Publications by authors named "Rodolfo Bracci"

7 Publications

  • Page 1 of 1

The timing of neonatal brain damage.

Biol Neonate 2006 1;90(3):145-55. Epub 2006 Mar 1.

Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Siena, Italy.

Although neonatal morbidity and mortality are less than in the past, the risk of pre-natal and neonatal brain damage has not been eliminated. In order to optimize pre-natal, perinatal and neonatal care, it is necessary to detect factors responsible for brain damage and obtain information about their timing. Knowledge of the timing of asphyxia, infections and circulatory abnormalities would enable obstetricians and neonatologists to improve prevention in pre-term and full-term neonates. Cardiotocography has been criticized as being too indirect a sign of fetal condition and as having various technical pitfalls, though its reliability seems to be improved by association with pulse oximetry, fetal blood pH and electrocardiography. Neuroimaging is particularly useful to determine the timing of hypoxic-ischemic brain damage. Cranial ultrasound has been used to determine the type and evolution of brain damage. Magnetic resonance has also been used to detect antenatal, perinatal and neonatal abnormalities and timing on the basis of standardized assessment of brain maturation. Advances in the interpretation of neonatal electroencephalograms have also made this technique useful for determining the timing of brain lesions. Nucleated red blood cell count in cord blood has been recognized as an important indication of the timing of pre-natal hypoxia, and even abnormal lymphocyte and thrombocyte counts may be used to establish pre-natal asphyxia. Cord blood pH and base excess are well-known markers of fetal hypoxia, but are best combined with heart rate and blood pressure. Other markers of fetal and neonatal hypoxia useful for determining the timing of brain damage are assays of lactate and markers of oxidative stress in cord blood and neonatal blood. Cytokines in blood and amniotic fluid may indicate chorioamnionitis or post-natal infections. The determination of activin and protein S100 has also been proposed. Obstetricians and neonatologists can therefore now rely on various methods for monitoring the risk of brain damage in the antenatal and post-natal periods.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1159/000092517DOI Listing
October 2006

Proteomic approach to the identification of voltage-dependent anion channel protein isoforms in guinea pig brain synaptosomes.

Proteomics 2004 May;4(5):1335-40

Department of Molecular Biology, University of Siena, Italy.

Voltage-dependent anion channel (VDAC) proteins are small, abundant, pore-forming proteins belonging to the eukaryotic mitochondrial porins. At least three different VDAC genes have been identified in vertebrates. VDAC proteins are known to play an essential role in cellular metabolism and in the early stages of apoptosis. A proteomic approach, consisting of two-dimensional gel electrophoresis followed by two-dimensional immunoblotting with anti-VDAC and anti-phosphotyrosine antibodies and by matrix-assisted laser desorption/ionization-time of flight mass spectrometry, was exploited to define the expression pattern of VDAC isoforms in guinea pig brain synaptosomes, both in normoxic and hypoxic conditions. In this way a total of five different VDAC isoforms were identified, as both VDAC1 and VDAC2 were detected in more than one electrophoretic spot. Moreover, VDAC isoforms selectively undergo hypoxia-induced tyrosine phosphorylation, suggesting that tyrosine phosphorylation may contribute to the modulation of VDAC protein function/conformation or interaction with other proteins in hypoxic conditions.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/pmic.200300734DOI Listing
May 2004

Non protein bound iron as early predictive marker of neonatal brain damage.

Brain 2003 May;126(Pt 5):1224-30

Department of Paediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.

Of the approximately 130 million births worldwide each year, four million infants will suffer from birth asphyxia and, of these, one million will die and a similar number will develop serious sequelae. Before being able to develop effective interventions, a better understanding of the pathophysiological mechanisms leading to brain injury and an early identification of babies at high risk for brain injury are required. This study tests the predictivity of traditional and new markers of foetal oxidative stress in relation to neurodevelopmental outcome in 384 newborn infants. The results indicate plasma non protein bound iron as the best early predictive marker of neurodevelopmental outcome, with 100% sensitivity and 100% specificity for good neurodevelopmental outcome at 0-1.16 micro mol/l, and for poor neurodevelopmental outcome at values >15.2 micro mol/l. The number of children with values between 1.16 and 15.2 were 195. Common use of this predictive marker in neonatology units will improve the ability of clinicians to identify those newborn babies who will develop neurodisability.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/brain/awg116DOI Listing
May 2003

Iron release in erythrocytes and plasma non protein-bound iron in hypoxic and non hypoxic newborns.

Free Radic Res 2003 Jan;37(1):51-8

Department of Pathophysiology and Experimental Medicine, University of Siena, Siena, Italy.

Iron is released in a desferrioxamine (DFO)-chelatable form (DCI) when erythrocytes are challenged by an oxidative stress. In beta-thalassemic erythrocytes, both DCI content and release (after aerobic incubation for 24h) are increased and correlated with the fetal hemoglobin (HbF) levels. Since erythrocytes from newborns have an extremely high content of HbF and are exposed to conditions of oxidative stress, the release of iron in these erythrocytes was investigated. The erythrocyte DCI content was increased in preterm but not in term newborns as compared to adults, while the release was increased in both preterm and term erythrocytes. The level of plasma non protein-bound iron (NPBI), which was not detectable in adults, was much higher in preterm than in term newborns. When term plus preterm newborns were divided in two groups, normoxic and hypoxic, according to cord blood pH, it was found that both iron release and NBPI were markedly higher in the hypoxic newborns compared to normoxic ones. Similar results were also obtained when the preterm and term infants were considered separately on the basis of cord blood pH. Therefore, iron release and NPBI are higher when conditions of hypoxia occur. In fact, when the values for iron release and NPBI were separately plotted against cord blood pH values, significant negative correlations were seen in both cases. NPBI was correlated with iron release seen in all the newborns and a significant part of the released iron could be recovered into the incubation medium at the end of the incubation.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/1071576021000032122DOI Listing
January 2003

Chorioamnionitis: a risk factor for fetal and neonatal morbidity.

Biol Neonate 2003 ;83(2):85-96

Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, Italy.

Despite widespread use of drugs to arrest preterm labor, there has been no decrease in the numbers of low-birth-weight or preterm infants in the last 20 years. Evidence from many sources links preterm birth to symptomatic and subclinical infections. Recently, an increasing body of evidence has suggested that not only is subclinical infection responsible for preterm birth but also for many serious neonatal sequelae, including periventricular leukomalacia, cerebral palsy, respiratory distress and even bronchopulmonary dysplasia and necrotizing enterocolitis. Proxies of intrauterine infection include clinical chorioamnionitis, histological chorioamnionitis and intraamniotic increase in cytokines, which have been found to be associated with acute neonatal morbidity and mortality and, at least to some degree, with neurological impairment, chronic lung disease and thymus involution in the preterm infant. The infectious/inflammatory mechanisms involved are not fully understood, and the types of microbes and genetic features of host adaptive and innate immune responses need to be better characterized.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1159/000067956DOI Listing
September 2003

Oxidative stress in preterm neonates at birth and on the seventh day of life.

Pediatr Res 2002 Jul;52(1):46-9

Department of Pediatrics, Obstetrics and Reproductive Medicine, University of Siena, 53100 Siena, Italy.

Previous studies have demonstrated increased oxidative damage to proteins and increased lipid peroxidation products in the plasma of hypoxic newborns at birth. We tested the hypothesis that hypoxic preterm newborns are at increased risk for oxidative stress in the first week of life. Heparinized blood samples of 34 hypoxic and 15 control preterm newborns were obtained at birth from the umbilical vein immediately after delivery and from a peripheral vein on postnatal d 7. Plasma levels of hypoxanthine, total hydroperoxide (TH), and advanced oxidation protein products (AOPP) were measured in cord blood and blood drawn on d 7. Hypoxanthine, TH, and AOPP levels were significantly higher in cord and d 7 blood samples of hypoxic newborn than control infants. Statistically significant correlations were observed between AOPP and hypoxanthine and between AOPP and TH plasma levels on d 7. AOPP and TH plasma levels significantly increased from cord to d 7 blood in neonates without hypoxia. These findings show that the oxidative stress observed in cord blood of hypoxic preterm newborns is still higher than control infants on d 7. The significant increase in TH and AOPP levels in nonhypoxic preterm newborns at the end of the first postnatal week indicates that damage caused by free radicals also occurs in nonhypoxic babies with normal clinical course. In summary, TH and AOPP production is prolonged for several days after birth in hypoxic preterm babies. The risk of free radical damage is lower but still exists in preterm neonates with normal clinical course.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1203/00006450-200207000-00010DOI Listing
July 2002