Recent research on changes in genomic regulation and protein expression in intracerebral haemorrhage

Intracerebral haemorrhage (ICH) is a devastating form of stroke that accounts for roughly 10% of all strokes and the effects on those that survive are often debilitating. To date, no suitable therapy exists. Recent work has examined alterations in gene and protein expression after ICH. The focus of this review is to outline the current knowledge of changes in genetic and protein expression after ICH and how those changes may affect the course of brain injury. Both animal and human data are reviewed.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73607/1/j.1747-4949.2007.00160.x.pd

Src Family Kinases in Brain Edema After Acute Brain Injury

Brain edema, the first stage of intracranial hypertension, has been associated with poor prognosis and increased mortality after acute brain injury, such as ischemic stroke, intracranial hemorrhage (ICH), and traumatic brain injury (TBI). The acute brain injury often initiates release of many molecules, including glutamate, adenosine, thrombin, oxyhemoglobin, cytokines, reactive oxygen species (ROS), damage associated molecular pattern molecules (DAMPs), and others. Most of those molecules activate Src family kinases (SFKs), a family of proto-oncogenic non-receptor tyrosine kinases, resulting in blood-brain barrier (BBB) disruption and brain edema at the acute stage after brain injury. However, SFKs also contributes to BBB self-repair and brain edema resolution in the chronic stage that follows brain injury. In this review we summarize possible pathways through which SFKs are implicated in both brain edema formation and its eventual resolution