@phdthesis{Ritter2002, author = {Ritter, Andreas}, title = {Wandlungen in der Steuerung des DDR-Hochleistungssports in den 1960er und 1970er Jahren}, publisher = {Universit{\"a}tsverlag Potsdam}, address = {Potsdam}, isbn = {978-3-935024-61-7}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-0000665}, school = {Universit{\"a}t Potsdam}, pages = {337}, year = {2002}, abstract = {Die intensive Auswertung unterschiedlicher schriftlicher und m{\"u}ndlicher Quellen sowie die Erschließung von damals "geheimer" Literatur f{\"u}r die Forschung heute erm{\"o}glicht eine differenzierte Rekonstruktion historischer Abl{\"a}ufe. Die vorliegende Arbeit nutzt diesen Zugang zur Darstellung von kleineren und gr{\"o}ßeren DDR-internen sportpolitischen Strukturwandlungen der 1960er und 1970er Jahre, die ihren H{\"o}hepunkt in einer dramatischen Umsteuerung des DDR-Hochleistungssports fanden. Es wird gezeigt, wie die Akteure unter F{\"u}hrung von Manfred EWALD, gew{\"a}hltem Mitglied des SED-Zentralkomitees, einer Zentralfigur des DDR-Sports (vergleichbar mit der Bedeutung eines Willi DAUME im Westen) zwischen Systemzw{\"a}ngen und individueller Handlungsfreiheit innerhalb des Rahmens einer Diktatur in der Phase des Wechsels von Walter ULBRICHT zu Erich HONECKER eine Effektivierung des zentralistischen Modells durchsetzten (eine Parallele zum Ansatz von Monika KAISER). Im Gegensatz zu vielen kontroversen Erkl{\"a}rungsmodellen belegt der Verf., dass die Medaillenerfolge durch die zentrale Steuerung aller Abl{\"a}ufe gew{\"a}hrleistet wurden. Ohne SED-Auftrag wurde 1967 die "Leistungssportkommission der DDR" (LSK der DDR) gebildet. Im Unterschied zu den zahlreichen vom Verf. erstmals dargestellten Vorg{\"a}ngermodellen war diese SED-LSK "oberhalb des DTSB" angesiedelt und erteilte ihm Parteiauftr{\"a}ge - die Unterordnung des organisierten Sports unter die Autorit{\"a}t des Zentralkomitee machte angesichts der "Nationalen Fronten" von Armeesportvereinigung "Vorw{\"a}rts" und Sportvereinigung "Dynamo" (SPITZER) jegliche zentrale Sportpolitik erst durchsetzbar. Zur "LSK der DDR" waren SED-Mitglieder abgeordnet, welche ihr Sachgebiet vertraten und nach gemeinsamer Beschlussfassung die Ergebnisse der LSK-Arbeit wiederum in ihrem jeweiligen T{\"a}tigkeitsfeld durchzusetzen hatten, was in der Diss. ausgef{\"u}hrt wird. Sportvertreter ebenso wie hochrangige Abgesandte der Ministerien, die mit der Produktion von G{\"u}tern f{\"u}r den Hochleistungssport befasst waren, geh{\"o}rten den LSK-Gremien an, die auch die DDR-Sportwissenschaft steuerten; es l{\"a}sst sich sogar nachweisen, dass die Herrschaft {\"u}ber diesen wichtigen Apparat sowie die Dopingforschung ein Hauptmotiv der LSK-Bildung gewesen ist. Durch seine Quellenorientierung und die F{\"u}lle an Belegen gibt die vorliegende Arbeit neue Anreize zur Auseinandersetzung mit dem Ph{\"a}nomen der Steuerung des Hochleistungssports in der DDR - auch {\"u}ber den Untersuchungszeitraum hinaus. Die Untersuchung wurde von der Humanwissenschaftlichen Fakult{\"a}t der Universit{\"a}t Potsdam als Dissertation angenommen. Sie geht auf ein Stipendium dieser Universit{\"a}t zur{\"u}ck; das Verfahren konnte mit einem Pr{\"a}dikat abgeschlossen werden. Gutachter waren Prof. Dr. Dr. Gertrud PFISTER, Kopenhagen, Prof. Dr. Christoph KLEßMANN, Potsdam, und der Betreuer, Steady Visiting Prof. Univ. Odense, Priv.-Doz. Dr. habil. Giselher SPITZER, Berlin / Potsdam / Odense (D{\"a}nemark).}, language = {de} } @article{HoffmannOsterlohStoneetal.2012, author = {Hoffmann, Anne and Osterloh, Lukas and Stone, Robert and Lampert, Astrid and Ritter, Christoph and Stock, Maria and Tunved, Peter and Hennig, Tabea and B{\"o}ckmann, Christine and Li, Shao-Meng and Eleftheriadis, Kostas and Maturilli, Marion and Orgis, Thomas and Herber, Andreas and Neuber, Roland and Dethloff, Klaus}, title = {Remote sensing and in-situ measurements of tropospheric aerosol, a PAMARCMiP case study}, series = {Atmospheric environment : air pollution ; emissions, transport and dispersion, transformation, deposition effects, micrometeorology, urban atmosphere, global atmosphere}, volume = {52}, journal = {Atmospheric environment : air pollution ; emissions, transport and dispersion, transformation, deposition effects, micrometeorology, urban atmosphere, global atmosphere}, number = {3}, publisher = {Elsevier}, address = {Oxford}, issn = {1352-2310}, doi = {10.1016/j.atmosenv.2011.11.027}, pages = {56 -- 66}, year = {2012}, abstract = {In this work, a closure experiment for tropospheric aerosol is presented. Aerosol size distributions and single scattering albedo from remote sensing data are compared to those measured in-situ. An aerosol pollution event on 4 April 2009 was observed by ground based and airborne lidar and photometer in and around Ny-Alesund, Spitsbergen, as well as by DMPS, nephelometer and particle soot absorption photometer at the nearby Zeppelin Mountain Research Station. The presented measurements were conducted in an area of 40 x 20 km around Ny-Alesund as part of the 2009 Polar Airborne Measurements and Arctic Regional Climate Model Simulation Project (PAMARCMiP). Aerosol mainly in the accumulation mode was found in the lower troposphere, however, enhanced backscattering was observed up to the tropopause altitude. A comparison of meteorological data available at different locations reveals a stable multi-layer-structure of the lower troposphere. It is followed by the retrieval of optical and microphysical aerosol parameters. Extinction values have been derived using two different methods, and it was found that extinction (especially in the UV) derived from Raman lidar data significantly surpasses the extinction derived from photometer AOD profiles. Airborne lidar data shows volume depolarization values to be less than 2.5\% between 500 m and 2.5 km altitude, hence, particles in this range can be assumed to be of spherical shape. In-situ particle number concentrations measured at the Zeppelin Mountain Research Station at 474 m altitude peak at about 0.18 mu m diameter, which was also found for the microphysical inversion calculations performed at 850 m and 1500 m altitude. Number concentrations depend on the assumed extinction values, and slightly decrease with altitude as well as the effective particle diameter. A low imaginary part in the derived refractive index suggests weakly absorbing aerosols, which is confirmed by low black carbon concentrations, measured at the Zeppelin Mountain as well as on board the Polar 5 aircraft.}, language = {en} } @misc{WardelmannRathCastroetal.2021, author = {Wardelmann, Kristina and Rath, Michaela and Castro, Jos{\´e} Pedro and Bl{\"u}mel, Sabine and Schell, Mareike and Hauffe, Robert and Schumacher, Fabian and Flore, Tanina and Ritter, Katrin and Wernitz, Andreas and Hosoi, Toru and Ozawa, Koichiro and Kleuser, Burkhard and Weiß, J{\"u}rgen and Sch{\"u}rmann, Annette and Kleinridders, Andr{\´e}}, title = {Central acting Hsp10 regulates mitochondrial function, fatty acid metabolism and insulin sensitivity in the hypothalamus}, series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, number = {5}, issn = {1866-8372}, doi = {10.25932/publishup-52298}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-522985}, pages = {24}, year = {2021}, abstract = {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.}, language = {en} } @misc{SchellChudobaLeboucheretal.2020, author = {Schell, Mareike and Chudoba, Chantal and Leboucher, Antoine and Alfine, Eugenia and Flore, Tanina and Ritter, Katrin and Weiper, Katharina and Wernitz, Andreas and Henkel, Janin and Kleinridders, Andr{\´e}}, title = {Interplay of Dietary Fatty Acids and Cholesterol Impacts Brain Mitochondria and Insulin Action}, series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, number = {946}, issn = {1866-8372}, doi = {10.25932/publishup-47077}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-470773}, pages = {24}, year = {2020}, abstract = {Overconsumption of high-fat and cholesterol-containing diets is detrimental for metabolism and mitochondrial function, causes inflammatory responses and impairs insulin action in peripheral tissues. Dietary fatty acids can enter the brain to mediate the nutritional status, but also to influence neuronal homeostasis. Yet, it is unclear whether cholesterol-containing high-fat diets (HFDs) with different combinations of fatty acids exert metabolic stress and impact mitochondrial function in the brain. To investigate whether cholesterol in combination with different fatty acids impacts neuronal metabolism and mitochondrial function, C57BL/6J mice received different cholesterol-containing diets with either high concentrations of long-chain saturated fatty acids or soybean oil-derived poly-unsaturated fatty acids. In addition, CLU183 neurons were stimulated with combinations of palmitate, linoleic acid and cholesterol to assess their effects on metabolic stress, mitochondrial function and insulin action. The dietary interventions resulted in a molecular signature of metabolic stress in the hypothalamus with decreased expression of occludin and subunits of mitochondrial electron chain complexes, elevated protein carbonylation, as well as c-Jun N-terminal kinase (JNK) activation. Palmitate caused mitochondrial dysfunction, oxidative stress, insulin and insulin-like growth factor-1 (IGF-1) resistance, while cholesterol and linoleic acid did not cause functional alterations. Finally, we defined insulin receptor as a novel negative regulator of metabolically stress-induced JNK activation.}, language = {en} } @article{WardelmannRathCastroetal.2021, author = {Wardelmann, Kristina and Rath, Michaela and Castro, Jos{\´e} Pedro and Bl{\"u}mel, Sabine and Schell, Mareike and Hauffe, Robert and Schumacher, Fabian and Flore, Tanina and Ritter, Katrin and Wernitz, Andreas and Hosoi, Toru and Ozawa, Koichiro and Kleuser, Burkhard and Weiß, J{\"u}rgen and Sch{\"u}rmann, Annette and Kleinridders, Andr{\´e}}, title = {Central acting Hsp10 regulates mitochondrial function, fatty acid metabolism and insulin sensitivity in the hypothalamus}, series = {Antioxidants}, volume = {10}, journal = {Antioxidants}, number = {5}, publisher = {MDPI}, address = {Basel}, issn = {2076-3921}, doi = {10.3390/antiox10050711}, pages = {22}, year = {2021}, abstract = {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.}, language = {en} } @article{SchellChudobaLeboucheretal.2020, author = {Schell, Mareike and Chudoba, Chantal and Leboucher, Antoine and Alfine, Eugenia and Flore, Tanina and Ritter, Katrin and Weiper, Katharina and Wernitz, Andreas and Henkel, Janin and Kleinridders, Andr{\´e}}, title = {Interplay of Dietary Fatty Acids and Cholesterol Impacts Brain Mitochondria and Insulin Action}, series = {Nutrients}, volume = {12}, journal = {Nutrients}, number = {5}, publisher = {MDPI}, address = {Basel}, issn = {2072-6643}, doi = {10.3390/nu12051518}, pages = {22}, year = {2020}, abstract = {Overconsumption of high-fat and cholesterol-containing diets is detrimental for metabolism and mitochondrial function, causes inflammatory responses and impairs insulin action in peripheral tissues. Dietary fatty acids can enter the brain to mediate the nutritional status, but also to influence neuronal homeostasis. Yet, it is unclear whether cholesterol-containing high-fat diets (HFDs) with different combinations of fatty acids exert metabolic stress and impact mitochondrial function in the brain. To investigate whether cholesterol in combination with different fatty acids impacts neuronal metabolism and mitochondrial function, C57BL/6J mice received different cholesterol-containing diets with either high concentrations of long-chain saturated fatty acids or soybean oil-derived poly-unsaturated fatty acids. In addition, CLU183 neurons were stimulated with combinations of palmitate, linoleic acid and cholesterol to assess their effects on metabolic stress, mitochondrial function and insulin action. The dietary interventions resulted in a molecular signature of metabolic stress in the hypothalamus with decreased expression of occludin and subunits of mitochondrial electron chain complexes, elevated protein carbonylation, as well as c-Jun N-terminal kinase (JNK) activation. Palmitate caused mitochondrial dysfunction, oxidative stress, insulin and insulin-like growth factor-1 (IGF-1) resistance, while cholesterol and linoleic acid did not cause functional alterations. Finally, we defined insulin receptor as a novel negative regulator of metabolically stress-induced JNK activation.}, language = {en} }