The interest of the laboratory is focused on stroke. Cerebral ischemia induces a significant early and sustained increase of the intracellular calcium concentration. It also has been observed that an increase of intracellular calcium lasting long enough could trigger delayed neuronal death. Preventing the intracellular calcium increase during an ischemic insult by reducing the extracellular calcium concentration prevents delayed neuronal death. The research in the laboratory is therefore focused on understanding the alteration of intracellular calcium signaling during an ischemic insult. The effort is currently concentrated on understanding the implication of a specific type of voltage-activated calcium channel present on the plasma membrane during ischemia. Neuronal ischemia is studied on three different models. Electrophysiology and calcium imaging is performed on dissociated neuronal cultures during ischemic insults. Pharamacology and neuroprotection studies are performed first in an in vitro model with organotypic hippocampal slice cultures and then in an in vivo model of global ischemia in rats.
Disturbed flow induces a sustained, stochastic NF-κB activation which may support intracranial aneurysm growth in vivo.
Correction to: Ruptured posterior circulation aneurysms: epidemiology, patterns of care, and outcomes from the Swiss SOS national registry.
Ruptured posterior circulation aneurysms: epidemiology, patterns of care, and outcomes from the Swiss SOS national registry.
External validation of cerebral aneurysm rupture probability model with data from two patient cohorts.
Departement des neurosciences cliniques