The Experts below are selected from a list of 198 Experts worldwide ranked by ideXlab platform
Romolo Di Iorio - One of the best experts on this subject based on the ideXlab platform.
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Effects of prenatal betamethasone administration on leptin and adiponectin concentrations in maternal and Fetal Circulation.
American journal of obstetrics and gynecology, 2008Co-Authors: Emanuela Marinoni, Claudio Letizia, Francesca Ciardo, Giovanna Corona, Massimo Moscarini, Romolo Di IorioAbstract:The aim of this study was to determine the effects of in vivo administration of prenatal betamethasone on leptin and adiponectin concentration in maternal and Fetal Circulation. Blood samples were collected from 35 pregnant women receiving betamethasone for threatened preterm delivery before and at different time points after drug administration. Cord blood was collected at delivery in infants born from mothers treated with betamethasone and in 15 infants who delivered at the same gestational age not receiving betamethasone. Betamethasone caused an approximately 170% increase in maternal leptin at 24 hours after betamethasone, whereas it had no effects on adiponectin concentration. Betamethasone affects neonatal leptin and adiponectin levels in a time-dependent manner. The glucocorticoid-induced changes in the relationship between these adipokines in maternal and Fetal Circulation was long lasting. These results provide the first evidence for in vivo effects of glucocorticoids on maternal and Fetal adipokines relationship in human pregnancy.
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Effects of prenatal betamethasone administration on leptin and adiponectin concentrations in maternal and Fetal Circulation
American Journal of Obstetrics and Gynecology, 2008Co-Authors: Emanuela Marinoni, Claudio Letizia, Francesca Ciardo, Massimo Moscarini, Corona G, Romolo Di IorioAbstract:Objective The aim of this study was to determine the effects of in vivo administration of prenatal betamethasone on leptin and adiponectin concentration in maternal and Fetal Circulation. Study Design Blood samples were collected from 35 pregnant women receiving betamethasone for threatened preterm delivery before and at different time points after drug administration. Cord blood was collected at delivery in infants born from mothers treated with betamethasone and in 15 infants who delivered at the same gestational age not receiving betamethasone. Results Betamethasone caused an approximately 170% increase in maternal leptin at 24 hours after betamethasone, whereas it had no effects on adiponectin concentration. Betamethasone affects neonatal leptin and adiponectin levels in a time-dependent manner. The glucocorticoid-induced changes in the relationship between these adipokines in maternal and Fetal Circulation was long lasting. Conclusion These results provide the first evidence for in vivo effects of glucocorticoids on maternal and Fetal adipokines relationship in human pregnancy.
Anne Cathrine Staff - One of the best experts on this subject based on the ideXlab platform.
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Asymmetric dimethylarginine in the maternal and Fetal Circulation in preeclampsia.
Pediatric research, 2009Co-Authors: Kristin Braekke, Nina Kittelsen Harsem, Per Magne Ueland, Anne Cathrine StaffAbstract:Preeclampsia is a leading cause of intrauterine growth restriction and preterm birth. Endothelial dysfunction is the common final pathway leading to clinical signs of preeclampsia including hypertension and proteinuria. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NOS and induces endothelial dysfunction by reversibly inhibiting NO production from l-arginine. The purpose of this study was to investigate maternal and Fetal concentrations of ADMA, l-arginine, and symmetric dimethylarginine (SDMA). Women with preeclampsia (n = 47) and controls (n = 51) who gave birth by cesarean section were included in the study. We analyzed the maternal plasma and umbilical vein and artery plasma. We found that not only maternal concentrations of ADMA and SDMA but also l-arginine were significantly higher in women with preeclampsia than in controls. In Fetal samples, only SDMA concentrations were higher in the preeclampsia group than in controls. The median ADMA concentration was three times higher in the Fetal Circulation than in the maternal Circulation, but there was no difference between the preeclampsia group and the control group, and the veno-arterious gradient indicated that the placenta was the source of ADMA.
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Oxidative Stress and Antioxidant Status in Fetal Circulation in Preeclampsia
Pediatric research, 2006Co-Authors: Kristin Braekke, Nina Kittelsen Harsem, Anne Cathrine StaffAbstract:Preeclampsia is associated with oxidative stress in maternal Circulation. The purpose of this study was to explore oxidative stress and antioxidants in the Fetal Circulation in preeclampsia. Women with preeclampsia (n = 19) or uncomplicated pregnancies (n = 33) delivered by cesarean section were included. Blood was sampled separately from the umbilical vein and artery. 8-Iso-prostaglandin F(2alpha) (8-isoprostane), a stable product of lipid peroxidation, is a reliable marker of oxidative stress. Concentration of total 8-isoprostane in cord plasma was analyzed by gas chromatography-mass spectrometry. Antioxidant status was evaluated measuring ferric reducing ability of plasma and vitamin E. There was no difference between preeclampsia and control groups regarding median plasma concentration of 8-isoprostane in umbilical vein (955 versus 780 pg/mL, p = 0.41) or in umbilical artery (233 versus 276 pg/mL, p = 0.65). Concentration of 8-isoprostane was much higher in plasma from the umbilical vein than artery, suggesting placenta as the source of 8-isoprostane. Median ferric reducing ability of plasma concentration was higher in preeclampsia than in controls, both in the umbilical vein and artery. Median vitamin E concentration in the umbilical vein was higher in preeclampsia, but no difference was found in the umbilical artery. In conclusion, no evidence of increased oxidative stress, evaluated by 8-isoprostane concentration, was found in Fetal Circulation in preeclampsia.
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39 Is There Evidence of Oxidative Stress in Maternal and Fetal Circulation in Preeclampsia|[quest]|
Pediatric Research, 2004Co-Authors: Kristin Braekke, Nina Kittelsen Harsem, Anne Cathrine StaffAbstract:Background: Preeclampsia (PE) is a pregnancy-induced syndrome associated with increased maternal and Fetal morbidity and mortality. The major Fetal consequences of PE are intrauterine growth restriction and premature delivery. It is hypothesized that placental oxidative stress results in shedding of circulating factors into the maternal Circulation, leading to endothelial dysfunction and inflammation in the maternal Circulation. This mediates the maternal characteristics of PE; hypertension and proteinuria. There are conflicting reports as to what extent Fetal Circulation is involved. Oxidative stress is a condition where prooxidants dominate over antioxidants. Several studies have associated PE with augmented oxidative stress. 8-isoprostane is a stable marker of oxidative stress; it is formed by free radicals attack on arachidonic acid in cell membranes phospholipids. The aim of this study was to compare the level of oxidative stress in both maternal and Fetal Circulation in PE and uneventful pregnancies.
Emanuela Marinoni - One of the best experts on this subject based on the ideXlab platform.
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Effects of prenatal betamethasone administration on leptin and adiponectin concentrations in maternal and Fetal Circulation.
American journal of obstetrics and gynecology, 2008Co-Authors: Emanuela Marinoni, Claudio Letizia, Francesca Ciardo, Giovanna Corona, Massimo Moscarini, Romolo Di IorioAbstract:The aim of this study was to determine the effects of in vivo administration of prenatal betamethasone on leptin and adiponectin concentration in maternal and Fetal Circulation. Blood samples were collected from 35 pregnant women receiving betamethasone for threatened preterm delivery before and at different time points after drug administration. Cord blood was collected at delivery in infants born from mothers treated with betamethasone and in 15 infants who delivered at the same gestational age not receiving betamethasone. Betamethasone caused an approximately 170% increase in maternal leptin at 24 hours after betamethasone, whereas it had no effects on adiponectin concentration. Betamethasone affects neonatal leptin and adiponectin levels in a time-dependent manner. The glucocorticoid-induced changes in the relationship between these adipokines in maternal and Fetal Circulation was long lasting. These results provide the first evidence for in vivo effects of glucocorticoids on maternal and Fetal adipokines relationship in human pregnancy.
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Effects of prenatal betamethasone administration on leptin and adiponectin concentrations in maternal and Fetal Circulation
American Journal of Obstetrics and Gynecology, 2008Co-Authors: Emanuela Marinoni, Claudio Letizia, Francesca Ciardo, Massimo Moscarini, Corona G, Romolo Di IorioAbstract:Objective The aim of this study was to determine the effects of in vivo administration of prenatal betamethasone on leptin and adiponectin concentration in maternal and Fetal Circulation. Study Design Blood samples were collected from 35 pregnant women receiving betamethasone for threatened preterm delivery before and at different time points after drug administration. Cord blood was collected at delivery in infants born from mothers treated with betamethasone and in 15 infants who delivered at the same gestational age not receiving betamethasone. Results Betamethasone caused an approximately 170% increase in maternal leptin at 24 hours after betamethasone, whereas it had no effects on adiponectin concentration. Betamethasone affects neonatal leptin and adiponectin levels in a time-dependent manner. The glucocorticoid-induced changes in the relationship between these adipokines in maternal and Fetal Circulation was long lasting. Conclusion These results provide the first evidence for in vivo effects of glucocorticoids on maternal and Fetal adipokines relationship in human pregnancy.
Eduard Gratacós - One of the best experts on this subject based on the ideXlab platform.
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placental exosomes profile in maternal and Fetal Circulation in intrauterine growth restriction liquid biopsies to monitoring Fetal growth
Placenta, 2018Co-Authors: Jezid Miranda, Eduard Gratacós, Cristina Paules, Soumyalekshmi Nair, Andrew Lai, Carlos Palma, Katherin Scholzromero, Gregory E Rice, F Crispi, Carlos SalomonAbstract:Abstract Introduction Placenta-derived exosomes may represent an additional pathway by which the placenta communicates with the maternal system to induce maternal vascular adaptations to pregnancy and it may be affected during Fetal growth restriction (FGR). The objective of this study was to quantify the concentration of total and placenta-derived exosomes in maternal and Fetal Circulation in small fetuses classified as FGR or small for gestational age (SGA). Methods Prospective cohort study in singleton term gestations including 10 normally grown fetuses and 20 small fetuses, sub-classified into SGA and FGR accordingly to birth weight (BW) percentile and fetoplacental Doppler. Exosomes were isolated from maternal and Fetal plasma and characterized by morphology, enrichment of exosomal proteins, and size distribution by electron microscopy, western blot, and nanoparticle tracking analysis, respectively. Total and specific placenta-derived exosomes were determined using quantum dots coupled with CD63+ve and placental-type alkaline phosphatase (PLAP)+ve antibodies, respectively. Results Maternal concentrations of CD63+ve and PLAP+ve exosomes were similar between the groups (all p > 0.05). However, there was a significant positive correlation between the ratio of placental-derived to total exosomes (PLAP+ve ratio) and BW percentile, [rho = 0.77 (95% CI: 0.57 to 0.89); p = 0.0001]. The contribution of placental exosomes to the total exosome concentration in maternal and Fetal Circulation showed a significant decrease among cases, with lower PLAP+ve ratios in FGR compared to controls and SGA cases. Discussion Quantification of placental exosomes in maternal plasma reflects Fetal growth and it may be a useful indicator of placental function.
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Understanding the Aortic Isthmus Doppler Profile and Its Changes with Gestational Age Using a Lumped Model of the Fetal Circulation.
Fetal diagnosis and therapy, 2016Co-Authors: Patricia Garcia-canadilla, Paula A. Rudenick, Fatima Crispi, Monica Cruz-lemini, Eduard Gratacós, Brenda Valenzuela-alcaraz, Bart BijnensAbstract:Objective: The aortic isthmus (AoI) blood flow has a characteristic shape with a small end-systolic notch observed during the third trimester of pregnancy. However, what causes the appearance of this notch is not fully understood. We used a lumped model of the Fetal Circulation to study the possible factors causing the end-systolic notch and the changes of AoI flow through gestation. Methods: A validation of the model was performed by fitting patient-specific data from two normal fetuses. Then, different parametric analyses were performed to evaluate the major determinants of the appearance of the end-systolic notch. The changes in the AoI flow profile through gestation were assessed. Results: Our model allows to simulate the AoI waveform. The delay in the onset of ejection together with the longer ejection duration of the right ventricle are the most relevant factors in the origin of the notch. It appears around 25 weeks of gestation and becomes more pronounced with advancing gestation. Discussion: We demonstrated that the end-systolic notch on the AoI flow occurs mainly as a result of a delayed and longer ejection of the right ventricle. Our findings improve the understanding of hemodynamic changes in the Fetal Circulation and the interpretation of clinical imaging.
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patient specific estimates of vascular and placental properties in growth restricted fetuses based on a model of the Fetal Circulation
Placenta, 2015Co-Authors: Paula A. Rudenick, F Crispi, Patricia Garciacanadilla, Monica Cruzlemini, Stefania Triunfo, Alfons Nadal, Brenda Valenzuelaalcaraz, Eduard GratacósAbstract:Abstract Introduction Intrauterine growth restriction (IUGR) due to placental insufficiency is associated with blood-flow redistribution in order to maintain perfusion to the brain. However, some hemodynamic parameters that might be more directly related to staging of the disease cannot be measured non-invasively in clinical practice. For this, we developed a patient-specific model of the Fetal Circulation to estimate vascular properties of each individual. Methods A lumped model of the Fetal Circulation was developed and personalized using measured echographic data from 37 normal and IUGR fetuses to automatically estimate model-based parameters. A multivariate regression analysis was performed to evaluate the association between the Doppler pulsatility indices (PI) and the model-based parameters. The correlation between model-based parameters and the placental lesions was analyzed in a set of 13 IUGR placentas. A logistic regression analysis was done to assess the added value of the model-based parameters relative to Doppler indices, for the detection of fetuses with adverse perinatal outcome. Results The estimated model-based placental and brain resistances were respectively increased and reduced in IUGR fetuses while placental compliance was increased in IUGR fetus. Umbilical and middle cerebral arteries PIs were most associated with both placental resistance and compliance, while uterine artery PI was more associated with the placental compliance. The logistic regression analysis showed that the model added significant information to the traditional analysis of Doppler waveforms for predicting adverse outcome in IUGR. Discussion The proposed patient-specific computational model seems to be a good approach to assess hemodynamic parameters than cannot be measured clinically.
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A computational model of the Fetal Circulation to quantify blood redistribution in intrauterine growth restriction.
PLoS computational biology, 2014Co-Authors: Patricia Garcia-canadilla, Paula A. Rudenick, Fatima Crispi, Monica Cruz-lemini, Georgina Palau, Eduard Gratacós, Oscar Camara, Bart H. BijensAbstract:Intrauterine growth restriction (IUGR) due to placental insufficiency is associated with blood flow redistribution in order to maintain delivery of oxygenated blood to the brain. Given that, in the fetus the aortic isthmus (AoI) is a key arterial connection between the cerebral and placental Circulations, quantifying AoI blood flow has been proposed to assess this brain sparing effect in clinical practice. While numerous clinical studies have studied this parameter, fundamental understanding of its determinant factors and its quantitative relation with other aspects of haemodynamic remodeling has been limited. Computational models of the cardiovascular Circulation have been proposed for exactly this purpose since they allow both for studying the contributions from isolated parameters as well as estimating properties that cannot be directly assessed from clinical measurements. Therefore, a computational model of the Fetal Circulation was developed, including the key elements related to Fetal blood redistribution and using measured cardiac outflow profiles to allow personalization. The model was first calibrated using patient-specific Doppler data from a healthy fetus. Next, in order to understand the contributions of the main parameters determining blood redistribution, AoI and middle cerebral artery (MCA) flow changes were studied by variation of cerebral and peripheral-placental resistances. Finally, to study how this affects an individual fetus, the model was fitted to three IUGR cases with different degrees of severity. In conclusion, the proposed computational model provides a good approximation to assess blood flow changes in the Fetal Circulation. The results support that while MCA flow is mainly determined by a fall in brain resistance, the AoI is influenced by a balance between increased peripheral-placental and decreased cerebral resistances. Personalizing the model allows for quantifying the balance between cerebral and peripheral-placental remodeling, thus providing potentially novel information to aid clinical follow up.
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FIMH - Understanding prenatal brain sparing by flow redistribution based on a lumped model of the Fetal Circulation
Functional Imaging and Modeling of the Heart, 2013Co-Authors: Patricia Garcia-canadilla, Paula A. Rudenick, Fatima Crispi, Monica Cruz-lemini, Georgina Palau, Eduard Gratacós, Bart BijnensAbstract:Intrauterine Growth Restriction due to placental insufficiency leads to cardiac dysfunction in utero which can persist postnatally. Brain sparing by flow redistribution is an adaptive mechanism used by the restricted fetus to ensure delivery of oxygenated blood to the brain. The quantification of reversed flow in the aortic isthmus is used in clinical practice to detect signs of brain sparing. Two parameters are used to quantify reversed flow: pulsatility index and isthmic flow index. We developed a simplified 0-D lumped model of the Fetal Circulation to simulate brain-sparing for better understanding this compensatory mechanism and its influence on the mentioned parameters. We were able to reproduce the clinical phenomenon and to quantify the effect of brain sparing on pulsatility and isthmic flow indexes. Therefore, our model seems to be a good approximation of the Fetal Circulation and offers potential to study hemodynamic changes in intrauterine growth restricted fetuses.
Kristin Braekke - One of the best experts on this subject based on the ideXlab platform.
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Asymmetric dimethylarginine in the maternal and Fetal Circulation in preeclampsia.
Pediatric research, 2009Co-Authors: Kristin Braekke, Nina Kittelsen Harsem, Per Magne Ueland, Anne Cathrine StaffAbstract:Preeclampsia is a leading cause of intrauterine growth restriction and preterm birth. Endothelial dysfunction is the common final pathway leading to clinical signs of preeclampsia including hypertension and proteinuria. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NOS and induces endothelial dysfunction by reversibly inhibiting NO production from l-arginine. The purpose of this study was to investigate maternal and Fetal concentrations of ADMA, l-arginine, and symmetric dimethylarginine (SDMA). Women with preeclampsia (n = 47) and controls (n = 51) who gave birth by cesarean section were included in the study. We analyzed the maternal plasma and umbilical vein and artery plasma. We found that not only maternal concentrations of ADMA and SDMA but also l-arginine were significantly higher in women with preeclampsia than in controls. In Fetal samples, only SDMA concentrations were higher in the preeclampsia group than in controls. The median ADMA concentration was three times higher in the Fetal Circulation than in the maternal Circulation, but there was no difference between the preeclampsia group and the control group, and the veno-arterious gradient indicated that the placenta was the source of ADMA.
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Oxidative Stress and Antioxidant Status in Fetal Circulation in Preeclampsia
Pediatric research, 2006Co-Authors: Kristin Braekke, Nina Kittelsen Harsem, Anne Cathrine StaffAbstract:Preeclampsia is associated with oxidative stress in maternal Circulation. The purpose of this study was to explore oxidative stress and antioxidants in the Fetal Circulation in preeclampsia. Women with preeclampsia (n = 19) or uncomplicated pregnancies (n = 33) delivered by cesarean section were included. Blood was sampled separately from the umbilical vein and artery. 8-Iso-prostaglandin F(2alpha) (8-isoprostane), a stable product of lipid peroxidation, is a reliable marker of oxidative stress. Concentration of total 8-isoprostane in cord plasma was analyzed by gas chromatography-mass spectrometry. Antioxidant status was evaluated measuring ferric reducing ability of plasma and vitamin E. There was no difference between preeclampsia and control groups regarding median plasma concentration of 8-isoprostane in umbilical vein (955 versus 780 pg/mL, p = 0.41) or in umbilical artery (233 versus 276 pg/mL, p = 0.65). Concentration of 8-isoprostane was much higher in plasma from the umbilical vein than artery, suggesting placenta as the source of 8-isoprostane. Median ferric reducing ability of plasma concentration was higher in preeclampsia than in controls, both in the umbilical vein and artery. Median vitamin E concentration in the umbilical vein was higher in preeclampsia, but no difference was found in the umbilical artery. In conclusion, no evidence of increased oxidative stress, evaluated by 8-isoprostane concentration, was found in Fetal Circulation in preeclampsia.
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39 Is There Evidence of Oxidative Stress in Maternal and Fetal Circulation in Preeclampsia|[quest]|
Pediatric Research, 2004Co-Authors: Kristin Braekke, Nina Kittelsen Harsem, Anne Cathrine StaffAbstract:Background: Preeclampsia (PE) is a pregnancy-induced syndrome associated with increased maternal and Fetal morbidity and mortality. The major Fetal consequences of PE are intrauterine growth restriction and premature delivery. It is hypothesized that placental oxidative stress results in shedding of circulating factors into the maternal Circulation, leading to endothelial dysfunction and inflammation in the maternal Circulation. This mediates the maternal characteristics of PE; hypertension and proteinuria. There are conflicting reports as to what extent Fetal Circulation is involved. Oxidative stress is a condition where prooxidants dominate over antioxidants. Several studies have associated PE with augmented oxidative stress. 8-isoprostane is a stable marker of oxidative stress; it is formed by free radicals attack on arachidonic acid in cell membranes phospholipids. The aim of this study was to compare the level of oxidative stress in both maternal and Fetal Circulation in PE and uneventful pregnancies.