Bernhard H. J. Juurlink

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Release of glutamate and aspartate was measured in mouse cerebellar granule cells in primary cultures grown for 4-16 days in serum-containing tissue culture medium with either a partially depolarizing (25 mM) or a physiological concentration of potassium (5.4 mM). The cells migrated to form aggregates connected by a network of processes during the first(More)
Much of the damage that occurs in the central nervous system (CNS) following trauma is due to secondary effects of glutamate excitotoxicity, Ca2+ overload, and oxidative stress, three mechanisms that in a spiraling interactive cascade end in neuronal death. Oxidative stress activates mechanisms that result in a neutrophil-mediated inflammation that also(More)
Astrocytes in primary cultures constitute an exceedingly useful preparation for studies of astroglial development and function. These cells, however, demonstrate a pronounced plasticity in their reactions to culturing conditions. Thus, species and spatiotemporal region of CNS chosen for source of cells, dissociation procedures used, cell density in culture,(More)
Imbalance between production and scavenging of superoxide anion results in hypertension by the inactivation of nitric oxide, and the increased oxidative stress from the resultant peroxynitrite that is produced promotes inflammatory processes such as atherosclerosis. Induction of phase 2 proteins promotes oxidant scavenging. We hypothesized that intake of(More)
A review of reactive oxygen species (ROS) is followed by a discussion on the differential susceptibility of astrocytes and oligodendroglia to ischemia-related insults. Astrocytes can survive chronic hypoxia as well as long periods of simulated ischemia, i.e. hypoglycemia and anoxia. Oligodendroglia are preferentially injured over astrocytes by chronic(More)
Astrocytes cope more readily with hypoxic insults than do neurons. We hypothesized that astrocytes can upregulate their glycolytic capacity, allowing anaerobic glycolysis to provide sufficient ATP for cell survival as well as for carrying out critical functions such as taking up glutamate. To test this hypothesis, astrocytes were subjected to hypoxia for 5(More)
An outline is given of mechanisms that generate oxidative stress and inflammation. Considered are the metabolic mechanisms that give rise to peroxides, the source of strong oxidants; the production of dicarbonyls that interact with macromolecules to form advanced glycation endproducts; and the role that activation of the transcription factor NFkB has in the(More)
Previous work showed that the susceptibility of oligodendroglial progenitors to oxidative stress is related to their low reduced-glutathione (GSH) and high iron contents. This suggests that these cells have a poor ability to scavenge peroxides. All peroxides are scavenged by glutathione peroxidase. Glutathione peroxidase activity requires GSH as an electron(More)
The destructive mechanisms associated with stroke are initiated by activation of glutamate receptors resulting in elevated intracellular Ca2+ and reactive oxygen species (ROS) formation. Three major approaches have been investigated to ameliorate ischemia-induced brain damage: (i) interfering with the excitatory action of glutamate; (ii) preventing(More)
A major problem in treating cancer is the development of drug resistance. We previously demonstrated doxorubicin (DOX) resistance in K562 human leukemia cells that was associated with upregulation of glyoxalase 1 (GLO-1) and histone H3 expression. The thiazolidinedione troglitazone (TRG) downregulated GLO-1 expression and further upregulated histone H3(More)