@article{SirenMcCarronLiuetal.1993,
  author    = {Sir{\´e}n, Anna-Leena and McCarron, R. M. and Liu, Y. and Barone, F. and Spatz, M. and Feuerstein, G. and Hallenbeck, J. M.},
  title     = {Perivascular monocyte/macrophage interaction with endothelium as a mechanism through which stroke-risk factors operate to increase stroke likelihood. Research Initiatives in Vascular Disease; SPECIAL COMMUNICATION},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63006},
  year      = {1993},
  abstract  = {No abstract available},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{FeuersteinLeaderSirenetal.1987,
  author    = {Feuerstein, G. and Leader, P. and Sir{\´e}n, Anna-Leena and Braquet, P.},
  title     = {Protective effect of PAF-acether antagonist, BN 52021, in trichothecen toxicosis},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63244},
  year      = {1987},
  abstract  = {Trichothecenes are mycotoxins which produce Iethai toxicosis in humans and animals, yet no adequate therapeutic regimen has been developed. This study provides evidence that the selective platelet activating factor (PAF) antagonist, BN 52021 (5-15 mg/kg i.v.) can prolong the survival of conscious rats exposed to a highly Iethai T -2 toxicosis. These data also suggest that P AF is an important mediator of this unique toxicosis.},
  subject      = {Neurobiologie},
  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}
}
@article{SirenHeldmanDoronetal.1992,
  author    = {Sir{\´e}n, Anna-Leena and Heldman, Eliahu and Doron, David and Yue, Tian-Li and Liu, Yong and Feuerstein, G. and Hallenbeck, JM},
  title     = {Release of proinflammatory and prothrombbtic mediators in the brain and peripheral circulation in spontaneously hypertensive and normotensive Wistar-Kyoto rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47469},
  year      = {1992},
  abstract  = {Background and Purpose: We reported previously that stroke risk factors prepared the brain stem for the development of ischemia and hemorrhage and induced the production of tumor necrosis factor following an intrathecal injection of Iipopolysaccharide, a prototypic monocyte-activating stimulus. This study evaluates whether blood or brain cells of hypertensive rats produce more proinflammatory and prothrombotic mediators than do blood or brain cells of normotensive rats. MethotJs: Levels of tumor necrosis factor, platelet-activating factor, 6-ketoprostaglandin F1a, and thromboxane B2 in the cerebrospinal fluid and blood of spontaneously hypertensive and normotensive Wistar-Kyoto rats were monitored before and after achallenge with Iipopolysaccharide. Results: Little or no activity from these media tors was found in the cerebrospinal fluid or blood of saline-injected control animals. Intravenous administration of Iipopolysaccharide (0.001, 0.1, and 1.8 mg/kg) produced dose-dependent increases in blood levels of all mediators in hypertensive rats. In normotensive rats the levels were less than in hypertensive rats and were not c1early dose-related. When Iipopolysaccharide was injected intracerebroventricularly, more tumor necrosis factor was measured in the cerebrospinal fluid than in the blood, suggesting local synthesis of this cytokine. Levels of tumor necrosis factor and platelet-activating factor in the cerebrospinal fluid were higher in hypertensive than in normotensive rats. The thromboxane A2/prostacyclin ratio was not aItered significantly between the two rat strains. Conclusions: It is suggested that the higher incidence of brain stem ischemia and hemorrhage after the intrathecal injection oflipopolysaccharide in hypertensive rats than in normotensive rats might be related to the higher levels of the two cytotoxic factors tumor necrosis factor and platelet-activating factor produced in response to such challenge.},
  subject      = {Gehirn},
  language  = {en}
}
@article{PaakkariPaakkariLandesetal.1993,
  author    = {Paakkari, P. and Paakkari, I. and Landes, P. and Sir{\´e}n, Anna-Leena and Feuerstein, G.},
  title     = {Respiratory \(\mu\)-Opioid and benzodiazepine interactions in the understrained rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-62974},
  year      = {1993},
  abstract  = {lnteractions of p-opioid receptors with the benzodiazepine system were studied by examining the modulatory effects of flumazenil (a benzodiazepine antagonist) and alprazolam (a benzodiazepine agonist) on the respiratory effects ofthe opioid peptide dermorphin. Dermorphin, 1-30 nmol administered i.c.v., to conscious, unrestrained rats decreased ventilation rate (VR) and minute volume (MV) dose-dependently. The ventilatory depression was antagonized by naloxone and by the benzodiazepine antagonist flumazenil. The benzodiazepine alprazolam potentiateri the respiratory inhibition of a small (I nmol) dose of dermorphin but antagonized that of a higher dos:~ (3 nmol). The results suggest that the benzodiazepine/GABA receptor complex modulates respiratory depression induced by centrat p-receptor Stimulation in the rat.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{PaakkariPaakkariSirenetal.1990,
  author    = {Paakkari, P. and Paakkari, I. and Sir{\´e}n, Anna-Leena and Feuerstein, G.},
  title     = {Respiratory and locomotor stimulation by low doses of dermorphin - a Mu\(_1\)-receptor mediated effect},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63110},
  year      = {1990},
  abstract  = {The selective opioid mu receptor agonist dermorphin increased the locomotor activity of rats dose dependently at 1 0 to 1 00 pmol/kg i.c.v. Respiratory rate, relative tidal volume and respiratory minute volume also increased unrelated to changes in locomotor activity. Higher doses, on the other hand, produced catalepsy and respiratory depression. Pretreatment of the rats with the mu,-selective antagonist naloxonazine (10 mg/kg i.v.) blocked the stimulant locomotor and respiratory effects of low doses of dermorphin (1 0--1 00 pmol/kg), but potentiated the respiratory depressant effect of a high dose (1 0 nmol/kg) of dermorphin. The selective benzodiazepine antagonist flumazenil (5 mg/kg), which has been shown previously to antagonize catalepsy and respiratory depression produced by relatively high doses of dermorphin, did not antagonize the respiratory or locomotor stimulant effect of dermorphin. The data suggest that mu\(_1\)-opioid receptors are responsible for the low dose stimulant effects of dermorphin on locomotor activity and respiration whereas mu\(_2\) receptors mediate the respiratory depressant effect of dermorphin.},
  subject      = {Neurobiologie},
  language  = {en}
}
@article{VonhofSiren1991,
  author    = {Vonhof, S. and Sir{\´e}n, Anna-Leena},
  title     = {Reversal of µ-opioid-mediated respiratory depression by α2-adrenoceptor antagonism},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47454},
  year      = {1991},
  abstract  = {The present study was performed in order to evaluate the effects of the selective 02- adrenoceptor antagonist 6-chloro-2,3,4,5-tetrahydro-3-methyl-1H-3-benzazepine (SK\&F 86466) on dermorphin-induced analgesia, respiratory depression and inhibition of locomotor activity in the conscious rat. Intracerebroventricular (icv) administration of dermorphin (3 nmol/rat) decreased respiration rate and relative ventilatory minute volume maximally by 38 \% and 50 \% of baseline respectively. SK\&F 86466 dose-dependently reversed the dermorphin-induced depression of ventilatory parameters, while SK\&F 86466 exerted no effect on dermorphin-induced analgesia or depression of locomotor activity due to catalepsia. It appears, therefore, that a 2-adrenoceptors selectively interact with Jl2-opioid-receptor mediated effects, such as respiratory depression, but are not involved in the modulation of Jl,-opioid-related effects, such as supraspinal analgesia and depression of locomotor activity.},
  subject      = {Biowissenschaften},
  language  = {en}
}
@article{AlbertWeissenbergerMenclHoppetal.2014,
  author    = {Albert-Weissenberger, Christiane and Mencl, Stine and Hopp, Sarah and Kleinschnitz, Christoph and Siren, Anna-Leena},
  title     = {Role of the kallikrein-kinin system in traumatic brain injury},
  series = {Frontiers in Cellular Neuroscience},
  volume    = {8},
  journal   = {Frontiers in Cellular Neuroscience},
  issn      = {1662-5102},
  doi       = {10.3389/fncel.2014.00345},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-118226},
  pages     = {345},
  year      = {2014},
  abstract  = {Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Despite improvements in acute intensive care, there are currently no specific therapies to ameliorate the effects of TBI. Successful therapeutic strategies for TBI should target multiple pathophysiologic mechanisms that occur at different stages of brain injury. The kallikrein-kinin system is a promising therapeutic target for TBI as it mediates key pathologic events of traumatic brain damage, such as edema formation, inflammation, and thrombosis. Selective and specific kinin receptor antagonists and inhibitors of plasma kallikrein and coagulation factor XII have been developed, and have already shown therapeutic efficacy in animal models of stroke and TBI. However, conflicting preclinical evaluation, as well as limited and inconclusive data from clinical trials in TBI, suggests that caution should be taken before transferring observations made in animals to humans. This review summarizes current evidence on the pathologic significance of the kallikrein-kinin system during TBI in animal models and, where available, the experimental findings are compared with human data.},
  language  = {en}
}
@article{MrestaniLichterSirenetal.2023,
  author    = {Mrestani, Achmed and Lichter, Katharina and Sir{\´e}n, Anna-Leena and Heckmann, Manfred and Paul, Mila M. and Pauli, Martin},
  title     = {Single-molecule localization microscopy of presynaptic active zones in Drosophila melanogaster after rapid cryofixation},
  series = {International Journal of Molecular Sciences},
  volume    = {24},
  journal   = {International Journal of Molecular Sciences},
  number    = {3},
  issn      = {1422-0067},
  doi       = {10.3390/ijms24032128},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-304904},
  year      = {2023},
  abstract  = {Single-molecule localization microscopy (SMLM) greatly advances structural studies of diverse biological tissues. For example, presynaptic active zone (AZ) nanotopology is resolved in increasing detail. Immunofluorescence imaging of AZ proteins usually relies on epitope preservation using aldehyde-based immunocompetent fixation. Cryofixation techniques, such as high-pressure freezing (HPF) and freeze substitution (FS), are widely used for ultrastructural studies of presynaptic architecture in electron microscopy (EM). HPF/FS demonstrated nearer-to-native preservation of AZ ultrastructure, e.g., by facilitating single filamentous structures. Here, we present a protocol combining the advantages of HPF/FS and direct stochastic optical reconstruction microscopy (dSTORM) to quantify nanotopology of the AZ scaffold protein Bruchpilot (Brp) at neuromuscular junctions (NMJs) of Drosophila melanogaster. Using this standardized model, we tested for preservation of Brp clusters in different FS protocols compared to classical aldehyde fixation. In HPF/FS samples, presynaptic boutons were structurally well preserved with ~22\% smaller Brp clusters that allowed quantification of subcluster topology. In summary, we established a standardized near-to-native preparation and immunohistochemistry protocol for SMLM analyses of AZ protein clusters in a defined model synapse. Our protocol could be adapted to study protein arrangements at single-molecule resolution in other intact tissue preparations.},
  language  = {en}
}
@article{HallenbeckDutkaKochaneketal.1988,
  author    = {Hallenbeck, JM and Dutka, AJ and Kochanek, PM and Sir{\´e}n, Anna-Leena and Pezeskpour, GH and Feuerstein, G.},
  title     = {Stroke risk factors prepare rat brainstem tissues for a modified localized Shwartzman reaction},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47971},
  year      = {1988},
  abstract  = {Stroke risk factors such as hypertension, diabetes, advanced age, and genetic predisposition to stroke were demonstrated to prepare rat brainstem tissues for a modified local Shwartzman reaction. A single intracisternal injection of endotoxin provoked the reaction, and affected rats manifested neurologie deficits accompanied by pathologie lesions. Brainstem infarcts developed in only a small proportion of rats without recognized risk factors after intracisternal injection of endotoxin. Thus, stroke risk factors, whieh are ordinarily regarded as operating through acceleration of atherosclerosis, may predispose to brain ischemia by local effects on brain mierocirculation such as those thought to underlie preparation of a tissue for the local Shwartzman reaction.},
  subject      = {Gehirn},
  language  = {en}
}