asphyxia neonatorum/hypoxia

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[An immunochemical analysis of the function of the hemato-encephalic barrier in acute fetal hypoxia and asphyxia neonatorum].

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The neurospecific protein alpha 1-globulin has been assayed in serum in order to evaluate the blood-brain barrier in newborns with acute intrapartum hypoxia. The study involved 35 term newborns with birth asphyxia of variable severity. The alpha 1-globulin levels correlated with severity of

Value of myocardial hypoxia markers (creatine kinase and its MB-fraction, troponin-T, QT-intervals) and serum creatinine for the retrospective diagnosis of perinatal asphyxia.

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Neonatal asphyxia is a major topic of neonatal research. However, no clear-cut physiologic parameters exist which enable an early identification of neonatal infants who are either at risk to develop brain damage or posthypoxic heart failure. Parameters indicating dysfunction of the heart and kidneys

mRNA levels of the hypoxia inducible factor (HIF-1) and DNA repair genes in perinatal asphyxia of the rat.

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Hypoxia inducible factor 1 (HIF-1) is a transcription factor which is expressed, when mammalian cells are subjected to hypoxia, activating the transcription of genes encoding proteins thought important for maintaining oxygen hemostasis. The aim of the study was to evaluate HIF-1 mRNA levels in a

Hypobaric hypoxia postconditioning reduces brain damage and improves antioxidative defense in the model of birth asphyxia in 7-day-old rats.

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Perinatal brain insult mostly resulting from hypoxia-ischemia (H-I) often brings lifelong permanent disability, which has a major impact on the life of individuals and their families. The lack of progress in clinically-applicable neuroprotective strategies for birth asphyxia has led to an increasing

Endogenous opioid-like substances in perinatal asphyxia and cerebral injury due to anoxia.

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Perinatal asphyxia is one of the major causes of cerebral injury in neonates. It may be due to the increased endogenous opioid-like substances (OLS) in the body. The levels of three OLS, namely leucine-enkephalin (LEK), beta-endorphin (beta-EP) and dynorphin A1-13 (DynoA1-13) of 44 cases with

[Observations on the use of analeptics in fetal anoxia and in asphyxia neonatorum].

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[Observations on the use of analeptics in fetal anoxia and in neonatal asphyxia].

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[Effects of fetal hypoxia on later life. Late prognosis of asphyxia neonatorum].

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[The early recognition of threatening fetal asphyxia (hypoxia and acidosis)].

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[Effect of fetal anoxia and asphyxia neonatorum on the main indicators of phosphorus-calcium metabolism].

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Contributions to the study of cerebral anoxia. III. Neonatal asphyxia and its relation to certain degenerative diseases of the brain in infancy and childhood.

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[Various causative factors of fetal anoxia, asphyxia neonatorum and different forms of acidosis during postnatal development of children with cerebral palsy].

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[Pathogenesis of fetal hypoxia and asphyxia neonatorum].

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[Use of cytochrome "C" for preventing and treating asphyxia neonatorum and intra-uterine fetal hypoxia].

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Erythropoietin prevents hypoxia/ischemia-induced DNA fragmentation in an experimental model of perinatal asphyxia.

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Erythropoietin (EPO) prevents neuronal damage following ischemic, metabolic and excitotoxic stress. Recent studies have shown that EPO plays a significant role in the developing brain. The present study investigates the effect of EPO administration on hypoxic-ischemic brain injury and the

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