Recent scientific results include demonstration of:

  • the role of cerebral mast cells in the course of experimental ischemic brain injury, blood-brain barrier damage and expansive brain edema (J Cereb Blood Flow Metab 2006, 2010, Stroke 2011)
  • the role of cerebral mast cells in the development of experimental cerebral hemorrhage, with and without administration of thrombolytics (Circulation 2007, J Cereb Blood Flow Metab 2007, 2014)
  • the transcriptome of symptomatic carotid artery disease: differential gene expression profiles in symptom-causing and asymptomatic carotid artery plaques (Arterioscler Thromb Vasc Biol 2007, J Mol Med 2011)
  • the significance of intraplaque hemorrhages, macrophage-monocyte lineage cells and lipid transport molecules (adipophilin, ABCA1, CD36, FABP4) in the transformation of a clinically silent carotid plaque into a dangerous one (Stroke 2007, 2010, Atherosclerosis 2013)
  • the potential value of apoptosis of human cerebral cells, caspace-3, PARP-1, and inflammatory cells as a target of neuroprotective therapeutic strategies in ischemic stroke (Brain 2006, Acta Neuropathol 2009)
  • the safety and efficacy of recanalization therapies in the therapy acute cerebrovascular occlusions, especially in its most devastating form basilar occlusion (Stroke 2006, 2010, 2011, 2014, Arch Neurol 2010, Ann Neurol 2013, Lancet Neurol 2009, 2011, BMJ 2010)
  • the safe and fast delivery of thrombolytic therapy and the occurrence of hemorrhagic events in acute stroke in humans (Stroke 2003, JAMA 2004, Neurology 2006, 2012)

In the future aims, the following examples are the most immediate:

  • to identify novel BBB breakdown biomarkers at the ultra-acute stage of ischemic and hemorrhagic stroke by EMS blood sampling in order, aiming to improve early differential diagnosis and the risk stratification of thrombolytic therapy of stroke
  • to examine  the wide therapeutic efficacy of mast cell blockers in treating ischemic brain edema, reperfusion injury and inflammation with and without recanalization therapies in acute stroke and in states with acutely increased intracranial pressure
  • to generate a clinical database for dissecting therapeutically important advances of recanalization therapies of stroke, especially its most devastating form basilar occlusion.
  • to characterize novel molecular mechanisms leading to human cerebral infarction through cell apoptosis, and to hazardous brain edema and hemorrhage through neutrophil and mast cell activation
  • to collect a representative clinical carotid plaque material and generate gene expression profiles in symptomatic and asymptomatic carotid plaques to identify novel therapeutic targets and biomarkers in cell signaling in atherosclerotic vascular lesions