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Pàgina 1 des de 1368 resultats
Blood genomic responses differ after stroke, seizures, hypoglycemia, and hypoxia: blood genomic fingerprints of disease.
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Using microarray technology, we investigated whether the gene expression profile in white blood cells could be used as a fingerprint of different disease states. Adult rats were subjected to ischemic strokes, hemorrhagic strokes, sham surgeries, kainate-induced seizures, hypoxia, or insulin-induced
Changes of evoked epileptic seizures after the short term hypobaric hypoxia in the young rats.
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Exposition to the acute intensive hypobaric hypoxia blocks the triggering mechanism of epileptic seizures only within a short time interval after the end of hypoxia period and it does not influence the progressive epileptogenesis in 12-day-old rats. In 25-day-old rats' hypobaric hypoxia suppresses
[A study of the sequelae of perinatal hypoxia and convulsions in full-term newborn infants].
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Perinatal hypoxia may result in neuromotor handicaps. The occurrence of convulsions after perinatal hypoxia is regarded as a bad prognostic sign. Thirty-two full-term babies with perinatal hypoxia were studied retrospectively. Post-hypoxic convulsions were seen in 20 newborns. In 26 out of 29
Nocturnal seizures are associated with more severe hypoxemia and increased risk of postictal generalized EEG suppression.
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Patients with epilepsy have 20-fold risk of sudden death when compared to the general population. Uncontrolled seizures is the most consistent risk factor, and death often occurs at night or in relation to sleep. We examined seizure-related respiratory disturbances in sleep versus wakefulness,
Does anoxemia play a role in the effects of neonatal seizures on brain growth? An experimental study in the rat.
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Groups of 4 Wistar rat littermates of matched sex and weight received the following daily treatment between the ages of 2 and 11 days: handling (untreated controls, UC), succinylcholine paralysis and ventilation with 100% O2 (respirator control, RC), electroconvulsive seizures (ECS) and ECS while
The dynamics of changes in hippocampal GABAergic system in rats exposed to early-life hypoxia-induced seizures.
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Hypoxia-evoked seizures (H/S) early in life lead to multiple chronic neurological deficits. Here, we present the results of studying GABA release and uptake in hippocampal axon terminals of rats exposed to H/S at 10-12 days of age. We characterized (i) exocytotic release of GABA; (ii) the initial
Ketogenic diet prevents seizure and reduces myoclonic jerks in rats with cardiac arrest-induced cerebral hypoxia.
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Although the mechanism underlying the anti-epileptic effects of a ketogenic diet (KD) is not known, KD is reported to be an effective treatment for intractable epilepsy, in particular among children. Here, we evaluated whether a KD can reduce posthypoxic seizure and myoclonic jerks in a rat model of
Perinatal exposure to anoxia alone does not alter the susceptibility to amygdaloid-kindled seizures in the adult rabbit.
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It is suggested that asphyxia on newborns increases the susceptibility to epileptic syndromes. The effect of perinatal and postnatal anoxia on subsequent seizure susceptibility was assessed by amygdaloid kindling in adult rabbits. Rabbits from 1 day pre-term to 53 days were exposed to 100% N2 for an
Pre-existing hypoxia is associated with greater EEG suppression and early onset of evolving seizure activity during brief repeated asphyxia in near-term fetal sheep.
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Spontaneous antenatal hypoxia is associated with high risk of adverse outcomes, however, there is little information on neural adaptation to labor-like insults. Chronically instrumented near-term sheep fetuses (125 ± 3 days, mean ± SEM) with baseline PaO2 < 17 mmHg (hypoxic group: n = 8) or > 17
Behavioral abnormalities and seizure susceptibility in rat after neonatal anoxia.
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Wistar rat pups were exposed to 99.99%-nitrogen gas for 10 minutes at 4 days of age, and then their behavior and susceptibility to pentylentetrazol (PTZ) induced seizure were investigated at the ages of 28 and 56 days. Neonatal anoxic rats exhibited hyperactivity in the open field examination and
Epileptic seizure-induced hypoxemia in infants with apparent life-threatening events.
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OBJECTIVE
To describe the physiologic changes that occur during epileptic seizure (ES)-induced apparent life-threatening events (ALTE) and to provide an explanation for the mechanism whereby the hypoxemia characterizing these events occurred.
METHODS
Six infants were retrospectively selected from a
Fetal seizures causing increased heart rate variability during terminal fetal hypoxia.
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Fetal seizures together with both abnormal breathing movements and fluctuations in fetal blood pressure and heart rate resulting in increased fetal heart rate variability have been observed in brain-damaged fetal sheep shortly after an asphyxial insult. We report a clinical example of convulsions
The effects of neonatal hypoxia on kindled seizure development and electroconvulsive shock profiles.
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OBJECTIVE
Our previous research indicated that the exposure of rat pups to an hypoxic environment during a discrete developmental period (postnatal days 10-15) produces short-term seizures and confers an enduring increase in susceptibility to pentylenetetrazol- and flurothyl-induced seizures. In
Sensitivity to seizure-like activity in Drosophila following acute hypoxia and hypercapnia.
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Human seizure disorders represent a heterogeneous collection of neuropathies, many of which are poorly understood. To investigate the etiology of seizure disorders, we have used a group of Drosophila mutants known as the bang-sensitive (BS) paralytics. The BS mutants exhibit seizure-like activity
Persistently decreased basal synaptic inhibition of hippocampal CA1 pyramidal neurons after neonatal hypoxia-induced seizures.
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Hypoxia is the most common cause of neonatal seizures and can lead to epilepsy, but the epileptogenic mechanisms are not yet understood. We have previously shown that hypoxia-induced seizures in the neonatal rat result in acutely decreased amplitudes and frequency of spontaneous and miniature
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