@phdthesis{Raslan2011,
  author    = {Raslan, Furat},
  title     = {Pathomechanismen und Therapie der Kallikrein-Kinin-System vermittelten Hirn{\"o}dembildung nach Neurotrauma},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-71407},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2011},
  abstract  = {In einem experimentellen Sch{\"a}del-Hirn-Trauma-Modell der fokalen K{\"a}ltel{\"a}sion bei der Maus wurde die Effektivit{\"a}t der B1R-Blockade untersucht. Die Ergebnisse dieser Untersuchung dokumentierten auf der Suche nach einer grundlegenden spezifischen Therapie des vasogenen traumatischen Hirn{\"o}dems die B1R-Blockade als einen potentiellen Ansatz zu Reduktion der sekund{\"a}ren Hirn-sch{\"a}den. Zum Einen konnte durch die selektive Blockade von B1R mit dem Pr{\"a}parat R-715 nach einer fokalen K{\"a}ltel{\"a}sion im Mausmodell die Hirnsch{\"a}digung um etwa 75 \% gegen{\"u}ber den Tieren der Kontrollgruppen reduziert werden. Zum Anderen l{\"a}sst sich nach der B1R-Blockade u. a. eine signifikante Abschw{\"a}chung des vasogenen Hirn{\"o}dems um etwa 50 \% im Vergleich zu den Tieren der Kontrollgruppen feststellen. Die Reduktion der sekund{\"a}ren Hirnsch{\"a}digung durch die B1R-Blockade 24 Stunden nach der L{\"a}sionsinduktion macht die selektive B1R-Blockade als kausaler Therapie-ansatz eine interessante Behandlungsoption des posttraumatischen vasogenen Hirn{\"o}dems.},
  subject      = {Sch{\"a}del-Hirn-Trauma},
  language  = {de}
}
@article{WestermaierStetterKunzeetal.2013,
  author    = {Westermaier, Thomas and Stetter, Christian and Kunze, Ekkehard and Willner, Nadine and Raslan, Furat and Vince, Giles H. and Ernestus, Ralf-Ingo},
  title     = {Magnesium treatment for neuroprotection in ischemic diseases of the brain},
  series = {Experimental and Translational Stroke Medicine},
  journal   = {Experimental and Translational Stroke Medicine},
  doi       = {10.1186/2040-7378-5-6},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-96729},
  year      = {2013},
  abstract  = {This article reviews experimental and clinical data on the use of magnesium as a neuroprotective agent in various conditions of cerebral ischemia. Whereas magnesium has shown neuroprotective properties in animal models of global and focal cerebral ischemia, this effect could not be reproduced in a large human stroke trial. These conflicting results may be explained by the timing of treatment. While treatment can be started before or early after ischemia in experimental studies, there is an inevitable delay of treatment in human stroke. Magnesium administration to women at risk for preterm birth has been investigated in several randomized controlled trials and was found to reduce the risk of neurological deficits for the premature infant. Postnatal administration of magnesium to babies after perinatal asphyxia has been studied in a number of controlled clinical trials. The results are promising but the trials have, so far, been underpowered. In aneurysmal subarachnoid hemorrhage (SAH), cerebral ischemia arises with the onset of delayed cerebral vasospasm several days after aneurysm rupture. Similar to perinatal asphyxia in impending preterm delivery, treatment can be started prior to ischemia. The results of clinical trials are conflicting. Several clinical trials did not show an additive effect of magnesium with nimodipine, another calcium antagonist which is routinely administered to SAH patients in many centers. Other trials found a protective effect after magnesium therapy. Thus, it may still be a promising substance in the treatment of secondary cerebral ischemia after aneurysmal SAH. Future prospects of magnesium therapy are discussed.},
  language  = {en}
}