@article{WuttkeLiLietal.2019, author = {Wuttke, Matthias and Li, Yong and Li, Man and Sieber, Karsten B. and Feitosa, Mary F. and Gorski, Mathias and Tin, Adrienne and Wang, Lihua and Chu, Audrey Y. and Hoppmann, Anselm and Kirsten, Holger and Giri, Ayush and Chai, Jin-Fang and Sveinbjornsson, Gardar and Tayo, Bamidele O. and Nutile, Teresa and Fuchsberger, Christian and Marten, Jonathan and Cocca, Massimiliano and Ghasemi, Sahar and Xu, Yizhe and Horn, Katrin and Noce, Damia and Van der Most, Peter J. and Sedaghat, Sanaz and Yu, Zhi and Akiyama, Masato and Afaq, Saima and Ahluwalia, Tarunveer Singh and Almgren, Peter and Amin, Najaf and Arnlov, Johan and Bakker, Stephan J. L. and Bansal, Nisha and Baptista, Daniela and Bergmann, Sven and Biggs, Mary L. and Biino, Ginevra and Boehnke, Michael and Boerwinkle, Eric and Boissel, Mathilde and B{\"o}ttinger, Erwin and Boutin, Thibaud S. and Brenner, Hermann and Brumat, Marco and Burkhardt, Ralph and Butterworth, Adam S. and Campana, Eric and Campbell, Archie and Campbell, Harry and Canouil, Mickael and Carroll, Robert J. and Catamo, Eulalia and Chambers, John C. and Chee, Miao-Ling and Chee, Miao-Li and Chen, Xu and Cheng, Ching-Yu and Cheng, Yurong and Christensen, Kaare and Cifkova, Renata and Ciullo, Marina and Concas, Maria Pina and Cook, James P. and Coresh, Josef and Corre, Tanguy and Sala, Cinzia Felicita and Cusi, Daniele and Danesh, John and Daw, E. Warwick and De Borst, Martin H. and De Grandi, Alessandro and De Mutsert, Renee and De Vries, Aiko P. J. and Degenhardt, Frauke and Delgado, Graciela and Demirkan, Ayse and Di Angelantonio, Emanuele and Dittrich, Katalin and Divers, Jasmin and Dorajoo, Rajkumar and Eckardt, Kai-Uwe and Ehret, Georg and Elliott, Paul and Endlich, Karlhans and Evans, Michele K. and Felix, Janine F. and Foo, Valencia Hui Xian and Franco, Oscar H. and Franke, Andre and Freedman, Barry I. and Freitag-Wolf, Sandra and Friedlander, Yechiel and Froguel, Philippe and Gansevoort, Ron T. and Gao, He and Gasparini, Paolo and Gaziano, J. Michael and Giedraitis, Vilmantas and Gieger, Christian and Girotto, Giorgia and Giulianini, Franco and Gogele, Martin and Gordon, Scott D. and Gudbjartsson, Daniel F. and Gudnason, Vilmundur and Haller, Toomas and Hamet, Pavel and Harris, Tamara B. and Hartman, Catharina A. and Hayward, Caroline and Hellwege, Jacklyn N. and Heng, Chew-Kiat and Hicks, Andrew A. and Hofer, Edith and Huang, Wei and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Indridason, Olafur S. and Ingelsson, Erik and Ising, Marcus and Jaddoe, Vincent W. V. and Jakobsdottir, Johanna and Jonas, Jost B. and Joshi, Peter K. and Josyula, Navya Shilpa and Jung, Bettina and Kahonen, Mika and Kamatani, Yoichiro and Kammerer, Candace M. and Kanai, Masahiro and Kastarinen, Mika and Kerr, Shona M. and Khor, Chiea-Chuen and Kiess, Wieland and Kleber, Marcus E. and Koenig, Wolfgang and Kooner, Jaspal S. and Korner, Antje and Kovacs, Peter and Kraja, Aldi T. and Krajcoviechova, Alena and Kramer, Holly and Kramer, Bernhard K. and Kronenberg, Florian and Kubo, Michiaki and Kuhnel, Brigitte and Kuokkanen, Mikko and Kuusisto, Johanna and La Bianca, Martina and Laakso, Markku and Lange, Leslie A. and Langefeld, Carl D. and Lee, Jeannette Jen-Mai and Lehne, Benjamin and Lehtimaki, Terho and Lieb, Wolfgang and Lim, Su-Chi and Lind, Lars and Lindgren, Cecilia M. and Liu, Jun and Liu, Jianjun and Loeffler, Markus and Loos, Ruth J. F. and Lucae, Susanne and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Magi, Reedik and Magnusson, Patrik K. E. and Mahajan, Anubha and Martin, Nicholas G. and Martins, Jade and Marz, Winfried and Mascalzoni, Deborah and Matsuda, Koichi and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Metspalu, Andres and Mikaelsdottir, Evgenia K. and Milaneschi, Yuri and Miliku, Kozeta and Mishra, Pashupati P. and Program, V. A. Million Veteran and Mohlke, Karen L. and Mononen, Nina and Montgomery, Grant W. and Mook-Kanamori, Dennis O. and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nalls, Mike A. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and Noordam, Raymond and Olafsson, Isleifur and Oldehinkel, Albertine J. and Orho-Melander, Marju and Ouwehand, Willem H. and Padmanabhan, Sandosh and Palmer, Nicholette D. and Palsson, Runolfur and Penninx, Brenda W. J. H. and Perls, Thomas and Perola, Markus and Pirastu, Mario and Pirastu, Nicola and Pistis, Giorgio and Podgornaia, Anna I. and Polasek, Ozren and Ponte, Belen and Porteous, David J. and Poulain, Tanja and Pramstaller, Peter P. and Preuss, Michael H. and Prins, Bram P. and Province, Michael A. and Rabelink, Ton J. and Raffield, Laura M. and Raitakari, Olli T. and Reilly, Dermot F. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Ridker, Paul M. and Rivadeneira, Fernando and Rizzi, Federica and Roberts, David J. and Robino, Antonietta and Rossing, Peter and Rudan, Igor and Rueedi, Rico and Ruggiero, Daniela and Ryan, Kathleen A. and Saba, Yasaman and Sabanayagam, Charumathi and Salomaa, Veikko and Salvi, Erika and Saum, Kai-Uwe and Schmidt, Helena and Schmidt, Reinhold and Ben Schottker, and Schulz, Christina-Alexandra and Schupf, Nicole and Shaffer, Christian M. and Shi, Yuan and Smith, Albert V. and Smith, Blair H. and Soranzo, Nicole and Spracklen, Cassandra N. and Strauch, Konstantin and Stringham, Heather M. and Stumvoll, Michael and Svensson, Per O. and Szymczak, Silke and Tai, E-Shyong and Tajuddin, Salman M. and Tan, Nicholas Y. Q. and Taylor, Kent D. and Teren, Andrej and Tham, Yih-Chung and Thiery, Joachim and Thio, Chris H. L. and Thomsen, Hauke and Thorleifsson, Gudmar and Toniolo, Daniela and Tonjes, Anke and Tremblay, Johanne and Tzoulaki, Ioanna and Uitterlinden, Andre G. and Vaccargiu, Simona and Van Dam, Rob M. and Van der Harst, Pim and Van Duijn, Cornelia M. and Edward, Digna R. Velez and Verweij, Niek and Vogelezang, Suzanne and Volker, Uwe and Vollenweider, Peter and Waeber, Gerard and Waldenberger, Melanie and Wallentin, Lars and Wang, Ya Xing and Wang, Chaolong and Waterworth, Dawn M. and Bin Wei, Wen and White, Harvey and Whitfield, John B. and Wild, Sarah H. and Wilson, James F. and Wojczynski, Mary K. and Wong, Charlene and Wong, Tien-Yin and Xu, Liang and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Weihua and Zonderman, Alan B. and Rotter, Jerome I. and Bochud, Murielle and Psaty, Bruce M. and Vitart, Veronique and Wilson, James G. and Dehghan, Abbas and Parsa, Afshin and Chasman, Daniel I. and Ho, Kevin and Morris, Andrew P. and Devuyst, Olivier and Akilesh, Shreeram and Pendergrass, Sarah A. and Sim, Xueling and Boger, Carsten A. and Okada, Yukinori and Edwards, Todd L. and Snieder, Harold and Stefansson, Kari and Hung, Adriana M. and Heid, Iris M. and Scholz, Markus and Teumer, Alexander and Kottgen, Anna and Pattaro, Cristian}, title = {A catalog of genetic loci associated with kidney function from analyses of a million individuals}, series = {Nature genetics}, volume = {51}, journal = {Nature genetics}, number = {6}, publisher = {Nature Publ. Group}, address = {New York}, organization = {Lifelines COHort Study}, issn = {1061-4036}, doi = {10.1038/s41588-019-0407-x}, pages = {957 -- +}, year = {2019}, abstract = {Chronic kidney disease (CKD) is responsible for a public health burden with multi-systemic complications. Through transancestry meta-analysis of genome-wide association studies of estimated glomerular filtration rate (eGFR) and independent replication (n = 1,046,070), we identified 264 associated loci (166 new). Of these,147 were likely to be relevant for kidney function on the basis of associations with the alternative kidney function marker blood urea nitrogen (n = 416,178). Pathway and enrichment analyses, including mouse models with renal phenotypes, support the kidney as the main target organ. A genetic risk score for lower eGFR was associated with clinically diagnosed CKD in 452,264 independent individuals. Colocalization analyses of associations with eGFR among 783,978 European-ancestry individuals and gene expression across 46 human tissues, including tubulo-interstitial and glomerular kidney compartments, identified 17 genes differentially expressed in kidney. Fine-mapping highlighted missense driver variants in 11 genes and kidney-specific regulatory variants. These results provide a comprehensive priority list of molecular targets for translational research.}, 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
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} } @article{KearneyShemlavanKnippenbergetal.2019, author = {Kearney, Eric and Shemla, Meir and van Knippenberg, Daan and Scholz, Florian A.}, title = {A paradox perspective on the interactive effects of visionary and empowering leadership}, series = {Organizational Behavior and Human Decision Processes}, volume = {155}, journal = {Organizational Behavior and Human Decision Processes}, publisher = {Elsevier}, address = {San Diego}, issn = {0749-5978}, doi = {10.1016/j.obhdp.2019.01.001}, pages = {20 -- 30}, year = {2019}, abstract = {In a multi-source, lagged design field study of 197 leader-follower dyads, we test a model that predicts positive interactive effects of visionary and empowering leadership on follower performance. Based on the paradox perspective, we argue that visionary and empowering leadership are synergistic in that their combination enables leaders to address a key paradox inherent to leader behavior identified by Waldman and Bowen (2016): Maintaining control while simultaneously letting go of control. We argue that visionary leadership addresses the former and empowering leadership addresses the latter pole of this pair of opposites. Hence, in line with paradox thinking, we posit that leaders will engender more positive effects on follower performance when they enact visionary and empowering leadership behaviors simultaneously and adopt a "both-and" approach, rather than focus on one of these behaviors without the other. Our results support our hypothesized interactive effect of visionary and empowering leadership on goal clarity, as well as a conditional indirect effect such that goal clarity mediates the interactive effect of visionary and empowering leadership on individual follower performance.}, language = {en} } @article{GuentherSchueleZurelletal.2023, author = {G{\"u}nther, Oliver and Sch{\"u}le, Manja and Zurell, Damaris and Jeltsch, Florian and Roeleke, Manuel and Kampe, Heike and Zimmermann, Matthias and Scholz, Jana and Engbert, Ralf and Elsner, Birgit and Schlangen, David and Agrofylax, Luisa and Georgi, Doreen and Weymar, Mathias and Wagener, Thorsten and Bookhagen, Bodo and Eibl, Eva P. S. and Korup, Oliver and Oswald, Sascha and Thieken, Annegret and van der Beek, Pieter A.}, title = {Portal Wissen = Exzellenz}, series = {Portal Wissen: Das Forschungsmagazin der Universit{\"a}t Potsdam}, journal = {Portal Wissen: Das Forschungsmagazin der Universit{\"a}t Potsdam}, number = {02/2023}, issn = {2194-4245}, doi = {10.25932/publishup-61144}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-611440}, pages = {98}, year = {2023}, abstract = {Was nicht nur gut oder sehr gut ist, nennen wir gern exzellent. Aber was meint das eigentlich? Vom lateinischen „excellere" kommend, beschreibt es Dinge, Personen oder Handlungen, die „hervor-" oder „herausragen" aus der Menge, sich „auszeichnen" gegen{\"u}ber anderen. Mehr geht nicht. Exzellenz ist das Mittel der Wahl, wenn es darum geht, der Erste oder Beste zu sein. Und das macht auch vor der Forschung nicht halt. Wer auf die Universit{\"a}t Potsdam schaut, findet zahlreiche ausgezeichnete Forschende, hervorragende Projekte und immer wieder auch aufsehenerregende Erkenntnisse, Ver{\"o}ffentlichungen und Ergebnisse. Aber ist die UP auch exzellent? Eine Frage, die 2023 ganz sicher andere Wellen schl{\"a}gt als vielleicht vor 20 Jahren. Denn seit dem Start der Exzellenzinitiative 2005 gelten als - w{\"o}rtlich - exzellent jene Hochschulen, denen es gelingt, in dem umfangreichsten F{\"o}rderprogramm f{\"u}r Wissenschaft in Deutschland einen Zuschlag zu erhalten. Egal ob in Form von Graduiertenschulen, Forschungsclustern oder - seit Fortsetzung des Programms ab 2019 unter dem Titel „Exzellenzstrategie" - ganzen Exzellenzuniversit{\"a}ten: Wer im Kreis der Forschungsuniversit{\"a}ten zu den Besten geh{\"o}ren will, braucht das Siegel der Exzellenz. In der gerade eingel{\"a}uteten neuen Wettbewerbsrunde der „Exzellenzstrategie des Bundes und der L{\"a}nder" bewirbt sich die Universit{\"a}t Potsdam mit drei Clusterskizzen um F{\"o}rderung. Ein Antrag kommt aus der {\"O}kologie- und Biodiversit{\"a}tsforschung. Ziel ist es, ein komplexes Bild {\"o}kologischer Prozesse zu zeichnen - und dabei die Rolle von einzelnen Individuen ebenso zu betrachten wie das Zusammenwirken vieler Arten in einem {\"O}kosystem, um die Funktion der Artenvielfalt genauer zu bestimmen. Eine zweite Skizze haben die Kognitionswissenschaften eingereicht. Hier soll das komplexe Nebeneinander von Sprache und Kognition, Entwicklung und Lernen sowie Motivation und Verhalten als dynamisches Miteinander erforscht werden - wobei auch mit den Erziehungswissenschaften kooperiert wird, um verkn{\"u}pfte Lernund Bildungsprozesse stets mitzudenken. Der dritte Antrag aus den Geo- und Umweltwissenschaften nimmt extreme und besonders folgenschwere Naturgefahren und -prozesse wie {\"U}berschwemmungen und D{\"u}rren in den Blick. Die Forschenden untersuchen die Extremereignisse mit besonderem Fokus auf deren Wechselwirkung mit der Gesellschaft, um mit ihnen einhergehende Risiken und Sch{\"a}den besser einsch{\"a}tzen sowie k{\"u}nftig rechtzeitig Maßnahmen einleiten zu k{\"o}nnen. „Alle drei Antr{\"a}ge zeichnen ein hervorragendes Bild unserer Leistungsf{\"a}higkeit", betont der Pr{\"a}sident der Universit{\"a}t, Prof. Oliver G{\"u}nther, Ph.D. „Die Skizzen dokumentieren eindrucksvoll unser Engagement, vorhandene Forschungsexzellenz sowie die Potenziale der Universit{\"a}t Potsdam insgesamt. Allein die Tatsache, dass sich drei schlagkr{\"a}ftige Konsortien in ganz unterschiedlichen Themenbereichen zusammengefunden haben, zeigt, dass wir auf unserem Weg in die Spitzengruppe der deutschen Universit{\"a}ten einen guten Schritt vorangekommen sind." In diesem Heft schauen wir, was sich in und hinter diesen Antr{\"a}gen verbirgt: Wir haben mit den Wissenschaftlerinnen und Wissenschaftlern gesprochen, die sie geschrieben haben, und sie gefragt, was sie sich vornehmen, sollten sie den Zuschlag erhalten und ein Cluster an die Universit{\"a}t holen. Wir haben aber auch auf die Forschung geschaut, die zu den Antr{\"a}gen gef{\"u}hrt hat und die schon l{\"a}nger das Profil der Universit{\"a}t pr{\"a}gt und ihr national wie international Anerkennung eingebracht hat. Wir stellen eine kleine Auswahl an Projekten, Methoden und Forschenden vor, um zu zeigen, warum in diesen Antr{\"a}gen tats{\"a}chlich exzellente Forschung steckt! {\"U}brigens: Auch „Exzellenz" ist nicht das Ende der Fahnenstange. Immerhin l{\"a}sst sich das Adjektiv exzellent sogar steigern. In diesem Sinne w{\"u}nschen wir exzellentestes Vergn{\"u}gen beim Lesen!}, language = {de} } @article{GuentherSchueleZurelletal.2023, author = {G{\"u}nther, Oliver and Sch{\"u}le, Manja and Zurell, Damaris and Jeltsch, Florian and Roeleke, Manuel and Kampe, Heike and Zimmermann, Matthias and Scholz, Jana and Mikulla, Stefanie and Engbert, Ralf and Elsner, Birgit and Schlangen, David and Agrofylax, Luisa and Georgi, Doreen and Weymar, Mathias and Wagener, Thorsten and Bookhagen, Bodo and Eibl, Eva P. S. and Korup, Oliver and Oswald, Sascha and Thieken, Annegret and van der Beek, Pieter A.}, title = {Portal Wissen = Excellence}, series = {Portal Wissen: The research magazine of the University of Potsdam}, journal = {Portal Wissen: The research magazine of the University of Potsdam}, number = {02/2023}, issn = {2198-9974}, doi = {10.25932/publishup-61145}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-611456}, pages = {58}, year = {2023}, abstract = {When something is not just good or very good, we often call it excellent. But what does that really mean? Coming from the Latin word "excellere," it describes things, persons, or actions that are outstanding or superior and distinguish themselves from others. It cannot get any better. Excellence is the top choice for being the first or the best. Research is no exception. At the university, you will find numerous exceptional researchers, outstanding projects, and, time and again, sensational findings, publications, and results. But is the University of Potsdam also excellent? A question that will certainly create a different stir in 2023 than it did perhaps 20 years ago. Since the launch of the Excellence Initiative in 2005, universities that succeed in winning the most comprehensive funding program for research in Germany have been considered - literally - excellent. Whether in the form of graduate schools, research clusters, or - since the program was continued in 2019 under the title "Excellence Strategy" - entire universities of excellence: Anyone who wants to be among the best research universities needs the seal of excellence. The University of Potsdam is applying for funding with three cluster proposals in the recently launched new round of the "Excellence Strategy of the German Federal and State Governments." One proposal comes from ecology and biodiversity research. The aim is to paint a comprehensive picture of ecological processes by examining the role of single individuals as well as the interactions among many species in an ecosystem to precisely determine the function of biodiversity. A second proposal has been submitted by the cognitive sciences. Here, the complex coexistence of language and cognition, development and learning, as well as motivation and behavior will be researched as a dynamic interrelation. The projects will include cooperation with the educational sciences to constantly consider linked learning and educational processes. The third proposal from the geo and environmental sciences concentrates on extreme and particularly devastating natural hazards and processes such as floods and droughts. The researchers examine these extreme events, focusing on their interaction with society, to be able to better assess the risks and damages they might involve and to initiate timely measures in the future. "All three proposals highlight the excellence of our performance," emphasizes University President Prof. Oliver G{\"u}nther, Ph.D. "The outlines impressively document our commitment, existing research excellence, and the potential of the University of Potsdam as a whole. The fact that three powerful consortia have come together in different subject areas shows that we have taken a good step forward on our way to becoming one of the top German universities." In this issue, we are looking at what is in and behind these proposals: We talked to the researchers who wrote them. We asked them about their plans in case their proposals are successful and they bring a cluster of excellence to the university. But we also looked at the research that has led to the proposals, has long shaped the university's profile, and earned it national and international recognition. We present a small selection of projects, methods, and researchers to illustrate why there really is excellent research in these proposals! By the way, "excellence" is also not the end of the flagpole. After all, the adjective "excellent" even has a comparative and a superlative. With this in mind, I wish you the most excellent pleasure reading this issue!}, language = {en} }