Vassiliki Soubasi

Aristotle University of Thessaloniki, Saloníki, Central Macedonia, Greece

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Publications (13)33.15 Total impact

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    ABSTRACT: In preterm infants with IVH the electrocortical background activity is affected and there is a correlation between the severity of cerebral injury to the degree of depression, however the usefulness of the early aEEG recordings has hardly been determined. To identify early aEEG features that could be used as prognostic markers for severe brain injury in prematures. In 115 infants, 25-32 wk GA, aEEG recordings during the first 72h of life were correlated with head ultrasound findings. Continuity (Co), sleep-wake cycling (Cy) and amplitude of the lower border (LB) of the aEEG were evaluated by semi-quantitative analysis. The infants were divided into four groups based on head ultrasound findings: A (n=72, normal), B [n=16, grades 1-2 intraventricular hemorrhage (IVH)], C (n=21, grades 3-4 IVH) and D (n=6, periventricular leukomalacia). 18 infants (16 of group C and 2 of group D) died during hospitalization. Significantly lower values of all aEEG features were found in group C infants. The presence of pathological tracings (burst-suppression, continuous low-voltage, flat trace) or discontinuous low-voltage (DLV), the absence of Cy and LB<3μV in the initial aEEG displayed a sensitivity of 88.9%, 63% and 51.9% respectively, for severe brain injury. Logistic regression of aEEG features and GA to the presence or absence of severe injury revealed that only Co was significantly correlated to outcome. Using this feature 83.19% of cases were correctly classified. Pathological tracings or DLV in the initial aEEG is predictive for poor short-term outcome in premature neonates.
    European journal of paediatric neurology: EJPN: official journal of the European Paediatric Neurology Society 03/2012; 16(6):625-30. DOI:10.1016/j.ejpn.2012.02.008 · 1.93 Impact Factor
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    ABSTRACT: Hypoxia-ischemia (HI) induced injury of the neonatal brain accounts for behavioral deficits concerning mainly neurological reflexes, sensorimotor functions and learning/memory disabilities that may evolve throughout development. The positive biological effects of resveratrol, a natural compound with anti-oxidant/anti-inflammatory properties found mainly in red wine have been indicated recently. Aim of this study was to investigate the delayed outcome of early administration of resveratrol in an experimental model of hypoxic-ischemic encephalopathy, by means of behavioral analysis and late neuropathological examination. Seven-day-old (P7) rats were separated into 3 groups: Group 1 underwent HI and treated with resveratrol. Group 2 (HI-treated) was subjected to HI and received same volume of saline. Group 3 (sham-operated) was the control group. A battery of behavioral tests was performed from days P8-P66, during which early reflexes (righting reflex, gait, geotaxis), sensorimotor (rope suspension, beam walking, rotarod) and learning/memory function (passive avoidance, Morris water-maze) were examined. Significant difference among the groups was observed in righting reflex, rotarod and water maze tests in which the resveratrol group almost reached the performance of the control animals. The other behavioral tests showed that control and resveratrol groups were better compared to HI, although not significant. Neuropathology study revealed a remarkable reduction of the infarct and preservation of myelination after resveratrol treatment, which was in most cases correlated with the better performance of the resveratrol group. These findings indicate that long-term neuroprotective effect of resveratrol on neonatal HI-induced gray and white matter damage might be associated with the preservation of behavioral functions.
    Brain research 11/2011; 1425:98-110. DOI:10.1016/j.brainres.2011.09.044 · 2.83 Impact Factor
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    ABSTRACT: To study, the maturational changes of the amplitude-integrated electroencephalogram (aEEG) in preterm infants without neurological disorders and especially the influence of the duration of extrauterine life, over this process. 96 preterm infants, 25-34weeks' gestational age (GA) at birth, clinically stable and without ultrasonographic evidence of neurological abnormalities, were studied. The aEEG recordings were obtained within 72 h of life and then weekly until discharge. Four aspects of each tracing (continuity, sleep-wake cycling, bandwidth, and lower border), were evaluated by visual analysis, applying pre-established criteria. We analysed 624 aEEG recordings at postmenstrual age (PMA) of 25-42weeks. With advanced GA the aEEG becomes more continuous (p: 0.022), it displays definite sleep-wake cycles (p: 0.011), and its bandwidth acquires the mature pattern (p: 0.012). A positive significant interaction of GA and PMA in the evolution of aEEG was found regarding continuity (p: 0.002), sleep-wake cycling (p: 0.002), and bandwidth (p: 0.02). The evolution of the aEEG tracing depends on both GA and PMA. The older the infants at birth the more mature the aEEG pattern. At the same PMA, preterm infants of lower GA display an advanced maturation of the aEEG comparing with others of higher GA.
    Early human development 11/2009; 85(12):761-5. DOI:10.1016/j.earlhumdev.2009.10.004 · 1.93 Impact Factor
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    ABSTRACT: Perinatal asphyxia (PA) is a major determinant for long-term sensorimotor and locomotor deficits. The model of neonatal hypoxia-ischemia (HI) in 7-day-old rats produces sensorimotor cortex, thalamus and striatum injury, which are all critical for the maintenance of sensory motor function. The aim of this study was to evaluate the long-term neurodevelopmental disturbances in the above experimental model and to assess the neuroprotective effect of MgSO(4) in terms of long-term behavioral and morphological changes. Seven-day-old rats were separated into three groups: A (control), neither ligated nor exposed to hypoxia; B (HI/MgSO(4)) ligated, exposed to hypoxia and treated with MgSO(4) (2 g/kg b.w., i.p.), and C (HI) ligated and exposed to hypoxia. At the age of 42 days, the behavior of the rats was evaluated using 5 sensorimotor tests. Muscle power, motor coordination, reflexes, and limb placing were tested to different sensory stimuli. The study was completed with the histopathological evaluation of brain tissue damage. In all individual tests the HI-treated rats performed significantly worse than the control and MgSO(4)-treated rats and this difference was more pronounced in the limb placing tests. Additionally, neonatal HI resulted in extensive neuronal damage that was limited after MgSO(4) administration. Behavioral alterations represent a useful endpoint for studying the consequences of a perinatal HI insult and the efficacy of potential neuroprotective treatments. MgSO(4) administration resulted in prevention of HI-induced sensorimotor deficits and brain injury.
    Neonatology 10/2008; 95(1):33-40. DOI:10.1159/000151753 · 2.37 Impact Factor
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    ABSTRACT: Previous studies have shown contradictory results regarding magnesium-mediated neuroprotection in animal models of perinatal asphyxia. The aim of this study is to investigate the effects of MgSO(4) postasphyxial treatment on hypoxia-ischemia (HI)-induced brain injury in neonatal rats and the possibility that this effect is related to the severity of brain damage. Seven-day-old rats underwent unilateral carotid artery ligation followed by 1 or 2 hours of hypoxia (8% O(2)) and MgSO(4) administration. Adenosine triphosphate/phosphocreatine and glutamate/glutamine measurements and neuropathological evaluation of the hippocampus were used to assess the effects of HI and MgSO(4). HI caused time-dependent changes in energy stores, amino acid concentrations, and brain damage. Administration of MgSO(4) after 1 hour but not after 2 hours of hypoxia resulted in significant prevention of HI-induced brain injury. MgSO(4) administration results in a significant protection against moderate HI-induced brain damage, whereas it fails to offer a similar effect against severe brain damage.
    Reproductive sciences (Thousand Oaks, Calif.) 11/2007; 14(7):667-77. DOI:10.1177/1933719107305864 · 2.18 Impact Factor
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    ABSTRACT: Perinatal asphyxia accounts for behavioral dysfunctions that often manifest as sensorimotor, learning or memory disabilities throughout development and into maturity. Erythropoietin (Epo) has been shown to exert neuroprotective effects in different models of brain injury including experimental models of perinatal asphyxia. However, the effect of Epo on functional abilities following cerebral hypoxia-ischemia (HI) in neonatal rats is not known. The aim of the present study is to investigate the effect of Epo on sensorimotor deficits and brain injury induced by hypoxia-ischemia. Seven-day-old rats underwent unilateral, permanent carotid artery ligation followed by 1 h of hypoxia. Epo was administered as a single dose immediately after the hypoxic insult (2000 U/kg). The neuroprotective effect of Epo was evaluated at postnatal day 42 by using a battery of behavioral tests and histological analysis. The results of the present study suggest that Epo treatment immediately after HI insult significantly facilitated recovery of sensorimotor function. Consistently, histopathological evaluation demonstrated that Epo significantly attenuated brain injury and preserved the integrity of cerebral cortex. These findings indicate that long-term neuroprotective effect of Epo on neonatal HI-induced brain injury might be associated with the preservation of sensorimotor functions.
    Brain Research 06/2005; 1045(1-2):22-30. DOI:10.1016/j.brainres.2005.03.013 · 2.83 Impact Factor
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    ABSTRACT: Erythropoietin (EPO), known for its role in erythroid differentiation, has been suggested to have non-hematopoietic functions in the brain, especially during development. In the present study, we investigated the expression of erythropoietin and erythropoietin receptor (EPOR) in the developing rat brain following hypoxia-ischemia. Seven-day-old rats underwent unilateral, permanent carotid artery ligation followed by 1 h of hypoxia, and their brains were examined immediately, 24 h or 4 days after hypoxia-ischemia. RT-PCR and Western blot analysis revealed that hypoxia-ischemia only marginally affected EPO expression. Immunohistochemical study of brains 4 days after hypoxia showed that 60 min of hypoxia (resulting in cortical infarction and severe neuronal loss in other regions) led to the increased EPO immunoreactivity, especially in the boundaries of the damaged cerebral cortex, associated with astrocytosis. In contrast, EPOR was dramatically upregulated within 24 h after hypoxia-ischemia. These results suggest that there is a rapid response of EPOR to the hypoxic-ischemic stimulus, which seems to precede that of EPO, leading to the hypothesis that the EPO/EPOR system is implicated in the processes of neuroprotection from hypoxia-ischemia.
    Brain Research 10/2004; 1021(2):167-72. DOI:10.1016/j.brainres.2004.06.057 · 2.83 Impact Factor
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    ABSTRACT: Background: Perinatal asphyxia (PA) accounts for the majority of developmental and cognitive deficits. Various therapeutic interventions after hypoxia-ischemia (HI) have been shown to reduce brain injury in the short-term perspective, although long-term functional and structural improvements are still uncertain.
    Pediatric Research 09/2004; 56(3). DOI:10.1203/00006450-200409000-00229 · 2.84 Impact Factor
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    ABSTRACT: 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 possibility that its neuroprotective action may be associated with anti-apoptotic activity. Seven-day-old rats were treated with EPO (2000 U/kg) and subjected to a modified Levine procedure. EPO administration before the hypoxic-ischemic insult significantly reduces the severity of brain damage and improved the short-term functional brain recovery. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling and DNA electrophoresis displayed no evidence of DNA fragmentation in EPO-treated animals. These results suggest that EPO might protect the neonatal rat brain by anti-apoptotic mechanisms.
    Neuroscience Letters 09/2004; 366(1):24-8. DOI:10.1016/j.neulet.2004.05.032 · 2.06 Impact Factor
  • Pediatric Research 06/1999; 45(6). DOI:10.1203/00006450-199906000-00198 · 2.84 Impact Factor
  • Pediatric Research 09/1998; 44(3). DOI:10.1203/00006450-199809000-00087 · 2.84 Impact Factor
  • Pediatric Research 09/1996; 40(3). DOI:10.1203/00006450-199609000-00252 · 2.84 Impact Factor
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    ABSTRACT: Objective: It is known that rHu-EPO treatment prevents successfully AOP during the period which administered (Soubasi et aL Pediatr Res 1993;34:675). However data on the duration and optimal timing of EPO administration is unavailable.
    Pediatric Research 07/1994; 36(1). DOI:10.1203/00006450-199407000-00215 · 2.84 Impact Factor