@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<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}
}
@article{RancanWieheNoebeletal.2005,
  author    = {Rancan, Fiorenza and Wiehe, Arno and N{\"o}bel, Maria and Senge, Mathias O and Al Omari, Saleh and B{\"o}hm, Fritz and John, Matthias and R{\"o}der, Beate},
  title     = {Influence of substitutions on asymmetric dihydroxychlorins with regard to intracellular uptake, subcellular localization and photosensitization of Jurkat cells},
  issn      = {1011-1344},
  year      = {2005},
  abstract  = {The search for new efficient sensitizers for photodynamic therapy (PDT) points to improve photophysical properties like absorption in the red region and singlet oxygen quantum yield as well as to control the localization of the sensitizer within the tumour cell. Depending on their physicochemical properties and their uptake mechanism, sensitizers can reach different intracellular concentrations and localize in different subcellular compartments. Moreover, the preferential localization of a sensitizer in target organelles, like mitochondria or lysosomes, could determine the cell death mechanism after PDT. This study aimed to investigate the influence of substitutions on dihydroxychlorins with regard to intracellular uptake, subcellular localization and cell death pathway. Moreover, the effect of a liposome-based delivery system was tested. The intracellular uptake was found to be strictly dependent on the sensitizer molecular structure and the means of its delivery. The most polar sensitizer in this study (compound 3) had, depending on incubation time, an intracellular concentration 2-8 times higher than the unsubstituted chlorin 1. All investigated photosensitizers localize predominantly in lysosomes but after longer incubation times weak fluorescence intensity was also detected in mitochondria and Golgi apparatus. The cell death pathway was found to be influenced by the sensitizer intracellular concentration and the applied light doses. In general, the increasing amphiphilicity of the sensitizer molecules is correlated with an increased sensitizer uptake and an increased rate of necrotic cells after irradiation. (C) 2004 Elsevier B.V. All rights reserved},
  language  = {en}
}
@article{WanjohiYenesewMidiwoetal.2005,
  author    = {Wanjohi, John M. and Yenesew, Abiy and Midiwo, Jacob O. and Heydenreich, Matthias and Peter, Martin G. and Dreyer, M. and Reichert, M. and Bringmann, Gerhard},
  title     = {Three dimeric anthracene derivatives from the fruits of Bulbine abyssinica},
  issn      = {0040-4020},
  year      = {2005},
  abstract  = {From the fruits of Bulbine abyssinica three new dimeric anthracene derivatives, (P)-8,9,1',8'- tetrahydroxy-3,3'-dimethyl[10,7'-bianthracene]-1,4,9',10'- tetraone (trivial name abyquinone A), (10R)-1,4,8,1',8-pentahydroxy-3,3'-dimethyl-[10,7'-bianthracene]9,9',10' (10H)-trione (trivial name abyquinone B), and (10R)-3,4'-dihydro-1,4,8,3',8',9'-hexahydroxy-3,3'- dimethyl-[10,7'-biant hracene]9,1'(10H,2'H)-dione (trivial name abyquinone Q were isolated. Despite their structural differences, these three compounds are connected to each other by the apparently biomimetic conversion of abyquinone C (a preanthraquinonylanthrone with two stereogenic centers) into B (an anthraquinonylanthrone with one stereogenic center) and finally into A (an axially chiral bianthraquinone) under mild conditions, involving a highly efficient center-to-axis chirality transfer. In addition, the known anthraquinones islandicin and chrysophanol were identified. The structures were determined on the basis of spectroscopical evidences, chemical transformations, and quantum chemical CD calculations. (C) 2005 Elsevier Ltd. All rights reserved},
  language  = {en}
}
@article{YenesewKiplagatDereseetal.2006,
  author    = {Yenesew, Abiy and Kiplagat, John T. and Derese, Solomon and Midiwo, Jacob O. and Kabaru, Jacques M. and Heydenreich, Matthias and Peter, Martin G.},
  title     = {Two unusual rotenoid derivatives, 7a-O-methyl-12a-hydroxydeguelol and spiro-13-homo-13-oxaelliptone, from the seeds of Derris trifoliata},
  doi       = {10.1016/j.phytochem.2006.01.002},
  year      = {2006},
  abstract  = {The crude methanol extract of the seeds of Derris trifoliata showed potent and dose dependent larvicidal activity against the 2nd instar larvae of Aedes aegypti. From this extract two unusual rotenoid derivatives, a rotenoloid (named 7a-O-methyl-12a-hydroxydeguelol) and a spirohomooxarotenoid (named spiro-13-homo-13-oxaelliptone), were isolated and characterised. In addition a rare natural chromanone (6,7-dimethoxy-4-chromanone) and the known rotenoids rotenone, tephrosin and dehydrodeguelin were identified. The structures were assigned on the basis of spectroscopic evidence. The larvicidal activity of the crude extract is mainly due to rotenone. (c) 2006 Elsevier Ltd. All rights reserved},
  language  = {en}
}
@article{InduliChelotiWasunaetal.2012,
  author    = {Induli, Martha and Cheloti, Michael and Wasuna, Antonina and Wekesa, Ingrid and Wanjohi, John M. and Byamukama, Robert and Heydenrich, Matthias and Makayoto, Moses and Yenesew, Abiy},
  title     = {Naphthoquinones from the roots of Aloe secundiflora},
  series = {Phytochemistry letters},
  volume    = {5},
  journal   = {Phytochemistry letters},
  number    = {3},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {1874-3900},
  doi       = {10.1016/j.phytol.2012.04.014},
  pages     = {506 -- 509},
  year      = {2012},
  abstract  = {Two new naphthoquinones, 5-hydroxy-3,6-dimethoxy-2-methylnaphthalene-1,4-dione and 5,8-dihydroxy-3-methoxy-2-methylnaphthalene-1,4-dione, were isolated from the roots of Aloe secundiflora together with the known compounds chrysophanol, helminthosporin, isoxanthorin, ancistroquinone C, aloesaponarins I and II, aloesaponols I and II, laccaic acid D methyl ester and asphodelin. The structures were elucidated based on spectroscopic evidence. This appears to be the first report on the occurrence of naphthoquinones in the genus Aloe. Aloesaponarin I and 5-hydroxy-3,6-dimethoxy-2-methylnaphthalene-1,4-dione showed anti-bacterial activity against Mycobacterium tuberculosis with MIC values of 21-23 mu g/mL in the Microplate Alamar Blue Assay (MABA) and Low Oxygen Recovery Assay (LORA); 5-hydroxy-3,6-dimethoxy-2-methylnaphthalene-1,4-dione also showed cytotoxicity against the Vero cell line (IC50 = 10.2 mu g/mL).},
  language  = {en}
}
@article{MarcoDeyouGruhonjicetal.2017,
  author    = {Marco, Makungu and Deyou, Tsegaye and Gruhonjic, Amra and Holleran, John and Duffy, Sandra and Heydenreich, Matthias and Firtzpatrick, Paul A. and Landberg, Goran and Koch, Andreas and Derese, Solomon and Pelletier, Jerry and Avery, Vicky M. and Erdelyi, Mate and Yenesew, Abiy},
  title     = {Pterocarpans and isoflavones from the root bark of Millettia micans and of Millettia dura},
  series = {Phytochemistry letters},
  volume    = {21},
  journal   = {Phytochemistry letters},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {1874-3900},
  doi       = {10.1016/j.phytol.2017.07.012},
  pages     = {216 -- 220},
  year      = {2017},
  language  = {en}
}
@misc{BringmannMutanyattaComarMaksimenkaetal.2008,
  author    = {Bringmann, Gerhard and Mutanyatta-Comar, Joan and Maksimenka, Katja and Wanjohi, John M. and Heydenreich, Matthias and Brun, Reto and M{\"u}ller, Werner E. G. and Peter, Martin and Midiwo, Jacob O. and Yenesew, Abiy},
  title     = {Joziknipholones A and B : the First Dimeric Phenylanthraquinones, from the Roots of Bulbine frutescens},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-42638},
  year      = {2008},
  abstract  = {From the roots of the African plant Bulbine frutescens (Asphodelaceae), two unprecedented novel dimeric phenylanthraquinones, named joziknipholones A and B, possessing axial and centrochirality, were isolated, together with six known compounds. Structural elucidation of the new metabolites was achieved by spectroscopic and chiroptical methods, by reductive cleavage of the central bond between the monomeric phenylanthraquinone and -anthrone portions with sodium dithionite, and by quantum chemical CD calculations. Based on the recently revised absolute axial configuration of the parent phenylanthraquinones, knipholone and knipholone anthrone, the new dimers were attributed to possess the P-configuration (i.e., with the acetyl portions below the anthraquinone plane) at both axes in the case of joziknipholone A, whereas in joziknipholone B, the knipholone part was found to be M-configured. Joziknipholones A and B are active against the chloroquine resistant strain K1 of the malaria pathogen, Plasmodium falciparum, and show moderate activity against murine leukemic lymphoma L5178y cells.},
  language  = {en}
}
@article{BringmannMutanyattaComarMaksimenkaetal.2008,
  author    = {Bringmann, Gerhard and Mutanyatta-Comar, Joan and Maksimenka, Katja and Wanjohi, John M. and Heydenreich, Matthias and Brun, Reto and M{\"u}ller, Werner E. G. and Peter, Martin G. and Midiwo, Jacob O. and Yenesew, Abiy},
  title     = {Joziknipholones A and B : the first dimeric phenylanthraquinones, from the roots of Bulbine frutescens},
  issn      = {0947-6539},
  year      = {2008},
  abstract  = {From the roots of the African plant Bulbine frutescens (Asphodelaceae), two unprecedented novel dimeric phenylanthraquinones, named joziknipholones A and B, possessing axial and centrochirality, were isolated, together with six known compounds. Structural elucidation of the new metabolites was achieved by spectroscopic and chiroptical methods, by reductive cleavage of the central bond between the monomeric phenylanthraquinone and -anthrone portions with sodium dithionite, and by quantum chemical CD calculations. Based on the recently revised absolute axial configuration of the parent phenylanthraquinones, knipholone and knipholone anthrone, the new dimers were attributed to possess the P- configuration (i.e., with the acetyl portions below the anthraquinone plane) at both axes in the case of joziknipholone A, whereas in joziknipholone B, the knipholone part was found to be M-configured. Joziknipholones A and B are active against the chloroquine resistant strain K1 of the malaria pathogen, Plasmodium falciparum, and show moderate activity against murine leukemic lymphoma L5178y cells.},
  language  = {en}
}
@article{AartsAndersonAndersonetal.2015,
  author    = {Aarts, Alexander A. and Anderson, Joanna E. and Anderson, Christopher J. and Attridge, Peter R. and Attwood, Angela and Axt, Jordan and Babel, Molly and Bahnik, Stepan and Baranski, Erica and Barnett-Cowan, Michael and Bartmess, Elizabeth and Beer, Jennifer and Bell, Raoul and Bentley, Heather and Beyan, Leah and Binion, Grace and Borsboom, Denny and Bosch, Annick and Bosco, Frank A. and Bowman, Sara D. and Brandt, Mark J. and Braswell, Erin and Brohmer, Hilmar and Brown, Benjamin T. and Brown, Kristina and Bruening, Jovita and Calhoun-Sauls, Ann and Callahan, Shannon P. and Chagnon, Elizabeth and Chandler, Jesse and Chartier, Christopher R. and Cheung, Felix and Christopherson, Cody D. and Cillessen, Linda and Clay, Russ and Cleary, Hayley and Cloud, Mark D. and Cohn, Michael and Cohoon, Johanna and Columbus, Simon and Cordes, Andreas and Costantini, Giulio and Alvarez, Leslie D. Cramblet and Cremata, Ed and Crusius, Jan and DeCoster, Jamie and DeGaetano, Michelle A. and Della Penna, Nicolas and den Bezemer, Bobby and Deserno, Marie K. and Devitt, Olivia and Dewitte, Laura and Dobolyi, David G. and Dodson, Geneva T. and Donnellan, M. Brent and Donohue, Ryan and Dore, Rebecca A. and Dorrough, Angela and Dreber, Anna and Dugas, Michelle and Dunn, Elizabeth W. and Easey, Kayleigh and Eboigbe, Sylvia and Eggleston, Casey and Embley, Jo and Epskamp, Sacha and Errington, Timothy M. and Estel, Vivien and Farach, Frank J. and Feather, Jenelle and Fedor, Anna and Fernandez-Castilla, Belen and Fiedler, Susann and Field, James G. and Fitneva, Stanka A. and Flagan, Taru and Forest, Amanda L. and Forsell, Eskil and Foster, Joshua D. and Frank, Michael C. and Frazier, Rebecca S. and Fuchs, Heather and Gable, Philip and Galak, Jeff and Galliani, Elisa Maria and Gampa, Anup and Garcia, Sara and Gazarian, Douglas and Gilbert, Elizabeth and Giner-Sorolla, Roger and Gl{\"o}ckner, Andreas and G{\"o}llner, Lars and Goh, Jin X. and Goldberg, Rebecca and Goodbourn, Patrick T. and Gordon-McKeon, Shauna and Gorges, Bryan and Gorges, Jessie and Goss, Justin and Graham, Jesse and Grange, James A. and Gray, Jeremy and Hartgerink, Chris and Hartshorne, Joshua and Hasselman, Fred and Hayes, Timothy and Heikensten, Emma and Henninger, Felix and Hodsoll, John and Holubar, Taylor and Hoogendoorn, Gea and Humphries, Denise J. and Hung, Cathy O. -Y. and Immelman, Nathali and Irsik, Vanessa C. and Jahn, Georg and Jaekel, Frank and Jekel, Marc and Johannesson, Magnus and Johnson, Larissa G. and Johnson, David J. and Johnson, Kate M. and Johnston, William J. and Jonas, Kai and Joy-Gaba, Jennifer A. and Kappes, Heather Barry and Kelso, Kim and Kidwell, Mallory C. and Kim, Seung Kyung and Kirkhart, Matthew and Kleinberg, Bennett and Knezevic, Goran and Kolorz, Franziska Maria and Kossakowski, Jolanda J. and Krause, Robert Wilhelm and Krijnen, Job and Kuhlmann, Tim and Kunkels, Yoram K. and Kyc, Megan M. and Lai, Calvin K. and Laique, Aamir and Lakens, Daniel and Lane, Kristin A. and Lassetter, Bethany and Lazarevic, Ljiljana B. and LeBel, Etienne P. and Lee, Key Jung and Lee, Minha and Lemm, Kristi and Levitan, Carmel A. and Lewis, Melissa and Lin, Lin and Lin, Stephanie and Lippold, Matthias and Loureiro, Darren and Luteijn, Ilse and Mackinnon, Sean and Mainard, Heather N. and Marigold, Denise C. and Martin, Daniel P. and Martinez, Tylar and Masicampo, E. J. and Matacotta, Josh and Mathur, Maya and May, Michael and Mechin, Nicole and Mehta, Pranjal and Meixner, Johannes and Melinger, Alissa and Miller, Jeremy K. and Miller, Mallorie and Moore, Katherine and M{\"o}schl, Marcus and Motyl, Matt and M{\"u}ller, Stephanie M. and Munafo, Marcus and Neijenhuijs, Koen I. and Nervi, Taylor and Nicolas, Gandalf and Nilsonne, Gustav and Nosek, Brian A. and Nuijten, Michele B. and Olsson, Catherine and Osborne, Colleen and Ostkamp, Lutz and Pavel, Misha and Penton-Voak, Ian S. and Perna, Olivia and Pernet, Cyril and Perugini, Marco and Pipitone, R. Nathan and Pitts, Michael and Plessow, Franziska and Prenoveau, Jason M. and Rahal, Rima-Maria and Ratliff, Kate A. and Reinhard, David and Renkewitz, Frank and Ricker, Ashley A. and Rigney, Anastasia and Rivers, Andrew M. and Roebke, Mark and Rutchick, Abraham M. and Ryan, Robert S. and Sahin, Onur and Saide, Anondah and Sandstrom, Gillian M. and Santos, David and Saxe, Rebecca and Schlegelmilch, Rene and Schmidt, Kathleen and Scholz, Sabine and Seibel, Larissa and Selterman, Dylan Faulkner and Shaki, Samuel and Simpson, William B. and Sinclair, H. Colleen and Skorinko, Jeanine L. M. and Slowik, Agnieszka and Snyder, Joel S. and Soderberg, Courtney and Sonnleitner, Carina and Spencer, Nick and Spies, Jeffrey R. and Steegen, Sara and Stieger, Stefan and Strohminger, Nina and Sullivan, Gavin B. and Talhelm, Thomas and Tapia, Megan and te Dorsthorst, Anniek and Thomae, Manuela and Thomas, Sarah L. and Tio, Pia and Traets, Frits and Tsang, Steve and Tuerlinckx, Francis and Turchan, Paul and Valasek, Milan and Van Aert, Robbie and van Assen, Marcel and van Bork, Riet and van de Ven, Mathijs and van den Bergh, Don and van der Hulst, Marije and van Dooren, Roel and van Doorn, Johnny and van Renswoude, Daan R. and van Rijn, Hedderik and Vanpaemel, Wolf and Echeverria, Alejandro Vasquez and Vazquez, Melissa and Velez, Natalia and Vermue, Marieke and Verschoor, Mark and Vianello, Michelangelo and Voracek, Martin and Vuu, Gina and Wagenmakers, Eric-Jan and Weerdmeester, Joanneke and Welsh, Ashlee and Westgate, Erin C. and Wissink, Joeri and Wood, Michael and Woods, Andy and Wright, Emily and Wu, Sining and Zeelenberg, Marcel and Zuni, Kellylynn},
  title     = {Estimating the reproducibility of psychological science},
  series = {Science},
  volume    = {349},
  journal   = {Science},
  number    = {6251},
  publisher = {American Assoc. for the Advancement of Science},
  address   = {Washington},
  organization    = {Open Sci Collaboration},
  issn      = {1095-9203},
  doi       = {10.1126/science.aac4716},
  pages     = {8},
  year      = {2015},
  abstract  = {Reproducibility is a defining feature of science, but the extent to which it characterizes current research is unknown. We conducted replications of 100 experimental and correlational studies published in three psychology journals using high-powered designs and original materials when available. Replication effects were half the magnitude of original effects, representing a substantial decline. Ninety-seven percent of original studies had statistically significant results. Thirty-six percent of replications had statistically significant results; 47\% of original effect sizes were in the 95\% confidence interval of the replication effect size; 39\% of effects were subjectively rated to have replicated the original result; and if no bias in original results is assumed, combining original and replication results left 68\% with statistically significant effects. Correlational tests suggest that replication success was better predicted by the strength of original evidence than by characteristics of the original and replication teams.},
  language  = {en}
}
@article{DiluisoWalkManychetal.2021,
  author    = {Diluiso, Francesca and Walk, Paula and Manych, Niccolo and Cerutti, Nicola and Chipiga, Vladislav and Workman, Annabelle and Ayas, Ceren and Cui, Ryna Yiyun and Cui, Diyang and Song, Kaihui and Banisch, Lucy A. and Moretti, Nikolaj and Callaghan, Max W. and Clarke, Leon and Creutzig, Felix and Hilaire, Jerome and Jotzo, Frank and Kalkuhl, Matthias and Lamb, William F. and L{\"o}schel, Andreas and M{\"u}ller-Hansen, Finn and Nemet, Gregory F. and Oei, Pao-Yu and Sovacool, Benjamin K. and Steckel, Jan Christoph and Thomas, Sebastian and Wiseman, John and Minx, Jan C.},
  title     = {Coal transitions - part 1},
  series = {Environmental research letters},
  volume    = {16},
  journal   = {Environmental research letters},
  number    = {11},
  publisher = {Institute of Physics Publishing (IOP)},
  address   = {Bristol},
  issn      = {1748-9326},
  doi       = {10.1088/1748-9326/ac1b58},
  pages     = {40},
  year      = {2021},
  abstract  = {A rapid coal phase-out is needed to meet the goals of the Paris Agreement, but is hindered by serious challenges ranging from vested interests to the risks of social disruption. To understand how to organize a global coal phase-out, it is crucial to go beyond cost-effective climate mitigation scenarios and learn from the experience of previous coal transitions. Despite the relevance of the topic, evidence remains fragmented throughout different research fields, and not easily accessible. To address this gap, this paper provides a systematic map and comprehensive review of the literature on historical coal transitions. We use computer-assisted systematic mapping and review methods to chart and evaluate the available evidence on historical declines in coal production and consumption. We extracted a dataset of 278 case studies from 194 publications, covering coal transitions in 44 countries and ranging from the end of the 19th century until 2021. We find a relatively recent and rapidly expanding body of literature reflecting the growing importance of an early coal phase-out in scientific and political debates. Previous evidence has primarily focused on the United Kingdom, the United States, and Germany, while other countries that experienced large coal declines, like those in Eastern Europe, are strongly underrepresented. An increasing number of studies, mostly published in the last 5 years, has been focusing on China. Most of the countries successfully reducing coal dependency have undergone both demand-side and supply-side transitions. This supports the use of policy approaches targeting both demand and supply to achieve a complete coal phase-out. From a political economy perspective, our dataset highlights that most transitions are driven by rising production costs for coal, falling prices for alternative energies, or local environmental concerns, especially regarding air pollution. The main challenges for coal-dependent regions are structural change transformations, in particular for industry and labor. Rising unemployment is the most largely documented outcome in the sample. Policymakers at multiple levels are instrumental in facilitating coal transitions. They rely mainly on regulatory instruments to foster the transitions and compensation schemes or investment plans to deal with their transformative processes. Even though many models suggest that coal phase-outs are among the low-hanging fruits on the way to climate neutrality and meeting the international climate goals, our case studies analysis highlights the intricate political economy at work that needs to be addressed through well-designed and just policies.},
  language  = {en}
}
@book{AsemissenBellinghausenBoeckeretal.2022,
  author    = {Asemissen, Konrad and Bellinghausen, Till and B{\"o}cker, Ulrich and Booth, John Leonhard and Dombert, Matthias and Witt, Karsten},
  title     = {M{\"u}nchener Anwaltshandbuch Agrarrecht},
  series = {Beck-online B{\"u}cher},
  journal   = {Beck-online B{\"u}cher},
  editor    = {Dombert, Matthias and Witt, Karsten},
  edition   = {3., {\"u}berarbeitete},
  publisher = {C.H. Beck},
  address   = {M{\"u}nchen},
  isbn      = {978-3-406-76324-3},
  pages     = {XXXIII, 1269 Seiten},
  year      = {2022},
  abstract  = {Das bew{\"a}hrte Handbuch befasst sich mit allen praxisrelevanten Aspekten dieses {\"a}ußerst facettenreichen Rechtsgebiets.Wie alle M{\"u}nchener Anwaltshandb{\"u}cher bereitet auch dieses Werk die behandelten Themen und Rechtsmaterien praxis- und mandatsorientiert auf. Die juristischen, wirtschaftlichen, gesellschaftspolitischen und technischen Besonderheiten agrarrechtlicher Mandatsverh{\"a}ltnisse werden anhand konkreter Handlungs- und Gestaltungshinweise ausf{\"u}hrlich erl{\"a}utert. Die systematische Darstellung der sehr breit gestreuten Themen wird durch vielf{\"a}ltige Checklisten, Formulierungsbeispiele, Muster und Praxistipps aufgelockert, so dass ein schnelles Auffinden der konkreten Problemlage und eine rasche, interessengerechte Fall-L{\"o}sung gew{\"a}hrleistet sind.Der gesamte Katalog des 14m FAO wird behandelt; auch dar{\"u}berhinausgehende, praxisrelevante Fragen werden mit eigenen Kapiteln oder Kapitelabschnitten bedacht.},
  language  = {de}
}
@misc{PerezCornagoCroweApplebyetal.2021,
  author    = {Perez-Cornago, Aurora and Crowe, Francesca L. and Appleby, Paul N. and Bradbury, Kathryn E. and Wood, Angela M. and Jakobsen, Marianne Uhre and Johnson, Laura and Sacerdote, Carlotta and Steur, Marinka and Weiderpass, Elisabete and Wurtz, Anne Mette L. and Kuhn, Tilman and Katzke, Verena and Trichopoulou, Antonia and Karakatsani, Anna and La Vecchia, Carlo and Masala, Giovanna and Tumino, Rosario and Panico, Salvatore and Sluijs, Ivonne and Skeie, Guri and Imaz, Liher and Petrova, Dafina and Quiros, J. Ramon and Yohar, Sandra Milena Colorado and Jakszyn, Paula and Melander, Olle and Sonestedt, Emily and Andersson, Jonas and Wennberg, Maria and Aune, Dagfinn and Riboli, Elio and Schulze, Matthias Bernd and di Angelantonio, Emanuele and Wareham, Nicholas J. and Danesh, John and Forouhi, Nita G. and Butterworth, Adam S. and Key, Timothy J.},
  title     = {Plant foods, dietary fibre and risk of ischaemic heart disease in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort},
  series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  journal   = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe},
  number    = {1},
  issn      = {1866-8372},
  doi       = {10.25932/publishup-56034},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-560340},
  pages     = {13},
  year      = {2021},
  abstract  = {Background: Epidemiological evidence indicates that diets rich in plant foods are associated with a lower risk of ischaemic heart disease (IHD), but there is sparse information on fruit and vegetable subtypes and sources of dietary fibre. This study examined the associations of major plant foods, their subtypes and dietary fibre with risk of IHD in the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods: We conducted a prospective analysis of 490 311 men and women without a history of myocardial infarction or stroke at recruitment (12.6 years of follow-up, n cases = 8504), in 10 European countries. Dietary intake was assessed using validated questionnaires, calibrated with 24-h recalls. Multivariable Cox regressions were used to estimate hazard ratios (HR) of IHD. Results: There was a lower risk of IHD with a higher intake of fruit and vegetables combined [HR per 200 g/day higher intake 0.94, 95\% confidence interval (CI): 0.90-0.99, P-trend = 0.009], and with total fruits (per 100 g/day 0.97, 0.95-1.00, P-trend = 0.021). There was no evidence for a reduced risk for fruit subtypes, except for bananas. Risk was lower with higher intakes of nuts and seeds (per 10 g/day 0.90, 0.82-0.98, Ptrend = 0.020), total fibre (per 10 g/day 0.91, 0.85-0.98, P-trend = 0.015), fruit and vegetable fibre (per 4 g/day 0.95, 0.91-0.99, P-trend = 0.022) and fruit fibre (per 2 g/day 0.97, 0.95-1.00, P-trend = 0.045). No associations were observed between vegetables, vegetables subtypes, legumes, cereals and IHD risk. Conclusions: In this large prospective study, we found some small inverse associations between plant foods and IHD risk, with fruit and vegetables combined being the most strongly inversely associated with risk. Whether these small associations are causal remains unclear.},
  language  = {en}
}
@article{PerezCornagoCroweApplebyetal.2021,
  author    = {Perez-Cornago, Aurora and Crowe, Francesca L. and Appleby, Paul N. and Bradbury, Kathryn E. and Wood, Angela M. and Jakobsen, Marianne Uhre and Johnson, Laura and Sacerdote, Carlotta and Steur, Marinka and Weiderpass, Elisabete and Wurtz, Anne Mette L. and Kuhn, Tilman and Katzke, Verena and Trichopoulou, Antonia and Karakatsani, Anna and La Vecchia, Carlo and Masala, Giovanna and Tumino, Rosario and Panico, Salvatore and Sluijs, Ivonne and Skeie, Guri and Imaz, Liher and Petrova, Dafina and Quiros, J. Ramon and Yohar, Sandra Milena Colorado and Jakszyn, Paula and Melander, Olle and Sonestedt, Emily and Andersson, Jonas and Wennberg, Maria and Aune, Dagfinn and Riboli, Elio and Schulze, Matthias Bernd and di Angelantonio, Emanuele and Wareham, Nicholas J. and Danesh, John and Forouhi, Nita G. and Butterworth, Adam S. and Key, Timothy J.},
  title     = {Plant foods, dietary fibre and risk of ischaemic heart disease in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort},
  series = {International journal of epidemiology},
  volume    = {50},
  journal   = {International journal of epidemiology},
  number    = {1},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {0300-5771},
  doi       = {10.1093/ije/dyaa155},
  pages     = {212 -- 222},
  year      = {2021},
  abstract  = {Background: Epidemiological evidence indicates that diets rich in plant foods are associated with a lower risk of ischaemic heart disease (IHD), but there is sparse information on fruit and vegetable subtypes and sources of dietary fibre. This study examined the associations of major plant foods, their subtypes and dietary fibre with risk of IHD in the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods: We conducted a prospective analysis of 490 311 men and women without a history of myocardial infarction or stroke at recruitment (12.6 years of follow-up, n cases = 8504), in 10 European countries. Dietary intake was assessed using validated questionnaires, calibrated with 24-h recalls. Multivariable Cox regressions were used to estimate hazard ratios (HR) of IHD. Results: There was a lower risk of IHD with a higher intake of fruit and vegetables combined [HR per 200 g/day higher intake 0.94, 95\% confidence interval (CI): 0.90-0.99, P-trend = 0.009], and with total fruits (per 100 g/day 0.97, 0.95-1.00, P-trend = 0.021). There was no evidence for a reduced risk for fruit subtypes, except for bananas. Risk was lower with higher intakes of nuts and seeds (per 10 g/day 0.90, 0.82-0.98, Ptrend = 0.020), total fibre (per 10 g/day 0.91, 0.85-0.98, P-trend = 0.015), fruit and vegetable fibre (per 4 g/day 0.95, 0.91-0.99, P-trend = 0.022) and fruit fibre (per 2 g/day 0.97, 0.95-1.00, P-trend = 0.045). No associations were observed between vegetables, vegetables subtypes, legumes, cereals and IHD risk. Conclusions: In this large prospective study, we found some small inverse associations between plant foods and IHD risk, with fruit and vegetables combined being the most strongly inversely associated with risk. Whether these small associations are causal remains unclear.},
  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 Bernd 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{AbdallaAbramowskiAharonianetal.2016,
  author    = {Abdalla, Hassan E. and Abramowski, Attila and Aharonian, Felix A. and Benkhali, Fai{\c{c}}al Ait and Akhperjanian, A. G. and Ang{\"u}ner, Ekrem Oǧuzhan and Arrieta, M. and Aubert, Pierre and Backes, Michael and Balzer, Arnim and Barnard, Michelle and Becherini, Yvonne and Tjus, Julia Becker and Berge, David and Bernhard, Sabrina and Bernl{\"o}hr, K. and Birsin, E. and Blackwell, R. and Bottcher, Markus and Boisson, Catherine and Bolmont, J. and Bordas, Pol and Bregeon, Johan and Brun, Francois and Brun, Pierre and Bryan, Mark and Bulik, Tomasz and Capasso, M. and Carr, John and Casanova, Sabrina and Chakraborty, N. and Chalme-Calvet, R. and Chaves, Ryan C. G. and Chen, Andrew and Chevalier, J. and Chretien, M. and Colafrancesco, Sergio and Cologna, Gabriele and Condon, B. and Conrad, Jan and Couturier, C. and Cui, Y. and Davids, I. D. and Degrange, B. and Deil, Christoph and deWilt, P. and Djannati-Atai, Arache and Domainko, Wilfried and Donath, Axel and Dubus, Guillaume and Dutson, Kate and Dyks, J. and Dyrda, M. and Edwards, T. and Egberts, Kathrin and Eger, P. and Ernenwein, J. -P. and Eschbach, S. and Farnier, C. and Fegan, Stuart and Fernandes, M. V. and Fiasson, A. and Fontaine, G. and Foerster, A. and Funk, S. and F{\"u}ßling, Matthias and Gabici, Stefano and Gajdus, M. and Gallant, Y. A. and Garrigoux, T. and Giavitto, Gianluca and Giebels, B. and Glicenstein, J. F. and Gottschall, Daniel and Goyal, A. and Grondin, M. -H. and Grudzinska, M. and Hadasch, Daniela and Hahn, J. and Hawkes, J. and Heinzelmann, G. and Henri, Gilles and Hermann, G. and Hervet, Olivier and Hillert, A. and Hinton, James Anthony and Hofmann, Werner and Hoischen, Clemens and Holler, M. and Horns, D. and Ivascenko, Alex and Jacholkowska, A. and Jamrozy, Marek and Janiak, M. and Jankowsky, D. and Jankowsky, Felix and Jingo, M. and Jogler, Tobias and Jouvin, Lea and Jung-Richardt, Ira and Kastendieck, M. A. and Katarzynski, Krzysztof and Katz, Uli and Kerszberg, D. and Khelifi, B. and Kieffer, M. and King, J. and Klepser, S. and Klochkov, Dmitry and Kluzniak, W. and Kolitzus, D. and Komin, Nu. and Kosack, K. and Krakau, S. and Kraus, Michael and Krayzel, F. and Kruger, P. P. and Laffon, H. and Lamanna, G. and Lau, Jeanie and Lees, J. -P. and Lefaucheur, J. and Lefranc, V. and Lemiere, A. and Lemoine-Goumard, M. and Lenain, J. -P. and Leser, Eva and Lohse, Thomas and Lorentz, M. and Lui, R. and Lypova, Iryna and Marandon, Vincent and Marcowith, Alexandre and Mariaud, C. and Marx, R. and Maurin, G. and Maxted, N. and Mayer, Michael and Meintjes, Petrus Johannes and Menzler, U. and Meyer, Manuel and Mitchell, A. M. W. and Moderski, R. and Mohamed, M. and Mora, K. and Moulin, Emmanuel and Murach, T. and de Naurois, Mathieu and Niederwanger, F. and Niemiec, J. and Oakes, L. and Odaka, Hirokazu and Ohm, Stefan and Oettl, S. and Ostrowski, M. and Oya, I. and Padovani, Marco and Panter, M. and Parsons, R. D. and Arribas, M. Paz and Pekeur, N. W. and Pelletier, G. and Petrucci, P. -O. and Peyaud, B. and Pita, S. and Poon, Helen and Prokhorov, Dmitry and Prokoph, Heike and Puehlhofer, Gerd and Punch, Michael and Quirrenbach, Andreas and Raab, S. and Reimer, Anita and Reimer, Olaf and Renaud, M. and de los Reyes, R. and Rieger, Frank and Romoli, Carlo and Rosier-Lees, S. and Rowell, G. and Rudak, B. and Rulten, C. B. and Sahakian, V. and Salek, David and Sanchez, David A. and Santangelo, Andrea and Sasaki, Manami and Schlickeiser, Reinhard and Schussler, F. and Schulz, Andreas and Schwanke, U. and Schwemmer, S. and Seyffert, A. S. and Shafi, N. and Simoni, R. and Sol, H. and Spanier, Felix and Spengler, G. and Spiess, F. and Stawarz, Lukasz and Steenkamp, R. and Stegmann, Christian and Stinzing, F. and Stycz, K. and Sushch, Iurii and Tavernet, J. -P. and Tavernier, T. and Taylor, A. M. and Terrier, R. and Tluczykont, Martin and Trichard, C. and Tuffs, R. and van der Walt, Johan and van Eldik, Christopher and van Soelen, Brian and Vasileiadis, Georges and Veh, J. and Venter, C. and Viana, A. and Vincent, P. and Vink, Jacco and Voisin, F. and Voelk, Heinrich J. and Vuillaume, Thomas and Wadiasingh, Z. and Wagner, Stefan J. and Wagner, P. and Wagner, R. M. and White, R. and Wierzcholska, Alicja and Willmann, P. and Woernlein, A. and Wouters, Denis and Yang, R. and Zabalza, Victor and Zaborov, D. and Zacharias, M. and Zdziarski, A. A. and Zech, Andreas and Zefi, F. and Ziegler, A. and Zywucka, Natalia},
  title     = {Search for Dark Matter Annihilations towards the Inner Galactic Halo from 10 Years of Observations with HESS},
  series = {Physical review letters},
  volume    = {117},
  journal   = {Physical review letters},
  publisher = {American Physical Society},
  address   = {College Park},
  organization    = {HESS Collaboration},
  issn      = {0031-9007},
  doi       = {10.1103/PhysRevLett.117.111301},
  pages     = {6},
  year      = {2016},
  abstract  = {The inner region of the Milky Way halo harbors a large amount of dark matter (DM). Given its proximity, it is one of the most promising targets to look for DM. We report on a search for the annihilations of DM particles using gamma-ray observations towards the inner 300 pc of the Milky Way, with the H.E.S.S. array of ground-based Cherenkov telescopes. The analysis is based on a 2D maximum likelihood method using Galactic Center (GC) data accumulated by H.E.S.S. over the last 10 years (2004-2014), and does not show any significant gamma-ray signal above background. Assuming Einasto and Navarro-Frenk-White DM density profiles at the GC, we derive upper limits on the annihilation cross section <sigma nu >. These constraints are the strongest obtained so far in the TeV DM mass range and improve upon previous limits by a factor 5. For the Einasto profile, the constraints reach <sigma nu > values of 6 x 10(-26) cm(3) s(-1) in the W+W- channel for a DM particle mass of 1.5 TeV, and 2 x 10(-26) cm(3) s(-1) in the tau(+)tau(-) channel for a 1 TeV mass. For the first time, ground-based gamma-ray observations have reached sufficient sensitivity to probe <sigma nu > values expected from the thermal relic density for TeV DM particles.},
  language  = {en}
}
@misc{AcharyaAramoBabicetal.2015,
  author    = {Acharya, B. S. and Aramo, C. and Babic, A. and Barrio, J. A. and Baushev, Anton N. and Tjus, J. Becker and Berge, David and Bohacova, M. and Bonardi, A. and Brown, A. and Bugaev, V. and Bulik, Tomasz and Burton, M. and Busetto, G. and Caraveo, P. A. and Carosi, R. and Carr, John and Chadwick, Paula M. and Chudoba, J. and Conforti, V. and Connaughton, V. and Contreras, J. L. and Cotter, G. and Dazzi, F. and De Franco, A. and de la Calle, I. and Lopez, R. de los Reyes and De Lotto, B. and De Palma, F. and Di Girolamo, T. and Di Giulio, C. and Di Pierro, F. and Dournaux, J. -L. and Dwarkadas, Vikram V. and Ebr, J. and Egberts, Kathrin and Fesquet, M. and Fleischhack, H. and Font, L. and Fontaine, G. and Foerster, A. and F{\"u}ßling, Matthias and Garcia, B. and Lopez, R. Garcia and Garczarczyk, M. and Gargano, F. and Garrido, D. and Gaug, M. and Giglietto, N. and Giordano, F. and Giuliani, A. and Godinovic, N. and Gonzalez, M. M. and Grabarczyk, T. and Hassan, T. and Hoerandel, J. and Hrabovsky, M. and Hrupec, D. and Humensky, T. B. and Huovelin, J. and Jamrozy, M. and Janecek, P. and Kaaret, P. E. and Katz, U. and Kaufmann, S. and Khelifi, B. and Kluzniak, W. and Kocot, J. and Komin, N. and Kubo, H. and Kushida, J. and Lamanna, G. and Lee, W. H. and Lenain, J. -P. and Lohse, T. and Lombardi, S. and Lopez-Coto, R. and Lopez-Oramas, A. and Lucarelli, F. and Maccarone, M. C. and Maier, G. and Majumdar, P. and Malaguti, G. and Mandat, D. and Mazziotta, Mario Nicola and Meagher, K. and Mirabal, N. and Morselli, A. and Moulin, Emmanuel and Niemiec, J. and Nievas, M. and Nishijima, K. and Nosek, D. and Nunio, F. and Ohishi, M. and Ohm, S. and Ong, R. A. and Orito, R. and Otte, N. and Palatka, M. and Pareschi, G. and Pech, M. and Persic, M. and Pohl, Manuela and Prouza, M. and Quirrenbach, A. and Raino, S. and Fernandez, G. Rodriguez and Romano, Patrizia and Rovero, A. C. and Rudak, B. and Schovanek, P. and Shayduk, M. and Siejkowski, H. and Sillanpaa, A. and Stefanik, S. and Stolarczyk, T. and Szanecki, M. and Szepieniec, T. and Tejedor, L. A. and Telezhinsky, Igor O. and Teshima, M. and Tibaldo, L. and Tibolla, O. and Tovmassian, G. and Travnicek, P. and Trzeciak, M. and Vallania, P. and van Eldik, C. and Vercellone, S. and Vigorito, C. and Wagner, S. J. and Wakely, S. P. and Weinstein, A. and Wierzcholska, A. and Wilhelm, Alina and Wojcik, P. and Yoshikoshi, T.},
  title     = {The Cherenkov Telescope Array potential for the study of young supernova remnants},
  series = {Astroparticle physics},
  volume    = {62},
  journal   = {Astroparticle physics},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0927-6505},
  doi       = {10.1016/j.astropartphys.2014.08.005},
  pages     = {152 -- 164},
  year      = {2015},
  abstract  = {Supernova remnants (SNRs) are among the most important targets for gamma-ray observatories. Being prominent non-thermal sources, they are very likely responsible for the acceleration of the bulk of Galactic cosmic rays (CRS). To firmly establish the SNR paradigm for the origin of cosmic rays, it should be confirmed that protons are indeed accelerated in, and released from, SNRs with the appropriate flux and spectrum. This can be done by detailed theoretical models which account for microphysics of acceleration and various radiation processes of hadrons and leptons. The current generation of Cherenkov telescopes has insufficient sensitivity to constrain theoretical models. A new facility, the Cherenkov Telescope Array (CTA), will have superior capabilities and may finally resolve this long standing issue of high-energy astrophysics. We want to assess the capabilities of CTA to reveal the physics of various types of SNRs in the initial 2000 years of their evolution. During this time, the efficiency to accelerate cosmic rays is highest. We perform time-dependent simulations of the hydrodynamics, the magnetic fields, the cosmic-ray acceleration, and the non-thermal emission for type Ia, Ic and IIP SNRs. We calculate the CTA response to the y-ray emission from these SNRs for various ages and distances, and we perform a realistic analysis of the simulated data. We derive distance limits for the detectability and resolvability of these SNR types at several ages. We test the ability of CTA to reconstruct their morphological and spectral parameters as a function of their distance. Finally, we estimate how well CTA data will constrain the theoretical models. (C) 2014 Elsevier B.V. All rights reserved.},
  language  = {en}
}