PubMed Health⌕ Search

Biomedical subjects

E Beinder

Publications and source records attributed to E Beinder.

At least 19 recordsLinked to original sources
PubMed2003

Hypoxia activates the human placental vascular endothelial growth factor system in vitro and in vivo: up-regulation of vascular endothelial growth factor in clinically relevant hypoxic ischemia in birth asphyxia.

OBJECTIVE: We investigated the influence of acute hypoxia on the placental vascular endothelial growth factor system in vitro and in vivo in acute birth asphyxia compared with pregnancies that were complicated by preeclampsia and with healthy control subjects. STUDY DESIGN: Messenger RNA levels for vascular endothelial growth factor, flt-1, and KDR were measured by TaqMan real-time polymerase chain reaction in human placental choriocarcinoma cells (BeWo) that were exposed to hypoxia (1% oxygen, 5% carbon dioxide, 94% nitrogen) and in placental tissue of neonates with birth asphyxia (n = 20), newborn infants of mothers with preeclampsia (n = 20), and gestational age-matched control subjects. Immunhistologically, placental vascular endothelial growth factor protein expression was compared among the groups. RESULTS: In BeWo cells, vascular endothelial growth factor, flt-1 and KDR messenger RNA increased in a time-dependent manner in response to hypoxia. In vivo, vascular endothelial growth factor/beta-actin and KDR/beta-actin messenger RNA were significantly higher in placental tissue of newborn infants with severe hypoxic-ischemic encephalopathy than with newborn infants with mild or no hypoxic-ischemic encephalopathy and control subjects. In chronic placental hypoxia (preeclampsia), vascular endothelial growth factor and both receptors were found to be up-regulated. Increased placental vascular endothelial growth factor expression was confirmed by immunohistologic examination. CONCLUSION: The vascular endothelial growth factor system is up-regulated in response to placental hypoxia and is assumed to be a potential early indicator of severe birth asphyxia.

Actins↗
PubMed2002

Surgery of a splenic artery aneurysm during pregnancy.

We report a case of ligation of the splenic artery with splenectomy during pregnancy due to a splenic artery aneurysm. The risk of aneurysmal rupture is increased in multipara and during pregnancy. As a result of high maternal and fetal morbidity and mortality elective surgery should be performed.

Adult↗
PubMed2002

Effect of endothelin-1 on intracellular glutathione and lipid peroxide availability and on the secretion of vasoactive substances by human umbilical vein endothelial cells.

BACKGROUND: The major pathophysiologic changes observed in preeclampsia suggest that endothelial cell dysfunction plays an important role in this disorder. The pathway mediating endothelial cell layer dysfunction is unknown. The concentration of endothelin-1 (ET-1), a potent mammalian vasoconstrictor peptide produced by the vascular endothelium, has been observed to be significantly increased in preeclampsia. In this study, we determined the in vitro effect of endothelin-1 on glutathione and lipid peroxide levels and on the secretion of vasoactive substances by human umbilical vein endothelial cells (HUVECs). METHODS: Human umbilical vein endothelial cells were incubated for 24 h in the presence of different concentrations of ET-1 (0-1000 pmol L(-1)), which were shown in an earlier experiment to have no effects on vitality and proliferation rate of HUVECs. The levels of glutathione (GSH) and lipid peroxides (LPO) were measured in endothelial cell lysates. For the measurement of vasoactive substances, levels of nitric oxide (NO), prostacyclin (PGI2) and thromboxane A2 (TXA2) were measured in endothelial cell supernatants. RESULTS: At lower concentrations (5-50 pmol L(-1)), ET-1 increases the intracellular content of LPO, stimulates the secretion of TXA2, but inhibits the secretion of PGI2 in endothelial cells compared with control cells. At higher concentrations (100-1000 pmol L(-1)), ET-1 increases the intracellular content of GSH, but results in a decrease of LPO, and increase of PGI2, back to control levels. ET-1 has no effect on NO secretion. CONCLUSION: These findings demonstrate that at concentrations corresponding to values in plasma from preeclamptic women, ET-1 induces oxidative stress and results in altered secretion of vasoactive substances in human endothelial cells. We conclude that ET-1 may participate in the pathway leading to endothelial cell dysfunction seen in preeclampsia.

Cells, Cultured↗
PubMed2002

Adrenomedullin gene expression in human placental tIssue and leukocytes: a potential marker of severe tIssue hypoxia in neonates with birth asphyxia.

OBJECTIVE: The aim of the present study was to investigate the role of adrenomedullin (ADM) as a hypoxia-inducible marker of clinically relevant tIssue hypoxia in acute birth asphyxia of term newborn infants. METHODS: For this purpose, ADM mRNA was determined in human placental tIssue of 20 term pregnancies complicated by birth asphyxia (pH and base deficit values, clinical score). In addition, ADM mRNA was measured in leukocytes of the asphyxiated newborn infants during the first 12 h of life (n=12). Controls were available from ten healthy term pregnancies. In vitro, hypoxia-inducible expression of ADM mRNA was evaluated in human choriocarcinoma cells (BeWo) and human leukocytes exposed to hypoxia (1% O(2)) for 1-24 h. mRNA levels were measured by TaqMan real-time PCR. RESULTS: In vitro, ADM mRNA related to porphobilinogen deaminase (PBGD) mRNA levels significantly increased in response to hypoxia within a period of 4 h in leukocytes and 12 h in BeWo cells. In human placental tIssue, significantly higher levels of ADM/PBGD mRNA were present in asphyxiated newborn infants with severe hypoxic-ischemic encephalopathy (HIE) (n=5) compared with patients with mild or no HIE (n=15). Increased levels of ADM/PBGD mRNA levels were found during the first hours of life in leukocytes of neonates with severe HIE compared with controls. CONCLUSIONS: Our results indicate an upregulation of ADM gene expression in human placenta and leukocytes in clinically relevant hypoxic-ischemic birth complications and suggest ADM gene expression as a promising marker for severe complications due to perinatal asphyxia such as HIE.

Adrenomedullin↗
PubMed2001

Production of vasoactive substances by human umbilical vein endothelial cells after incubation with serum from preeclamptic patients.

OBJECTIVE: To determine the in vitro effect of serum from preeclamptic patients on the proliferation, viability and secretion of vasoactive substances by human umbilical vein endothelial cells (HUVEC). STUDY DESIGN: HUVEC were incubated for 24h with sera from 16 preeclamptic, 19 healthy pregnant and 8 healthy nonpregnant women. Proliferation rates were determined by cell counting and vitality by trypan blue staining. The vasoactive substances, 6-keto-prostaglandin F(1alpha), nitrite and nitrate, and endothelin-1 (ET-1) were measured in endothelial cell supernatants. RESULTS: The preeclamptic serum had no effect on cell proliferation or vitality compared with control sera. It induced more HUVEC production of ET-1, but not of prostacyclin (PGI2) or nitric oxide compared with control serum. CONCLUSION: Preeclamptic serum appears to contain a factor(s) that specifically stimulates ET-1 secretion from HUVEC without altering cell growth or vitality.

6-Ketoprostaglandin F1 alpha↗
PubMed2001

Deletion 15q24-26 in prenatally detected diaphragmatic hernia: increasing evidence of a candidate region for diaphragmatic development.

Survival of children with congenital diaphragmatic hernia (CDH) is mainly dependent on the extent of lung hypoplasia and the presence of additional congenital anomalies or chromosomal aberrations. A chromosomal deletion 15q25-q26.2 in a fetus with prenatally diagnosed CDH and growth retardation is reported. Despite optimal pre- and neonatal management the baby died shortly after birth. There is increasing evidence that the long arm of chromosome 15, and especially the region 15q24 to 15q26, plays a crucial role in the development of the diaphragm. The finding of a deletion within 15q24-26 in a fetus with CDH has to be considered a predictor of poor prognosis. It is of utmost interest for proper parental counselling to search in fetuses with CDH for subtle chromosomal lesions paying special attention to chromosome 15q.

Abnormalities, Multiple↗
PubMed2001

Skin flux during reactive hyperemia and local hyperthermia in patients with preeclampsia.

OBJECTIVE: To test the contribution of the endothelium to the maximum vasodilatation in patients with preeclampsia and healthy pregnant controls. METHODS: Laser-Doppler flowmetry, which is a noninvasive method for the continuous measurement of skin blood flow, was used to test the response of skin microcirculation to the above-mentioned stimuli in 14 patients with preeclampsia and 20 normotensive pregnant controls. RESULTS: In normotensive pregnant controls, the reactive hyperemic response after a 3-minute ischemia in the forearm reaches values of 77 +/- 16% of the maximum vasodilatation, which was induced by local hyperthermia of 42C. In patients with preeclampsia, this response was significantly (P <.05) reduced (43 +/- 9%). CONCLUSION: Vascular reactivity is altered in skin vessels of patients with preeclampsia in vivo. This alteration seems to be attributable mainly to the endothelium.

Adult↗
PubMed2001

Surgical treatment of HELLP syndrome-associated liver rupture -- an update.

In some 2% of the cases of the HELLP syndrome, severe spontaneous bleeding into the liver accompanied by haemorrhagic liver cell necrosis and rupture of the organ occurs and represents one of the main cause of death. On the basis of our own experience with four cases, a review of the literature is presented with particular focus on a therapeutic concept based on appropriate surgery. Within a MEDLINE search covering the period 1990-1999, the case reports of this kind of liver complication in the literature were analysed in terms of clinical course and outcome.In addition to our own four patients, a total of 49 cases with rupture of the liver were found in the literature. Despite surgical interventions, HELLP syndrome-associated liver rupture carried a mortality of 39%. Most patients died of haemorrhagic shock and organ failure. In order to improve survival, patients with ruptured liver or hepatic failure should be transferred to a centre with the necessary experience in liver surgery including liver transplantation. An interdisciplinary approach is required, including the use of temporary packing of the liver to control the bleeding, and during the further course of the condition, possibly even liver transplantation, as in one of our own cases.

Adult↗
PubMed2001

Fetal sinus bradycardia and the long QT syndrome.

OBJECTIVE: Recent evidence in literature shows that the long QT syndrome accounts for a fraction of the sudden infant death syndrome. Newborn infants with prolongation of the Q-T interval often show sinus bradycardia, which led us to test whether children who were diagnosed with long QT syndrome also show sinus bradycardia in the cardiotocogram before birth. STUDY DESIGN: We identified 18 children who were born from singleton pregnancies at or near term in whom long QT syndrome (corrected QT interval, >0.440 second) was diagnosed after birth or in childhood. Cardiograms during pregnancy and delivery were available from 17 of the 18 children. RESULTS: The cardiotocogram showed persistent fetal sinus bradycardia (baseline heart rate permanently below 120 beats/min) in 12 of 17 fetuses (71%) with long QT syndrome. Two fetuses had additional intermittent tachyarrhythmias. CONCLUSION: Sinus bradycardia in the cardiotocogram during delivery or in pregnancy may indicate long QT syndrome in the fetus. Postnatal electrocardiography should be performed in these children to rule out or confirm a prolongation of the Q-T interval.

Arrhythmia, Sinus↗
PubMed2001

Influence of reduced intracellular glutathione availability on the secretion of vasoactive substances by human umbilical vein endothelial cells.

OBJECTIVE: Oxidative stress might be the reason for endothelial dysfunction in preeclampsia. The glutathione-peroxidase system is one of the primary antioxidants in the endothelium. We tested the effect of oxidative stress by reduction of glutathione availability on the secretion of vasoactive substances in endothelial cells. METHODS: Endothelial cells in culture were incubated with different concentrations of buthionine-[S,R]-sulfoximine (BSO) or 1-chloro-2,4-dinitrobenzene (CDNB), both leading to a reduced intracellular availability of glutathione. The secretion of the vasoactive substances nitric oxide (NO), endothelin-I (ET-1), and prostacyclin (PGI2) was measured with respect to vitality and proliferation rate of the endothelial cells in culture. MAIN OUTCOME MEASURE: Effect of oxidative stress on the secretion of vasoactive substances from endothelial cells. RESULTS: The oxidants CDNB and BSO have (in concentrations before evidence of cytotoxicity) a stimulating effect on the production of PGI2, they inhibit NO availability, and they do not significantly interfere with ET-1 production. Conclusion Oxidative stress in vitro induces an imbalance in the secretion of NO, ET-1, and PGI2 in endothelial cells.

Biological Availability↗
PubMed2000

Prenatal diagnosis of heterokaryotypic mosaic twins discordant for fetal sex.

The presence of a monozygotic twin gestation with discordant sex of the twins is a very rare constellation, which is referred to as heterokaryotypic monozygotic pregnancy. This constellation can develop either due to a chromosomal aberration after twinning or is - as in the following case - due to a mitotic error before twinning and an unequal distribution of mosaicism in both embryos. So far the diagnosis of heterokaryotypic monozygotic pregnancy has always been made postnatally, with only one exception (Gonsoulin et al., 1990). In this case we suspected the presence of monozygotic twins ultrasonically because of the chorionic and amniotic membrane characteristics. Surprisingly the sex of the fetuses was discrepant. As one of them had hydrops and a structural heart defect, we carried out an amniocentesis, which revealed mosaicism [45,X/46,X,i(Y)(p10)] of both fetuses. The female fetus with a predominant 45,X set of chromosomes and the typical intrauterine signs of the Ullrich-Turner syndrome (massive hygroma colli, hydrops fetalis and multiple cardiac defects) died during the 25th week of gestation due to cardiac decompensation. The other fetus appeared to be male with a predominance of a 46,X,i(Y)(p10) set of chromosomes and was born a few days after the intrauterine death of the hydropic fetus. In conclusion, our observation shows that ultrasonic evidence of discordant fetal sex in twins does not necessarily exclude monozygosity.

Amniocentesis↗
PubMed2000

Prenatal diagnosis of QT prolongation by magnetocardiography.

Magnetocardiography constitutes a new tool for monitoring fetal cardiac activity. The fetal magnetocardiogram (FMCG) recorded noninvasively over the maternal abdomen is detectable with high temporal resolution and permits analysis of all parts of the PQRST waveform. In this way measurements of cardiac time intervals, including the QT interval, become possible. The following article constitutes the first report of antenatal detection of QT prolongation in two fetuses by FMCG.

Adult↗
PubMed1999

Rapid development of hydrops fetalis in the donor twin following death of the recipient twin in twin-twin transfusion syndrome.

Intrauterine death of one fetus in monochorionic twinning is associated with high rates of perinatal morbidity and mortality in the surviving fetus. Subsequent development of hydrops fetalis in the donor twin after fetal demise of the recipient twin has been described in only two case reports and pathophysiology remains unclear. We report on a monochorionic-diamniotic twin pregnancy complicated by severe twin-twin transfusion syndrome. Ultrasound examination at 20 weeks of gestation showed discrepant twins with oligohydramnios in the smaller twins' sac and polyhydramnios in that of the larger twin. Repeated amniocenteses permitted prolongation of the pregnancy. However, the recipient twin developed deteriorating hydrops fetalis and died at 28 weeks of gestation. After this event, subsequent development of hydrops fetalis in the surviving donor twin could be observed, as well as an increase of amniotic fluid. An elective cesarean section was performed at 29 weeks of gestation. Initial hypoxemia could be effectively treated by high frequency oscillatory ventilation, surfactant therapy and inotropic support. The infant was discharged in good condition at the age of 2 months. Although rare, antenatal demise of the recipient twin in a monochorionic pregnancy can be associated with the subsequent development of hydrops fetalis in the surviving donor twin. We speculate that this phenomenon is due to ischemia-reperfusion injury of the previously poorly perfused twin.

Adult↗
PubMed1999

Nitric oxide synthase activity and Doppler parameters in the fetoplacental and uteroplacental circulation in preeclampsia.

OBJECTIVE: We investigated the hypothesis that changes in blood flow in the uteroplacental and fetoplacental circulation in preeclampsia are associated with an abnormality of placental or uterine placental bed nitric oxide (NO) synthesis. METHODS: We measured pulsatility indices on Doppler waveform analysis from uterine and umbilical arteries in 20 patients with preeclampsia and 14 healthy pregnant controls before elective cesarean section. During cesarean section, biopsies from the uterine placental bed and the placenta were taken and the nitric oxide synthase (NOS) activity was measured by the [3H] L-arginine-[3H] L-citrulline conversion assay in these samples. RESULTS: The NOS activity was significantly lower in the uterine placental bed in comparison to the placental tissue (p < 0.01). Placental NOS activity was similar between patients with preeclampsia and healthy controls and in the groups with either a pathological or a normal Doppler flow in the umbilical artery. In the uterine placental bed however, NOS activity from patients with preeclampsia was significantly lower (p < 0.01), whereas the blood flow resistance in the uterine arteries was elevated (p < 0.01) in comparison to healthy controls. CONCLUSIONS: Our data show that pathological Doppler waveforms in the uterine arteries of patients with preeclampsia are paralleled by diminished NOS activity in the uterine placental bed. Therefore, the compromised NO production in the uterine placental bed may play an important role in the impaired uteroplacental blood flow and potentially in some pathological features of preeclampsia such as intervillous thrombosis formation and fetal growth retardation.

Adult↗