@techreport{McCarronDoronSirenetal.1994,
  author    = {McCarron, R. M. and Doron, D. A. and Sir{\´e}n, Anna-Leena and Feuerstein, G. Z. and Heldman, E. and Pollard, H. B. and Spatz, M. and Hallenbeck, J. M.},
  title     = {Agonist-stimulated release of von Willebrand factor and procoagulant factor VIII in rats with and without risk factors for stroke [Research Report]},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-62945},
  year      = {1994},
  abstract  = {Lipopolysaccharidc (LPS)-induced (i.v. or i.c.v., 1.8 mg/kg) release of von Willebrand factor (vWF) ·was examined in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. SHR rats releascd significantly (P < 0.05) more vWF than WKY rats in response to LPS. LPS also inhibited factor VIII procoagulant activity (FVIII: c) which may indicate an increase in thrombin activity. Cultured cerebrovascular endothelial cells (EC) derived from both SHR and WKY rats, as weil as human umbilical vein EC (HUVEC) cultures constitutively released vWF. Treatment with agonists including LPS, thrombin and tumor necrosis factor-a (TNFa) did not affect the in vitro secretion of vWF by cerebrovascular EC cultures but significantly upregulated vWF release by HUVEC cultur~s. Preincubation of cerebrovascular EC cultures with interleukin-1 OL-l) ± TNFa or co-culturing in the presence of LPS-activated syngeneic monocytes had no effect on vWF secretion. The findings demoostrate that conditions of hypertension may affect endothelial cells and make them more responsive to agonist Stimulation and thereby increase secretion of vWF, an important factqr in hemostasis as weil as thrombosis. The capacity of LPS to significantly affect the in vivo secretion of vWF in SHR and WKY rats but not cultured cerebrovascular EC indicates that observed elevations in plasma vWF were not derived from cerebrovascular EC. lt is suggested that hypertension may function as a risk factor for thrombotic stroke by influencing factors involved in coagulation processes, such as vWF and factor VIII : c.},
  subject      = {Neurobiologie},
  language  = {en}
}
@techreport{WangSirenLiuetal.1994,
  author    = {Wang, X. and Sir{\´e}n, Anna-Leena and Liu, Y. and Yue, T-L. and Barone, F. C. and Feuerstein, G. Z.},
  title     = {Upregulation of intercellular adhesion molecule-1 (ICAM-1) on brain microvascular endothelial cells in rat ischemic cortex [Research Report]},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-62952},
  year      = {1994},
  abstract  = {The expression of intercellular adhesion molecule 1 (ICAM-1) was studied in rat focal ischemic cortex. A significant increase in ICAM-1 mRNA expression in the ischemic cortex over Ievels in contralateral (nonischemic) site was observed by means of Northern blot analysis following either permanent or temporary occlusion with reperfusion of the middle cerebral artery (PMCAO or MCAO with reperfusion) in spontaneously hypertensive rats. In the ischemic cortex, Ievels of ICAM-1 mRNA increased significantly at 3 h (2.6-fold, n = 3, P < 0.05), peaked at 6 to 12 h (6.0-fold, P < 0.01) and remained elevated up to 5 days (2.5-fold, P < 0.05) after PMCAO. The profile of ICAM-1 mRNA expression in the ischemic cortex following MCAO with reperfusion was similar to that following PMCAO, except that ICAM-1 mRNA was significantly increased as early as 1 h (6.3-fold, n = 3, P < 0.05) and then gradually reached a peak at 12 h (12-fold, P < 0.01) after reperfusion. ICAM-1 mRNA expression in ischemic cortex following PMCAO was significantly greater in hypertensive rats than in two normotensive rat strains. Immunostaining using anti-ICAM-1 antiborlies indicated that upregulated ICAM-1 expressionwas localized to endotheIial cells of intraparenchymal blood vessels in the ischemic but not contralateral cortex. The data suggest that an upregulation of ICAM-1 mRNA and protein on brain capillary endothelium may play an important rote in leukocyte migration into ischemic brain tissue.},
  subject      = {Neurobiologie},
  language  = {en}
}
@techreport{LuettickenWegenkaYuanetal.1994,
  author    = {L{\"u}tticken, Claudia and Wegenka, Ursula M. and Yuan, Juping and Buschmann, Jan and Schindler, Chris and Ziemiecki, Andrew and Harpur, Alisa G. and Wilks, Andrew F. and Yasukawa, Kiyoshi and Taga, Tetsuya and Kishimoto, Tadamitsu and Barbieri, Giovanna and Sendtner, Michael and Pellegrini, Sandra and Heinrich, Peter C. and Horn, Friedemann},
  title     = {Association of transcription factor APRF and protein kinase JAK1 with the IL-6 signal transducer gp130},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42577},
  year      = {1994},
  abstract  = {Interleukin-6, leukemia inhibitory factor, oncostatin M. Interleukin-11, and cilialy neurotrophic factor bind to receptor complexes that share the signal transducer gp130. Upon binding, the ligands rapidly activate DNA binding of acute-phase response factor (APRF), a protein antigenicaly relaled to the p91 subunit of the interferon-stimulated gene factor-(ISGF-3a). These cytokines caused tyrosine phosphorylation of APRF and ISGF-3a p91. Protein kinases of the Jak family were also rapidly tyrosine phosphorylated, and both APRF and Jak1 associated with gp130. These data indicate that Jak family protein kinases may participate in IL-6 signaling and that APRF may be activated in a complex with gp130.},
  language  = {en}
}
@techreport{SendtnerKreutzbergJennekens1992,
  author    = {Sendtner, Michael and Kreutzberg, Georg W. and Jennekens, Frans G.},
  title     = {Workshop on trophic factors in the peripheral nervous system. Capri, October 1991.},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31451},
  year      = {1992},
  abstract  = {No abstract available},
  language  = {en}
}
@techreport{GesslerSimolaBruns1989,
  author    = {Gessler, Manfred and Simola, Kalle O. and Bruns, Gail A. P.},
  title     = {Cloning of breakpoints of a chromosome translocation identifies the AN2 locus},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-30177},
  year      = {1989},
  abstract  = {Chromosome translocations involving llpl3 have been associated with familial aniridia in two kindreds highlighting the chromosomal localization of the AN2 locus. This locus is also part of the WAGR complex (Wilros tumor, aniridia, genitourinary abnormalities, and mental retardation). In one kindred, the translocation is associated with a deletion, and probes for this region were used to identify and clone the breakpoints of the translocation in the second kindred. Comparison of phage restriction maps exclude the presence of any sizable deletion in this case. Sequences at the chromosome 11 breakpoint are conserved in multiple species, suggesting that the translocation falls within the AN2 gene.},
  language  = {en}
}
@techreport{Hommers1988,
  author    = {Hommers, Wilfried},
  title     = {Recompense as Stimulus and Response: Toward an Exchange of Law and Psychology},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-43743},
  year      = {1988},
  abstract  = {Recompense denotes a more or less complete undoing of a harm which may combine the tWO aspects: compensation for the victim and the apology of the harmdoer. The present empirical research on recompense started with an analysis of the judgmental structures of recompense in legal thought and law, as such analysis has been neglected in prior research. The obtained results on recompense as stimulus and response reinforce the general idea of the present approach of using the framework of law and legal history in the empirical research of cognitive science. Since the traditionahelationship of jurisprudence and psychology is reversed by that research strategy, law and psychology appear to interact mutually, and a more comprehensive concept of legal psychology is implemented.},
  language  = {en}
}
@techreport{Christl1986,
  author    = {Christl, Manfred},
  title     = {Cycloadditions of 1,3,4-Oxadiazin-6-ones},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-41677},
  year      = {1986},
  abstract  = {No abstract available},
  language  = {en}
}