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At least 145 records · Page 8Linked to original sources
PubMed1995

Amniotic fluid and plasma levels of parathyroid hormone-related protein and hormonal modulation of its secretion by amniotic fluid cells.

Parathyroid hormone-related (PTHrP), the major mediator of humoral hypercalcemia of malignancy, may also regulate placental calcium flux, uterine contraction and fetal tissue development. In the present study, we demonstrated that the mean immunoreactive PTHrP concentrations in amniotic fluid at mid-gestation (21.2 +/- 3.7 pmol/l) and at term (19.0 +/- 2.7 pmol/l) were 13-16-fold higher than levels measured in either fetal (1.6 +/- 0.1 pmol/l) or maternal plasma (1.4 +/- 0.3 pmol/l) at term and equal to levels found in plasma of patients with humoral hypercalcemia of malignancy. In vitro studies pointed to three possible sources of PTHrP in amniotic fluid: cultured amniotic fluid cells, cells derived from the amniotic membrane overlying the placenta and placental villous core mesenchymal cells. Treatment of cultured amniotic fluid cells with human prolactin, human placental lactogen (hPL) or human growth hormone (100 micrograms/l) increased PTHrP secretion after 24 h by 43%, 109% and 90%, respectively. Insulin-like growth factors I and II (100 micrograms/l), insulin (100 micrograms/l) and epidermal growth factor (EGF) (10 micrograms/l) increased PTHrP secretion by 53%, 46%, 68% and 118%, respectively. The stimulation of PTHrP secretion by EGF or by hPL was both time- and dose-dependent. In contrast, calcitriol and dexamethasone (10 nmol/l) decreased PTHrP secretion by 32% and 75%, respectively. Estradiol, progesterone, dihydrotestosterone and human chorionic gonadotropin had no effect on PTHrP secretion. These findings support the notion that PTHrP may play a physiological role in the uteroplacental unit and demonstrate that human amniotic fluid cells could be a useful model for studying the regulation of PTHrP production and secretion by hormones and growth factors.

Amniotic Fluid↗
PubMed2003

Interferon-alpha-like biological activity in human seminal plasma, follicular fluid, embryo culture medium, amniotic fluid and fetal blood.

Interferons (IFNs) are a group of cytokines exhibiting antiviral, antiproliferative and immunoregulatory properties. The principal stimulus for the synthesis of IFNs is the presence of viral double-stranded RNA, although rare examples of constitutive synthesis have also been described. The aim of the present study was to determine IFN-alpha-like biological activity in the seminal plasma, follicular and amniotic fluid, embryo culture medium, and fetal blood obtained from patients without apparent viral or bacterial infections. Interferon-alpha-like biological activity was determined by a standard cytopathic effect inhibition bioassay. The study included two groups of patients. The first group consisted of 30 married couples participating in the programme for assisted reproduction and the second group consisted of 23 patients scheduled for prenatal diagnosis (15 for amniocentesis and eight for cordocentesis). The seminal plasma of infertile men (asthenozoospermia, oligoasthenozoospermia) contained a high titre of IFN-alpha-like antiviral activity. Asthenozoospermia was diagnosed in men with a normal sperm concentration but less than 50% progressively motile sperm and oligoasthenozoospermia was diagnosed in men with a sperm count less than 1 x 10(6) mL(-1). Despite slightly higher antiviral titres in the seminal plasma obtained from asthenozoospermic patients, no clear association between IFN-alpha-like biological activity and sperm concentration was found. Interferon-alpha-like biological activity was found in all samples of follicular and amniotic fluid and in fetal blood of patients with intrauterine growth retardation and trisomy 18. Antiviral titres from seminal plasma and follicular fluids were significantly higher compared with amniotic fluids and fetal blood. Embryo culture medium did not contain IFN-alpha-like biological activity. Our results demonstrate that IFN-alpha-like activity in biological fluids is relevant for reproduction, even in the absence of infection.

Amniotic Fluid↗
PubMed1987

Stable isotope dilution analysis of pipecolic acid in cerebrospinal fluid, plasma, urine and amniotic fluid using electron capture negative ion mass fragmentography.

A sensitive and accurate stable isotope dilution assay was developed for the measurement of pipecolic acid in body fluids using electron capture negative ion mass fragmentography. The method utilizes [2H11]pipecolic acid as the internal standard. Sample preparation consisted of derivatization in aqueous solution (pH 11.5) of the amine moiety with methyl chloroformate to the N-methylcarbamate, followed by acidic ethyl acetate extraction (pH 2) and further derivatization of the carboxyl moiety to the pentafluorobenzyl ester. Normal values have been determined in cerebrospinal fluid (mean means = 0.041 mumol/l, range 0.010-0.120 mumol/l), in plasma of at term infants (age less than 1 wk, means = 5.73 mumol/l, range 3.75-10.8 mumol/l; age greater than 1 wk, means = 1.46 mumol/l, range 0.70-2.46 mumol/l), in urine of at term infants (age less than 6 mth, means = 32.5 mumol/g. creat., range 9.81-84.5 mumol/g. creat; age greater than 6 mth, means = 6.35 mumol/g. creat., range 0.15-13.6 mumol/g. creat.) and in amniotic fluid (means = 4.65 mumol/l, range 2.24-8.40 mumol/l). The utility of the method was demonstrated for the pipecolic acid quantification in these biofluids of patients with peroxisomal disorders. As affected fetuses with infantile Refsum's disease and Zellweger syndrome showed no significant elevation of pipecolic acid in their surrounding amniotic fluids, the measurement of pipecolic acid in amniotic fluid seemed not to be useful for prenatal diagnosis in these disorders.

Adult↗
PubMed1977

Bacterial growth inhibition by amniotic fluid. VII. The effect of zinc supplementation on bacterial inhibitory activity of amniotic fluids from gestation of 20 weeks.

Twenty human amniotic fluids obtained from gestations of 20 weeks' duration supported bacterial growth. Nine of the 20 fluids could be made inhibitory by adjusting the phosphate to zinc ratios of the fluids to less than 200 mug per milliliter. These fluids contained the phosphate-sensitive bacterial inhibitor previously, but the fluids contained sufficient phosphate to inactivate the antibacterial system. The remaining 11 amniotic fluids did not contain the peptide component of the phosphate-sensitive bacterial inhibitor and could not be made inhibitory by adjusting the phosphate to zinc ratio to less than 200 mug per milliliter. The data obtained suggested synthesis of the peptide component may occur at a gestational age of approximately 20 weeks. The peptide may indirectly be detected in fluids by determining whether antibacterial activity is obtained when the phosphate to zinc ratio of the fluids is adjusted to less than 200 mug per milliliter.

Amniotic Fluid↗
PubMed1977

Changes in the concentration of cortisol in amniotic fluid after intra-amniotic prostaglandin for midtrimester abortion.

The effects of intra-amniotic prostaglandin E2 (PGE2) and PGF2alpha on the concentration of cortisol in amniotic fluid and in maternal peripheral plasma of patients undergoing abortion between 16 and 23 weeks gestation have been examined. There was a significant (P less than 0-01) increase in the concentration of cortisol in amniotic fluid for hours after PGE2, but not after PGF2alpha. The concentration of cortisol in the maternal peripheral plasma increased in both groups with the progression of abortion, but the levels were not significantly correlated with those in amniotic fluid. These results suggest that by mid-pregnancy fetal cortisol production can be stimulated by PGE2 but the mechanism of this action remains to be elucidated.

Abortifacient Agents↗
PubMed1982

Measurement of thyroid-stimulating hormone in human amniotic fluid.

TSH was measured in human amniotic fluid after 3- to 8-fold concentration of the fluids. Amniotic fluid TSH was identical to standard pituitary TSH by immunological and gel chromatographic criteria. In 201 samples of normal second trimester amniotic fluid (16-19 weeks of pregnancy), amniotic fluid TSH concentrations had a mean value of 0.4 microunits/ml (range, less than 0.15 to 1.7 microunits/ml). In 21 samples of third trimester amniotic fluid (obtained to check fetal lung maturity), amniotic fluid TSH concentrations had a mean value of 0.25 microunits/ml (range, less than 0.15 to 0.55 microunits/ml). The capability of measuring TSH in amniotic fluid and the relative constancy of these values between the second and third trimesters of pregnancy suggest that the determination of TSH levels in amniotic fluid may be useful in the diagnosis of fetal hypothyroidism in utero.

Amniotic Fluid↗
PubMed1983

[Amniotic fluid cytology and foetal lung maturity--a comparison with the dynamic surface tension measurement of the amniotic fluid for predicting foetal lung maturity].

79 samples of amniotic fluid in 69 pregnancies between 29-40 weeks of gestation were examined for foetal lung maturity (dynamic surface tension) and general maturity (Nile Blue cytological test). Both parameters were compared with the pulmonary maturity of the newborn post partum in 24 cases born within 72 hours after the last amniotic fluid examination. In 49 cases the Nile Blue cytological test showed mature values, in 24 cases immature - and in 6 cases borderline values. The dynamic surface tension measurement showed 55 mature, 19 immature and 5 borderline results. These findings show an earlier maturation of the foetal lung compared with the foetal sebaceous glands. Between 36 and 40 weeks of gestation we found a significant (p less than 0.01) correlation between the two methods. Between 32 and 35 weeks of gestation, the significance was less (p less than 0.05) and between 29 and 31 weeks of gestation no correlation could be found. The Nile Blue cytological test for lipid cells is easy to perform, requires less than 1 ml amniotic fluid and is not influenced by blood and meconium and shows no false positive results. Immature findings with the Nile Blue cytological test should be confirmed by other lung maturity tests, like LS-ratio or amniotic dynamic tension measurement. Therefore we can recommend this simple method for the screening of foetal lung maturity as well.

Amniotic Fluid↗
PubMed2005

Amniotic fluid embolism.

INCIDENCE: Amniotic fluid embolism is a catastrophic syndrome that occurs during pregnancy or in the immediate postpartum period. Multiple case reports have described the clinical findings and have reported variable success with supportive care. There has been discrepancy with respect to the incidence and mortality of amniotic fluid embolism. One likely explanation for this inconsistency is the lack of sensitive and specific diagnostic studies to definitively identify cases of amniotic fluid embolism, leading to both over- and underreporting. Despite the variation in reported incidence and mortality, amniotic fluid embolism remains a life-threatening condition with significant morbidity and mortality for the pregnant woman. It is the fifth most common cause of maternal mortality in the world. DIAGNOSIS: The diagnosis of amniotic fluid embolism continues to be a clinical diagnosis and a diagnosis of exclusion based on the rapid development of a complex constellation of findings with sudden cardiovascular collapse, acute left ventricular failure with pulmonary edema, disseminated intravascular coagulation, and neurologic impairment. Given the significant morbidity and mortality associated with this condition, a high index of suspicion is warranted. Suspected risk factors have included tumultuous labor, trauma, multiparity, increased gestational age, and increased maternal age. However, many patients who develop amniotic fluid embolism have no obvious risk factors. MANAGEMENT: Patients with amniotic fluid embolus are best managed using a multidisciplinary approach. There are no pharmacologic or other therapies that prevent or treat the amniotic fluid embolism syndrome, and supportive care typically involves aggressive treatment of multiple types of shock simultaneously. In this article we discuss the clinical presentation of amniotic fluid embolism syndrome as well as current opinions regarding pathophysiology, diagnosis, and management.

Critical Care↗
PubMed2005

Activation of ectopic Oct-4 and Rex-1 promoters in human amniotic fluid cells.

Recently, amniotic fluid was suggested as a new source for stem-cell research and tissue engineering approaches. In order to enable isolation of stem cells and establishment of lines of such cells with an undifferentiated phenotype we have introduced green fluorescent protein regulated by the promoters of the stem cell-specific genes, Oct-4 or Rex-1, into human amniotic fluid cells. For the introduction of DNA into human amniotic fluid cells, we have optimized a specific transfection protocol. We found that human amniotic fluid contains cell populations which are able to activate these promoters. These undifferentiated cells expressing green fluorescent protein can be analysed on a flow cytometer. In addition, we have introduced a plasmid harboring a neomycin-resistance gene under the control of the Oct-4 promoter. G418 selection allowed the isolation of undifferentiated stem cells expressing Oct-4 protein out of human amniotic fluid samples. Our findings confirm the existence of stem cells within amniotic fluid. In addition, the ability to transfect human amniotic fluid cells and to isolate stem-cell marker-positive cells will provide the means to study and manipulate these cells for the purpose of basic and applied research.

Amniotic Fluid↗
PubMed1988

Hormone release by primary amniotic fluid cell cultures.

Amniotic fluid cells have been widely used in prenatal diagnosis; however, there is great heterogeneity of the cells and their origin. In this study we analyze the karyotype and release of human chorionic gonadotropin (hCG), human chorionic somatomammotropin (hCS), free estriol (E 3), prolactin (PRL) and progesterone (P) of amniotic fluid cells from primary cultures of six normal and two anencephalic fetuses. In all the amniotic fluid samples there was release of hCG; in one amniotic fluid, in which several tetraploid colonies were found. PRL and P were also released. The heterogeneity of amniotic fluid cell morphology and their hormone release in culture was confirmed. The presence of hormones like hCG supports the trophoblastic origin of some amniotic fluid cells from normal and anencephalic fetuses. Other hormones, such as PRL and P could be used in the differential diagnosis between the karyotype of fetal membranes and the true fetal karyotype. Amniotic fluid cell cultures used in prenatal diagnosis yielded second trimester placental cells without any elaborate methods that could be used as cell models for hormone studies.

Amniotic Fluid↗
PubMed1986

Fetal recirculation of amniotic fluid arginine vasopressin.

Amniotic fluid volume reflects a balance between fetal lung fluid and fetal urine production and fluid reabsorption via fetal swallowing. Arginine vasopressin (AVP) infusion decreases both fetal lung fluid and urine production and increases amniotic fluid osmolality and AVP concentration. In the present study we assessed the effect of amniotic fluid AVP injection on plasma AVP (n = 6) and renal function (n = 4) in chronically catheterized fetal lambs (X gestation = 130 days). Thirty minutes after addition of 25 micrograms of synthetic AVP into the amniotic cavity, mean +/- SE fetal plasma AVP increased from a base line of 2.7 +/- 0.2 to 14.6 +/- 3.4 pg/ml (P less than 0.01). One hundred and twenty minutes after injection, plasma AVP had increased to 26.9 +/- 5.7 pg/ml. Fetal urine volume did not change (0.78 +/- 0.01 ml/min) but significant increases in urine osmolality (169 +/- 19 to 315 +/- 25 mosm) and urine sodium (64 +/- 11 to 125 +/- 11 mueq/ml) were observed 120 min after AVP administration. In conclusion, amniotic fluid AVP levels can affect fetal plasma AVP concentration, and AVP absorbed from the amniotic fluid by the fetus remains biologically active.

Amniotic Fluid↗
PubMed1978

Arachidonic acid in amniotic fluid after extra-amniotic instillation of rivanol for midtrimester abortion.

Free arachidonic acid was measured by gas liquid chromatography in amniotic fluid in 13 women during induction of midtrimester abortion. The abortions were induced by extraamniotic instillation of 0.1% Rivanol. Serial sampling of amniotic fluid were performed through a transabdominal catheter up to 22 hrs. Free, total arachidonic acid showed a significant increase from 26 +/- 8 ng/ml to 293 +/- 102 ng/ml at 22 hrs. The percentage of free arachidonic acid in total free fatty acids increased significantly from 2.2 +/- 0.5 to 6.1 +/- 1.6+ during the same time. The results suggest a selective release of arachidonic acid during Rivanol-induced abortion.

Abortion, Induced↗
PubMed1991

Amniotic fluid embolism.

Amniotic fluid embolism is an almost universally fatal complication of pregnancy. We have presented a case and reviewed the literature concerning this rare but catastrophic problem.

Adult↗
PubMed1985

Structure of the carbohydrate units of human amniotic fluid fibronectin.

Human amniotic fluid fibronectin was found to contain three types of carbohydrates: complex-type N-glycosidic glycans, lactosaminoglycans, and O-glycosidic glycans. The structures of the complex-type glycans were established by carbohydrate and methylation analysis, Smith degradation, sequential exoglycosidase treatments, lectin chromatography, and DEAE-Sephadex chromatography. Lactosaminoglycans were analyzed by fast atom bombardment mass spectrometry, and the O-glycosidically-linked oligosaccharides by gas-liquid chromatography-mass spectrometry and high-pressure liquid chromatography. The results show that amniotic fluid fibronectin contains 2 mol of biantennary and 2-3 mol of triantennary, complex-type N-glycosidic glycans. Unlike the N-glycosidic glycans of human adult plasma fibronectin, which contain only traces of fucose and are completely sialylated, the glycans from amniotic fluid fibronectin are fucosylated and only partially sialylated. The complex-type N-glycosidic glycans present in amniotic fluid fibronectin also include a fractional amount (0.1 mol) of glycans with a polylactosaminyl structure. In addition, 4 mol of O-glycosidic oligosaccharides, which have not previously been described in fibronectins, were found in amniotic fluid fibronectin. The major oligosaccharides in this fraction have the structures Gal beta 1----3GalNAcol, NeuNAc alpha 2----3Gal beta 1----3GalNAcol and NeuNAc alpha 2----3Gal beta 1----3(NeuNAc alpha 2----6)GalNAcol. O-glycosidically linked oligosaccharides were also detected in human adult plasma fibronectin but in smaller amounts than in amniotic fluid fibronectin. These results show that amniotic fluid fibronectin differs from plasma fibronectin with regard to the number of glycans attached to the polypeptide and that the glycans present in these two fibronectins differ in structure.

Amniotic Fluid↗