@misc{Winkler1995,
  author    = {Winkler, Rainer},
  title     = {Deutschlands geopolitische Lage im sich wandelnden Europa},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-11067},
  year      = {1995},
  abstract  = {Based on the discussion on Germany´s new 'central location', the author tries to sketch Germany´s geopolitical position in view of the constellation of powers in Europe from a national point of view. This favourable position offers a great chance for the country to play an active role in Europe's integration. However, German historical heritage as well as the delicate relationship of Germany´s political elite to the use of power are reasons for the country´s hesitation to fulfill her neighbours' and her allies' expectations. Anyhow, Summaries 192 rooted in the West-European and transatlantic integration is Germany the natural dooropener for its Eastern, South-Eastern and Baltic neighbours to become 'members of the club'. )</a> Jahresabo: 40,00 € (erm{\"a}ßigt: 25,00 €)},
  language  = {de}
}
@misc{vFrankenbergSeidlSchultheissetal.2012,
  author    = {v. Frankenberg, Jenny and Seidl, Rainer Ottis and Schultheiss, Corinna and Frank, Ulrike and Fuß, Sophia and Stefke, Michaela and Honekamp, Andrea and Winkler, Silke and J{\"a}ckel, Annemarie and Schindler, Wencke and Wenglarczyk, Anke and Weise, Stefanie and Heide, Judith and Stadie, Nicole and Schr{\"o}der, Astrid and Baer-Henney, Dinah and van de Vijver, Ruben and Sauerland, Uli and Yatsushiro, Kazuko and Sch{\"o}ppe, Doreen and Blatter, Kristine and Faust, Verena and J{\"a}ger, Dana and Artelt, Cordula and Schneider, Wolfgang and Stanat, Petra and Bruchm{\"u}ller, Wiebke and Sj{\"o}str{\"o}m, Saana and Sch{\"u}tz, Susann and Swietza, Romy and Zielina, Marie and Freymann, Marie and Hausmann, Nadin and K{\"o}ntopp, Isabelle and Liebig, Johanna and Schnell, Annemarie and Wegener, Viktoria and Heinemann, Steffi and Haensel, Diana and M{\"u}rbe, Dirk and Pomnitz, Patricia and Siegm{\"u}ller, Julia},
  title     = {Spektrum Patholinguistik = Schwerpunktthema: Schluck f{\"u}r Schluck: Dysphagietherapie bei Kindern und Erwachsenen},
  number    = {5},
  editor    = {Heide, Judith and Fritzsche, Tom and Meyer, Corinna B. and Ott, Susan},
  publisher = {Universit{\"a}tsverlag Potsdam},
  address   = {Potsdam},
  organization    = {Verband f{\"u}r Patholinguistik e.V.},
  isbn      = {978-3-86956-199-8},
  issn      = {1866-9433},
  doi       = {10.25932/publishup-5866},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-59877},
  year      = {2012},
  abstract  = {Das Herbsttreffen Patholinguistik wird seit 2007 j{\"a}hrlich vom Verband f{\"u}r Patholinguistik e.V. (vpl) durchgef{\"u}hrt. Die Jubil{\"a}umsveranstaltung am 19.11.2011 in Potsdam war nicht nur die 5. Auflage der Veranstaltung, sondern auch ein Fest zum 10j{\"a}hrigen Bestehen des Verbandes. Das Thema lautete "Schluck f{\"u}r Schluck: Dysphagietherapie bei Kindern und Erwachsenen". Im vorliegenden Tagungsband finden sich die Artikel der Hauptvortr{\"a}ge sowie die Abstracts der Posterpr{\"a}sentationen.},
  language  = {de}
}
@misc{AichertStaigerSchulteMaeteretal.2010,
  author    = {Aichert, Ingrid and Staiger, Anja and Schulte-M{\"a}ter, Anne and Becker-Redding, Ulrike and Stahn, Corinna and Peschke, Claudia and Heide, Judith and Ott, Susan and Herrmann, Heike and V{\"o}lsch, Juliane and Mayer, J{\"o}rg and Rohnke, Lucie and Frank, Ulrike and Stadie, Nicole and Jentsch, Nadine and Blech, Anke and Kurtenbach, Stephanie and Thieke, Johanna and Schr{\"o}der, Astrid and Stahn, Corinna and H{\"o}rnig, Robin and Burchert, Frank and De Bleser, Ria and Heister, Julian and Bartels, Luise and W{\"u}rzner, Kay-Michael and B{\"o}hme, Romy and Burmester, Juliane and Krajewski, Melanie and Nager, Wido and Jungeh{\"u}lsing, Gerhard Jan and Wartenburger, Isabell and J{\"o}bges, Michael and Schwilling, Eleonore and Lidzba, Karen and Winkler, Susanne and Konietzko, Andreas and Kr{\"a}geloh-Mann, Ingeborg and Rilling, Eva and Wilken, Rainer and Wismann, Kathrin and Glandorf, Birte and Hoffmann, Hannah and Hinnenkamp, Christiane and Rohlmann, Insa and Ludewigt, Jacqueline and Bittner, Christian and Orlov, Tatjana and Claus, Katrin and Ehemann, Christine and Winnecken, Andreas and Hummel, Katja and Breitenstein, Sarah},
  title     = {Spektrum Patholinguistik = Schwerpunktthema: Von der Programmierung zur Artikulation : Sprechapraxie bei Kindern und Erwachsenen},
  number    = {3},
  editor    = {Wahl, Michael and Stahn, Corinna and Hanne, Sandra and Fritzsche, Tom},
  publisher = {Universit{\"a}tsverlag Potsdam},
  address   = {Potsdam},
  organization    = {Verband f{\"u}r Patholinguistik e. V. (vpl)},
  isbn      = {978-3-86956-079-3},
  issn      = {1869-3822},
  doi       = {10.25932/publishup-4578},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-45470},
  year      = {2010},
  abstract  = {Das 3. Herbsttreffen Patholinguistik fand am 21. November 2009 an der Universit{\"a}t Potsdam statt. Der vorliegende Tagungsband enth{\"a}lt die drei Hauptvortr{\"a}ge zum Schwerpunktthema „Von der Programmierung zu Artikulation: Sprechapraxie bei Kindern und Erwachsenen". Dar{\"u}ber hinaus enth{\"a}lt der Band die Beitr{\"a}ge aus dem Spektrum Patholinguistik, sowie die Abstracts der Posterpr{\"a}sentationen.},
  language  = {de}
}
@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}
}