Results 161 to 170 of about 120,663 (190)

Oxidant Mechanisms in Neonatal Hypoxia-Ischemia

Developmental Neuroscience, 2001
The neonatal brain appears to be selectively vulnerable to oxidative stress. Several potential mechanisms associated with altered reactive oxygen species metabolism would explain the increased susceptibility. They include increased accumulation of hydrogen peroxide with subsequent neurotoxicity. This enhanced neurotoxicity from H₂
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Regional Changes in Metabolism in Hypoxia-Ischemia

1977
The purpose of this study is to describe regional metabolic changes following an episode of cerebral ischemia in the cat. Regional characterization of metabolic derangements is imperative because it is unlikely that cerebral blood flow is uniformly reduced in most hypoxic-ischemic episodes.1, 2, 3 Furthermore, neurons in discrete anatomic regions such ...
F A, Welsh, M J, O'Connor, W, Rieder, V R, Marcy   +3 more
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Cerebral hypoxia-ischemia in immature rats: Methodological considerations

Experimental Neurology, 1988
We used a model of perinatal hypoxic/ischemic brain damage which combines unilateral common carotid artery ligation and hypoxia (8% O2). Protein synthesis inhibition and cell loss were found in the ipsilateral forebrain of 11-day-old rats when hypoxia was initiated 4 h but not 24 h after carotid ligation. [14C]Iodoantipyrine uptake studies suggest that
B E, Dwyer, R N, Nishimura, D G, Fujikawa   +2 more
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Hypoxia/Ischemia and the pH Paradox

1996
Hydrogen ions play an important role in cellular processes. There are intimate links between energy metabolism and the control of cell and tissue acid/base balance. Control of this balance is threatened or lost during severe hypoxia or ischemia. Re-establishment of pH balance must occur before the tissue can be considered to have returned to normal ...
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Transgenerational effects of neonatal hypoxia‐ischemia in progeny

International Journal of Developmental Neuroscience, 2013
AbstractNeonatal hypoxia‐ischemia (HI) affects 60% of low birth weight infants and up to 40% of preterm births. Cell death and brain injury after HI have been shown to cause long‐lasting behavioral deficits. By using a battery of behavioral tests on second generation 3‐week‐old rodents, we found that neonatal HI is associated with behavioral outcomes ...
Smitha K, Infante, Harriett C, Rea, J R, Perez-Polo   +2 more
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Hypoxia-ischemia and thiamine deficiency.

Clinical neuropathology, 1993
In order to test the hypothesis that Wernicke's encephalopathy is of topographic rather than of pathogenetic specificity we examined the brains of 49 patients without any evidence of chronic alcoholism. They had died at least four days after an event of severe hypoxia-ischemia.
A O, Vortmeyer, C, Hagel, R, Laas
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Annexin V labels apoptotic neurons following hypoxia-ischemia

NeuroReport, 1997
The translocation of phosphatidylserine from the cytosol to the external surface of the plasma membrane has been documented as a characteristic feature of apoptosis in a number of cell types. Annexin V is a calcium-dependent phospholipid binding protein that has high affinity for phosphatidylserine. To investigate whether Annexin V provides a marker of
M, Walton, E, Sirimanne, C, Reutelingsperger, C, Williams, P, Gluckman, M, Dragunow   +5 more
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ORP150 protects against hypoxia/ischemia-induced neuronal death

Nature Medicine, 2001
Oxygen-regulated protein 150 kD (ORP150) is a novel endoplasmic-reticulum-associated chaperone induced by hypoxia/ischemia. Although ORP150 was sparingly upregulated in neurons from human brain undergoing ischemic stress, there was robust induction in astrocytes.
M, Tamatani, T, Matsuyama, A, Yamaguchi, N, Mitsuda, Y, Tsukamoto, M, Taniguchi, Y H, Che, K, Ozawa, O, Hori, H, Nishimura, A, Yamashita, M, Okabe, H, Yanagi, D M, Stern, S, Ogawa, M, Tohyama   +15 more
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Perspectives on Neonatal Hypoxia/Ischemia-Induced Edema Formation

Neurochemical Research, 2010
Neonatal hypoxia/ischemia (HI) is the most common cause of developmental neurological, cognitive and behavioral deficits in children, with hyperoxia (HHI) treatment being a clinical therapy for newborn resuscitation. Although cerebral edema is a common outcome after HI, the mechanisms leading to excessive fluid accumulation in the brain are poorly ...
Ferrari, Diana Carolina, Taylor,, Olivera Nesic, Perez-Polo, Jose Regino   +2 more
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Matrix Metalloproteinases in Cerebral Hypoxia-Ischemia

2009
Matrix metalloproteinase enzymes (MMPs) have been implicated in the pathogenesis of cerebral ischemia (stroke) and neurodegenerative diseases. Until recently, however, the mechanism of activation of MMPs in these disorders remained unclear. Following a hypoxic-ischemic insult, we identified a novel posttranslational modification (PTM) of MMPs involving
Zezong Gu, Jiankun Cui, Stuart A. Lipton
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