The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform
Amato Maurizio - One of the best experts on this subject based on the ideXlab platform.
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perinatal aSphyxia in preterm neonateS leadS to Serum changeS in Protein S 100 and neuron Specific enolaSe
Current Neurovascular Research, 2009Co-Authors: Distefano Giuseppe, Curreri Sergio, Betta Pasqua, Li Volti Giovanni, Cilauro Salvatore, Alessandro Frigiola, Huppi Petra, Amato MaurizioAbstract:In preterm infantS, neurological SignS and clinical manifeStationS of brain damage are limited criteria for diagnoSiS of neurologic Sequelae. Early indicatorS of brain damage are needed and currently Some Specific biochemical markerS of brain injury are inveStigated to aSSeSS regional brain damage after perinatal aSphyxia in neonateS. In thiS Study Protein S-100 (PS-100) and Neuron Specific EnolaSe (NSE) Serum levelS were Studied Serially during the perinatal period in preterm neonateS with perinatal aSphyxia aS markerS of glial and neuronal damage reSpectively. Thirty outborn preterm infantS with perinatal aSphyxia were Studied at 3, 24, 48 hourS and 7 dayS of life. According to Apgar ScoreS at 1 and cord blood pH and lacticidemia (LA), patientS were divided in two groupS: 15 of them (GA 33±1.2 wk, BW 1790±383 g) with Severe aSphyxia (Apgar < 4, pH7.0±0.08, LA 6.29±0.79 mM/L) and 15 (GA 32±1.8 wk, BW 1810±290 g) with mild aSphyxia (Apgar between 4-6, pH 7.18±0.05, LA 2.59±0.61 mM/L). Ten geStational age matched healthy preterm neonateS were Studied aS control group. Cerebral ultraSound examinationS (7 MHz) were performed at birth and repeated at 3 weekS of life. The reSultS of thiS Study Show that neonateS with Severe aSphyxia at any time had Significantly more elevated mean Serum levelS of both markerS compared to the group with mild aSphyxia and to the control group (p < 0.05). The valueS of control group were alSo Significantly lower in compariSon with that of mild aSphyxia. In neonateS with Severe aSphyxia, NSE valueS decreaSed conStantly from birth to the Seventh day of life, while PS-100 Showed a different pattern increaSing progreSSively between 3 h and 7 dayS. In neonateS with mild aSphyxia Serum valueS of both markerS Showed decreaSing levelS through the Study period. The reSultS of thiS Study SuggeSt that perinatal aSphyxia iS aSSociated with the releaSe of different brain cellular ProteinS in the blood of preterm infantS with different time courSe indicating Specific regional cellular injury. The more elevated levelS of NSE at birth found in the newbornS with Severe aSphyxia could be conSidered aS an early biomarker of neuronal necrotic damage in the iSchaemic phaSe of perinatal cerebral hypoxic-iSchaemic inSult; progreSSive increaSe of PS-100 during the firSt week of life in the Same neonateS could be expreSSion of apoptotic damage of glial cellS occurring in the reperfuSion phaSe of cerebral iSchaemia.
Alexander Sartorius - One of the best experts on this subject based on the ideXlab platform.
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Protein S 100 and neuron Specific enolaSe Serum levelS remain unaffected by electroconvulSive therapy in patientS with depreSSion
Journal of Neural Transmission, 2014Co-Authors: Laura Kranaster, Christoph Janke, Sonani Mindt, Michael Neumaier, Alexander SartoriusAbstract:The mechaniSm of the reverSible cognitive deficitS that might occur within an electroconvulSive therapy (ECT) treatment haS not been clarified in a SubStantial way yet. Although the data available So far do not point towardS a cauSe due to any Structural or diffuSe damage, further clarification, eSpecially of the role of S-100 SeemS to be neceSSary before robuSt concluSionS can be drawn. Serum levelS of Protein S-100 and neuron-Specific enolaSe (NSE) were analySed in 19 patientS with depreSSion, who received ECT. The Sampling waS adjuSted for the Short half-life of Protein S-100. Several outcome parameterS Such aS Hamilton DepreSSion Rating Scale and Mini-mental State examination before and after the ECT, reSponSe and remiSSion to the treatment were recorded. S-100 and NSE levelS at baSeline, 30 and 60 min after the third SeSSion and after the end of the ECT remained Stable. S-100 and NSE levelS were neither aSSociated with antidepreSSant reSponSe or remiSSion nor with alterationS in the cognitive performance. Although aiming for detecting potential riSe in theSe eStabliShed brain damage markerS, an increaSe due to ECT waS not obServed, which iS in line with the previouS StudieS concerning the Safety of ECT on a cellular baSiS.
H Przuntek - One of the best experts on this subject based on the ideXlab platform.
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relation between electroconvulSive therapy cognitive Side effectS neuron Specific enolaSe and Protein S 100
Journal of Neurology Neurosurgery and Psychiatry, 2001Co-Authors: M W Agelink, Jurgen Andrich, Thomas Postert, U Wurzinger, T Zeit, P Klotz, H PrzuntekAbstract:OBJECTIVE To inveStigate whether electroconvulSive therapy (ECT) induceS brain tiSSue damage expreSSed aS an increaSe in neuron Specific enolaSe and Protein S-100. METHODS A total of 179 Serial meaSurementS of S-100 and NSE Serum concentrationS were performed on 14 patientS during the courSe of a bilaterally Stimulated ECT SerieS. Cognitive performance waS aSSeSSed by pSychometric teSting carried out on the day before the Start of ECT aS well aS on the dayS after the third, Sixth, and laSt ECT. Pre-ECT and poSt-ECT concentrationS of NSE and S-100 were compared by non-parametric teStS. RESULTS On average, 9.5 (SD 2.9) (range 3–12) ECTS were applied; 13 of 14 patientS received at leaSt Six ECTS. The average duration of convulSion (computed for all ECTS) waS 29.0 (SD 10.5) SecondS. At no point during the ECT SerieS waS there a Significant increaSe in the average NSE or S-100 concentrationS compared with the baSeline inveStigation before the Start of the ECT SerieS. The maximal meaSured poSt-ECT valueS of NSE and S-100 were 26.6 ng/ml and 0.46 ng/ml, reSpectively. The cumulative energy doSeS applied, Seizure durationS, and ECT induced changeS in cognitive performance ScoreS were never Significantly correlated with the NSE or S-100 Serum concentrationS. CONCLUSION ThiS pattern of findingS SuggeStS that a modern ECT, fulfilling current quality StandardS, induceS no brain tiSSue damage detectable by changeS in NSE or Protein S-100.
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Serum levelS of neuron Specific enolaSe and S 100 Protein after Single tonic clonic SeizureS
Journal of Neurology, 1999Co-Authors: T Buttner, H Przuntek, Birgit Lack, Matthias Jager, Wolfgang Wunsche, W Kuhn, Thomas Muller, Thomas PostertAbstract:Serum neuron-Specific enolaSe (S-NSE) and S-100 Protein (S-100) are SenSitive markerS of variouS brain diSeaSeS. We inveStigated both of theSe markerS in nine patientS within 5 min, 6 h, 12 h, and 48 h after a Single tonic-clonic Seizure. The mean peak S-NSE level waS Significantly higher after 5 min (11.97 ± 8.56 μg/l) and 48 h (10.31 ± 8.92 μg/l, P < 0.05) than the levelS of Seizure-free, age-matched controlS. Five patientS had increaSed S-NSE levelS regarding the upper limit of normal aS mean + 3 SD. S-100 waS not detected either in controlS or epileptic patientS. TheSe data indicate that S-NSE in contraSt to S-100 may be an in vivo marker after generalized SeizureS in Some patientS.
Distefano Giuseppe - One of the best experts on this subject based on the ideXlab platform.
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perinatal aSphyxia in preterm neonateS leadS to Serum changeS in Protein S 100 and neuron Specific enolaSe
Current Neurovascular Research, 2009Co-Authors: Distefano Giuseppe, Curreri Sergio, Betta Pasqua, Li Volti Giovanni, Cilauro Salvatore, Alessandro Frigiola, Huppi Petra, Amato MaurizioAbstract:In preterm infantS, neurological SignS and clinical manifeStationS of brain damage are limited criteria for diagnoSiS of neurologic Sequelae. Early indicatorS of brain damage are needed and currently Some Specific biochemical markerS of brain injury are inveStigated to aSSeSS regional brain damage after perinatal aSphyxia in neonateS. In thiS Study Protein S-100 (PS-100) and Neuron Specific EnolaSe (NSE) Serum levelS were Studied Serially during the perinatal period in preterm neonateS with perinatal aSphyxia aS markerS of glial and neuronal damage reSpectively. Thirty outborn preterm infantS with perinatal aSphyxia were Studied at 3, 24, 48 hourS and 7 dayS of life. According to Apgar ScoreS at 1 and cord blood pH and lacticidemia (LA), patientS were divided in two groupS: 15 of them (GA 33±1.2 wk, BW 1790±383 g) with Severe aSphyxia (Apgar < 4, pH7.0±0.08, LA 6.29±0.79 mM/L) and 15 (GA 32±1.8 wk, BW 1810±290 g) with mild aSphyxia (Apgar between 4-6, pH 7.18±0.05, LA 2.59±0.61 mM/L). Ten geStational age matched healthy preterm neonateS were Studied aS control group. Cerebral ultraSound examinationS (7 MHz) were performed at birth and repeated at 3 weekS of life. The reSultS of thiS Study Show that neonateS with Severe aSphyxia at any time had Significantly more elevated mean Serum levelS of both markerS compared to the group with mild aSphyxia and to the control group (p < 0.05). The valueS of control group were alSo Significantly lower in compariSon with that of mild aSphyxia. In neonateS with Severe aSphyxia, NSE valueS decreaSed conStantly from birth to the Seventh day of life, while PS-100 Showed a different pattern increaSing progreSSively between 3 h and 7 dayS. In neonateS with mild aSphyxia Serum valueS of both markerS Showed decreaSing levelS through the Study period. The reSultS of thiS Study SuggeSt that perinatal aSphyxia iS aSSociated with the releaSe of different brain cellular ProteinS in the blood of preterm infantS with different time courSe indicating Specific regional cellular injury. The more elevated levelS of NSE at birth found in the newbornS with Severe aSphyxia could be conSidered aS an early biomarker of neuronal necrotic damage in the iSchaemic phaSe of perinatal cerebral hypoxic-iSchaemic inSult; progreSSive increaSe of PS-100 during the firSt week of life in the Same neonateS could be expreSSion of apoptotic damage of glial cellS occurring in the reperfuSion phaSe of cerebral iSchaemia.
Thomas Postert - One of the best experts on this subject based on the ideXlab platform.
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relation between electroconvulSive therapy cognitive Side effectS neuron Specific enolaSe and Protein S 100
Journal of Neurology Neurosurgery and Psychiatry, 2001Co-Authors: M W Agelink, Jurgen Andrich, Thomas Postert, U Wurzinger, T Zeit, P Klotz, H PrzuntekAbstract:OBJECTIVE To inveStigate whether electroconvulSive therapy (ECT) induceS brain tiSSue damage expreSSed aS an increaSe in neuron Specific enolaSe and Protein S-100. METHODS A total of 179 Serial meaSurementS of S-100 and NSE Serum concentrationS were performed on 14 patientS during the courSe of a bilaterally Stimulated ECT SerieS. Cognitive performance waS aSSeSSed by pSychometric teSting carried out on the day before the Start of ECT aS well aS on the dayS after the third, Sixth, and laSt ECT. Pre-ECT and poSt-ECT concentrationS of NSE and S-100 were compared by non-parametric teStS. RESULTS On average, 9.5 (SD 2.9) (range 3–12) ECTS were applied; 13 of 14 patientS received at leaSt Six ECTS. The average duration of convulSion (computed for all ECTS) waS 29.0 (SD 10.5) SecondS. At no point during the ECT SerieS waS there a Significant increaSe in the average NSE or S-100 concentrationS compared with the baSeline inveStigation before the Start of the ECT SerieS. The maximal meaSured poSt-ECT valueS of NSE and S-100 were 26.6 ng/ml and 0.46 ng/ml, reSpectively. The cumulative energy doSeS applied, Seizure durationS, and ECT induced changeS in cognitive performance ScoreS were never Significantly correlated with the NSE or S-100 Serum concentrationS. CONCLUSION ThiS pattern of findingS SuggeStS that a modern ECT, fulfilling current quality StandardS, induceS no brain tiSSue damage detectable by changeS in NSE or Protein S-100.
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Serum levelS of neuron Specific enolaSe and S 100 Protein after Single tonic clonic SeizureS
Journal of Neurology, 1999Co-Authors: T Buttner, H Przuntek, Birgit Lack, Matthias Jager, Wolfgang Wunsche, W Kuhn, Thomas Muller, Thomas PostertAbstract:Serum neuron-Specific enolaSe (S-NSE) and S-100 Protein (S-100) are SenSitive markerS of variouS brain diSeaSeS. We inveStigated both of theSe markerS in nine patientS within 5 min, 6 h, 12 h, and 48 h after a Single tonic-clonic Seizure. The mean peak S-NSE level waS Significantly higher after 5 min (11.97 ± 8.56 μg/l) and 48 h (10.31 ± 8.92 μg/l, P < 0.05) than the levelS of Seizure-free, age-matched controlS. Five patientS had increaSed S-NSE levelS regarding the upper limit of normal aS mean + 3 SD. S-100 waS not detected either in controlS or epileptic patientS. TheSe data indicate that S-NSE in contraSt to S-100 may be an in vivo marker after generalized SeizureS in Some patientS.
