@article{DenglerWagnerDembiczetal.2018,
  author    = {Dengler, J{\"u}rgen and Wagner, Viktoria and Dembicz, Iwona and Garcia-Mijangos, Itziar and Naqinezhad, Alireza and Boch, Steffen and Chiarucci, Alessandro and Conradi, Timo and Filibeck, Goffredo and Guarino, Riccardo and Janisova, Monika and Steinbauer, Manuel J. and Acic, Svetlana and Acosta, Alicia T. R. and Akasaka, Munemitsu and Allers, Marc-Andre and Apostolova, Iva and Axmanova, Irena and Bakan, Branko and Baranova, Alina and Bardy-Durchhalter, Manfred and Bartha, Sandor and Baumann, Esther and Becker, Thomas and Becker, Ute and Belonovskaya, Elena and Bengtsson, Karin and Benito Alonso, Jose Luis and Berastegi, Asun and Bergamini, Ariel and Bonini, Ilaria and Bruun, Hans Henrik and Budzhak, Vasyl and Bueno, Alvaro and Antonio Campos, Juan and Cancellieri, Laura and Carboni, Marta and Chocarro, Cristina and Conti, Luisa and Czarniecka-Wiera, Marta and De Frenne, Pieter and Deak, Balazs and Didukh, Yakiv P. and Diekmann, Martin and Dolnik, Christian and Dupre, Cecilia and Ecker, Klaus and Ermakov, Nikolai and Erschbamer, Brigitta and Escudero, Adrian and Etayo, Javier and Fajmonova, Zuzana and Felde, Vivian A. and Fernandez Calzado, Maria Rosa and Finckh, Manfred and Fotiadis, Georgios and Fracchiolla, Mariano and Ganeva, Anna and Garcia-Magro, Daniel and Gavilan, Rosario G. and Germany, Markus and Giladi, Itamar and Gillet, Francois and Giusso del Galdo, Gian Pietro and Gonzalez, Jose M. and Grytnes, John-Arvid and Hajek, Michal and Hajkova, Petra and Helm, Aveliina and Herrera, Mercedes and Hettenbergerova, Eva and Hobohm, Carsten and Huellbusch, Elisabeth M. and Ingerpuu, Nele and Jandt, Ute and Jeltsch, Florian and Jensen, Kai and Jentsch, Anke and Jeschke, Michael and Jimenez-Alfaro, Borja and Kacki, Zygmunt and Kakinuma, Kaoru and Kapfer, Jutta and Kavgaci, Ali and Kelemen, Andras and Kiehl, Kathrin and Koyama, Asuka and Koyanagi, Tomoyo F. and Kozub, Lukasz and Kuzemko, Anna and Kyrkjeeide, Magni Olsen and Landi, Sara and Langer, Nancy and Lastrucci, Lorenzo and Lazzaro, Lorenzo and Lelli, Chiara and Leps, Jan and Loebel, Swantje and Luzuriaga, Arantzazu L. and Maccherini, Simona and Magnes, Martin and Malicki, Marek and Marceno, Corrado and Mardari, Constantin and Mauchamp, Leslie and May, Felix and Michelsen, Ottar and Mesa, Joaquin Molero and Molnar, Zsolt and Moysiyenko, Ivan Y. and Nakaga, Yuko K. and Natcheva, Rayna and Noroozi, Jalil and Pakeman, Robin J. and Palpurina, Salza and Partel, Meelis and Paetsch, Ricarda and Pauli, Harald and Pedashenko, Hristo and Peet, Robert K. and Pielech, Remigiusz and Pipenbaher, Natasa and Pirini, Chrisoula and Pleskova, Zuzana and Polyakova, Mariya A. and Prentice, Honor C. and Reinecke, Jennifer and Reitalu, Triin and Pilar Rodriguez-Rojo, Maria and Rolecek, Jan and Ronkin, Vladimir and Rosati, Leonardo and Rosen, Ejvind and Ruprecht, Eszter and Rusina, Solvita and Sabovljevic, Marko and Maria Sanchez, Ana and Savchenko, Galina and Schuhmacher, Oliver and Skornik, Sonja and Sperandii, Marta Gaia and Staniaszek-Kik, Monika and Stevanovic-Dajic, Zora and Stock, Marin and Suchrow, Sigrid and Sutcliffe, Laura M. E. and Swacha, Grzegorz and Sykes, Martin and Szabo, Anna and Talebi, Amir and Tanase, Catalin and Terzi, Massimo and Tolgyesi, Csaba and Torca, Marta and Torok, Peter and Tothmeresz, Bela and Tsarevskaya, Nadezda and Tsiripidis, Ioannis and Tzonev, Rossen and Ushimaru, Atushi and Valko, Orsolya and van der Maarel, Eddy and Vanneste, Thomas and Vashenyak, Iuliia and Vassilev, Kiril and Viciani, Daniele and Villar, Luis and Virtanen, Risto and Kosic, Ivana Vitasovic and Wang, Yun and Weiser, Frank and Went, Julia and Wesche, Karsten and White, Hannah and Winkler, Manuela and Zaniewski, Piotr T. and Zhang, Hui and Ziv, Yaron and Znamenskiy, Sergey and Biurrun, Idoia},
  title     = {GrassPlot - a database of multi-scale plant diversity in Palaearctic grasslands},
  series = {Phytocoenologia},
  volume    = {48},
  journal   = {Phytocoenologia},
  number    = {3},
  publisher = {Cramer},
  address   = {Stuttgart},
  issn      = {0340-269X},
  doi       = {10.1127/phyto/2018/0267},
  pages     = {331 -- 347},
  year      = {2018},
  abstract  = {GrassPlot is a collaborative vegetation-plot database organised by the Eurasian Dry Grassland Group (EDGG) and listed in the Global Index of Vegetation-Plot Databases (GIVD ID EU-00-003). GrassPlot collects plot records (releves) from grasslands and other open habitats of the Palaearctic biogeographic realm. It focuses on precisely delimited plots of eight standard grain sizes (0.0001; 0.001;... 1,000 m(2)) and on nested-plot series with at least four different grain sizes. The usage of GrassPlot is regulated through Bylaws that intend to balance the interests of data contributors and data users. The current version (v. 1.00) contains data for approximately 170,000 plots of different sizes and 2,800 nested-plot series. The key components are richness data and metadata. However, most included datasets also encompass compositional data. About 14,000 plots have near-complete records of terricolous bryophytes and lichens in addition to vascular plants. At present, GrassPlot contains data from 36 countries throughout the Palaearctic, spread across elevational gradients and major grassland types. GrassPlot with its multi-scale and multi-taxon focus complements the larger international vegetationplot databases, such as the European Vegetation Archive (EVA) and the global database " sPlot". Its main aim is to facilitate studies on the scale-and taxon-dependency of biodiversity patterns and drivers along macroecological gradients. GrassPlot is a dynamic database and will expand through new data collection coordinated by the elected Governing Board. We invite researchers with suitable data to join GrassPlot. Researchers with project ideas addressable with GrassPlot data are welcome to submit proposals to the Governing Board.},
  language  = {en}
}
@article{FoersterLindenauLeyendeckeretal.2015,
  author    = {F{\"o}rster, Daniel F. and Lindenau, Bernd and Leyendecker, Marko and Janssen, Franz and Winkler, Carsten and Schumann, Frank O. and Kirschner, Juergen and Holldack, Karsten and F{\"o}hlisch, Alexander},
  title     = {Phase-locked MHz pulse selector for x-ray sources},
  series = {Optics letters : a publication of the Optical Society of America},
  volume    = {40},
  journal   = {Optics letters : a publication of the Optical Society of America},
  number    = {10},
  publisher = {Optical Society of America},
  address   = {Washington},
  issn      = {0146-9592},
  doi       = {10.1364/OL.40.002265},
  pages     = {2265 -- 2268},
  year      = {2015},
  abstract  = {Picosecond x-ray pulses are extracted with a phase-locked x-ray pulse selector at 1.25 MHz repetition rate from the pulse trains of the accelerator-driven multiuser x-ray source BESSY II preserving the peak brilliance at high pulse purity. The system consists of a specially designed in-vacuum chopper wheel rotating with approximate to 1 kHz angular frequency. The wheel is driven in an ultrahigh vacuum and is levitated on magnetic bearings being capable of withstanding high centrifugal forces. Pulses are picked by 1252 high-precision slits of 70 mu m width on the outer rim of the wheel corresponding to a temporal opening window of the chopper of 70 ns. We demonstrate how the electronic phase stabilization of +/- 2 ns together with an arrival time jitter of the individual slits of the same order of magnitude allows us to pick short single bunch x-ray pulses out of a 200 ns ion clearing gap in a multibunch pulse train as emitted from a synchrotron facility at 1.25 MHz repetition rate with a pulse purity below the shot noise detection limit. The approach is applicable to any high-repetition pulsed radiation source, in particular in the x-ray spectral range up to 10 keV. The opening window in a real x-ray beamline, its stability, as well as the limits of mechanical pulse picking techniques in the MHz range are discussed. (C) 2015 Optical Society of America},
  language  = {en}
}
@misc{GorskiJungLietal.2020,
  author    = {Gorski, Mathias and Jung, Bettina and Li, Yong and Matias-Garcia, Pamela R. and Wuttke, Matthias and Coassin, Stefan and Thio, Chris H. L. and Kleber, Marcus E. and Winkler, Thomas W. and Wanner, Veronika and Chai, Jin-Fang and Chu, Audrey Y. and Cocca, Massimiliano and Feitosa, Mary F. and Ghasemi, Sahar and Hoppmann, Anselm and Horn, Katrin and Li, Man and Nutile, Teresa and Scholz, Markus and Sieber, Karsten B. and Teumer, Alexander and Tin, Adrienne and Wang, Judy and Tayo, Bamidele O. and Ahluwalia, Tarunveer S. and Almgren, Peter and Bakker, Stephan J. L. and Banas, Bernhard and Bansal, Nisha and Biggs, Mary L. and Boerwinkle, Eric and B{\"o}ttinger, Erwin and Brenner, Hermann and Carroll, Robert J. and Chalmers, John and Chee, Miao-Li and Chee, Miao-Ling and Cheng, Ching-Yu and Coresh, Josef and de Borst, Martin H. and Degenhardt, Frauke and Eckardt, Kai-Uwe and Endlich, Karlhans and Franke, Andre and Freitag-Wolf, Sandra and Gampawar, Piyush and Gansevoort, Ron T. and Ghanbari, Mohsen and Gieger, Christian and Hamet, Pavel and Ho, Kevin and Hofer, Edith and Holleczek, Bernd and Foo, Valencia Hui Xian and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Josyula, Navya Shilpa and Kahonen, Mika and Khor, Chiea-Chuen and Koenig, Wolfgang and Kramer, Holly and Kraemer, Bernhard K. and Kuehnel, Brigitte and Lange, Leslie A. and Lehtimaki, Terho and Lieb, Wolfgang and Loos, Ruth J. F. and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Milaneschi, Yuri and Mishra, Pashupati P. and Mononen, Nina and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and O'Donoghue, Michelle L. and Orho-Melander, Marju and Pendergrass, Sarah A. and Penninx, Brenda W. J. H. and Preuss, Michael H. and Psaty, Bruce M. and Raffield, Laura M. and Raitakari, Olli T. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Rosenkranz, Alexander R. and Rossing, Peter and Rotter, Jerome and Sabanayagam, Charumathi and Schmidt, Helena and Schmidt, Reinhold and Schoettker, Ben and Schulz, Christina-Alexandra and Sedaghat, Sanaz and Shaffer, Christian M. and Strauch, Konstantin and Szymczak, Silke and Taylor, Kent D. and Tremblay, Johanne and Chaker, Layal and van der Harst, Pim and van der Most, Peter J. and Verweij, Niek and Voelker, Uwe and Waldenberger, Melanie and Wallentin, Lars and Waterworth, Dawn M. and White, Harvey D. and Wilson, James G. and Wong, Tien-Yin and Woodward, Mark and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Yan and Snieder, Harold and Wanner, Christoph and Boger, Carsten A. and Kottgen, Anna and Kronenberg, Florian and Pattaro, Cristian and Heid, Iris M.},
  title     = {Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline},
  series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Reihe der Digital Engineering Fakult{\"a}t},
  journal   = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Reihe der Digital Engineering Fakult{\"a}t},
  number    = {19},
  doi       = {10.25932/publishup-56537},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-565379},
  pages     = {14},
  year      = {2020},
  abstract  = {Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25\% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95\% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.},
  language  = {en}
}
@article{GorskiJungLietal.2020,
  author    = {Gorski, Mathias and Jung, Bettina and Li, Yong and Matias-Garcia, Pamela R. and Wuttke, Matthias and Coassin, Stefan and Thio, Chris H. L. and Kleber, Marcus E. and Winkler, Thomas W. and Wanner, Veronika and Chai, Jin-Fang and Chu, Audrey Y. and Cocca, Massimiliano and Feitosa, Mary F. and Ghasemi, Sahar and Hoppmann, Anselm and Horn, Katrin and Li, Man and Nutile, Teresa and Scholz, Markus and Sieber, Karsten B. and Teumer, Alexander and Tin, Adrienne and Wang, Judy and Tayo, Bamidele O. and Ahluwalia, Tarunveer S. and Almgren, Peter and Bakker, Stephan J. L. and Banas, Bernhard and Bansal, Nisha and Biggs, Mary L. and Boerwinkle, Eric and B{\"o}ttinger, Erwin and Brenner, Hermann and Carroll, Robert J. and Chalmers, John and Chee, Miao-Li and Chee, Miao-Ling and Cheng, Ching-Yu and Coresh, Josef and de Borst, Martin H. and Degenhardt, Frauke and Eckardt, Kai-Uwe and Endlich, Karlhans and Franke, Andre and Freitag-Wolf, Sandra and Gampawar, Piyush and Gansevoort, Ron T. and Ghanbari, Mohsen and Gieger, Christian and Hamet, Pavel and Ho, Kevin and Hofer, Edith and Holleczek, Bernd and Foo, Valencia Hui Xian and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Josyula, Navya Shilpa and Kahonen, Mika and Khor, Chiea-Chuen and Koenig, Wolfgang and Kramer, Holly and Kraemer, Bernhard K. and Kuehnel, Brigitte and Lange, Leslie A. and Lehtimaki, Terho and Lieb, Wolfgang and Loos, Ruth J. F. and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Milaneschi, Yuri and Mishra, Pashupati P. and Mononen, Nina and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and O'Donoghue, Michelle L. and Orho-Melander, Marju and Pendergrass, Sarah A. and Penninx, Brenda W. J. H. and Preuss, Michael H. and Psaty, Bruce M. and Raffield, Laura M. and Raitakari, Olli T. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Rosenkranz, Alexander R. and Rossing, Peter and Rotter, Jerome and Sabanayagam, Charumathi and Schmidt, Helena and Schmidt, Reinhold and Schoettker, Ben and Schulz, Christina-Alexandra and Sedaghat, Sanaz and Shaffer, Christian M. and Strauch, Konstantin and Szymczak, Silke and Taylor, Kent D. and Tremblay, Johanne and Chaker, Layal and van der Harst, Pim and van der Most, Peter J. and Verweij, Niek and Voelker, Uwe and Waldenberger, Melanie and Wallentin, Lars and Waterworth, Dawn M. and White, Harvey D. and Wilson, James G. and Wong, Tien-Yin and Woodward, Mark and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Yan and Snieder, Harold and Wanner, Christoph and Boger, Carsten A. and Kottgen, Anna and Kronenberg, Florian and Pattaro, Cristian and Heid, Iris M.},
  title     = {Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline},
  series = {Kidney international : official journal of the International Society of Nephrology},
  volume    = {99},
  journal   = {Kidney international : official journal of the International Society of Nephrology},
  number    = {4},
  publisher = {Elsevier},
  address   = {New York},
  organization    = {Lifelines Cohort Study<br /> Regeneron Genetics Ctr},
  issn      = {0085-2538},
  doi       = {10.1016/j.kint.2020.09.030},
  pages     = {926 -- 939},
  year      = {2020},
  abstract  = {Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25\% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95\% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.},
  language  = {en}
}