The laboratory is interested in the molecular mechanisms involved in blood-brain barrier disruption and neuronal degeneration in ischemic brain injury. Brain edema and hemorrhagic transformation are the main cause of early mortality in ischemic stroke patients. Gelatinase B, an inducible matrix metalloproteinase overexpressed during cerebral ischemia, is associated to the proteolysis of the basal lamina resulting in blood-brain barrier disruption, brain edema and cerebral hemorrhage after stroke. We currently explore different therapeutic strategies focused on the role of gelatinase B to reduce the risk of hemorrhage and brain edema both in animal models of embolic stroke and in patients. We also investigate the mechanisms of ischemic brain injury in patients following cardiac arrest and in patients developing delayed ischemic injury due to vasospasm after subarachnoid hemorrhage.
Protein S100 as outcome predictor after out-of-hospital cardiac arrest and targeted temperature management at 33 °C and 36 °C.
Single versus Serial Measurements of Neuron-Specific Enolase and Prediction of Poor Neurological Outcome in Persistently Unconscious Patients after Out-Of-Hospital Cardiac Arrest - A TTM-Trial Substudy.
Infectious complications after out-of-hospital cardiac arrest-A comparison between two target temperatures.
Life-threatening neuroleptic withdrawal emergent syndrome resembling status dystonicus.
Département d’Anesthésiologie, Pharmacologie et Soins Intensifs