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Temperature disturbances are common in patients with severe traumatic brain injury. The possibility of an adaptive, potentially beneficial role for fever in patients with severe brain trauma has been dismissed, but without good justification. Fever might, in some patients, confer benefit. A cadre of clinicians and scientists met to debate the clinically relevant, but often controversial issue abou

The levels of protein kinase C-γ (PKC-γ) and the calcium/calmodulin-dependent kinase II-α (CaMKII-α) were measured in crude synaptosomal (P2), particulate (P3), and cytosolic (S3) fractions of the neocortex of rats exposed to 1-hour and 2-hour middle cerebral artery occlusion (MCAO) and 2-hour MCAO followed by 2-hour reperfusion. During MCAO, PKC levels increased in P2 and P3 in the most severe is

Inom ramen för Svenska kyrkans forskningsenhets projekt "I vems tjänst?", som är ett teologiskt aktionsforskningsprojekt om kyrka och välfärd, har under 2015 denna rapport arbetats fram för att ge en kunskapsöversiktom fält där kyrka och välfärd kopplas till varandra. Syftet med dennaförberedande undersökning är att bidra till underlag för att formulera frågeställningar och problem mer precist. Ra

The Benguela Upwelling System (BUS), located between 30 and 20°S, is one of the fundamental high-productivity systems of the world ocean. The BUS has previously been studied in terms of primary productivity and ecology over glacial-interglacial timescales; however, the response and coupling with the benthic environment have received little attention. Here, for the first time, we present a high-res

The tumor suppressor protein p53 is implicated in cell cycle arrest and DNA repair as well as in apoptosis. In the CNS, p53 has been associated with neuronal cell death following various insults, including cerebral ischemia. We investigated the expression of p53 messenger RNA and protein, and the messenger RNA expression of the p53-responsive gene p21(WAF1/Cip1), in specific hippocampal regions fo

Proliferating cell nuclear antigen (PCNA) is required for completion of the DNA synthesis step of DNA replication as well as nucleotide excision repair (NER) of damaged DNA. We investigated the expression of PCNA mRNA and the levels of PCNA protein in the adult rat hippocampus following normo- and hypothermic global forebrain ischemia. Hypothermia protected the CA1 neurons from ischemic damage. A

Hypothermia diminishes the ischemia-induced protein kinase C (PKC) translocation and inhibition, and also reduces transmitter release during ischemia. To study the role of PKC in the mechanism of glutamate release during ischemia, we measured extracellular glutamate levels in the striatum with the microdialysis technique, in the presence and absence in the dialysate of the PKC activator 4β-phorbol

Induction of the mitochondrial permeability transition (MPT) has been implicated in cellular apoptosis and in ischemia-reperfusion injury. During MPT, a channel in the inner mitochondrial membrane, the mitochondrial megachannel, opens and causes isolated mitochondria to swell. MPT and mitochondrial swelling is inhibited by cyclosporin A (CsA), which may also inhibit apoptosis in some cells. Treatm

The expression of the mRNAs of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3) and the neurotrophin receptor, TrkB, was studied in the rat hippocampus by in situ hybridization following normothermic (37°C) and protective hypothermic (33°C) transient cerebral ischemia of 15 min duration. In the resistant dentate gyms, normothermic ischemia transiently induc

Hypothermia (33°C) dramatically diminishes ischemic but not hypoglycemic brain damage. The beneficial effects of hypothermia in ischemia have been partly attributed to a reduction in the ischemia-induced increase in synaptic levels of glutamate or aspartate. With the microdialysis technique, we studied the effects of hypothermia (33°C) on the brain extracellular levels of glutamate and aspartate d

The mechanisms underlying secondary or delayed cell death following traumatic brain injury are poorly understood. Recent evidence from experimental models suggests that widespread neuronal loss is progressive and continues in selectively vulnerable brain regions for months to years after the initial insult. The mechanisms underlying delayed cell death are believed to result, in part, from the rele

The regional selectivity and mechanisms underlying the toxicity of the serine/threonine protein phosphatase inhibitor okadaic acid (OA) were investigated in hippocampal slice cultures. Image analysis of propidium iodide-labeled cultures revealed that okadaic acid caused a dose- and time- dependent injury to hippocampal neurons. Pyramidal cells in the CA3 region and granule cells in the dentate gyr

Rat and gerbil hippocampus exposed to a sublethal period of ischemia becomes resistant to a subsequent period of lethal ischemia induced several days later, a phenomenon referred to as ischemic preconditioning. Here we describe ischemic preconditioning induced in vitro in cultured hippocampal neurons. Mixed neuroglial hippocampal cell cultures of 14-17 DIV were exposed to a combined glucose and ox