27 research outputs found

    Intra-uterine fetal demise caused by amniotic band syndrome after standard amniocentesis

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    The amniotic band syndrome represents a prime example of exogenous disruption of an otherwise normal feta I development. It may be a sequel of invasive diagnostic procedures such as amniocentesis or fetal blood sampling. A 38-year-old gravida II, para II delivered a morphologically normal male stillborn at term. The pregnancy history had been unremarkable but for an early 2nd-trimester amniocentesis. Cause of the intra-uterine fetal demise was noted to be an amniotic band constricting the umbilical cord, An amniotic band is a rare but potentially fatal condition which may be induced by, e.g., invasive prenatal procedures. Such bands are not usually diagnosed prenatally; however, selected patients with augmented risk may profit from intensive ultrasound evaluation including Doppler studies. Copyright (C) 2000 S. Karger AG, Basel

    Myomectomy as a pregnancy-preserving option in the carefully selected patient

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    Objectives: To present the indications for myomectomy during pregnancy and to discuss complications possibly related and unrelated to the procedure. Method and Results: A 33-year-old patient at 18 weeks of gestation underwent removal of a 1,570-gram symptomatic fundic myoma. Histologically the patient had a leiomyomatous neoplasm of uncertain malignant potential. The pregnancy was continued under sequential observation with magnetic resonance imaging and ultrasound. At 36 weeks of gestation a healthy girl with an upper extremity limb defect was born via cesarean section. Follow-up of the mother and the child was uneventful. Conclusions: Certain known risk factors in pregnant women with myomas can predispose to complications during pregnancy. Women with such risk factors or women who have failed medical therapy should be offered the option of undergoing myomectomy as a pregnancy-preserving procedure. Copyright (C) 2002 S. Karger AG, Basel

    Twin Town in South Brazil: A Nazi's Experiment or a Genetic Founder Effect?

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    Cândido Godói (CG) is a small municipality in South Brazil with approximately 6,000 inhabitants. It is known as the “Twins' Town” due to its high rate of twin births. Recently it was claimed that such high frequency of twinning would be connected to experiments performed by the German Nazi doctor Joseph Mengele. It is known, however, that this town was founded by a small number of families and therefore a genetic founder effect may represent an alternatively explanation for the high twinning prevalence in CG. In this study, we tested specific predictions of the “Nazi's experiment” and of the “founder effect” hypotheses. We surveyed a total of 6,262 baptism records from 1959–2008 in CG catholic churches, and identified 91 twin pairs and one triplet. Contrary to the “Nazi's experiment hypothesis”, there is no spurt in twinning between the years (1964–1968) when Mengele allegedly was in CG (P = 0.482). Moreover, there is no temporal trend for a declining rate of twinning since the 1960s (P = 0.351), and no difference in twinning among CG districts considering two different periods: 1927–1958 and 1959–2008 (P = 0.638). On the other hand, the “founder effect hypothesis” is supported by an isonymy analysis that shows that women who gave birth to twins have a higher inbreeding coefficient when compared to women who never had twins (0.0148, 0.0081, respectively, P = 0.019). In summary, our results show no evidence for the “Nazi's experiment hypothesis” and strongly suggest that the “founder effect hypothesis” is a much more likely alternative for explaining the high prevalence of twinning in CG. If this hypothesis is correct, then this community represents a valuable population where genetic factors linked to twinning may be identified

    „GEBDOK“— Datenmanagement von Schwangerschaft, Geburt und Wochenbett

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    Metastatic Colon Cancer in pregnancy: a treatment concept

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    Poor sleep quality is associated with impaired glucose tolerance in women after gestational diabetes.

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    We analyzed the association of sleep quality and glucose metabolism in women after gestational diabetes (pGDM) and in women after normoglycemic pregnancy (controls). Data during pregnancy and a visit within the first 15 months after delivery were collected from 61 pGDM and 30 controls in a prospective cohort study. This included a medical history, physical examination, questionnaires (Pittsburgh Sleep Quality Index (PSQI), and Perceived Stress Scale (PSS)), and 5-point oral glucose tolerance test with insulin measurements to determine indices of insulin sensitivity and insulin secretion. We used Spearman correlation coefficients and multivariate regression models for analysis.9.3 ± 3.2 months after delivery, pGDM had significantly higher fasting and 2 h glucose levels and lower insulin sensitivity than controls. There was no significant difference in age, BMI and sleep quality as assessed with the PSQI between the two groups. The PSQI score correlated with the ogtt-2 h plasma glucose in pGDM (δ = 0.41; p = 0.0012), but not in controls. This association was confirmed with a multivariate linear regression model with adjustment for age, BMI and months post-delivery. Perceived stress was an independent risk factor (OR 1.12; 95% CI 1.02-1.23) for impaired sleep. Our findings suggest that post-delivery sleep quality significantly influences glucose tolerance in women after GDM and that impaired sleep is associated with increased stress perception. Measures to improve of sleep quality and reduce perceived stress should therefore be tested as additional strategies to prevent progression to type 2 diabetes after GDM

    Activation of the NF-kappa B pathway alters the phenotype of MSCs in the tracheal aspirates of preterm infants with severe BPD.

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    Mesenchymal stromal cells (MSCs) are released into the airways of preterm infants following lung injury. These cells display a proinflammatory phenotype and are associated with development of severe bronchopulmonary dysplasia (BPD). We aimed to characterize the functional properties of MSCs obtained from tracheal aspirates of 50 preterm infants who required invasive ventilation. Samples were separated by disease severity. The increased proliferative capacity of MSCs was associated with longer duration of mechanical ventilation and higher severity of BPD. Augmented growth depended on nuclear accumulation of NF kappa Bp65 and was accompanied by reduced expression of cytosolic alpha-smooth muscle actin (alpha-SMA). The central role of NF-kappa B signaling was confirmed by inhibition of I kappa B alpha phosphorylation. The combined score of proliferative capacity, accumulation of NF kappa Bp65, and expression of alpha-SMA was used to predict the development of severe BPD with an area under the curve (AUC) of 0.847. We mimicked the clinical situation in vitro, and stimulated MSCs with IL-1 beta and TNF-alpha. Both cytokines induced similar and persistent changes as was observed in MSCs obtained from preterm infants with severe BPD. RNA interference was employed to investigate the mechanistic link between NF kappa Bp65 accumulation and alterations in phenotype. Our data indicate that determining the phenotype of resident pulmonary MSCs represents a promising biomarker-based approach. The persistent alterations in phenotype, observed in MSCs from preterm infants with severe BPD, were induced by the pulmonary inflammatory response. NF kappa Bp65 accumulation was identified as a central regulatory mechanism. Future preclinical and clinical studies, aimed to prevent BPD, should focus on phenotype changes in pulmonary MSCs

    The diabetes risk phenotype of young women with recent gestational diabetes.

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    Context: The pathogenesis of type 2 diabetes (T2D) is still incompletely understood. In-depth phenotyping of young individuals at risk for T2D can contribute to the understanding of this process. Objective: To metabolically characterize women with recent gestational diabetes (GDM), an at-risk cohort for T2D. Study participants: 147 consecutively recruited women 3-16 months after pregnancy, women who had GDM and women after a normoglycemic pregnancy (controls) in a 2:1 ratio Design: Mono-center cross-sectional analysis (PPS-Diab study) Methods: 5-point OGTT with calculation of insulin sensitivity (ISI) and disposition index (DI; validation by euglycemic clamp and IVGTT), anthropometrics, medical and family history, clinical chemistry and biomarkers, statistical modelling, MRI/MRS substudy (body fat distribution, liver and muscle fat; n=66) Results: Compared to control subjects, women post GDM had a reduced DI, higher levels of plasma fetuin-A and a lower ISI. A low ISI was also the major determinant of pathologic glucose tolerance after GDM. The factors most strongly predictive of low insulin sensitivity were high plasma leptin, BMI, triglycerides, and waist circumference. Ectopic lipids showed no BMI-independent associations with having had GDM or low insulin sensitivity in an MRI substudy. Conclusions: We found that beta cell function is already impaired in women with recent GDM, a young at-risk cohort for T2D. Additionally, our data suggest that fetuin-A and leptin signaling may be important early contributors to the pathogenesis of T2D, at this disease stage equally or more relevant than ectopic lipids and low-grade inflammation
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