TY - JOUR A1 - Räder, Andy A1 - Schubarth, Wilfried A1 - Resch-Esser, Ursula A1 - Kube, Christian A1 - Strigin, Natalia A1 - Finschow, Michael A1 - Bode, Anja A1 - Püschel, Almuth T1 - Portal = Zukunftsinvestition: Förderung des wissenschaftlichen Nachwuchses BT - Die Potsdamer Universitätszeitung N2 - Aus dem Inhalt: - Zukunftsinvestition: Förderung des wissenschaftlichen Nachwuchses - Nobelpreisträger in Potsdam - Aktionen gegen Studiengebühren - Erdbebenanalyse in Minuten T3 - Portal: Das Potsdamer Universitätsmagazin - 07-09/2005 Y1 - 2005 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-439906 SN - 1618-6893 IS - 07-09/2005 ER - TY - GEN A1 - Hespeling, Ursula A1 - Jungermann, Kurt A1 - Püschel, Gerhard Paul T1 - Feedback-inhibition of glucagon-stimulated glycogenolysis in hepatocyte/kupffer cell cocultures by glucagon-elicited prostaglandin production in kupffer cells N2 - Prostaglandins, released from Kupffer cells, have been shown to mediate the increase in hepatic glycogenolysis by various stimuli such as zymosan, endotoxin, immune complexes, and anaphylotoxin C3a involving prostaglandin (PG) receptors coupled to phospholipase C via a G(0) protein. PGs also decreased glucagon-stimulated glycogenolysis in hepatocytes by a different signal chain involving PGE(2) receptors coupled to adenylate cyclase via a G(i) protein (EP(3) receptors). The source of the prostaglandins for this latter glucagon-antagonistic action is so far unknown. This study provides evidence that Kupffer cells may be one source: in Kupffer cells, maintained in primary culture for 72 hours, glucagon (0.1 to 10 nmol/ L) increased PGE(2), PGF(2 alpha), and PGD(2) synthesis rapidly and transiently. Maximal prostaglandin concentrations were reached after 5 minutes. Glucagon (1 nmol/L) elevated the cyclic adenosine monophosphate (cAMP) and inositol triphosphate (InsP(3)) levels in Kupffer cells about fivefold and twofold, respectively. The increase in glyco gen phosphorylase activity elicited by 1 nmol/L glucagon was about twice as large in monocultures of hepatocytes than in cocultures of hepatocytes and Kupffer cells with the same hepatocyte density. Treatment of cocultures with 500 mu mol/L acetylsalicylic acid (ASA) to irreversibly inhibit cyclooxygenase (PGH-synthase) 30 minutes before addition of glucagon abolished this difference. These data support the hypothesis that PGs produced by Kupffer cells in response to glucagon might participate in a feedback loop inhibiting glucagon-stimulated glycogenolysis in hepatocytes. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - paper 036 KW - perfused-rat-liver KW - aggregated immunoglobulin-g KW - intercellular communication KW - adenylate-cyclase KW - arachidonic-acid KW - activation KW - glucose Y1 - 1995 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus-16697 ER - TY - GEN A1 - Püschel, Gerhard Paul A1 - Hespeling, Ursula A1 - Oppermann, Martin A1 - Dieter, Peter T1 - Increase in prostanoid formation in rat liver macrophages (Kupffer cells) by human anaphylatoxin C3a N2 - Human anaphylatoxin C3a increases glycogenolysis in perfused rat liver. This action is inhibited by prostanoid synthesis inhibitors and prostanoid antagonists. Because prostanoids but not anaphylatoxin C3a can increase glycogenolysis in hepatocytes, it has been proposed that prostanoid formation in nonparenchymal cells represents an important step in the C3a-dependent increase in hepatic glycogenolysis. This study shows that (a) human anaphylatoxin C3a (0.1 to 10 mug/ml) dose-dependently increased prostaglandin D2, thromboxane B, and prostaglandin F2alpha formation in rat liver macrophages (Kupffer cells); (b) the C3a-mediated increase in prostanoid formation was maximal after 2 min and showed tachyphylaxis; and (c) the C3a-elicited prostanoid formation could be inhibited specifically by preincubation of C3a with carboxypeptidase B to remove the essential C-terminal arginine or by preincubation of C3a with Fab fragments of a neutralizing monoclonal antibody. These data support the hypothesis that the C3a-dependent activation of hepatic glycogenolysis is mediated by way of a C3a-induced prostanoid production in Kupffer cells. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - paper 037 KW - lactate output KW - glucose KW - complement KW - flow KW - prostaglandin-f2-alpha Y1 - 1993 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus-16716 ER - TY - GEN A1 - Hespeling, Ursula A1 - Püschel, Gerhard Paul A1 - Jungermann, Kurt A1 - Götze, Otto A1 - Zwirner, Jörg T1 - Stimulation of glycogen phosphorylase in rat hepatocytes via prostanoid release from Kupffer cells by recombinant rat anaphylatoxin C5a but not by native human C5a in hepatocyte/Kupffer cell co-cultures N2 - Human anaphylatoxin C3a had previously been shown to increase glycogenolysis in perfused rat liver and prostanoid formation in rat liver macrophages. Surprisingly, human C5a, which in other systems elicited stronger responses than C3a, did not increase glycogenolysis in perfused rat liver. Species incompatibilities within the experimental system had been supposed to be the reason. The current study supports this hypothesis: (1) In rat liver macrophages that had been maintained in primary culture for 72 h recombinant rat anaphylatoxin C5a in concentrations between 0.1 and 10 pg/ml increased the formation of thromboxane A₂, prostaglandin D₂, E₂ and F₂α6- to 12-fold over basal within 10 min. In contrast, human anaphylatoxin C5a did not increase prostanoid formation in rat Kupffer cells. (2) The increase in prostanoid formation by recombinant rat C5a was specific. It was inhibited by a neutralizing monoclonal antibody. (3) In co-cultures of rat hepatocytes and rat Kupffer cells but not in hepatocyte mono-cultures recombinant rat C5a increased glycogen phosphorylase activity 3-fold over basal. This effect was inhibited by incubation of the co-cultures with 500 μM acetylsalicyclic acid. Thus, C5a generated either locally in the liver or systemically e.g. in the course of sepsis, may increase hepatic glycogenolysis by a prostanoid-mediated intercellular communication between Kupffer cells and hepatocytes. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - paper 117 Y1 - 1995 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus-45909 ER - TY - BOOK A1 - Bircken, Margrid A1 - Lüdecke, Marianne A1 - Peitsch, Helmut A1 - Runge, Anita A1 - Meier, Monika A1 - Püschel, Ursula A1 - Bock, Helmut A1 - Dahlke, Birgit A1 - Kaufmann, Eva A1 - Schlenstedt, Silvia A1 - Maydell, Miriam von A1 - Lorenz, Natalie A1 - Schiller, Dieter A1 - Fetscher, Justus A1 - Klapdor, Heike A1 - Barck, Simone A1 - Jacobeit, Sigrid A1 - Melchert, Monika A1 - Künzel, Christine A1 - Rudolph, Andrea ED - Bircken, Margrid ED - Lüdecke, Marianne ED - Peitsch, Helmut T1 - Brüche und Umbrüche BT - Frauen, Literatur und soziale Bewegungen N2 - Einen Überblick über historische Veränderungen der Bedingungen, unter denen Frauen geschrieben haben, sollte eine Ringvorlesung vermitteln, die das Institut für Germanistik der Universität Potsdam in zwei Semestern der Jahre 2005/06 veranstaltete. Unter dem Titel »Lesen und Schreiben in Umbrüchen« macht der Lehrplan in Brandenburg und Berlin für die Sekundarstufe II mindestens zwei der drei Umbrüche von 1933, 1945 und 1989 verbindlich zum Gegenstand des Literaturunterrichts. Als Institut der einzigen lehrerbildenden Universität des Landes wollten wir nicht nur Vorschläge machen, welche Autoren sich zur Behandlung dieser Umbrüche des zwanzigsten Jahrhunderts anbieten, sondern zum einen durch die Beschränkung auf weibliche Autoren in den Umbrüchen, der Veränderung gesellschaftlichen Verhältnisse, die Geschlechterverhältnisse hervorheben und über ihnen die Brüche in den Biographien nicht aussparen, zum anderen dem Blick auf die Umbrüche zwischen 1933 und 1989 durch eine Einbeziehung früherer Umbrüche historische Tiefenschärfe geben. Von der Französischen Revolution bis zur ›Wende‹ haben gesellschaftliche Umbrüche nicht nur das Leben weiblicher Autoren im Allgemeinen bestimmt, sondern auch ihr Schreiben als eine Auseinandersetzung mit ganz individuellen Brüchen. KW - soziale Bewegung KW - Frauenliteratur Y1 - 2010 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus-46029 SN - 978-3-86956-085-4 PB - Universitätsverlag Potsdam CY - Potsdam ER -