widen, Elisabeth and Hakonarson, Hakon and Smith, George Davey and Heinrich, Joachim and Jarvelin, Marjo-Riitta and Jaddoe, Vincent W. V. and Adair, Linda S. and Ang, Wei and Atalay, Mustafa and van Beijsterveldt, Toos and Bergen, Nienke and Benke, Kelly and Berry, Diane J. and Bradfield, Jonathan P. and Charoen, Pimphen and Coin, Lachlan and Cousminer, Diana L. and Das, Shikta and Davis, Oliver S. P. and Elliott, Paul and Evans, David M. and Feenstra, Bjarke and Flexeder, Claudia and Frayling, Tim and Freathy, Rachel M. and Gaillard, Romy and Geller, Frank and Groen-Blokhuis, Maria and Goh, Liang-Kee and Guxens, Monica and Haworth, Claire M. A. and Hadley, Dexter and Hebebrand, Johannes and Hinney, Anke and Hirschhorn, Joel N. and Holloway, John W. and Holst, Claus and Hottenga, Jouke Jan and Horikoshi, Momoko and Huikari, Ville and Hypponen, Elina and Iniguez, Carmen and Kaakinen, Marika and Kilpelainen, Tuomas O. and Kirin, Mirna and Kowgier, Matthew and Lakka, Hanna-Maaria and Lange, Leslie A. and Lawlor, Debbie A. and Lehtimaki, Terho and Lewin, Alex and Lindgren, Cecilia and Lindi, Virpi and Maggi, Reedik and Marsh, Julie and Middeldorp, Christel and Millwood, Iona and Mook-Kanamori, Dennis O. and Murray, Jeffrey C. and Nivard, Michel and Nohr, Ellen Aagaard and Ntalla, Ioanna and Oken, Emily and O'Reilly, Paul F. and Palmer, Lyle J. and Panoutsopoulou, Kalliope and Pararajasingham, Jennifer and Prokopenko, Inga and Rodriguez, Alina and Salem, Rany M. and Sebert, Sylvain and Siitonen, Niina and Sovio, Ulla and St Pourcain, Beate and Strachan, David P. and Sunyer, Jordi and Taal, H. Rob and Teo, Yik-Ying and Thiering, Elisabeth and Tiesler, Carla and Uitterlinden, Andre G. and Valcarcel, Beatriz and Warrington, Nicole M. and White, Scott and Willemsen, Gonneke and Yaghootkar, Hanieh and Zeggini, Eleftheria and Boomsma, Dorret I. and Cooper, Cyrus and Estivill, Xavier and Gillman, Matthew and Grant, Struan F. A. and Hakonarson, Hakon and Hattersley, Andrew T. and Heinrich, Joachim and Hocher, Berthold and Jaddoe, Vincent W. V. and Jarvelin, Marjo-Riitta and Lakka, Timo A. and McCarthy, Mark I. and Melbye, Mads and Mohlke, Karen L. and Dedoussis, George V. and Ong, Ken K. and Pearson, Ewan R. and Pennell, Craig E. and Price, Thomas S. and Power, Chris and Raitakari, Olli T. and Saw, Seang-Mei and Scherag, Andre and Simell, Olli and Sorensen, Thorkild I. A. and Timpson, Nicholas J. and Widen, Elisabeth and Wilson, James F. and Ang, Wei and van Beijsterveldt, Toos and Bergen, Nienke and Benke, Kelly and Berry, Diane J. and Bradfield, Jonathan P. and Charoen, Pimphen and Coin, Lachlan and Cousminer, Diana L. and Das, Shikta and Elliott, Paul and Evans, David M. and Frayling, Tim and Freathy, Rachel M. and Gaillard, Romy and Groen-Blokhuis, Maria and Guxens, Monica and Hadley, Dexter and Hottenga, Jouke Jan and Huikari, Ville and Hypponen, Elina and Kaakinen, Marika and Kowgier, Matthew and Lawlor, Debbie A. and Lewin, Alex and Lindgren, Cecilia and Marsh, Julie and Middeldorp, Christel and Millwood, Iona and Mook-Kanamori, Dennis O. and Nivard, Michel and O'Reilly, Paul F. and Palmer, Lyle J. and Prokopenko, Inga and Rodriguez, Alina and Sebert, Sylvain and Sovio, Ulla and St Pourcain, Beate and Standl, Marie and Strachan, David P. and Sunyer, Jordi and Taal, H. Rob and Thiering, Elisabeth and Tiesler, Carla and Uitterlinden, Andre G. and Valcarcel, Beatriz and Warrington, Nicole M. and White, Scott and Willemsen, Gonneke and Yaghootkar, Hanieh and Boomsma, Dorret I. and Estivill, Xavier and Grant, Struan F. A. and Hakonarson, Hakon and Hattersley, Andrew T. and Heinrich, Joachim and Jaddoe, Vincent W. V. and Jarvelin, Marjo-Riitta and McCarthy, Mark I. and Pennell, Craig E. and Power, Chris and Timpson, Nicholas J. and Widen, Elisabeth and Ikram, M. Arfan and Fornage, Myriam and Smith, Albert V. and Seshadri, Sudha and Schmidt, Reinhold and Debette, Stephanie and Vrooman, Henri A. and Sigurdsson, Sigurdur and Ropele, Stefan and Coker, Laura H. and Longstreth, W. T. and Niessen, Wiro J. and DeStefano, Anita L. and Beiser, Alexa and Zijdenbos, Alex P. and Struchalin, Maksim and Jack, Clifford R. and Nalls, Mike A. and Au, Rhoda and Hofman, Albert and Gudnason, Haukur and van der Lugt, Aad and Harris, Tamara B. and Meeks, William M. and Vernooij, Meike W. and van Buchem, Mark A. and Catellier, Diane and Gudnason, Vilmundur and Windham, B. Gwen and Wolf, Philip A. and van Duijn, Cornelia M. and Mosley, Thomas H. and Schmidt, Helena and Launer, Lenore J. and Breteler, Monique M. B. and DeCarli, Charles},
  title     = {Common variants at 12q15 and 12q24 are associated with infant head circumference},
  series = {Nature genetics},
  volume    = {44},
  journal   = {Nature genetics},
  number    = {5},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {Cohorts Heart Aging Res Genetic Ep, Early Genetics Lifecourse Epidemio, Early Growth Genetics EGG Consorti},
  issn      = {1061-4036},
  doi       = {10.1038/ng.2238},
  pages     = {532 -- +},
  year      = {2012},
  abstract  = {To identify genetic variants associated with head circumference in infancy, we performed a meta-analysis of seven genome-wide association studies (GWAS) (N = 10,768 individuals of European ancestry enrolled in pregnancy and/or birth cohorts) and followed up three lead signals in six replication studies (combined N = 19,089). rs7980687 on chromosome 12q24 (P = 8.1 x 10(-9)) and rs1042725 on chromosome 12q15 (P = 2.8 x 10(-10)) were robustly associated with head circumference in infancy. Although these loci have previously been associated with adult height(1), their effects on infant head circumference were largely independent of height (P = 3.8 x 10(-7) for rs7980687 and P = 1.3 x 10(-7) for rs1042725 after adjustment for infant height). A third signal, rs11655470 on chromosome 17q21, showed suggestive evidence of association with head circumference (P = 3.9 x 10(-6)). SNPs correlated to the 17q21 signal have shown genome-wide association with adult intracranial volume(2), Parkinson's disease and other neurodegenerative diseases(3-5), indicating that a common genetic variant in this region might link early brain growth with neurological disease in later life.},
  language  = {en}
}
@article{HavingaKoolAchilleetal.2016,
  author    = {Havinga, Reinout and Kool, Anneleen and Achille, Frederic and Bavcon, Joze and Berg, Christian and Bonomi, Costantino and Burkart, Michael and De Meyere, Dirk and Havstrom, Mats and Kessler, Paul and Knickmann, Barbara and Koester, Nils and Martinez, Remy and Ostgaard, Havard and Ravnjak, Blanka and Scheen, Anne-Cathrine and Smith, Pamela and Smith, Paul and Socher, Stephanie A. and Vange, Vibekke},
  title     = {The Index Seminum: Seeds of change for seed exchange},
  series = {Taxon},
  volume    = {65},
  journal   = {Taxon},
  publisher = {International Association for Plant Taxonomy},
  address   = {Bratislava},
  issn      = {0040-0262},
  doi       = {10.12705/652.9},
  pages     = {333 -- 336},
  year      = {2016},
  abstract  = {Botanic gardens have been exchanging seeds through seed catalogues for centuries. In many gardens, these catalogues remain an important source of plant material. Living collections have become more relevant for genetic analysis and derived research, since genomics of non-model organisms heavily rely on living material. The range of species that is made available annually on all seed lists combined, provides an unsurpassed source of instantly accessible plant material for research collections. Still, the Index Seminum has received criticism in the past few decades. The current exchange model dictates that associated data is manually entered into each database. The amount of time involved and the human errors occurring in this process are difficult to justify when the data was initially produced as a report from another database. The authors propose that an online marketplace for seed exchange should be established, with enhanced search possibilities and downloadable accession data in a standardised format. Such online service should preferably be supervised and coordinated by Botanic Gardens Conservation International (BGCI). This manuscript is the outcome of a workshop on July 9th, 2015, at the European botanic gardens congress "Eurogard VII" in Paris, where the first two authors invited members of the botanic garden community to discuss how the anachronistic Index Seminum can be transformed into an improved and modern tool for seed exchange.},
  language  = {en}
}
@misc{HetenyiMolinariClintonetal.2018,
  author    = {Hetenyi, Gyorgy and Molinari, Irene and Clinton, John and Bokelmann, Gotz and Bondar, Istvan and Crawford, Wayne C. and Dessa, Jean-Xavier and Doubre, Cecile and Friederich, Wolfgang and Fuchs, Florian and Giardini, Domenico and Graczer, Zoltan and Handy, Mark R. and Herak, Marijan and Jia, Yan and Kissling, Edi and Kopp, Heidrun and Korn, Michael and Margheriti, Lucia and Meier, Thomas and Mucciarelli, Marco and Paul, Anne and Pesaresi, Damiano and Piromallo, Claudia and Plenefisch, Thomas and Plomerova, Jaroslava and Ritter, Joachim and Rumpker, Georg and Sipka, Vesna and Spallarossa, Daniele and Thomas, Christine and Tilmann, Frederik and Wassermann, Joachim and Weber, Michael and Weber, Zoltan and Wesztergom, Viktor and Zivcic, Mladen and Abreu, Rafael and Allegretti, Ivo and Apoloner, Maria-Theresia and Aubert, Coralie and Besancon, Simon and de Berc, Maxime Bes and Brunel, Didier and Capello, Marco and Carman, Martina and Cavaliere, Adriano and Cheze, Jerome and Chiarabba, Claudio and Cougoulat, Glenn and Cristiano, Luigia and Czifra, Tibor and Danesi, Stefania and Daniel, Romuald and Dannowski, Anke and Dasovic, Iva and Deschamps, Anne and Egdorf, Sven and Fiket, Tomislav and Fischer, Kasper and Funke, Sigward and Govoni, Aladino and Groschl, Gidera and Heimers, Stefan and Heit, Ben and Herak, Davorka and Huber, Johann and Jaric, Dejan and Jedlicka, Petr and Jund, Helene and Klingen, Stefan and Klotz, Bernhard and Kolinsky, Petr and Kotek, Josef and Kuhne, Lothar and Kuk, Kreso and Lange, Dietrich and Loos, Jurgen and Lovati, Sara and Malengros, Deny and Maron, Christophe and Martin, Xavier and Massa, Marco and Mazzarini, Francesco and Metral, Laurent and Moretti, Milena and Munzarova, Helena and Nardi, Anna and Pahor, Jurij and Pequegnat, Catherine and Petersen, Florian and Piccinini, Davide and Pondrelli, Silvia and Prevolnik, Snjezan and Racine, Roman and Regnier, Marc and Reiss, Miriam and Salimbeni, Simone and Santulin, Marco and Scherer, Werner and Schippkus, Sven and Schulte-Kortnack, Detlef and Solarino, Stefano and Spieker, Kathrin and Stipcevic, Josip and Strollo, Angelo and Sule, Balint and Szanyi, Gyongyver and Szucs, Eszter and Thorwart, Martin and Ueding, Stefan and Vallocchia, Massimiliano and Vecsey, Ludek and Voigt, Rene and Weidle, Christian and Weyland, Gauthier and Wiemer, Stefan and Wolf, Felix and Wolyniec, David and Zieke, Thomas},
  title     = {The AlpArray seismic network},
  series = {Surveys in Geophysics},
  volume    = {39},
  journal   = {Surveys in Geophysics},
  number    = {5},
  publisher = {Springer},
  address   = {Dordrecht},
  organization    = {ETHZ SED Elect Lab AlpArray Seismic Network Team AlpArray OBS Cruise Crew AlpArray Working Grp},
  issn      = {0169-3298},
  doi       = {10.1007/s10712-018-9472-4},
  pages     = {1009 -- 1033},
  year      = {2018},
  abstract  = {The AlpArray programme is a multinational, European consortium to advance our understanding of orogenesis and its relationship to mantle dynamics, plate reorganizations, surface processes and seismic hazard in the Alps-Apennines-Carpathians-Dinarides orogenic system. The AlpArray Seismic Network has been deployed with contributions from 36 institutions from 11 countries to map physical properties of the lithosphere and asthenosphere in 3D and thus to obtain new, high-resolution geophysical images of structures from the surface down to the base of the mantle transition zone. With over 600 broadband stations operated for 2 years, this seismic experiment is one of the largest simultaneously operated seismological networks in the academic domain, employing hexagonal coverage with station spacing at less than 52 km. This dense and regularly spaced experiment is made possible by the coordinated coeval deployment of temporary stations from numerous national pools, including ocean-bottom seismometers, which were funded by different national agencies. They combine with permanent networks, which also required the cooperation of many different operators. Together these stations ultimately fill coverage gaps. Following a short overview of previous large-scale seismological experiments in the Alpine region, we here present the goals, construction, deployment, characteristics and data management of the AlpArray Seismic Network, which will provide data that is expected to be unprecedented in quality to image the complex Alpine mountains at depth.},
  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{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 B. 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}
}
@article{FrodlJanowitzSchmaaletal.2017,
  author    = {Frodl, Thomas and Janowitz, Deborah and Schmaal, Lianne and Tozzi, Leonardo and Dobrowolny, Henrik and Stein, Dan J. and Veltman, Dick J. and Wittfeld, Katharina and van Erp, Theo G. M. and Jahanshad, Neda and Block, Andrea and Hegenscheid, Katrin and Voelzke, Henry and Lagopoulos, Jim and Hatton, Sean N. and Hickie, Ian B. and Frey, Eva Maria and Carballedo, Angela and Brooks, Samantha J. and Vuletic, Daniella and Uhlmann, Anne and Veer, Ilya M. and Walter, Henrik and Schnell, Knut and Grotegerd, Dominik and Arolt, Volker and Kugel, Harald and Schramm, Elisabeth and Konrad, Carsten and Zurowski, Bartosz and Baune, Bernhard T. and van der Wee, Nic J. A. and van Tol, Marie-Jose and Penninx, Brenda W. J. H. and Thompson, Paul M. and Hibar, Derrek P. and Dannlowski, Udo and Grabe, Hans J.},
  title     = {Childhood adversity impacts on brain subcortical structures relevant to depression},
  series = {Journal of psychiatric research},
  volume    = {86},
  journal   = {Journal of psychiatric research},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0022-3956},
  doi       = {10.1016/j.jpsychires.2016.11.010},
  pages     = {58 -- 65},
  year      = {2017},
  abstract  = {Childhood adversity plays an important role for development of major depressive disorder (MDD). There are differences in subcortical brain structures between patients with MDD and healthy controls, but the specific impact of childhood adversity on such structures in MDD remains unclear. Thus, aim of the present study was to investigate whether childhood adversity is associated with subcortical volumes and how it interacts with a diagnosis of MDD and sex. Within the ENIGMA-MDD network, nine university partner sites, which assessed childhood adversity and magnetic resonance imaging in patients with MDD and controls, took part in the current joint mega-analysis. In this largest effort world-wide to identify subcortical brain structure differences related to childhood adversity, 3036 participants were analyzed for subcortical brain volumes using FreeSurfer. A significant interaction was evident between childhood adversity, MDD diagnosis, sex, and region. Increased exposure to childhood adversity was associated with smaller caudate volumes in females independent of MDD. All subcategories of childhood adversity were negatively associated with caudate volumes in females - in particular emotional neglect and physical neglect (independently from age, ICV, imaging site and MDD diagnosis). There was no interaction effect between childhood adversity and MDD diagnosis on subcortical brain volumes. Childhood adversity is one of the contributors to brain structural abnormalities. It is associated with subcortical brain abnormalities that are relevant to psychiatric disorders such as depression. (C) 2016 Published by Elsevier Ltd.},
  language  = {en}
}
@article{KroegerMeidtnerStefanetal.2018,
  author    = {Kroeger, Janine and Meidtner, Karina and Stefan, Norbert and Guevara, Marcela and Kerrison, Nicola D. and Ardanaz, Eva and Aune, Dagfinn and Boeing, Heiner and Dorronsoro, Miren and Dow, Courtney and Fagherazzi, Guy and Franks, Paul W. and Freisling, Heinz and Gunter, Marc J. and Maria Huerta, Jose and Kaaks, Rudolf and Key, Timothy J. and Khaw, Kay Tee and Krogh, Vittorio and Kuehn, Tilman and Mancini, Francesca Romana and Mattiello, Amalia and Nilsson, Peter M. and Olsen, Anja and Overvad, Kim and Palli, Domenico and Ramon Quiros, J. and Rolandsson, Olov and Sacerdote, Carlotta and Sala, Nuria and Salamanca-Fernandez, Elena and Sluijs, Ivonne and Spijkerman, Annemieke M. W. and Tjonneland, Anne and Tsilidis, Konstantinos K. and Tumino, Rosario and van der Schouw, Yvonne T. and Forouhi, Nita G. and Sharp, Stephen J. and Langenberg, Claudia and Riboli, Elio and Schulze, Matthias B. and Wareham, Nicholas J.},
  title     = {Circulating Fetuin-A and Risk of Type 2 Diabetes},
  series = {Diabetes : a journal of the American Diabetes Association},
  volume    = {67},
  journal   = {Diabetes : a journal of the American Diabetes Association},
  number    = {6},
  publisher = {American Diabetes Association},
  address   = {Alexandria},
  issn      = {0012-1797},
  doi       = {10.2337/db17-1268},
  pages     = {1200 -- 1205},
  year      = {2018},
  abstract  = {Fetuin-A, a hepatic-origin protein, is strongly positively associated with risk of type 2 diabetes in human observational studies, but it is unknown whether this association is causal. Weaimed to study the potential causal relation of circulating fetuin-A to risk of type 2 diabetes in a Mendelian randomization study with single nucleotide polymorphisms located in the fetuin-A-encoding AHSG gene. We used data from eight European countries of the European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct case-cohort study including 10,020 incident cases. Plasma fetuin-A concentration was measured in a subset of 965 subcohort participants and 654 case subjects. A genetic score of the AHSG single nucleotide polymorphisms was strongly associated with fetuin-A (28\% explained variation). Using the genetic score as instrumental variable of fetuin-A, we observed no significant association of a 50 mu g/mL higher fetuin-A concentration with diabetes risk (hazard ratio 1.02 [95\% CI 0.97, 1.07]). Combining our results with those from the DIAbetes Genetics Replication And Meta-analysis (DIAGRAM) consortium (12,171 case subjects) also did not suggest a clear significant relation of fetuin-A with diabetes risk. In conclusion, although there is mechanistic evidence for an effect of fetuin-A on insulin sensitivity and secretion, this study does not support a strong, relevant relationship between circulating fetuin-A and diabetes risk in the general population.},
  language  = {en}
}
@article{JannaschKroegerAgnolietal.2019,
  author    = {Jannasch, Franziska and Kr{\"o}ger, Janine and Agnoli, Claudia and Barricarte, Aurelio and Boeing, Heiner and Cayssials, Val{\´e}rie and Colorado-Yohar, Sandra and Dahm, Christina C. and Dow, Courtney and Fagherazzi, Guy and Franks, Paul W. and Freisling, Heinz and Gunter, Marc J. and Kerrison, Nicola D. and Key, Timothy J. and Khaw, Kay-Tee and K{\"u}hn, Tilman and Kyro, Cecilie and Mancini, Francesca Romana and Mokoroa, Olatz and Nilsson, Peter and Overvad, Kim and Palli, Domenico and Panico, Salvatore and Quiros Garcia, Jose Ramon and Rolandsson, Olov and Sacerdote, Carlotta and Sanchez, Maria-Jose and Sahrai, Mohammad Sediq and Sch{\"u}bel, Ruth and Sluijs, Ivonne and Spijkerman, Annemieke M. W. and Tjonneland, Anne and Tong, Tammy Y. N. and Tumino, Rosario and Riboli, Elio and Langenberg, Claudia and Sharp, Stephen J. and Forouhi, Nita G. and Schulze, Matthias Bernd and Wareham, Nicholas J.},
  title     = {Generalizability of a Diabetes-Associated Country-Specific Exploratory Dietary Pattern Is Feasible Across European Populations},
  series = {The Journal of Nutrition},
  volume    = {149},
  journal   = {The Journal of Nutrition},
  number    = {6},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {0022-3166},
  doi       = {10.1093/jn/nxz031},
  pages     = {1047 -- 1055},
  year      = {2019},
  abstract  = {Background: Population-specificity of exploratory dietary patterns limits their generalizability in investigations with type 2 diabetes incidence. Objective: The aim of this study was to derive country-specific exploratory dietary patterns, investigate their association with type 2 diabetes incidence, and replicate diabetes-associated dietary patterns in other countries. Methods: Dietary intake data were used, assessed by country-specific questionnaires at baseline of 11,183 incident diabetes cases and 14,694 subcohort members (mean age 52.9 y) from 8 countries, nested within the European Prospective Investigation into Cancer and Nutrition study (mean follow-up time 6.9 y). Exploratory dietary patterns were derived by principal component analysis. HRs for incident type 2 diabetes were calculated by Prentice-weighted Cox proportional hazard regression models. Diabetes-associated dietary patterns were simplified or replicated to be applicable in other countries. A meta-analysis across all countries evaluated the generalizability of the diabetes-association. Results: Two dietary patterns per country/UK-center, of which overall 3 dietary patterns were diabetes-associated, were identified. A risk-lowering French dietary pattern was not confirmed across other countries: pooled HRFrance per 1 SD: 1.00; 95\% CI: 0.90, 1.10. Risk-increasing dietary patterns, derived in Spain and UK-Norfolk, were confirmed, but only the latter statistically significantly: HRSpain: 1.09; 95\% CI: 0.97, 1.22 and HRUK-Norfolk: 1.12; 95\% CI: 1.04, 1.20. Respectively, this dietary pattern was characterized by relatively high intakes of potatoes, processed meat, vegetable oils, sugar, cake and cookies, and tea. Conclusions: Only few country/center-specific dietary patterns (3 of 18) were statistically significantly associated with diabetes incidence in this multicountry European study population. One pattern, whose association with diabetes was confirmed across other countries, showed overlaps in the food groups potatoes and processed meat with identified diabetes-associated dietary patterns from other studies. The study demonstrates that replication of associations of exploratory patterns with health outcomes is feasible and a necessary step to overcome population-specificity in associations from such analyses.},
  language  = {en}
}
@article{SchraplauScheweNeuschaeferRubeetal.2015,
  author    = {Schraplau, Anne and Schewe, Bettina and Neusch{\"a}fer-Rube, Frank and Ringel, Sebastian and Neuber, Corinna and Kleuser, Burkhard and P{\"u}schel, Gerhard Paul},
  title     = {Enhanced thyroid hormone breakdown in hepatocytes by mutual induction of the constitutive androstane receptor (CAR, NR1I3) and arylhydrocarbon receptor by benzo[a]pyrene and phenobarbital},
  series = {Toxicology},
  volume    = {328},
  journal   = {Toxicology},
  publisher = {Elsevier},
  address   = {Clare},
  issn      = {0300-483X},
  doi       = {10.1016/j.tox.2014.12.004},
  pages     = {21 -- 28},
  year      = {2015},
  abstract  = {Xenobiotics may interfere with the hypothalamic-pituitary-thyroid endocrine axis by inducing enzymes that inactivate thyroid hormones and thereby reduce the metabolic rate. This induction results from an activation of xeno-sensing nuclear receptors. The current study shows that benzo[a]pyrene, a frequent contaminant of processed food and activator of the arylhydrocarbon receptor (AhR) activated the promoter and induced the transcription of the nuclear receptor constitutive androstane receptor (CAR, NR1I3) in rat hepatocytes. Likewise, phenobarbital induced the AhR transcription. This mutual induction of the nuclear receptors enhanced the phenobarbital-dependent induction of the prototypic CAR target gene Cyp2b1 as well as the AhR-dependent induction of UDP-glucuronosyltransferases. In both cases, the induction by the combination of both xenobiotics was more than the sum of the induction by either substance alone. By inducing the AhR, phenobarbital enhanced the benzo[a]pyrene-dependent reduction of thyroid hormone half-life and the benzo[a]pyrene-dependent increase in the rate of thyroid hormone glucuronide formation in hepatocyte cultures. CAR ligands might thus augment the endocrine disrupting potential of AhR activators by an induction of the AhR. (C) 2014 Elsevier Ireland Ltd. All rights reserved.},
  language  = {en}
}
@article{NeuschaeferRubeSchraplauScheweetal.2015,
  author    = {Neuschaefer-Rube, Frank and Schraplau, Anne and Schewe, Bettina and Lieske, Stefanie and Kruetzfeldt, Julia-Mignon and Ringel, Sebastian and Henkela, Janin and Birkenfeld, Andreas L. and P{\"u}schel, Gerhard Paul},
  title     = {Arylhydrocarbon receptor-dependent mIndy (SIc13a5) induction as possible contributor to benzo[a]pyrene-induced lipid accumulation in hepatocytes},
  series = {Toxicology},
  volume    = {337},
  journal   = {Toxicology},
  publisher = {Elsevier},
  address   = {Clare},
  issn      = {0300-483X},
  doi       = {10.1016/j.tox.2015.08.007},
  pages     = {1 -- 9},
  year      = {2015},
  abstract  = {Non-alcoholic fatty liver disease is a growing problem in industrialized and developing countries. Hepatic lipid accumulation is the result of an imbalance between fatty acid uptake, fatty acid de novo synthesis, beta-oxidation and secretion of triglyceride-rich lipoproteins from the hepatocyte. A central regulator of hepatic lipid metabolism is cytosolic citrate that can either be derived from the mitochondrium or be taken up from the blood via the plasma membrane sodium citrate transporter NaCT, the product of the mammalian INDY gene (SLC13A5). mINDY ablation protects against diet-induced steatosis whereas mINDY expression is increased in patients with hepatic steatosis. Diet-induced hepatic steatosis is also enhanced by activation of the arylhyrocarbon receptor (AhR) both in humans and animal models. Therefore, the hypothesis was tested whether the mINDY gene might be a target of the AhR. In accordance with such a hypothesis, the AhR activator benzo[a]pyrene induced the mINDY expression in primary cultures of rat hepatocytes in an AhR-dependent manner. This induction resulted in an increased citrate uptake and citrate incorporation into lipids which probably was further enhanced by the benzo[a]pyrene-dependent induction of key enzymes of fatty acid synthesis. A potential AhR binding site was identified in the mINDY promoter that appears to be conserved in the human promoter. Elimination or mutation of this site largely abolished the activation of the mINDY promoter by benzo[a]pyrene. This study thus identified the mINDY as an AhR target gene. AhR-dependent induction of the mINDY gene might contribute to the development of hepatic steatosis. (C) 2015 Elsevier Ireland Ltd. All rights reserved.},
  language  = {en}
}
@misc{HenkelColemanMacGregorofInneregnySchraplauetal.2018,
  author    = {Henkel, Janin and Coleman Mac Gregor of Inneregny, Charles Dominic and Schraplau, Anne and J{\"o}hrens, Korinna and Weiss, Thomas Siegfried and Jonas, Wenke and Sch{\"u}rmann, Annette and P{\"u}schel, Gerhard Paul},
  title     = {Augmented liver inflammation in a microsomal prostaglandin E synthase 1 (mPGES-1)-deficient diet-induced mouse NASH model},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {483},
  issn      = {1866-8372},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-420879},
  pages     = {11},
  year      = {2018},
  abstract  = {In a subset of patients, non-alcoholic fatty liver disease (NAFLD) is complicated by cell death and inflammation resulting in non-alcoholic steatohepatitis (NASH), which may progress to fibrosis and subsequent organ failure. Apart from cytokines, prostaglandins, in particular prostaglandin E-2 (PGE(2)), play a pivotal role during inflammatory processes. Expression of the key enzymes of PGE(2) synthesis, cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), was increased in human NASH livers in comparison to controls and correlated with the NASH activity score. Both enzymes were also induced in NASH-diet-fed wild-type mice, resulting in an increase in hepatic PGE(2) concentration that was completely abrogated in mPGES-1-deficient mice. PGE(2) is known to inhibit TNF-alpha synthesis in macrophages. A strong infiltration of monocyte-derived macrophages was observed in NASH-diet-fed mice, which was accompanied with an increase in hepatic TNF-alpha expression. Due to the impaired PGE(2) production, TNF-alpha expression increased much more in livers of mPGES-1-deficient mice or in the peritoneal macrophages of these mice. The increased levels of TNF-alpha resulted in an enhanced IL-1 beta production, primarily in hepatocytes, and augmented hepatocyte apoptosis. In conclusion, attenuation of PGE(2) production by mPGES-1 ablation enhanced the TNF-alpha-triggered inflammatory response and hepatocyte apoptosis in diet-induced NASH.},
  language  = {en}
}
@article{HenkelColemanMacGregorofInneregnySchraplauetal.2018,
  author    = {Henkel, Janin and Coleman Mac Gregor of Inneregny, Charles Dominic and Schraplau, Anne and J{\"o}hrens, Korinna and Weiss, Thomas Siegfried and Jonas, Wenke and Sch{\"u}rmann, Annette and P{\"u}schel, Gerhard Paul},
  title     = {Augmented liver inflammation in a microsomal prostaglandin E synthase 1 (mPGES-1)-deficient diet-induced mouse NASH model},
  series = {Scientific Reports},
  journal   = {Scientific Reports},
  number    = {8},
  publisher = {Nature Research},
  address   = {London},
  issn      = {2045-2322},
  doi       = {10.1038/s41598-018-34633-y},
  pages     = {1 -- 11},
  year      = {2018},
  abstract  = {In a subset of patients, non-alcoholic fatty liver disease (NAFLD) is complicated by cell death and inflammation resulting in non-alcoholic steatohepatitis (NASH), which may progress to fibrosis and subsequent organ failure. Apart from cytokines, prostaglandins, in particular prostaglandin E-2 (PGE(2)), play a pivotal role during inflammatory processes. Expression of the key enzymes of PGE(2) synthesis, cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), was increased in human NASH livers in comparison to controls and correlated with the NASH activity score. Both enzymes were also induced in NASH-diet-fed wild-type mice, resulting in an increase in hepatic PGE(2) concentration that was completely abrogated in mPGES-1-deficient mice. PGE(2) is known to inhibit TNF-alpha synthesis in macrophages. A strong infiltration of monocyte-derived macrophages was observed in NASH-diet-fed mice, which was accompanied with an increase in hepatic TNF-alpha expression. Due to the impaired PGE(2) production, TNF-alpha expression increased much more in livers of mPGES-1-deficient mice or in the peritoneal macrophages of these mice. The increased levels of TNF-alpha resulted in an enhanced IL-1 beta production, primarily in hepatocytes, and augmented hepatocyte apoptosis. In conclusion, attenuation of PGE(2) production by mPGES-1 ablation enhanced the TNF-alpha-triggered inflammatory response and hepatocyte apoptosis in diet-induced NASH.},
  language  = {en}
}
@article{HenkelColemanSchraplauetal.2017,
  author    = {Henkel, Janin and Coleman, Charles Dominic and Schraplau, Anne and J{\"o}hrens, Korinna and Weber, Daniela and Castro, Jose Pedro and Hugo, Martin and Schulz, Tim Julius and Kr{\"a}mer, Stephanie and Sch{\"u}rmann, Annette and P{\"u}schel, Gerhard Paul},
  title     = {Induction of Steatohepatitis (NASH) with Insulin Resistance in Wild-type B6 Mice by a Western-type Diet Containing Soybean Oil and Cholesterol},
  series = {Molecular medicine},
  volume    = {23},
  journal   = {Molecular medicine},
  publisher = {Feinstein Inst. for Medical Research},
  address   = {Manhasset},
  issn      = {1076-1551},
  doi       = {10.2119/molmed.2016.00203},
  pages     = {70 -- 82},
  year      = {2017},
  abstract  = {Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are hepatic manifestations of the metabolic syndrome. Many currently used animal models of NAFLD/NASH lack clinical features of either NASH or metabolic syndrome such as hepatic inflammation and fibrosis (e.g., high-fat diets) or overweight and insulin resistance (e.g., methionine-choline-deficient diets), or they are based on monogenetic defects (e.g., ob/ob mice). In the current study, a Western-type diet containing soybean oil with high n-6-PUFA and 0.75\% cholesterol (SOD + Cho) induced steatosis, inflammation and fibrosis accompanied by hepatic lipid peroxidation and oxidative stress in livers of C57BL/6-mice, which in addition showed increased weight gain and insulin resistance, thus displaying a phenotype closely resembling all clinical features of NASH in patients with metabolic syndrome. In striking contrast, a soybean oil-containing Western-type diet without cholesterol (SOD) induced only mild steatosis but not hepatic inflammation, fibrosis, weight gain or insulin resistance. Another high-fat diet, mainly consisting of lard and supplemented with fructose in drinking water (LAD + Fru), resulted in more prominent weight gain, insulin resistance and hepatic steatosis than SOD + Cho, but livers were devoid of inflammation and fibrosis. Although both LAD + Fru-and SOD + Cho-fed animals had high plasma cholesterol, liver cholesterol was elevated only in SOD + Cho animals. Cholesterol induced expression of chemotactic and inflammatory cytokines in cultured Kupffer cells and rendered hepatocytes more susceptible to apoptosis. In summary, dietary cholesterol in the SOD + Cho diet may trigger hepatic inflammation and fibrosis. SOD + Cho-fed animals may be a useful disease model displaying many clinical features of patients with the metabolic syndrome and NASH.},
  language  = {en}
}
@article{HenkelColemanSchraplauetal.2018,
  author    = {Henkel, Janin and Coleman, Charles Dominic and Schraplau, Anne and Joehrens, Korinna and Weiss, Thomas Siegfried and Jonas, Wenke and Sch{\"u}rmann, Annette and P{\"u}schel, Gerhard Paul},
  title     = {Augmented liver inflammation in a microsomal prostaglandin E synthase 1 (mPGES-1)-deficient diet-induced mouse NASH model},
  series = {Scientific reports},
  volume    = {8},
  journal   = {Scientific reports},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {2045-2322},
  doi       = {10.1038/s41598-018-34633-y},
  pages     = {11},
  year      = {2018},
  abstract  = {In a subset of patients, non-alcoholic fatty liver disease (NAFLD) is complicated by cell death and inflammation resulting in non-alcoholic steatohepatitis (NASH), which may progress to fibrosis and subsequent organ failure. Apart from cytokines, prostaglandins, in particular prostaglandin E-2 (PGE(2)), play a pivotal role during inflammatory processes. Expression of the key enzymes of PGE(2) synthesis, cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), was increased in human NASH livers in comparison to controls and correlated with the NASH activity score. Both enzymes were also induced in NASH-diet-fed wild-type mice, resulting in an increase in hepatic PGE(2) concentration that was completely abrogated in mPGES-1-deficient mice. PGE(2) is known to inhibit TNF-alpha synthesis in macrophages. A strong infiltration of monocyte-derived macrophages was observed in NASH-diet-fed mice, which was accompanied with an increase in hepatic TNF-alpha expression. Due to the impaired PGE(2) production, TNF-alpha expression increased much more in livers of mPGES-1-deficient mice or in the peritoneal macrophages of these mice. The increased levels of TNF-alpha resulted in an enhanced IL-1 beta production, primarily in hepatocytes, and augmented hepatocyte apoptosis. In conclusion, attenuation of PGE(2) production by mPGES-1 ablation enhanced the TNF-alpha-triggered inflammatory response and hepatocyte apoptosis in diet-induced NASH.},
  language  = {en}
}
@misc{JolivetFaccennaHuetetal.2013,
  author    = {Jolivet, Laurent and Faccenna, Claudio and Huet, Benjamin and Labrousse, Loic and Le Pourhiet, Laetitia and Lacombe, Olivier and Lecomte, Emmanuel and Burov, Evguenii and Denele, Yoann and Brun, Jean-Pierre and Philippon, Melody and Paul, Anne and Salaue, Gwenaelle and Karabulut, Hayrullah and Piromallo, Claudia and Monie, Patrick and Gueydan, Frederic and Okay, Aral I. and Oberh{\"a}nsli, Roland and Pourteau, Amaury and Augier, Romain and Gadenne, Leslie and Driussi, Olivier},
  title     = {Aegean tectonics strain localisation, slab tearing and trench retreat},
  series = {Tectonophysics : international journal of geotectonics and the geology and physics of the interior of the earth},
  volume    = {597},
  journal   = {Tectonophysics : international journal of geotectonics and the geology and physics of the interior of the earth},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0040-1951},
  doi       = {10.1016/j.tecto.2012.06.011},
  pages     = {1 -- 33},
  year      = {2013},
  abstract  = {We review the geodynamic evolution of the Aegean-Anatolia region and discuss strain localisation there over geological times. From Late Eocene to Present, crustal deformation in the Aegean backarc has localised progressively during slab retreat. Extension started with the formation of the Rhodope Metamorphic Core Complex (Eocene) and migrated to the Cyclades and the northern Menderes Massif (Oligocene and Miocene), accommodated by crustal-scale detachments and a first series of core complexes (MCCs). Extension then localised in Western Turkey, the Corinth Rift and the external Hellenic arc after Messinian times, while the North Anatolian Fault penetrated the Aegean Sea. Through time the direction and style of extension have not changed significantly except in terms of localisation. The contributions of progressive slab retreat and tearing, basal drag, extrusion tectonics and tectonic inheritance are discussed and we favour a model (I) where slab retreat is the main driving engine, (2) successive slab tearing episodes are the main causes of this stepwise strain localisation and (3) the inherited heterogeneity of the crust is a major factor for localising detachments. The continental crust has an inherited strong heterogeneity and crustal-scale contacts such as major thrust planes act as weak zones or as zones of contrast of resistance and viscosity that can localise later deformation. The dynamics of slabs at depth and the asthenospheric flow due to slab retreat also have influence strain localisation in the upper plate. Successive slab ruptures from the Middle Miocene to the late Miocene have isolated a narrow strip of lithosphere, still attached to the African lithosphere below Crete. The formation of the North Anatolian Fault is partly a consequence of this evolution. The extrusion of Anatolia and the Aegean extension are partly driven from below (asthenospheric flow) and from above (extrusion of a lid of rigid crust).},
  language  = {en}
}
@article{HessSaffertLiebetonetal.2015,
  author    = {Hess, Anne-Katrin and Saffert, Paul and Liebeton, Klaus and Ignatova, Zoya},
  title     = {Optimization of Translation Profiles Enhances Protein Expression and Solubility},
  series = {PLoS one},
  volume    = {10},
  journal   = {PLoS one},
  number    = {5},
  publisher = {PLoS},
  address   = {San Fransisco},
  issn      = {1932-6203},
  doi       = {10.1371/journal.pone.0127039},
  pages     = {14},
  year      = {2015},
  abstract  = {mRNA is translated with a non-uniform speed that actively coordinates co-translational folding of protein domains. Using structure-based homology we identified the structural domains in epoxide hydrolases (EHs) and introduced slow-translating codons to delineate the translation of single domains. These changes in translation speed dramatically improved the solubility of two EHs of metagenomic origin in Escherichia coli. Conversely, the importance of transient attenuation for the folding, and consequently solubility, of EH was evidenced with a member of the EH family from Agrobacterium radiobacter, which partitions in the soluble fraction when expressed in E. coli. Synonymous substitutions of codons shaping the slow-transiting regions to fast-translating codons render this protein insoluble. Furthermore, we show that low protein yield can be enhanced by decreasing the free folding energy of the initial 5'-coding region, which can disrupt mRNA secondary structure and enhance ribosomal loading. This study provides direct experimental evidence that mRNA is not a mere messenger for translation of codons into amino acids but bears an additional layer of information for folding, solubility and expression level of the encoded protein. Furthermore, it provides a general frame on how to modulate and fine-tune gene expression of a target protein.},
  language  = {en}
}
@article{SzymanskiToenniesBecheretal.2012,
  author    = {Szymanski, Kolja V. and T{\"o}nnies, Mario and Becher, Anne and Fatykhova, Diana and N'Guessan, Philippe D. and Gutbier, Birgitt and Klauschen, Frederick and Neusch{\"a}fer-Rube, Frank and Schneider, Paul and R{\"u}ckert, Jens and Neudecker, Jens and Bauer, Torsten T. and Dalhoff, Klaus and Droemann, Daniel and Gruber, Achim D. and Kershaw, Olivia and Temmesfeld-Wollbrueck, Bettina and Suttorp, Norbert and Hippenstiel, Stefan and Hocke, Andreas C.},
  title     = {Streptococcus pneumoniae-induced regulation of cyclooxygenase-2 in human lung tissue},
  series = {The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology},
  volume    = {40},
  journal   = {The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology},
  number    = {6},
  publisher = {European Respiratory Society},
  address   = {Sheffield},
  issn      = {0903-1936},
  doi       = {10.1183/09031936.00186911},
  pages     = {1458 -- 1467},
  year      = {2012},
  abstract  = {The majority of cases of community-acquired pneumonia are caused by Streptococcus pneumoniae and most studies on pneumococcal host interaction are based on cell culture or animal experiments. Thus, little is known about infections in human lung tissue. Cyclooxygenase-2 and its metabolites play an important regulatory role in lung inflammation. Therefore, we established a pneumococcal infection model on human lung tissue demonstrating mitogen-activated protein kinase (MAPK)-dependent induction of cyclooxygenase-2 and its related metabolites. In addition to alveolar macrophages and the vascular endothelium, cyclooxygenase-2 was upregulated in alveolar type II but not type I epithelial cells, which was confirmed in lungs of patients suffering from acute pneumonia. Moreover, we demonstrated the expression profile of all four E prostanoid receptors at the mRNA level and showed functionality of the E prostanoid(4) receptor by cyclic adenosine monophosphate production. Additionally, in comparison to previous studies, cyclooxygenase-2/prostaglandin E-2 related pro- and anti-inflammatory mediator regulation was partly confirmed in human lung tissue after pneumococcal infection. Overall, cell type-specific and MAPK-dependent cyclooxygenase-2 expression and prostaglandin E-2 formation in human lung tissue may play an important role in the early phase of pneumococcal infections.},
  language  = {en}
}
@misc{HessSaffertLiebetonetal.2015,
  author    = {Hess, Anne-Katrin and Saffert, Paul and Liebeton, Klaus and Ignatova, Zoya},
  title     = {Optimization of translation profiles enhances protein expression and solubility},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {518},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-40957},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-409574},
  pages     = {14},
  year      = {2015},
  abstract  = {mRNA is translated with a non-uniform speed that actively coordinates co-translational folding of protein domains. Using structure-based homology we identified the structural domains in epoxide hydrolases (EHs) and introduced slow-translating codons to delineate the translation of single domains. These changes in translation speed dramatically improved the solubility of two EHs of metagenomic origin in Escherichia coli. Conversely, the importance of transient attenuation for the folding, and consequently solubility, of EH was evidenced with a member of the EH family from Agrobacterium radiobacter, which partitions in the soluble fraction when expressed in E. coli. Synonymous substitutions of codons shaping the slow-transiting regions to fast-translating codons render this protein insoluble. Furthermore, we show that low protein yield can be enhanced by decreasing the free folding energy of the initial 5'-coding region, which can disrupt mRNA secondary structure and enhance ribosomal loading. This study provides direct experimental evidence that mRNA is not a mere messenger for translation of codons into amino acids but bears an additional layer of information for folding, solubility and expression level of the encoded protein. Furthermore, it provides a general frame on how to modulate and fine-tune gene expression of a target protein.},
  language  = {en}
}
@article{WeckGrikscheitHoeflingetal.2016,
  author    = {Weck, Florian and Grikscheit, Florian and H{\"o}fling, Volkmar and Kordt, Anne and Hamm, Alfons O. and Gerlach, Alexander L. and Alpers, Georg W. and Arolt, Volker and Kircher, Tilo and Pauli, Paul and Rief, Winfried and Lang, Thomas},
  title     = {The role of treatment delivery factors in exposure-based cognitive behavioral therapy for panic disorder with agoraphobia},
  series = {Journal of anxiety disorders},
  volume    = {42},
  journal   = {Journal of anxiety disorders},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0887-6185},
  doi       = {10.1016/j.janxdis.2016.05.007},
  pages     = {10 -- 18},
  year      = {2016},
  abstract  = {Treatment delivery factors (i.e., therapist adherence, therapist competence, and therapeutic alliance) are considered to be important for cognitive behavioral therapy (CBT) for panic disorder and agoraphobia (PD/AG). In the current study, four independent raters conducted process evaluations based on 168 two-hour videotapes of 84 patients with PD/AG treated with exposure-based CBT. Two raters evaluated patients' interpersonal behavior in Session 1. Two raters evaluated treatment delivery factors in Session 6, in which therapists provided the rationale for conducting exposure exercises. At the 6-month follow-up, therapists' adherence (r = 0.54) and therapeutic alliance (r = 0.31) were significant predictors of changes in agoraphobic avoidance behavior; therapist competence was not associated with treatment outcomes. Patients' interpersonal behavior in Session 1 was a significant predictor of the therapeutic alliance in Session 6 (r = 0.17). The findings demonstrate that treatment delivery factors, particularly therapist adherence, are relevant to the long-term success of CBT for PD/AG.},
  language  = {en}
}
@article{HenkelKlauderStatzetal.2021,
  author    = {Henkel, Janin and Klauder, Julia and Statz, Meike and Wohlenberg, Anne-Sophie and Kuipers, Sonja and Vahrenbrink, Madita and P{\"u}schel, Gerhard Paul},
  title     = {Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin E-2},
  series = {Biomedicines},
  volume    = {9},
  journal   = {Biomedicines},
  number    = {5},
  publisher = {MDPI},
  address   = {Basel},
  issn      = {2227-9059},
  doi       = {10.3390/biomedicines9050449},
  pages     = {10},
  year      = {2021},
  abstract  = {Macrophages in pathologically expanded dysfunctional white adipose tissue are exposed to a mix of potential modulators of inflammatory response, including fatty acids released from insulin-resistant adipocytes, increased levels of insulin produced to compensate insulin resistance, and prostaglandin E-2 (PGE(2)) released from activated macrophages. The current study addressed the question of how palmitate might interact with insulin or PGE(2) to induce the formation of the chemotactic pro-inflammatory cytokine interleukin-8 (IL-8). Human THP-1 cells were differentiated into macrophages. In these macrophages, palmitate induced IL-8 formation. Insulin enhanced the induction of IL-8 formation by palmitate as well as the palmitate-dependent stimulation of PGE(2) synthesis. PGE(2) in turn elicited IL-8 formation on its own and enhanced the induction of IL-8 release by palmitate, most likely by activating the EP4 receptor. Since IL-8 causes insulin resistance and fosters inflammation, the increase in palmitate-induced IL-8 formation that is caused by hyperinsulinemia and locally produced PGE(2) in chronically inflamed adipose tissue might favor disease progression in a vicious feed-forward cycle.},
  language  = {en}
}