TY - CHAP A1 - Ritz, Thomas A1 - Strauch, Jakob ED - Bick, Markus T1 - „Offline Strategie"-Patterns für mobile SOA Prozesse T2 - Mobile und ubiquitäre Informationssysteme : Technologien, Anwendungen und Dienste zur Unterstützung von mobiler Kollaboration ; Proceedings zur 5. Konferenz Mobile und Ubiquitäre Informationssysteme (MMS 2010) ; 23. - 25. Februar 2010 in Göttingen, Germany. - (GI-Edition : Proceedings ; 163) Y1 - 2010 SN - 978-3-88579-257-4 SP - 174 EP - 180 PB - Gesellschaft für Informatik CY - Bonn ER - TY - JOUR A1 - Ross, Jillian A1 - Plummer, Simon M. A1 - Rode, Anja A1 - Scheer, Nico A1 - Bower, Conrad C. A1 - Vogel, Ortwin A1 - Henderson, Colin J. A1 - Wolf, C. Roland A1 - Elcombe, Clifford R. T1 - Human constitutive androstane receptor (CAR) and pregnane X receptor (PXR) support the hypertrophic but not the hyperplastic response to the murine nongenotoxic hepatocarcinogens phenobarbital and chlordane in vivo JF - Toxicological Sciences N2 - Mouse nongenotoxic hepatocarcinogens phenobarbital (PB) and chlordane induce hepatomegaly characterized by hypertrophy and hyperplasia. Increased cell proliferation is implicated in the mechanism of tumor induction. The relevance of these tumors to human health is unclear. The xenoreceptors, constitutive androstane receptors (CARs), and pregnane X receptor (PXR) play key roles in these processes. Novel “humanized” and knockout models for both receptors were developed to investigate potential species differences in hepatomegaly. The effects of PB (80 mg/kg/4 days) and chlordane (10 mg/kg/4 days) were investigated in double humanized PXR and CAR (huPXR/huCAR), double knockout PXR and CAR (PXRKO/CARKO), and wild-type (WT) C57BL/6J mice. In WT mice, both compounds caused increased liver weight, hepatocellular hypertrophy, and cell proliferation. Both compounds caused alterations to a number of cell cycle genes consistent with induction of cell proliferation in WT mice. However, these gene expression changes did not occur in PXRKO/CARKO or huPXR/huCAR mice. Liver hypertrophy without hyperplasia was demonstrated in the huPXR/huCAR animals in response to both compounds. Induction of the CAR and PXR target genes, Cyp2b10 and Cyp3a11, was observed in both WT and huPXR/huCAR mouse lines following treatment with PB or chlordane. In the PXRKO/CARKO mice, neither liver growth nor induction of Cyp2b10 and Cyp3a11 was seen following PB or chlordane treatment, indicating that these effects are CAR/PXR dependent. These data suggest that the human receptors are able to support the chemically induced hypertrophic responses but not the hyperplastic (cell proliferation) responses. At this time, we cannot be certain that hCAR and hPXR when expressed in the mouse can function exactly as the genes do when they are expressed in human cells. However, all parameters investigated to date suggest that much of their functionality is maintained. Y1 - 2010 U6 - https://doi.org/10.1093/toxsci/kfq118 SN - 1096-0929 VL - 116 IS - 2 SP - 452 EP - 466 PB - Oxford University Press CY - Oxford ER - TY - JOUR A1 - Scheer, Nico A1 - Ross, Jillian A1 - Kapelyukh, Yury A1 - Rode, Anja A1 - Wolf, C. Roland T1 - In vivo responses of the human and murine pregnane X receptor to dexamethasone in mice JF - Drug Metabolism and Disposition N2 - Dexamethasone (DEX) is a potent and widely used anti-inflammatory and immunosuppressant glucocorticoid. It can bind and activate the pregnane X receptor (PXR), which plays a critical role as xenobiotic sensor in mammals to induce the expression of many enzymes, including cytochromes P450 in the CYP3A family. This induction results in its own metabolism. We have used a series of transgenic mouse lines, including a novel, improved humanized PXR line, to compare the induction profile of PXR-regulated drug-metabolizing enzymes after DEX administration, as well as looking at hepatic responses to rifampicin (RIF). The new humanized PXR model has uncovered further intriguing differences between the human and mouse receptors in that RIF only induced Cyp2b10 in the new humanized model. DEX was found to be a much more potent inducer of Cyp3a proteins in wild-type mice than in mice humanized for PXR. To assess whether PXR is involved in the detoxification of DEX in the liver, we analyzed the consequences of high doses of the glucocorticoid on hepatotoxicity on different PXR genetic backgrounds. We also studied these effects in an additional mouse model in which functional mouse Cyp3a genes have been deleted. These strains exhibited different sensitivities to DEX, indicating a protective role of the PXR and CYP3A proteins against the hepatotoxicity of this compound. Y1 - 2010 U6 - https://doi.org/10.1124/dmd.109.031872 SN - 1521-009X VL - 38 IS - 7 SP - 1046 EP - 1053 PB - ASPET CY - Bethesda ER - TY - BOOK A1 - Schelthoff, Christof T1 - Mathematik im ingenieurwissenschaftlichen Bachelorstudium / 4., überarb. Aufl. Y1 - 2010 SN - 978-3-8322-9288-1 PB - Shaker CY - Aachen ER - TY - BOOK A1 - Schelthoff, Christof T1 - Mathematik im ingenieurwissenschaftlichen Bachelorstudium : Lösung der Übungs- und Klausuraufgaben Y1 - 2010 SN - 978-3-8322-9502-8 PB - Shaker CY - Aachen ER - TY - JOUR A1 - Schermutzki, Margret T1 - In Modulen lehren, lernen und prüfen JF - In Modulen lehren, lernen und prüfen. Herausforderungen an die Hochschuldidaktik / Terbuyken, Gregor [Hrsg.] Y1 - 2010 SN - 978-3-8172-7809-1 N1 - Loccumer Protokoll 78/09 SP - 81 EP - 106 CY - Rehburg-Loccum ER - TY - JOUR A1 - Schiffer, Stefan A1 - Ferrein, Alexander A1 - Lakemeyer, Gerhard T1 - Proceedings of the Fourth International Conference on Intelligent Robotics and Applications (ICIRA 2011) JF - Proceedings of the Fourth International Conference on Intelligent Robotics and Applications (ICIRA 2011) Y1 - 2010 SP - 1 EP - 10 ER - TY - JOUR A1 - Schlamann, Marc A1 - Voigt, Melanie A. A1 - Maderwald, Stefan A1 - Bitz, Andreas A1 - Kraff, Oliver A1 - Ladd, Susanne C. A1 - Ladd, Mark E. A1 - Forsting, Michael A1 - Wilhelm, Hans T1 - Exposure to high-field MRI does not affect cognitive function JF - Journal of Magnetic Resonance Imaging N2 - Purpose To assess potential cognitive deficits under the influence of static magnetic fields at various field strengths some studies already exist. These studies were not focused on attention as the most vulnerable cognitive function. Additionally, mostly no magnetic resonance imaging (MRI) sequences were performed. Materials and Methods In all, 25 right-handed men were enrolled in this study. All subjects underwent one MRI examination of 63 minutes at 1.5 T and one at 7 T within an interval of 10 to 30 days. The order of the examinations was randomized. Subjects were referred to six standardized neuropsychological tests strictly focused on attention immediately before and after each MRI examination. Differences in neuropsychological variables between the timepoints before and after each MRI examination were assessed and P-values were calculated Results Only six subtests revealed significant differences between pre- and post-MRI. In these tests the subjects achieved better results in post-MRI testing than in pre-MRI testing (P = 0.013–0.032). The other tests revealed no significant results. Conclusion The improvement in post-MRI testing is only explicable as a result of learning effects. MRI examinations, even in ultrahigh-field scanners, do not seem to have any persisting influence on the attention networks of human cognition immediately after exposure. Y1 - 2010 U6 - https://doi.org/10.1002/jmri.22065 SN - 1522-2586 VL - 31 IS - 5 SP - 1061 EP - 1066 PB - Wiley-Liss CY - New York ER - TY - JOUR A1 - Schlamann, Marc A1 - Yoon, Min-Suk A1 - Maderwald, Stefan A1 - Pietrzyk, Thomas A1 - Bitz, Andreas A1 - Gerwig, Marcus A1 - Forsting, Michael A1 - Ladd, Susanne C. A1 - Ladd, Mark E. A1 - Kastrup, Oliver T1 - Short term effects of magnetic resonance imaging on excitability of the motor cortex at 1.5T and 7T JF - Academic Radiology N2 - Rationale and Objectives The increasing spread of high-field and ultra-high-field magnetic resonance imaging (MRI) scanners has encouraged new discussion of the safety aspects of MRI. Few studies have been published on possible cognitive effects of MRI examinations. The aim of this study was to examine whether changes are measurable after MRI examinations at 1.5 and 7 T by means of transcranial magnetic stimulation (TMS). Materials and Methods TMS was performed in 12 healthy, right-handed male volunteers. First the individual motor threshold was specified, and then the cortical silent period (SP) was measured. Subsequently, the volunteers were exposed to the 1.5-T MRI scanner for 63 minutes using standard sequences. The MRI examination was immediately followed by another TMS session. Fifteen minutes later, TMS was repeated. Four weeks later, the complete setting was repeated using a 7-T scanner. Control conditions included lying in the 1.5-T scanner for 63 minutes without scanning and lying in a separate room for 63 minutes. TMS was performed in the same way in each case. For statistical analysis, Wilcoxon's rank test was performed. Results Immediately after MRI exposure, the SP was highly significantly prolonged in all 12 subjects at 1.5 and 7 T. The motor threshold was significantly increased. Fifteen minutes after the examination, the measured value tended toward normal again. Control conditions revealed no significant differences. Conclusion MRI examinations lead to a transient and highly significant alteration in cortical excitability. This effect does not seem to depend on the strength of the static magnetic field. Y1 - 2010 U6 - https://doi.org/10.1016/j.acra.2009.10.004 SN - 1076-6332 VL - 17 IS - 3 SP - 277 EP - 281 PB - Elsevier CY - Amsterdam ER - TY - CHAP A1 - Schmiegel, A. A1 - Koch, K. A1 - Dittmer, M. A1 - Braun, M. A1 - Landau, M. A1 - Dick, C. A1 - Bragard, Michael A1 - [u.a.], T1 - Das Sol-ion System : ein System zur Optimierung des Eigenverbrauchs von PV-Strom T2 - Photovoltaische Solarenergie : 25. Symposium ; 03. - 05. März 2010, Kloster Banz, Bad Staffelstein. - (Wissen für Profis) Y1 - 2010 SN - 978-3-941785-23-6 SP - 354 EP - 359 PB - OTTI, Ostbayerisches Technologie-Transfer-Inst. CY - Regensburg ER -