@article{FeuersteinSiren1987,
  author    = {Feuerstein, Giora and Sir{\´e}n, Anna-Leena},
  title     = {The Opioid System in cardiac and vascular regulation of normal and hypertensive states},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47418},
  year      = {1987},
  abstract  = {The endogenous opioid system includes three major families of peptides: dynorphins (derived from pre-proenkephalin B), endorphins (derived from pre-proopiomelanocortin), and enkephalins (derived from pre-proenkephalin A). Multiple species of opioid peptides are derived from these major precursors and many of them possess potent cardiovascular properties. Opioid peptides and opioid receptors, of which multiple forms have been defined, are present in the central nervous system and peripheral neural elements. In the central nervous system, opioid peptides and receptors are found in forebrain and hindbrain nuclei involved in baroregulation, sympathoadrenal activation, and several other vital autonomic functions. In the periphery, opioid peptides are found in autonomic ganglia, adrenal gland, heart, and other organs; multiple opioid receptors are also found in vascular tissue, heart, and kidneys. Although little is known to date on the regulatory mechanisms of the opioid system in normal cardiovascular states, it became clear that cardiovascular stress situations substantially modify the activity of the endogenous opioid system. The purpose of this review is to clarify the sites of interaction of the opioid system with all major components of the cardiovascular system and indicate the potential role of this system in the ontogenesis of cardiac malfunction, vascular diseases, and hypertension.},
  subject      = {Medizin},
  language  = {en}
}
@article{VonhofSirenFeuerstein1990,
  author    = {Vonhof, S. and Sir{\´e}n, Anna-Leena and Feuerstein, Giora},
  title     = {Volume-dependent spatial distribution of microinjected thyrotropin-releasing hormone (TRH) into the medial preoptic nucleus of the rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47421},
  year      = {1990},
  abstract  = {The present study was performed to qua ntify the distribution of a peptide neurotransmitter after microinjection into the medial preoptic area (POM), using a technique suitable for conscious animal preparations. The results indicate that only 50-ni volumes of injected tracer were sufficiently localized with 77 ± 9\% recovery in the POM. Injections of higher volumes resulted in an increasing spread of tracer into distant anatomical regions and structures, including the needle tract and cerebral ventricles. The amount of tracer localized in the POM decreased to 38±4\% (200 nl) (P < 0.05) and 41 ±8\% (500 nl) (P <0.05), respectively. The data suggest that the volume of injection is critical for intraparenchymal injections into structures of a diameter of I mm or less, such as the POM and should not exceed 50 nl in conscious animal preparations.},
  subject      = {Neurophysiologie},
  language  = {en}
}
@article{ShuaibXuCrainetal.1990,
  author    = {Shuaib, A. and Xu, K. and Crain, B. and Sir{\´e}n, Anna-Leena and Feuerstein, Giora and Hallenbeck, J. and Davis, JN},
  title     = {Assessment of damage from implantation of microdialysis probes in the rat hippocampus with silver degeneration staining},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47433},
  year      = {1990},
  abstract  = {We used a sensitive silver degeneration staining method to study the effects of insertion of microdialysis probes in rat dorsal hippocampus and neocortex. Nine animals were sacrificed 24 h, 3 days or 7 days after implantation of dialysis tubing. Although mild neuronal cell death and small petechial hemorrhages were seen in elose proximity to the implantation site, the striking finding was the presence of degenerating axons both adjacent to the implantation site and in remote sites such as the corpus callosum and contralateral hippocampus. The observed changes could alter brain function near or remote from the implantation site and should be considered in analysis of dialysis experiments.},
  subject      = {Neurophysiologie},
  language  = {en}
}
@article{LiuMcDonnellYoungetal.1993,
  author    = {Liu, T. and McDonnell, PC and Young, PR and White, RF and Sir{\`e}n, Anna-Leena and Hallenbeck, JM and Barone, FC and Feuerstein, Giora},
  title     = {Interleukin-1ß mRNA expression in ischemic rat cortex},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47442},
  year      = {1993},
  abstract  = {Background and Pur pose: Interleukin-1ß is a proinftammatory cytokine produced by blood-borne and resident brain inftammatory cells. The present study was conducted to determine if interleukin-1ß mRNA was produced in the brain of rats subjected to permanent focal ischemia. Methods: Rat interleukin-1ß cDNA, synthesized from stimulated rat peritoneal macrophage RNA by reverse transcription and polymerase chain reaction and c10ned in plasmid Bluescript KS+, was used to evaluate the expression of interleukin-1ß mRNA in cerebral cortex from spontaneously hypertensive rats and normotensive rats subjected to permanent middle cerebral artery occlusion. Interleukin-1ß mRNA was quantified by Northern blot analysis and compared with rat macrophage RNA standard. To correct for gel loading, blots were also analyzed with cyclophilin cDNA, which encodes an abundant, conserved protein that was unchanged by the experimental conditions. Results: Interleukin-1ß mRNA produced in the ischemic zone was significantly increased from 6 hours to 120 hours, with a maximum of211±24\% ofinterleukin-1ß reference standard, ie, 0.2 ng stimulated rat macrophage RNA, mRNA compared with the level in nonischemic cortices (4±2\%) at 12 hours after ischemia (P<.OI; n=6). Interleukin-1ß mRNA at 12 hours after ischemia was markedly elevated in hypertensive rats over levels found in two normotensive rat strains. Neurological deficits were also apparent only in the hypertensive rats. Conclusions: Brain interleukin-1ß mRNA is elevated acutely after permanent focal ischemia and especially in hypertensive rats. These data suggest that this potent proinflammatory and procoagulant cytokine might have a role in brain damage following ischemia.},
  subject      = {Gehirn},
  language  = {en}
}
@article{YongJacobowitzBaroneetal.1994,
  author    = {Yong, Liu and Jacobowitz, David M. and Barone, Frank and McCarron, Richard and Spatz, Maria and Feuerstein, Giora and Hallenbeck, John M. and Sir{\´e}n, Anna-Leena},
  title     = {Quantitation of perivascular monocyte / macrophages around cerebral blood vessels of hypertensive and aged rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-86800},
  year      = {1994},
  abstract  = {The numbers of monocytes and macrophages in the walls of cerebral blood vessels were counted on perfusion-fixed frozen brain sections (16 JLffi) of spontaneously hypertensive rats (SHR), stroke-prone SHR (SHR-SP), normotensive Wistar-Kyoto (WKY) rats, and young (16-week-old) and old (2-year-old) normotensive Sprague-Dawley rats (SD-l6w and SD-2y, respectively) using monoclonal antiborlies against rat macrophages (ED2). The staining was visualized with fluoresceinlabeled second antiborlies. The ED2-specific staining in brain sections was restricted to macrophages in a perivascular location. The number of perivascular cells per square millimeter of high-power field was significantly greater in SHR-SP (8.6 ± 2.1; n = 4) and SHR (6. 7 ± 0.9; n = 6) than in normotensive WKY (4.0 ± 0.5; n = 6; p <0.01). The number of perivascular macrophages was also greater in SD-2y (7.5 ± 2.7; n = 9) than in SD-l6w (2.9 ± 1.8; n = 8; p < 0.01). No ED2 staining was found in the resident microglia or in the endothelial cells, which were identified by double staining with rhodamine-labeled anti-factor VIII-related antigen antiborlies. The results suggest that the stroke risk factors hypertension and advanced age are associated with increased subendothelial accumulation of monocytes and macrophages. This accumulation could increase the tendency for the endothelium to convert from an anticoagulant to a procoagulant surface in response to mediators released from these subendothelial cells.},
  subject      = {Willebrand-Faktor},
  language  = {en}
}