Hypoxic Ischemic Brain
Mostrando 13-24 de 26 artigos, teses e dissertações.
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13. BrdU-positive cells in the neonatal mouse hippocampus following hypoxic-ischemic brain injury
BioMed Central.
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14. Calcium-permeable AMPA/kainate receptors mediate toxicity and preconditioning by oxygen-glucose deprivation in oligodendrocyte precursors
Hypoxic–ischemic brain injury in premature infants results in cerebral white matter lesions with prominent oligodendroglial injury and loss, a disorder termed periventricular leukomalacia (PVL). We have previously shown that glutamate receptors mediate hypoxic–ischemic injury to oligodendroglial precursor cells (OPCs) in a model of PVL in the develop
National Academy of Sciences.
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15. Caspase inhibitor affords neuroprotection with delayed administration in a rat model of neonatal hypoxic-ischemic brain injury.
Programmed cell death (apoptosis) is a normal process in the developing nervous system. Recent data suggest that certain features seen in the process of programmed cell death may be favored in the developing versus the adult brain in response to different brain injuries. In a well characterized model of neonatal hypoxia-ischemia, we demonstrate marked but de
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16. Developmental amnesia: Effect of age at injury
Hypoxic–ischemic events sustained within the first year of life can result in developmental amnesia, a disorder characterized by markedly impaired episodic memory and relatively preserved semantic memory, in association with medial temporal pathology that appears to be restricted to the hippocampus. Here we compared children who had hypoxic–ischemic
National Academy of Sciences.
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17. Hypoxic Preconditioning Protects against Ischemic Brain Injury
Summary: Animals exposed to brief periods of moderate hypoxia (8% to 10% oxygen for 3 hours) are protected against cerebral and cardiac ischemia between 1 and 2 days later. This hypoxia preconditioning requires new RNA and protein synthesis. The mechanism of this hypoxia-induced tolerance correlates with the induction of the hypoxia-inducible factor (HIF), a
The American Society for Experimental NeuroTherapeutics.
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18. Neuroglobin is up-regulated by and protects neurons from hypoxic-ischemic injury
Globins are oxygen-binding heme proteins present in bacteria, protists, fungi, plants, and animals. Their functions have diverged widely in evolution, and include binding, transport, scavenging, detoxification, and sensing of gases like oxygen, nitric oxide, and carbon monoxide. Neuroglobin (Ngb) is a recently discovered monomeric globin with high affin
The National Academy of Sciences.
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19. Insulin-like growth factor-1 is a potent neuronal rescue agent after hypoxic-ischemic injury in fetal lambs.
This study was designed to determine the potential of IGF-1 as a neuronal rescue agent after cerebral ischemia. Unanesthetized late gestation fetal sheep were subjected to 30-min cerebral ischemia by inflation of carotid artery occluder cuffs. 2 h later either 0.1 microgram rhIGF-1, 1 microgram rhIGF-1, 10 micrograms rhIGF-1, or vehicle was infused into a la
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20. Can a simple blood test quantify brain injury?
Despite significant advances in neurocritical care, it remains difficult to precisely measure the extent of neurological injury in patients affected by stroke, trauma, or cardiac arrest. In the intensive care unit the extent of primary and secondary injury often eludes clinicians, making prognostication imprecise and difficult. Derwall and colleagues present
BioMed Central.
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21. Systemic hypoxia changes the organ-specific distribution of vascular endothelial growth factor and its receptors
Vascular endothelial growth factor (VEGF) plays a key role in physiological blood vessel formation and pathological angiogenesis such as tumor growth and ischemic diseases. Hypoxia is a potent inducer of VEGF in vitro. Here we demonstrate that VEGF is induced in vivo by exposing mice to systemic hypoxia. VEGF induction was highest in brain, but also occurred
The National Academy of Sciences.
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22. Caspases determine the vulnerability of oligodendrocytes in the ischemic brain
Although oligodendrocytes (OLGs) are thought to be vulnerable to hypoxia and ischemia, little is known about the detailed mechanism by which these insults induce OLG death. From the clinical viewpoint, it is imperative to protect OLGs as well as neurons against ischemic injury (stroke), because they are the only myelin-forming cells of the central nervous sy
American Society for Clinical Investigation.
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23. Stanniocalcin: A molecular guard of neurons during cerebral ischemia
Stanniocalcin (STC) is a glycoprotein hormone originally found in bony fish, in which it regulates calcium/phosphate homeostasis and protects against hypercalcemia. The recently characterized human STC shows about 70% homology with fish STC. We previously reported a constitutive expression of STC in terminally differentiated neurons. Here, we show that expos
The National Academy of Sciences.
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24. Role of metabotropic glutamate receptors in oligodendrocyte excitotoxicity and oxidative stress
Developing oligodendrocytes (OLs) are highly vulnerable to excitotoxicity and oxidative stress, both of which are important in the pathogenesis of many brain disorders. OL excitotoxicity is mediated by ionotropic glutamate receptors (iGluRs) of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate type on these cells. Here we report that metabotr
National Academy of Sciences.