23 research outputs found

    Bau und Test von drei Dish/Stirling-Einheiten auf dem deutsch-spanischen Testzentrum in Almeria Schlussbericht

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    A report is given on the results of the BMFT research project which has now been finished. The aim of the project was the development, the construction and the test of a Dish-Stirling-system. The permanent test was carried out at a system of the third generation. The following project targets were fully achieved: Proof of the efficiency, Proof of the reliability, Proof of the permanent operationability, Reduction of the system costs. The systems have been in continuous operation since September 1993 and have worked more than 10.000 operating hours at an availability exceeding 90%. (HW)Es wird ueber das Ergebnis eines jetzt abgeschlossenen BMFT-Forschungsvorhabens berichtet. Ziel des Vorhabens war die Entwicklung, der Bau und der Test eines Disk-Stirling-Systems. Der Dauertest wurde am in der 3. Generation befindlichen System durchgefuehrt. Die Projektziele Nachweis der Leistungsfaehigkeit; Nachweis der Zuverlaessigkeit; Nachweis der Dauerbetriebsfaehigkeit; Systemkostenreduzierung konnten in vollem Umfang erreicht werden. Die Systeme befinden sich seit Dezember 1993 im Dauerbetrieb und haben bei einer Verfuegbarkeit von ueber 90% mehr als 10000 Betriebsstunden akkumuliert. (HW)Available from TIB Hannover: F95B305+a / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEBundesministerium fuer Forschung und Technologie (BMFT), Bonn (Germany)DEGerman

    Dauerbetrieb von drei Dish-Stirling-Einheiten auf dem deutsch-spanischen Testzentrum in Almeria Abschlussbericht

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    The report describes a BMFT research project at the Spanish test center at Almeria. Three 9kW dish-Stirling passenger car engines were tested in continuous operation. The report comprises the following chapters: Research goals; Research findings; Cooperation with other institutions; Further prospects of the research project. (HW)Es wird berichtet ueber ein Forschungsvorhaben des BMFT im spanischen Testzentrum Almeria. Drei 9 kW Dish-Stirling-Einheiten wurden im Dauerbetrieb erprobt. Der Bericht enthaelt folgende Kapitel: - Aufgabenstellung - Ergebnisse des Forschungsvorhabens - Zusammenarbeit mit anderen Stellen - Weiterentwicklung des Forschungsvorhabens. (HW)Available from TIB Hannover: F96B656+a / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEBundesministerium fuer Bildung, Wissenschaft, Forschung und Technologie, Bonn (Germany)DEGerman

    Inhibition of PI-3-K and AKT amplifies Kv1.3 Inhibitor-induced death of human T leukemia cells

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    Background/Aims: We have previously shown that inhibition of the mitochondrial Kv1.3 channel results in an initial mitochondrial hyperpolarization and a release of oxygen radicals that mediate mitochondrial depolarization, cytochrome c release and death. Here, we investigated whether inhibition of Kv1.3 channels can also induce cellular resistance mechanisms that counteract the induction of cell death under certain conditions. Methods: We treated leukemic T cells with the mitochondria-targeted Kv1.3 inhibitor PCARBTP and determined the activity of different kinases associated with cell survival including ZAP70, PI-3-K, AKT, JNK and ERK by measuring the activation-associated phosphorylation of these proteins. Furthermore, we inhibited AKT and JNK and determined the effect of PCARBTP-induced tumor cell death. Results: We demonstrate that treatment of Jurkat T leukemia cells with low doses of the mitochondria-targeted inhibitor of Kv1.3 PCARBTP (0.25 \u3bcM or 1 \u3bcM) for 10 minutes induced a constitutive phosphorylation/activation of the pro-survival signaling molecules ZAP70, PI- 3-K, AKT and JNK, while the phosphorylation/activation of ERK was not affected. Stimulation of Jurkat cells via the TCR/CD3 complex induced an additional activation of a similar pattern of signaling events. Higher doses of the Kv1.3 inhibitor, i.e. 10 \u3bcM PCARBTP, reduced the basal phosphorylation/activation of these signaling molecules and also impaired their activation upon stimulation via the TCR/CD3 complex. A low dose of PCARBTP, i.e. 0.25 \u3bcM PCARBTP, was almost without any effect on cell death. In contrast, concomitant inhibition of PI-3-K or AKT greatly sensitized Jurkat leukemia cells to the Kv1.3 inhibitor PCARBTP and allowed induction of cell death already at 0.25 \u3bcM PCARBTP. Conclusion: These studies indicate that Jurkat leukemia cells respond to low doses of the mitochondria-targeted Kv1.3 inhibitor PCARBTP with an activation of survival signals counteracting cell death. Inhibition of these T cell survival signals sensitizes leukemia cells to death induced by mitochondria-targeted Kv1.3 inhibitors. High doses of the Kv1.3 inhibitor inactivate these signals directly permitting death
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