Search for dissertations about: "Hypoxia-Ischemia"
Showing result 1 - 5 of 33 swedish dissertations containing the word Hypoxia-Ischemia.
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1. Apoptosis-related mechanisms in the immature brain after hypoxia-ischemia
Abstract : Aims: To characterize the activation of caspases-3 and extracellular signal-regulated kinase (ERK) in the neonatal brain after hypoxia-ischemia (HI) injury and evaluate the neuroprotective effect of X-linked inhibitor of apoptosis (XIAP) protein, erythropoietin (EPO) and the non-erythropoietic derivative asialoEPO. Methods: Seven-day-old rats or 9-day-old mice were subjected to HI. READ MORE
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2. Aspects of pathological apoptosis in the immature brain after hypoxia-ischemia
Abstract : The cause of mechanisms underlying perinatal brain injury is not fully known, but it results in a wide variety of neurological impairments in the affected children. When injured, neurons of the newborn brain are prone to undergo programmed cell death, apoptosis, since this genetic program is normally activated in some cells during development of the nervous system, even in the perinatal period. READ MORE
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3. Inflammatory response in the immature brainafter hypoxia-ischemia. Application of microarray and transgenic technology
Abstract : Hypoxic-ischemic (HI) brain injury remains a common problem encountered during theneonatal period, and it is a major cause of perinatal mortality and long term neurologicalimpairments. After HI, an inflammatory reaction is elicited in the brain, which is believedto contribute to the secondary progression of brain injury. READ MORE
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4. Apoptotic mechanisms in the neonatal brain following hypoxia-ischemia
Abstract : Neonatal encephalopathy is often perinatally acquired and caused by hypoxia-ischemia (HI). Brain injury develops with a delay, over 12-48 hours, after the insult. Hypothermia, an established neuroprotective treatment, saves 1 infant in 9 from neurological deficits suggesting that there is room for further improvement. READ MORE
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5. Glutathione in the brain. Studies on efflux and possible implications in neurotoxicity
Abstract : Neuronal cell death in acute insults such as stroke, trauma and epilepsy involves overactivation of glutamate receptors, calcium influx and increased formation of potentially toxic reactive oxygen species. Glutathione is a key component in the antioxidant defense system against reactive oxygen species. READ MORE