Peter Siesjö

TL;DR: GFI1 and GFI1B are identified as prominent medulloblastoma oncogenes and ‘enhancer hijacking’ is implicate as an efficient mechanism driving oncogene activation in a childhood cancer.

TL;DR: It has now been found that the secondary deterioration of the bioenergetic state of core and penumbral tissues are mirrored by corresponding changes in the respiratory functions of isolated mitochondria, suggesting that, also in this type of ischaemia, the mitochondria suffer secondary damage.

TL;DR: In vitro and in vivo experiments suggest that the main route of entry is through channels gated by glutamate receptors, leading to the excitotoxic hypothesis of cell death and in vitro experiments further support the role of calcium as a mediator of cellDeath.

TL;DR: The objective of this article is to amalgamate previous results into a speculative synthesis that sheds light on the causes of secondary brain damage following either global/forebrain or focal ischemia, based on the well-founded assumption that the pathophysiology of the brain damage incurred by global or forebrain ischemIA is different from that of focal isChemia.

TL;DR: It is shown that a large proportion of primary medulloblastomas and medullOBlastoma cell lines are infected with HCMV and that COX-2 expression, along with PGE2 levels, in tumors is directly modulated by the virus.