TY - JOUR A1 - Mantzouki, Evanthia A1 - Lurling, Miquel A1 - Fastner, Jutta A1 - Domis, Lisette Nicole de Senerpont A1 - Wilk-Wozniak, Elzbieta A1 - Koreiviene, Judita A1 - Seelen, Laura A1 - Teurlincx, Sven A1 - Verstijnen, Yvon A1 - Krzton, Wojciech A1 - Walusiak, Edward A1 - Karosiene, Jurate A1 - Kasperoviciene, Jurate A1 - Savadova, Ksenija A1 - Vitonyte, Irma A1 - Cillero-Castro, Carmen A1 - Budzynska, Agnieszka A1 - Goldyn, Ryszard A1 - Kozak, Anna A1 - Rosinska, Joanna A1 - Szelag-Wasielewska, Elzbieta A1 - Domek, Piotr A1 - Jakubowska-Krepska, Natalia A1 - Kwasizur, Kinga A1 - Messyasz, Beata A1 - Pelechata, Aleksandra A1 - Pelechaty, Mariusz A1 - Kokocinski, Mikolaj A1 - Garcia-Murcia, Ana A1 - Real, Monserrat A1 - Romans, Elvira A1 - Noguero-Ribes, Jordi A1 - Parreno Duque, David A1 - Fernandez-Moran, Elisabeth A1 - Karakaya, Nusret A1 - Haggqvist, Kerstin A1 - Demir, Nilsun A1 - Beklioglu, Meryem A1 - Filiz, Nur A1 - Levi, Eti E. A1 - Iskin, Ugur A1 - Bezirci, Gizem A1 - Tavsanoglu, Ulku Nihan A1 - Ozhan, Koray A1 - Gkelis, Spyros A1 - Panou, Manthos A1 - Fakioglu, Ozden A1 - Avagianos, Christos A1 - Kaloudis, Triantafyllos A1 - Celik, Kemal A1 - Yilmaz, Mete A1 - Marce, Rafael A1 - Catalan, Nuria A1 - Bravo, Andrea G. A1 - Buck, Moritz A1 - Colom-Montero, William A1 - Mustonen, Kristiina A1 - Pierson, Don A1 - Yang, Yang A1 - Raposeiro, Pedro M. A1 - Goncalves, Vitor A1 - Antoniou, Maria G. A1 - Tsiarta, Nikoletta A1 - McCarthy, Valerie A1 - Perello, Victor C. A1 - Feldmann, Tonu A1 - Laas, Alo A1 - Panksep, Kristel A1 - Tuvikene, Lea A1 - Gagala, Ilona A1 - Mankiewicz-Boczek, Joana A1 - Yagci, Meral Apaydin A1 - Cinar, Sakir A1 - Capkin, Kadir A1 - Yagci, Abdulkadir A1 - Cesur, Mehmet A1 - Bilgin, Fuat A1 - Bulut, Cafer A1 - Uysal, Rahmi A1 - Obertegger, Ulrike A1 - Boscaini, Adriano A1 - Flaim, Giovanna A1 - Salmaso, Nico A1 - Cerasino, Leonardo A1 - Richardson, Jessica A1 - Visser, Petra M. A1 - Verspagen, Jolanda M. H. A1 - Karan, Tunay A1 - Soylu, Elif Neyran A1 - Maraslioglu, Faruk A1 - Napiorkowska-Krzebietke, Agnieszka A1 - Ochocka, Agnieszka A1 - Pasztaleniec, Agnieszka A1 - Antao-Geraldes, Ana M. A1 - Vasconcelos, Vitor A1 - Morais, Joao A1 - Vale, Micaela A1 - Koker, Latife A1 - Akcaalan, Reyhan A1 - Albay, Meric A1 - Maronic, Dubravka Spoljaric A1 - Stevic, Filip A1 - Pfeiffer, Tanja Zuna A1 - Fonvielle, Jeremy Andre A1 - Straile, Dietmar A1 - Rothhaupt, Karl-Otto A1 - Hansson, Lars-Anders A1 - Urrutia-Cordero, Pablo A1 - Blaha, Ludek A1 - Geris, Rodan A1 - Frankova, Marketa A1 - Kocer, Mehmet Ali Turan A1 - Alp, Mehmet Tahir A1 - Remec-Rekar, Spela A1 - Elersek, Tina A1 - Triantis, Theodoros A1 - Zervou, Sevasti-Kiriaki A1 - Hiskia, Anastasia A1 - Haande, Sigrid A1 - Skjelbred, Birger A1 - Madrecka, Beata A1 - Nemova, Hana A1 - Drastichova, Iveta A1 - Chomova, Lucia A1 - Edwards, Christine A1 - Sevindik, Tugba Ongun A1 - Tunca, Hatice A1 - OEnem, Burcin A1 - Aleksovski, Boris A1 - Krstic, Svetislav A1 - Vucelic, Itana Bokan A1 - Nawrocka, Lidia A1 - Salmi, Pauliina A1 - Machado-Vieira, Danielle A1 - de Oliveira, Alinne Gurjao A1 - Delgado-Martin, Jordi A1 - Garcia, David A1 - Cereijo, Jose Luis A1 - Goma, Joan A1 - Trapote, Mari Carmen A1 - Vegas-Vilarrubia, Teresa A1 - Obrador, Biel A1 - Grabowska, Magdalena A1 - Karpowicz, Maciej A1 - Chmura, Damian A1 - Ubeda, Barbara A1 - Angel Galvez, Jose A1 - Ozen, Arda A1 - Christoffersen, Kirsten Seestern A1 - Warming, Trine Perlt A1 - Kobos, Justyna A1 - Mazur-Marzec, Hanna A1 - Perez-Martinez, Carmen A1 - Ramos-Rodriguez, Eloisa A1 - Arvola, Lauri A1 - Alcaraz-Parraga, Pablo A1 - Toporowska, Magdalena A1 - Pawlik-Skowronska, Barbara A1 - Niedzwiecki, Michal A1 - Peczula, Wojciech A1 - Leira, Manel A1 - Hernandez, Armand A1 - Moreno-Ostos, Enrique A1 - Maria Blanco, Jose A1 - Rodriguez, Valeriano A1 - Juan Montes-Perez, Jorge A1 - Palomino, Roberto L. A1 - Rodriguez-Perez, Estela A1 - Carballeira, Rafael A1 - Camacho, Antonio A1 - Picazo, Antonio A1 - Rochera, Carlos A1 - Santamans, Anna C. A1 - Ferriol, Carmen A1 - Romo, Susana A1 - Miguel Soria, Juan A1 - Dunalska, Julita A1 - Sienska, Justyna A1 - Szymanski, Daniel A1 - Kruk, Marek A1 - Kostrzewska-Szlakowska, Iwona A1 - Jasser, Iwona A1 - Zutinic, Petar A1 - Udovic, Marija Gligora A1 - Plenkovic-Moraj, Andelka A1 - Frak, Magdalena A1 - Bankowska-Sobczak, Agnieszka A1 - Wasilewicz, Michal A1 - Ozkan, Korhan A1 - Maliaka, Valentini A1 - Kangro, Kersti A1 - Grossart, Hans-Peter A1 - Paerl, Hans W. A1 - Carey, Cayelan C. A1 - Ibelings, Bas W. T1 - Temperature effects explain continental scale distribution of cyanobacterial toxins JF - Toxins N2 - Insight into how environmental change determines the production and distribution of cyanobacterial toxins is necessary for risk assessment. Management guidelines currently focus on hepatotoxins (microcystins). Increasing attention is given to other classes, such as neurotoxins (e.g., anatoxin-a) and cytotoxins (e.g., cylindrospermopsin) due to their potency. Most studies examine the relationship between individual toxin variants and environmental factors, such as nutrients, temperature and light. In summer 2015, we collected samples across Europe to investigate the effect of nutrient and temperature gradients on the variability of toxin production at a continental scale. Direct and indirect effects of temperature were the main drivers of the spatial distribution in the toxins produced by the cyanobacterial community, the toxin concentrations and toxin quota. Generalized linear models showed that a Toxin Diversity Index (TDI) increased with latitude, while it decreased with water stability. Increases in TDI were explained through a significant increase in toxin variants such as MC-YR, anatoxin and cylindrospermopsin, accompanied by a decreasing presence of MC-LR. While global warming continues, the direct and indirect effects of increased lake temperatures will drive changes in the distribution of cyanobacterial toxins in Europe, potentially promoting selection of a few highly toxic species or strains. KW - microcystin KW - anatoxin KW - cylindrospermopsin KW - temperature KW - direct effects KW - indirect effects KW - spatial distribution KW - European Multi Lake Survey Y1 - 2018 U6 - https://doi.org/10.3390/toxins10040156 SN - 2072-6651 VL - 10 IS - 4 PB - MDPI CY - Basel ER - TY - JOUR A1 - Mantzouki, Evanthia A1 - Campbell, James A1 - van Loon, Emiel A1 - Visser, Petra A1 - Konstantinou, Iosif A1 - Antoniou, Maria A1 - Giuliani, Gregory A1 - Machado-Vieira, Danielle A1 - de Oliveira, Alinne Gurjao A1 - Maronic, Dubravka Spoljaric A1 - Stevic, Filip A1 - Pfeiffer, Tanja Zuna A1 - Vucelic, Itana Bokan A1 - Zutinic, Petar A1 - Udovic, Marija Gligora A1 - Plenkovic-Moraj, Andelka A1 - Tsiarta, Nikoletta A1 - Blaha, Ludek A1 - Geris, Rodan A1 - Frankova, Marketa A1 - Christoffersen, Kirsten Seestern A1 - Warming, Trine Perlt A1 - Feldmann, Tonu A1 - Laas, Alo A1 - Panksep, Kristel A1 - Tuvikene, Lea A1 - Kangro, Kersti A1 - Haggqvist, Kerstin A1 - Salmi, Pauliina A1 - Arvola, Lauri A1 - Fastner, Jutta A1 - Straile, Dietmar A1 - Rothhaupt, Karl-Otto A1 - Fonvielle, Jeremy Andre A1 - Grossart, Hans-Peter A1 - Avagianos, Christos A1 - Kaloudis, Triantafyllos A1 - Triantis, Theodoros A1 - Zervou, Sevasti-Kiriaki A1 - Hiskia, Anastasia A1 - Gkelis, Spyros A1 - Panou, Manthos A1 - McCarthy, Valerie A1 - Perello, Victor C. A1 - Obertegger, Ulrike A1 - Boscaini, Adriano A1 - Flaim, Giovanna A1 - Salmaso, Nico A1 - Cerasino, Leonardo A1 - Koreiviene, Judita A1 - Karosiene, Jurate A1 - Kasperoviciene, Jurate A1 - Savadova, Ksenija A1 - Vitonyte, Irma A1 - Haande, Sigrid A1 - Skjelbred, Birger A1 - Grabowska, Magdalena A1 - Karpowicz, Maciej A1 - Chmura, Damian A1 - Nawrocka, Lidia A1 - Kobos, Justyna A1 - Mazur-Marzec, Hanna A1 - Alcaraz-Parraga, Pablo A1 - Wilk-Wozniak, Elzbieta A1 - Krzton, Wojciech A1 - Walusiak, Edward A1 - Gagala, Ilona A1 - Mankiewicz-Boczek, Joana A1 - Toporowska, Magdalena A1 - Pawlik-Skowronska, Barbara A1 - Niedzwiecki, Michal A1 - Peczula, Wojciech A1 - Napiorkowska-Krzebietke, Agnieszka A1 - Dunalska, Julita A1 - Sienska, Justyna A1 - Szymanski, Daniel A1 - Kruk, Marek A1 - Budzynska, Agnieszka A1 - Goldyn, Ryszard A1 - Kozak, Anna A1 - Rosinska, Joanna A1 - Szelag-Wasielewska, Elzbieta A1 - Domek, Piotr A1 - Jakubowska-Krepska, Natalia A1 - Kwasizur, Kinga A1 - Messyasz, Beata A1 - Pelechata, Aleksandra A1 - Pelechaty, Mariusz A1 - Kokocinski, Mikolaj A1 - Madrecka, Beata A1 - Kostrzewska-Szlakowska, Iwona A1 - Frak, Magdalena A1 - Bankowska-Sobczak, Agnieszka A1 - Wasilewicz, Michal A1 - Ochocka, Agnieszka A1 - Pasztaleniec, Agnieszka A1 - Jasser, Iwona A1 - Antao-Geraldes, Ana M. A1 - Leira, Manel A1 - Hernandez, Armand A1 - Vasconcelos, Vitor A1 - Morais, Joao A1 - Vale, Micaela A1 - Raposeiro, Pedro M. A1 - Goncalves, Vitor A1 - Aleksovski, Boris A1 - Krstic, Svetislav A1 - Nemova, Hana A1 - Drastichova, Iveta A1 - Chomova, Lucia A1 - Remec-Rekar, Spela A1 - Elersek, Tina A1 - Delgado-Martin, Jordi A1 - Garcia, David A1 - Luis Cereijo, Jose A1 - Goma, Joan A1 - Carmen Trapote, Mari A1 - Vegas-Vilarrubia, Teresa A1 - Obrador, Biel A1 - Garcia-Murcia, Ana A1 - Real, Monserrat A1 - Romans, Elvira A1 - Noguero-Ribes, Jordi A1 - Parreno Duque, David A1 - Fernandez-Moran, Elisabeth A1 - Ubeda, Barbara A1 - Angel Galvez, Jose A1 - Marce, Rafael A1 - Catalan, Nuria A1 - Perez-Martinez, Carmen A1 - Ramos-Rodriguez, Eloisa A1 - Cillero-Castro, Carmen A1 - Moreno-Ostos, Enrique A1 - Maria Blanco, Jose A1 - Rodriguez, Valeriano A1 - Juan Montes-Perez, Jorge A1 - Palomino, Roberto L. A1 - Rodriguez-Perez, Estela A1 - Carballeira, Rafael A1 - Camacho, Antonio A1 - Picazo, Antonio A1 - Rochera, Carlos A1 - Santamans, Anna C. A1 - Ferriol, Carmen A1 - Romo, Susana A1 - Soria, Juan Miguel A1 - Hansson, Lars-Anders A1 - Urrutia-Cordero, Pablo A1 - Ozen, Arda A1 - Bravo, Andrea G. A1 - Buck, Moritz A1 - Colom-Montero, William A1 - Mustonen, Kristiina A1 - Pierson, Don A1 - Yang, Yang A1 - Verspagen, Jolanda M. H. A1 - Domis, Lisette N. de Senerpont A1 - Seelen, Laura A1 - Teurlincx, Sven A1 - Verstijnen, Yvon A1 - Lurling, Miquel A1 - Maliaka, Valentini A1 - Faassen, Elisabeth J. A1 - Latour, Delphine A1 - Carey, Cayelan C. A1 - Paerl, Hans W. A1 - Torokne, Andrea A1 - Karan, Tunay A1 - Demir, Nilsun A1 - Beklioglu, Meryem A1 - Filiz, Nur A1 - Levi, Eti E. A1 - Iskin, Ugur A1 - Bezirci, Gizem A1 - Tavsanoglu, Ulku Nihan A1 - Celik, Kemal A1 - Ozhan, Koray A1 - Karakaya, Nusret A1 - Kocer, Mehmet Ali Turan A1 - Yilmaz, Mete A1 - Maraslioglu, Faruk A1 - Fakioglu, Ozden A1 - Soylu, Elif Neyran A1 - Yagci, Meral Apaydin A1 - Cinar, Sakir A1 - Capkin, Kadir A1 - Yagci, Abdulkadir A1 - Cesur, Mehmet A1 - Bilgin, Fuat A1 - Bulut, Cafer A1 - Uysal, Rahmi A1 - Koker, Latife A1 - Akcaalan, Reyhan A1 - Albay, Meric A1 - Alp, Mehmet Tahir A1 - Ozkan, Korhan A1 - Sevindik, Tugba Ongun A1 - Tunca, Hatice A1 - Onem, Burcin A1 - Richardson, Jessica A1 - Edwards, Christine A1 - Bergkemper, Victoria A1 - Beirne, Eilish A1 - Cromie, Hannah A1 - Ibelings, Bastiaan W. T1 - Data Descriptor: A European Multi Lake Survey dataset of environmental variables, phytoplankton pigments and cyanotoxins JF - Scientific Data N2 - Under ongoing climate change and increasing anthropogenic activity, which continuously challenge ecosystem resilience, an in-depth understanding of ecological processes is urgently needed. Lakes, as providers of numerous ecosystem services, face multiple stressors that threaten their functioning. Harmful cyanobacterial blooms are a persistent problem resulting from nutrient pollution and climate-change induced stressors, like poor transparency, increased water temperature and enhanced stratification. Consistency in data collection and analysis methods is necessary to achieve fully comparable datasets and for statistical validity, avoiding issues linked to disparate data sources. The European Multi Lake Survey (EMLS) in summer 2015 was an initiative among scientists from 27 countries to collect and analyse lake physical, chemical and biological variables in a fully standardized manner. This database includes in-situ lake variables along with nutrient, pigment and cyanotoxin data of 369 lakes in Europe, which were centrally analysed in dedicated laboratories. Publishing the EMLS methods and dataset might inspire similar initiatives to study across large geographic areas that will contribute to better understanding lake responses in a changing environment. KW - Climate-change ecology KW - Limnology KW - Water resources Y1 - 2018 U6 - https://doi.org/10.1038/sdata.2018.226 SN - 2052-4463 VL - 5 PB - Nature Publ. Group CY - London ER - TY - GEN A1 - Mantzouki, Evanthia A1 - Lürling, Miquel A1 - Fastner, Jutta A1 - Domis, Lisette Nicole de Senerpont A1 - Wilk-Woźniak, Elżbieta A1 - Koreiviene, Judita A1 - Seelen, Laura A1 - Teurlincx, Sven A1 - Verstijnen, Yvon A1 - Krztoń, Wojciech A1 - Walusiak, Edward A1 - Karosienė, Jūratė A1 - Kasperovičienė, Jūratė A1 - Savadova, Ksenija A1 - Vitonytė, Irma A1 - Cillero-Castro, Carmen A1 - Budzyńska, Agnieszka A1 - Goldyn, Ryszard A1 - Kozak, Anna A1 - Rosińska, Joanna A1 - Szeląg-Wasielewska, Elżbieta A1 - Domek, Piotr A1 - Jakubowska-Krepska, Natalia A1 - Kwasizur, Kinga A1 - Messyasz, Beata A1 - Pełechata, Aleksandra A1 - Pełechaty, Mariusz A1 - Kokocinski, Mikolaj A1 - García-Murcia, Ana A1 - Real, Monserrat A1 - Romans, Elvira A1 - Noguero-Ribes, Jordi A1 - Duque, David Parreño A1 - Fernández-Morán, Elísabeth A1 - Karakaya, Nusret A1 - Häggqvist, Kerstin A1 - Beklioğlu, Meryem A1 - Filiz, Nur A1 - Levi, Eti E. A1 - Iskin, Uğur A1 - Bezirci, Gizem A1 - Tavşanoğlu, Ülkü Nihan A1 - Özhan, Koray A1 - Gkelis, Spyros A1 - Panou, Manthos A1 - Fakioglu, Özden A1 - Avagianos, Christos A1 - Kaloudis, Triantafyllos A1 - Çelik, Kemal A1 - Yilmaz, Mete A1 - Marcé, Rafael A1 - Catalán, Nuria A1 - Bravo, Andrea G. A1 - Buck, Moritz A1 - Colom-Montero, William A1 - Mustonen, Kristiina A1 - Pierson, Don A1 - Yang, Yang A1 - Raposeiro, Pedro M. A1 - Gonçalves, Vítor A1 - Antoniou, Maria G. A1 - Tsiarta, Nikoletta A1 - McCarthy, Valerie A1 - Perello, Victor C. A1 - Feldmann, Tõnu A1 - Laas, Alo A1 - Panksep, Kristel A1 - Tuvikene, Lea A1 - Gagala, Ilona A1 - Mankiewicz-Boczek, Joana A1 - Yağcı, Meral Apaydın A1 - Çınar, Şakir A1 - Çapkın, Kadir A1 - Yağcı, Abdulkadir A1 - Cesur, Mehmet A1 - Bilgin, Fuat A1 - Bulut, Cafer A1 - Uysal, Rahmi A1 - Obertegger, Ulrike A1 - Boscaini, Adriano A1 - Flaim, Giovanna A1 - Salmaso, Nico A1 - Cerasino, Leonardo A1 - Richardson, Jessica A1 - Visser, Petra M. A1 - Verspagen, Jolanda M. H. A1 - Karan, Tünay A1 - Soylu, Elif Neyran A1 - Maraşlıoğlu, Faruk A1 - Napiórkowska-Krzebietke, Agnieszka A1 - Ochocka, Agnieszka A1 - Pasztaleniec, Agnieszka A1 - Antão-Geraldes, Ana M. A1 - Vasconcelos, Vitor A1 - Morais, João A1 - Vale, Micaela A1 - Köker, Latife A1 - Akçaalan, Reyhan A1 - Albay, Meriç A1 - Maronić, Dubravka Špoljarić A1 - Stević, Filip A1 - Pfeiffer, Tanja Žuna A1 - Fonvielle, Jeremy Andre A1 - Straile, Dietmar A1 - Rothhaupt, Karl-Otto A1 - Hansson, Lars-Anders A1 - Urrutia-Cordero, Pablo A1 - Bláha, Luděk A1 - Geriš, Rodan A1 - Fránková, Markéta A1 - Koçer, Mehmet Ali Turan A1 - Alp, Mehmet Tahir A1 - Remec-Rekar, Spela A1 - Elersek, Tina A1 - Triantis, Theodoros A1 - Zervou, Sevasti-Kiriaki A1 - Hiskia, Anastasia A1 - Haande, Sigrid A1 - Skjelbred, Birger A1 - Madrecka, Beata A1 - Nemova, Hana A1 - Drastichova, Iveta A1 - Chomova, Lucia A1 - Edwards, Christine A1 - Sevindik, Tuğba Ongun A1 - Tunca, Hatice A1 - Önem, Burçin A1 - Aleksovski, Boris A1 - Krstić, Svetislav A1 - Vucelić, Itana Bokan A1 - Nawrocka, Lidia A1 - Salmi, Pauliina A1 - Machado-Vieira, Danielle A1 - Oliveira, Alinne Gurjão De A1 - Delgado-Martín, Jordi A1 - García, David A1 - Cereijo, Jose Luís A1 - Gomà, Joan A1 - Trapote, Mari Carmen A1 - Vegas-Vilarrúbia, Teresa A1 - Obrador, Biel A1 - Grabowska, Magdalena A1 - Karpowicz, Maciej A1 - Chmura, Damian A1 - Úbeda, Bárbara A1 - Gálvez, José Ángel A1 - Özen, Arda A1 - Christoffersen, Kirsten Seestern A1 - Warming, Trine Perlt A1 - Kobos, Justyna A1 - Mazur-Marzec, Hanna A1 - Pérez-Martínez, Carmen A1 - Ramos-Rodríguez, Eloísa A1 - Arvola, Lauri A1 - Alcaraz-Párraga, Pablo A1 - Toporowska, Magdalena A1 - Pawlik-Skowronska, Barbara A1 - Niedźwiecki, Michał A1 - Pęczuła, Wojciech A1 - Leira, Manel A1 - Hernández, Armand A1 - Moreno-Ostos, Enrique A1 - Blanco, José María A1 - Rodríguez, Valeriano A1 - Montes-Pérez, Jorge Juan A1 - Palomino, Roberto L. A1 - Rodríguez-Pérez, Estela A1 - Carballeira, Rafael A1 - Camacho, Antonio A1 - Picazo, Antonio A1 - Rochera, Carlos A1 - Santamans, Anna C. A1 - Ferriol, Carmen A1 - Romo, Susana A1 - Soria, Juan Miguel A1 - Dunalska, Julita A1 - Sieńska, Justyna A1 - Szymański, Daniel A1 - Kruk, Marek A1 - Kostrzewska-Szlakowska, Iwona A1 - Jasser, Iwona A1 - Žutinić, Petar A1 - Udovič, Marija Gligora A1 - Plenković-Moraj, Anđelka A1 - Frąk, Magdalena A1 - Bańkowska-Sobczak, Agnieszka A1 - Wasilewicz, Michał A1 - Özkan, Korhan A1 - Maliaka, Valentini A1 - Kangro, Kersti A1 - Grossart, Hans-Peter A1 - Paerl, Hans W. A1 - Carey, Cayelan C. A1 - Ibelings, Bas W. T1 - Temperature effects explain continental scale distribution of cyanobacterial toxins T2 - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe N2 - Insight into how environmental change determines the production and distribution of cyanobacterial toxins is necessary for risk assessment. Management guidelines currently focus on hepatotoxins (microcystins). Increasing attention is given to other classes, such as neurotoxins (e.g., anatoxin-a) and cytotoxins (e.g., cylindrospermopsin) due to their potency. Most studies examine the relationship between individual toxin variants and environmental factors, such as nutrients, temperature and light. In summer 2015, we collected samples across Europe to investigate the effect of nutrient and temperature gradients on the variability of toxin production at a continental scale. Direct and indirect effects of temperature were the main drivers of the spatial distribution in the toxins produced by the cyanobacterial community, the toxin concentrations and toxin quota. Generalized linear models showed that a Toxin Diversity Index (TDI) increased with latitude, while it decreased with water stability. Increases in TDI were explained through a significant increase in toxin variants such as MC-YR, anatoxin and cylindrospermopsin, accompanied by a decreasing presence of MC-LR. While global warming continues, the direct and indirect effects of increased lake temperatures will drive changes in the distribution of cyanobacterial toxins in Europe, potentially promoting selection of a few highly toxic species or strains. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 1105 KW - microcystin KW - anatoxin KW - cylindrospermopsin KW - temperature KW - direct effects KW - indirect effects KW - spatial distribution KW - European Multi Lake Survey Y1 - 2021 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-427902 SN - 1866-8372 IS - 1105 ER - TY - JOUR A1 - Henkel, Janin A1 - Coleman, Charles Dominic A1 - Schraplau, Anne A1 - Jöhrens, Korinna A1 - Weber, Daniela A1 - Castro, Jose Pedro A1 - Hugo, Martin A1 - Schulz, Tim Julius A1 - Krämer, Stephanie A1 - Schürmann, Annette A1 - Püschel, Gerhard Paul T1 - Induction of Steatohepatitis (NASH) with Insulin Resistance in Wild-type B6 Mice by a Western-type Diet Containing Soybean Oil and Cholesterol JF - Molecular medicine N2 - Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are hepatic manifestations of the metabolic syndrome. Many currently used animal models of NAFLD/NASH lack clinical features of either NASH or metabolic syndrome such as hepatic inflammation and fibrosis (e.g., high-fat diets) or overweight and insulin resistance (e.g., methionine-choline-deficient diets), or they are based on monogenetic defects (e.g., ob/ob mice). In the current study, a Western-type diet containing soybean oil with high n-6-PUFA and 0.75% cholesterol (SOD + Cho) induced steatosis, inflammation and fibrosis accompanied by hepatic lipid peroxidation and oxidative stress in livers of C57BL/6-mice, which in addition showed increased weight gain and insulin resistance, thus displaying a phenotype closely resembling all clinical features of NASH in patients with metabolic syndrome. In striking contrast, a soybean oil-containing Western-type diet without cholesterol (SOD) induced only mild steatosis but not hepatic inflammation, fibrosis, weight gain or insulin resistance. Another high-fat diet, mainly consisting of lard and supplemented with fructose in drinking water (LAD + Fru), resulted in more prominent weight gain, insulin resistance and hepatic steatosis than SOD + Cho, but livers were devoid of inflammation and fibrosis. Although both LAD + Fru-and SOD + Cho-fed animals had high plasma cholesterol, liver cholesterol was elevated only in SOD + Cho animals. Cholesterol induced expression of chemotactic and inflammatory cytokines in cultured Kupffer cells and rendered hepatocytes more susceptible to apoptosis. In summary, dietary cholesterol in the SOD + Cho diet may trigger hepatic inflammation and fibrosis. SOD + Cho-fed animals may be a useful disease model displaying many clinical features of patients with the metabolic syndrome and NASH. KW - Nonalcoholic Steatohepatitis (NASH) KW - Typical Western Diet KW - Nonalcoholic Fatty Liver Disease (NAFLD) KW - Dietary Cholesterol KW - Kupffer Cells Y1 - 2017 U6 - https://doi.org/10.2119/molmed.2016.00203 SN - 1076-1551 SN - 1528-3658 VL - 23 SP - 70 EP - 82 PB - Feinstein Inst. for Medical Research CY - Manhasset ER - TY - GEN A1 - Henkel, Janin A1 - Buchheim-Dieckow, Katja A1 - Castro, José Pedro A1 - Laeger, Thomas A1 - Wardelmann, Kristina A1 - Kleinridders, André A1 - Jöhrens, Korinna A1 - Püschel, Gerhard Paul T1 - Reduced Oxidative Stress and Enhanced FGF21 Formation in Livers of Endurance-Exercised Rats with Diet-Induced NASH T2 - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe N2 - Non-alcoholic fatty liver diseases (NAFLD) including the severe form with steatohepatitis (NASH) are highly prevalent ailments to which no approved pharmacological treatment exists. Dietary intervention aiming at 10% weight reduction is efficient but fails due to low compliance. Increase in physical activity is an alternative that improved NAFLD even in the absence of weight reduction. The underlying mechanisms are unclear and cannot be studied in humans. Here, a rat NAFLD model was developed that reproduces many facets of the diet-induced NAFLD in humans. The impact of endurance exercise was studied in this model. Male Wistar rats received control chow or a NASH-inducing diet rich in fat, cholesterol, and fructose. Both diet groups were subdivided into a sedentary and an endurance exercise group. Animals receiving the NASH-inducing diet gained more body weight, got glucose intolerant and developed a liver pathology with steatosis, hepatocyte hypertrophy, inflammation and fibrosis typical of NAFLD or NASH. Contrary to expectations, endurance exercise did not improve the NASH activity score and even enhanced hepatic inflammation. However, endurance exercise attenuated the hepatic cholesterol overload and the ensuing severe oxidative stress. In addition, exercise improved glucose tolerance possibly in part by induction of hepatic FGF21 production. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 807 KW - NAFLD KW - NASH KW - endurance exercise KW - FGF21 KW - glucose intolerance KW - cholesterol KW - oxidative stress Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-442384 SN - 1866-8372 IS - 807 ER - TY - JOUR A1 - Henkel, Janin A1 - Buchheim-Dieckow, Katja A1 - Castro, José Pedro A1 - Laeger, Thomas A1 - Wardelmann, Kristina A1 - Kleinridders, André A1 - Jöhrens, Korinna A1 - Püschel, Gerhard Paul T1 - Reduced Oxidative Stress and Enhanced FGF21 Formation in Livers of Endurance-Exercised Rats with Diet-Induced NASH JF - Nutrients N2 - Non-alcoholic fatty liver diseases (NAFLD) including the severe form with steatohepatitis (NASH) are highly prevalent ailments to which no approved pharmacological treatment exists. Dietary intervention aiming at 10% weight reduction is efficient but fails due to low compliance. Increase in physical activity is an alternative that improved NAFLD even in the absence of weight reduction. The underlying mechanisms are unclear and cannot be studied in humans. Here, a rat NAFLD model was developed that reproduces many facets of the diet-induced NAFLD in humans. The impact of endurance exercise was studied in this model. Male Wistar rats received control chow or a NASH-inducing diet rich in fat, cholesterol, and fructose. Both diet groups were subdivided into a sedentary and an endurance exercise group. Animals receiving the NASH-inducing diet gained more body weight, got glucose intolerant and developed a liver pathology with steatosis, hepatocyte hypertrophy, inflammation and fibrosis typical of NAFLD or NASH. Contrary to expectations, endurance exercise did not improve the NASH activity score and even enhanced hepatic inflammation. However, endurance exercise attenuated the hepatic cholesterol overload and the ensuing severe oxidative stress. In addition, exercise improved glucose tolerance possibly in part by induction of hepatic FGF21 production. KW - NAFLD KW - NASH KW - endurance exercise KW - FGF21 KW - glucose intolerance KW - cholesterol KW - oxidative stress Y1 - 2019 U6 - https://doi.org/10.3390/nu11112709 SN - 2072-6643 VL - 11 IS - 11 PB - MDPI CY - Basel ER - TY - JOUR A1 - Henkel, Janin A1 - Alfine, Eugenia A1 - Saín, Juliana A1 - Jöhrens, Korinna A1 - Weber, Daniela A1 - Castro, José Pedro A1 - König, Jeannette A1 - Stuhlmann, Christin A1 - Vahrenbrink, Madita A1 - Jonas, Wenke A1 - Kleinridders, André A1 - Püschel, Gerhard Paul T1 - Soybean Oil-Derived Poly-Unsaturated Fatty Acids Enhance Liver Damage in NAFLD Induced by Dietary Cholesterol JF - Nutrients N2 - While the impact of dietary cholesterol on the progression of atherosclerosis has probably been overestimated, increasing evidence suggests that dietary cholesterol might favor the transition from blunt steatosis to non-alcoholic steatohepatitis (NASH), especially in combination with high fat diets. It is poorly understood how cholesterol alone or in combination with other dietary lipid components contributes to the development of lipotoxicity. The current study demonstrated that liver damage caused by dietary cholesterol in mice was strongly enhanced by a high fat diet containing soybean oil-derived ω6-poly-unsaturated fatty acids (ω6-PUFA), but not by a lard-based high fat diet containing mainly saturated fatty acids. In contrast to the lard-based diet the soybean oil-based diet augmented cholesterol accumulation in hepatocytes, presumably by impairing cholesterol-eliminating pathways. The soybean oil-based diet enhanced cholesterol-induced mitochondrial damage and amplified the ensuing oxidative stress, probably by peroxidation of poly-unsaturated fatty acids. This resulted in hepatocyte death, recruitment of inflammatory cells, and fibrosis, and caused a transition from steatosis to NASH, doubling the NASH activity score. Thus, the recommendation to reduce cholesterol intake, in particular in diets rich in ω6-PUFA, although not necessary to reduce the risk of atherosclerosis, might be sensible for patients suffering from non-alcoholic fatty liver disease. KW - non-alcoholic fatty liver disease (NAFLD) KW - NASH KW - cholesterol KW - PUFA KW - inflammation KW - oxidative stress Y1 - 2018 U6 - https://doi.org/10.3390/nu10091326 SN - 2072-6643 VL - 10 IS - 9 SP - 1 EP - 17 PB - Molecular Diversity Preservation International (MDPI) CY - Basel ER - TY - GEN A1 - Henkel, Janin A1 - Alfine, Eugenia A1 - Saín, Juliana A1 - Jöhrens, Korinna A1 - Weber, Daniela A1 - Castro, José Pedro A1 - König, Jeannette A1 - Stuhlmann, Christin A1 - Vahrenbrink, Madita A1 - Jonas, Wenke A1 - Kleinridders, André A1 - Püschel, Gerhard Paul T1 - Soybean Oil-Derived Poly-Unsaturated Fatty Acids Enhance Liver Damage in NAFLD Induced by Dietary Cholesterol T2 - Nutrients N2 - While the impact of dietary cholesterol on the progression of atherosclerosis has probably been overestimated, increasing evidence suggests that dietary cholesterol might favor the transition from blunt steatosis to non-alcoholic steatohepatitis (NASH), especially in combination with high fat diets. It is poorly understood how cholesterol alone or in combination with other dietary lipid components contributes to the development of lipotoxicity. The current study demonstrated that liver damage caused by dietary cholesterol in mice was strongly enhanced by a high fat diet containing soybean oil-derived ω6-poly-unsaturated fatty acids (ω6-PUFA), but not by a lard-based high fat diet containing mainly saturated fatty acids. In contrast to the lard-based diet the soybean oil-based diet augmented cholesterol accumulation in hepatocytes, presumably by impairing cholesterol-eliminating pathways. The soybean oil-based diet enhanced cholesterol-induced mitochondrial damage and amplified the ensuing oxidative stress, probably by peroxidation of poly-unsaturated fatty acids. This resulted in hepatocyte death, recruitment of inflammatory cells, and fibrosis, and caused a transition from steatosis to NASH, doubling the NASH activity score. Thus, the recommendation to reduce cholesterol intake, in particular in diets rich in ω6-PUFA, although not necessary to reduce the risk of atherosclerosis, might be sensible for patients suffering from non-alcoholic fatty liver disease. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 479 KW - non-alcoholic fatty liver disease (NAFLD) KW - NASH KW - cholesterol KW - PUFA KW - inflammation KW - oxidative stress Y1 - 2018 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-419773 ER - TY - GEN A1 - Wardelmann, Kristina A1 - Rath, Michaela A1 - Castro, José Pedro A1 - Blümel, Sabine A1 - Schell, Mareike A1 - Hauffe, Robert A1 - Schumacher, Fabian A1 - Flore, Tanina A1 - Ritter, Katrin A1 - Wernitz, Andreas A1 - Hosoi, Toru A1 - Ozawa, Koichiro A1 - Kleuser, Burkhard A1 - Weiß, Jürgen A1 - Schürmann, Annette A1 - Kleinridders, André T1 - Central acting Hsp10 regulates mitochondrial function, fatty acid metabolism and insulin sensitivity in the hypothalamus T2 - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe N2 - Mitochondria are critical for hypothalamic function and regulators of metabolism. Hypothalamic mitochondrial dysfunction with decreased mitochondrial chaperone expression is present in type 2 diabetes (T2D). Recently, we demonstrated that a dysregulated mitochondrial stress response (MSR) with reduced chaperone expression in the hypothalamus is an early event in obesity development due to insufficient insulin signaling. Although insulin activates this response and improves metabolism, the metabolic impact of one of its members, the mitochondrial chaperone heat shock protein 10 (Hsp10), is unknown. Thus, we hypothesized that a reduction of Hsp10 in hypothalamic neurons will impair mitochondrial function and impact brain insulin action. Therefore, we investigated the role of chaperone Hsp10 by introducing a lentiviral-mediated Hsp10 knockdown (KD) in the hypothalamic cell line CLU-183 and in the arcuate nucleus (ARC) of C57BL/6N male mice. We analyzed mitochondrial function and insulin signaling utilizing qPCR, Western blot, XF96 Analyzer, immunohistochemistry, and microscopy techniques. We show that Hsp10 expression is reduced in T2D mice brains and regulated by leptin in vitro. Hsp10 KD in hypothalamic cells induced mitochondrial dysfunction with altered fatty acid metabolism and increased mitochondria-specific oxidative stress resulting in neuronal insulin resistance. Consequently, the reduction of Hsp10 in the ARC of C57BL/6N mice caused hypothalamic insulin resistance with acute liver insulin resistance. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 1165 KW - brain insulin signaling KW - mitochondria KW - oxidative stress KW - fatty acid metabolism Y1 - 2021 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-522985 SN - 1866-8372 IS - 5 ER - TY - JOUR A1 - Wardelmann, Kristina A1 - Rath, Michaela A1 - Castro, José Pedro A1 - Blümel, Sabine A1 - Schell, Mareike A1 - Hauffe, Robert A1 - Schumacher, Fabian A1 - Flore, Tanina A1 - Ritter, Katrin A1 - Wernitz, Andreas A1 - Hosoi, Toru A1 - Ozawa, Koichiro A1 - Kleuser, Burkhard A1 - Weiß, Jürgen A1 - Schürmann, Annette A1 - Kleinridders, André T1 - Central acting Hsp10 regulates mitochondrial function, fatty acid metabolism and insulin sensitivity in the hypothalamus JF - Antioxidants N2 - Mitochondria are critical for hypothalamic function and regulators of metabolism. Hypothalamic mitochondrial dysfunction with decreased mitochondrial chaperone expression is present in type 2 diabetes (T2D). Recently, we demonstrated that a dysregulated mitochondrial stress response (MSR) with reduced chaperone expression in the hypothalamus is an early event in obesity development due to insufficient insulin signaling. Although insulin activates this response and improves metabolism, the metabolic impact of one of its members, the mitochondrial chaperone heat shock protein 10 (Hsp10), is unknown. Thus, we hypothesized that a reduction of Hsp10 in hypothalamic neurons will impair mitochondrial function and impact brain insulin action. Therefore, we investigated the role of chaperone Hsp10 by introducing a lentiviral-mediated Hsp10 knockdown (KD) in the hypothalamic cell line CLU-183 and in the arcuate nucleus (ARC) of C57BL/6N male mice. We analyzed mitochondrial function and insulin signaling utilizing qPCR, Western blot, XF96 Analyzer, immunohistochemistry, and microscopy techniques. We show that Hsp10 expression is reduced in T2D mice brains and regulated by leptin in vitro. Hsp10 KD in hypothalamic cells induced mitochondrial dysfunction with altered fatty acid metabolism and increased mitochondria-specific oxidative stress resulting in neuronal insulin resistance. Consequently, the reduction of Hsp10 in the ARC of C57BL/6N mice caused hypothalamic insulin resistance with acute liver insulin resistance. KW - brain insulin signaling KW - mitochondria KW - oxidative stress KW - fatty acid metabolism Y1 - 2021 U6 - https://doi.org/10.3390/antiox10050711 SN - 2076-3921 VL - 10 IS - 5 PB - MDPI CY - Basel ER -