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PubMed1993

Trophic influences of human and rat amniotic fluid on neural tube-derived rat fetal cells.

Normal human (week 17-20) and rat (E16-17) amniotic fluids were used as culture media for primary cultures of rat fetal (E 16) cortical, mesencephalic and striatal cell dissociates, or astroglial subcultures from the same brain regions. Phase-bright and dark cells were identified under phase contrast microscopy and their cell processes were measured utilizing semi-automated procedures. Subcultured astroglia were immuno-reacted against glial fibrillary acidic protein and fibronectin. Rat and human amniotic fluid allowed survival and growth of neuronal and non-neuronal cells. Human amniotic fluid samples were trophic in variable degrees. Cerebral cortex subcultured astroglia usually expressed a radial-like morphotype. Although charcoal-adsorbed human amniotic fluid was trophic for primary cultures, its ability to sustain neuritic growth depended on its degree of trophism before treatment. Growth of cell processes in neuronal- and glial-like cells in primary cultures was inhibited to different degrees by the addition of antisera towards nerve or epidermal growth factors. It is concluded that amniotic fluid constitutes a trophic medium for astroglia and neurons. Both, nerve and epidermal growth factors appear to be necessary for growth of cell processes in neuronal and glial primary cultures in amniotic fluid. Trophic effect of amniotic fluid on subcultured astroglia did not seem to be diminished by nerve growth factor antiserum. The role of amniotic fluid during the early phases of brain organogenesis is discussed.

Amniotic Fluid↗
PubMed1988

Antenatal diagnosis of neural tube defects using a coated bead immunoassay for acetylcholinesterase in amniotic fluid.

The development and validation of a coated bead immunoassay for amniotic fluid acetylcholinesterase is outlined. The assay has good precision (between assay CV of 6.8% within the normal range), and is linear up to 250 arbitrary units/L. The clinical validity of this assay has been assessed using a panel of amniotic fluid samples from normal and abnormal pregnancies. At an assay cut off level of 200 arbitrary units/L, all cases of neural tube defect-affected pregnancies were identified and the number of false positives was very small. False positives resulted from severe blood staining of the amniotic fluid. Since the monoclonal antibody used recognises red cell membrane acetylcholinesterase and the stored amniotic fluids had been frozen and thawed a number of times, the extent of this problem needs to be further assessed using freshly collected samples. The performance of this assay was found to be superior to the differential inhibitor colorimetric method and close to that of the electrophoretic procedure. The quantitative nature of the assay and the independence from operator technique makes it a useful adjunct to the measurement of amniotic fluid AFP in the prenatal diagnosis of neural tube defects.

Acetylcholinesterase↗
PubMed2005

A novel model of polyhydramnios: amniotic fluid volume is increased in aquaporin 1 knockout mice.

OBJECTIVE: To test the hypothesis that amniotic fluid volume is increased in aquaporin 1 knockout mice. STUDY DESIGN: Transgenic mice deficient in aquaporin 1 protein were generated by targeted gene disruption, as described previously. After a cesarean section was performed, intact, individual gestational sacs were removed from the uterus and weighed. Amniotic fluid volume, osmolality, and fetal and placental weights were determined. Data were analyzed by a 1-way analysis of variance for ranks; Dunn's post hoc test was used to analyze significant trends. RESULTS: Analysis of 16 litters showed 35 wild-type, 52 heterozygote, and 33 aquaporin 1 knockout mice. The knockout mice had a greater volume of amniotic fluid and lower amniotic fluid osmolality than their wild-type and heterozygote counterparts. There were no significant differences in fetal or placental weights among the groups. CONCLUSIONS: Aquaporin 1 null fetuses produce a greater volume of more dilute amniotic fluid. Our findings show that aquaporin 1 water channels in fetal membranes may contribute to amniotic fluid volume regulation. We speculate that idiopathic polyhydramnios may be associated with a deficiency of aquaporin 1 channels in human fetal membranes. Transgenic aquaporin 1 knockout mice provide a unique animal of polyhydramnios.

Amniotic Fluid↗
PubMed1995

Reproducibility of the amniotic fluid index: its effect on clinical practice.

Two methods of measuring the amniotic fluid index (AFI) were subjected to tests of intra- and interobserver reproducibility. In the first method, amniotic fluid in each quadrant was measured by using the deepest pool perpendicular to the floor; in the second method, amniotic fluid in each quadrant was measured by using the deepest pool perpendicular to the uterine contour. Intraobserver and interobserver variability were assessed by using one-way analysis of variance and limits of agreement, respectively. Intraobserver standard deviations were all < 9 mm. When the AFI was measured using the first method, there was an inverse relationship between the interobserver difference and mean values of AFI. Plots of the differences between observers against their means showed that the lower the AFI, the greater the interobserver variability. No such correlation was noted when the AFI was measured by the second method. The limits of agreement (within which 95% of interobserver differences lie) were comparable for the two methods [(-42 mm to 29.4 mm) and (-46.4 mm to 41.6 mm), respectively]. The results suggest that the amniotic fluid index measured by the second method is more reproducible, especially in the presence of reduced amniotic fluid.

Amniotic Fluid↗
PubMed2003

First-trimester echogenic amniotic fluid in the acrania-anencephaly sequence.

OBJECTIVE: To describe the association between echogenic amniotic fluid and first-trimester fetal acrania. METHODS: Nine fetuses with acrania were examined between 11 weeks' and 13 weeks 6 days' menstrual age for the presence of echogenic free-floating particles in the amniotic fluid. Cases were classified into 3 types according to the echogenicity of the amniotic fluid: similar to (type 0), slightly greater than (type 1), and clearly more echogenic than (type 2) that of the extracelomic fluid. RESULTS: In 1 pregnancy, no free-floating particles were identified (type 0). In 6 cases, small free-floating particles scattered within the amniotic cavity were identified, making the amniotic fluid slightly more echogenic than the extracelomic fluid (type 1). In the remaining 2 cases, the amniotic fluid was homogeneously and clearly more echogenic than the extracelomic fluid (type 2). CONCLUSIONS: A high percentage (89%) of fetuses with acrania had echogenic amniotic fluid, suggesting that this finding could potentially be used as a marker of fetal acrania in the first trimester. This finding also supports the hypothesis of the transition from acrania to anencephaly, with the unprotected brain undergoing progressive destruction from the first trimester, leading to the classic finding of anencephaly in the second trimester.

Amniotic Fluid↗
PubMed1993

The diagnostic and prognostic value of amniotic fluid white blood cell count, glucose, interleukin-6, and gram stain in patients with preterm labor and intact membranes.

OBJECTIVE: Our goal was to compare the value of amniotic fluid tests in the detection of microbial invasion of the amniotic cavity and in the relationship with the amniocentesis-to-delivery interval and neonatal complications in patients with preterm labor and intact membranes. STUDY DESIGN: Amniotic fluid was retrieved by transabdominal amniocentesis from 120 patients with preterm labor and intact membranes. Fluid was cultured for aerobic and anaerobic bacteria and for mycoplasmas. Amniotic fluid analysis included a Gram stain, white blood cell count, glucose and interleukin-6 determinations. Logistic regression and Cox's proportional hazards model were used for analysis. RESULTS: (1) The prevalence of positive amniotic fluid cultures was 9.2% (11/120); (2) patients with microbial invasion had a shorter amniocentesis-to-delivery interval and a higher neonatal complications rate than patients with a negative culture; (3) the most sensitive test for the detection of microbial invasion of the amniotic cavity was amniotic fluid interleukin-6 determinations (cutoff 11.3 ng/ml) (sensitivity; for interleukin-6 100%, for glucose 81.8%, for white blood cell count 63.6%, and for Gram stain 63.6%; p < 0.05 for all comparisons); (4) the most specific test was the Gram stain of amniotic fluid (specificity: for Gram stain 99.1%, for white blood cell count 94.5%, for interleukin-6 82.6%, and for glucose 81.6%; p < 0.01 for all); (5) of all amniotic fluid tests, interleukin-6 determinations were the only ones that had significant relationship with the amniocentesis-to-delivery interval and neonatal complications. CONCLUSION: Interleukin-6 concentrations in amniotic fluid are better indicators of microbial invasion of the amniotic cavity, amniocentesis-to-delivery interval, and neonatal complications than the amniotic fluid Gram stain, glucose concentration, or white blood cell count.

Adult↗
PubMed1981

Technical and theoretical considerations in the HLA typing of amniotic fluid cells for prenatal diagnosis and paternity testing.

HLA typing of amniotic fluid cells has been used for the prenatal diagnosis of the HLA linked diseases congenital adrenal hyperplasia (21-OH-deficiency (21-OH-def) type) and complement C4 deficiency and it has also been used for the prenatal determination of paternity. There are, however, technical difficulties in this test associated with the weak expression of some B locus antigens on amniotic fluid cells, and theoretical difficulties related to associations between particular HLA antigens and the 21-OH-def allele. Since certain HLA-B locus antigens are found in significantly increased frequencies among patients with 21-OH-def, there is a relatively high incidence of HLA-B homozygosity among the patients and over 40 per cent of the parents of these patients share one or more HLA-B locus antigens. Results of some prenatal HLA typing tests may thus be difficult to interpret, and supplementary tests should be used whenever possible. HLA typing of amniotic cells is, however, the only available procedure for prenatal diagnosis of C4 deficiency and it is the best available procedure for prenatal determination of paternity. A modification of our original procedure allows HLA typing to be performed with increased numbers of HLA typing sera, and sera with optimum reactivity for amniotic fluid cells have now been selected for the definition of most of the more commonly expressed HLA antigens. Although amniotic fluid cells do not express DR Antigens, amniotic fluid cells can be typed for the HLA-linked marker glyoxalase I (GLO) and this may be the informative for prenatal diagnosis in some cases.

Adrenal Hyperplasia, Congenital↗
PubMed1983

Measurement of sex hormone binding globulin in human amniotic fluid: its relationship to protein and testosterone concentrations, and fetal sex.

Sex hormone binding globulin (SHBG) has been identified and quantified in human amniotic fluid. Identification was based on its electrophoretic mobility on polyacrylamide gels and its steroid binding characteristics, which were identical to those attributed to SHBG in pregnancy serum. Amniotic fluid SHBG binding capacity was measured by competitive saturation analysis using [3H]-5 alpha-dihydrotestosterone as the labelled ligand, after removal of endogenous steroids with dextran-coated charcoal. Similar amniotic fluid SHBG binding capacities were found in samples taken during early (13-20 weeks, 8.5 +/- 5.1 (SD) nmol/l, n = 10) and late (36-37 weeks, 8.7 +/- 3.0 nmol/l, n = 28) pregnancy. In comparison with pregnancy serum SHBG levels (390 +/- 140 nmol/l, n = 5), amniotic fluid SHBG was not enriched in relation to the relative concentrations of total proteins, albumin or transferrin. Amniotic fluid is therefore not a better source for the purification of SHBG than pregnancy serum. There were no differences in amniotic fluid SHBG levels with respect to fetal sex, but positive correlations were observed between SHBG binding capacities and testosterone concentrations in amniotic fluid from both male (r = 0.68, P less than 0.001) and female (r = 0.53, P less than 0.05) fetuses. It is suggested that SHBG may sequester free testosterone in amniotic fluid, and that measurements of SHBG in amniotic fluid may help to more accurately identify fetal sex in cases where borderline amniotic fluid testosterone concentrations are found.

Amniotic Fluid↗
PubMed1990

Amniotic fluid prolactin in the third trimester of pregnancies complicated by gestational or pregestational diabetes mellitus.

Amniotic fluid concentrations of immunoreactive prolactin were measured during the third trimester in 184 diabetic gravidas and correlated with concurrent levels of prolactin in maternal plasma. Prolactin measurements concorded with previously published estimates in normal gravid women and averaged 825 +/- 32 ng/mL (mean +/- SEM) in amniotic fluid and 168 +/- 6.5 ng/mL in simultaneously sampled plasma. Cross-sectional and longitudinal analyses indicated that the prolactin levels in amniotic fluid of pregnant diabetics declined significantly between weeks 32 and 40 of gestation, whereas plasma levels did not change consistently during the same interval. Mean values for amniotic fluid prolactin did not correlate with simultaneous prolactin concentrations in plasma, nor with maternal age, clinical estimates of polyhydramnios, amniotic fluid creatinine content, or lecithin/sphingomyelin (L/S) ratios or subsequent birth weight of the offspring. Clear-cut correlations with overall maternal glucose regulation could not be demonstrated. However, subtle effects may be operative since amniotic fluid prolactin displayed weak but significant correlations with concurrent levels of maternal plasma glucose, and mean values for hemoglobin A1c (HbA1c) but not with mean values for fasting plasma glucose (FPG). Amniotic fluid prolactin concentrations were significantly greater in patients with pregestational diabetes (White classes C, D, and F) than in women with gestational diabetes mellitus (GDM) (our classes A1, A2, and B1). The differences could not be accounted for by differences in metabolic regulation, maternal age, or weights of these two populations.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗
PubMed1989

Amniotic fluid arachidonate lipoxygenase metabolites in preterm labor.

This study was conducted to determine if preterm labor with intact membranes is associated with changes in the amniotic fluid concentrations of arachidonate lipoxygenase metabolites. Amniotic fluid was obtained by transabdominal amniocentesis from 68 women with preterm labor. The patients were classified into three groups according to their response to tocolysis and their amniotic fluid culture results: Group 1 - women with a negative amniotic fluid culture who responded to tocolysis (n = 32); Group 2 - women with a negative culture, but who failed to respond to tocolysis (n = 22); and Group 3 - women with intraamniotic infection (n = 14). The following arachidonate lipoxygenase products were measured by radioimmunoassay: leukotriene B4 (LTB4); leukotriene C4 (LTC4); 12-hydroxyeicosatetraenoic acid (12-HETE); and 15-hydroxyeicosatetraenoic acid (15-HETE). The median concentrations of LTB4 were significantly different among the three study groups (26 pg/ml, 67 pg/ml and 885 pg/ml, respectively, p greater than 0.05). Amniotic fluid concentrations of 12-HETE and LTC4 did not vary among the three study groups. On the other hand, a significant difference in the distribution of amniotic fluid concentrations of 15-HETE was noted only between women with intraamniotic infection (Group 3) and women responding to tocolysis (Group 1). These results indicate that the arachidonate lipoxygenase pathway is activated during the course of preterm labor. Selective changes in the concentrations of the assayed metabolites were noted. Amniotic fluid LTB4 concentrations may be a marker for the patient with preterm labor who is unresponsive to tocolysis.

Amniocentesis↗
PubMed1980

Reaction of 4-methylumbelliferylguanidinobenzoate with proteases in human amniotic fluid.

An arginine esterase activity similar to that observed in plasma has been demonstrated in second trimester and term human amniotic fluid. Like plasma, the protease(s) hydrolyzed esters of arginine, were reactive towards 4-methylumbelliferylguanidinobenzoate (MUGB), a sensitive active site titrant of trypsin-like enzymes, and had a pI of 5.1--5.4. The pH optimum for proteolytic activity was 8.0. This protease activity was inhibited by soybean trypsin inhibitor (STI), benzamidine and (p-nitrophenyl)-p'-guanidinobenzoate (NPGB), and was insensitive to 1-chloro-3-tosylamido-7-amino-2-heptanone (TLCK) and p-hydroxymercuribenzoic acid (HMB). Upon gel filtration, two MUGB-reactive fractions were observed, one with an apparent molecular weight of 200,000 and the other, 100,000. Both fractions had arginine esterase activity and appeared to be sensitive to inhibition by STI and benzamidine. The mean MUGB titre value (nmoles of 4-methylumbelliferone released per ml amniotic fluid) for 300 mid-trimester amniotic fluids was 11.40 +/- 2.40 nmoles MU/ml. The mean specific activity was 2.36 +/- 0.41 nmoles MU/mg protein. Two amniotic fluids from pregnancies which delivered children with cystic fibrosis (CF) were analyzed in blind samples sent from other laboratories. The MU titre values obtained were 4.73 and 4.32 with specific activities of 1.24 and 1.30 respectively. A third was identified in our screening program of amniotic fluids obtained from amniocenteses done for the intrauterine detection of genetic abnormalities. The MU titre value was 5.52 nmoles/ml with a specific activity of 1.34. The specific activities of these fluids when compared to the controls were significantly different (p less than 0.001). The mean titre value for 23 term amniotic fluids samples was 8.14 +/- 1.69 nmoles MU/ml. The mean specific activity was 3.37 +/- 0.76 nmoles MU/mg protein. A term amniotic fluid obtained from a woman who delivered a baby with CF showed a markedly reduced level of MUGB reactivity (3.01 nmole/ml). The specific activity was 1.06 which was significantly different from the control term fluids. The MU titre values and specific activities of amniotic fluids obtained from abnormal pregnancies (such as those with neural tube defects, chromosomal abnormalities and polymorphisms, abortions and stillbirths) and fluids with elevated alphafetoprotein and maternal blood contaminants did not significantly vary from the mean control values (Table 3).

Amniotic Fluid↗
PubMed1987

Effect of amniotic fluid on platelet thromboxane production.

We have studied the effect of amniotic fluid on thromboxane A2 (TXA2) production as an initial step in an evaluation of the role of this metabolite as the mediator of the pulmonary hypertension that accompanies perinatal aspiration. Term amniotic fluid enhanced platelet thromboxane B2 (TXB2) production in the presence of the aggregating agents thrombin and arachidonic acid, activity being confined to the lipid fraction. Compared with a baseline production of 1.4 +/- 0.45 pmol TXB2/10(6) platelets in response to thrombin (1 U/ml), unfractionated amniotic fluid or its lipid fraction enhanced TXB2 production to 2.87 +/- 0.53 and 2.81 +/- 0.62 pmol, respectively (P less than 0.01). Values for the aqueous extract were no different from buffer control values (1.14 +/- 0.5). No enhancement of platelet TXB2 production was observed in amniotic fluid obtained at 15 to 17 weeks. Similar activity was observed with either adult or neonatal platelets. This thromboxane enhancing property of amniotic fluid appears to be distinct from its thrombin generating property. Following perinatal aspiration, in situ production of thrombin and proaggregatory TXA2 could recruit more platelets, enhance local TXA2 production, and be responsible for the platelet thrombi that have been documented at autopsy in the pulmonary microcirculation in infants with perinatal aspiration syndrome.

Amniotic Fluid↗
PubMed1983

A controlled study of amniotic fluid immunoglobulin levels in intraamniotic infection.

The authors studied the levels of immunoglobulins (Ig) in the amniotic fluid of 46 patients with intraamniotic infection and of 46 matched controls. Amniotic fluid was collected through a transcervical intrauterine catheter. All infected patients had clinical signs of intraamniotic infection and at least 10(2) colony-forming units/milliliter of a high-virulence organism. None of the controls became infected. The matching criteria were gestational age, labor, interval from rupture of the membranes to delivery, and interval from rupture of the membranes to amniotic fluid collection. The authors tested each amniotic fluid sample for immunoglobulins G, M, and A by a single radial immunodiffusion technique. The mean IgG level in amniotic fluid for the intraamniotic infection group was 33.9 +/- 38.5 mg/dl, and the mean level for the control group was 17.9 +/- 11.1 mg/dl. The authors concluded that the mean IgG level in amniotic fluid from patients with intraamniotic infection is significantly higher than in controls (P less than .02).

Amniotic Fluid↗
PubMed1982

The presence of alpha-interferon in human amniotic fluid.

Almost all the samples of amniotic fluid from 62 pregnant women from the 16th week to the end of the pregnancy contained detectable amounts of alpha-type interferon. The presence of this substance in amniotic fluid during pregnancy raises the question of the physiological significance of this finding. It is postulated that the amniotic type of alpha-interferon might be a product of a constitutive gene, rather than induced by latent virus infection.

Amniotic Fluid↗
PubMed1999

The effect of amniotic fluid on the human omental artery in vitro.

OBJECTIVE: The aim of the study was to determine the effect of amniotic fluid on the in vitro contractility of the human omental artery. STUDY DESIGN: Amniotic fluid and a segment of omentum were obtained from each of 5 patients at the time of planned cesarean delivery at normal term gestation for the indication of previous cesarean delivery. The omental artery was cleaned and cut into 3-mm rings, which were placed in 10-mL organ chambers for isometric tension recording. The chambers were filled with Krebs-Henseleit solution bubbled with 5% carbon dioxide in air and maintained at 37 C, pH 7.4. The rings were then equilibrated at 1 g passive tension for 90 minutes. The amniotic fluid was centrifuged for 10 minutes at 3000 rpm to remove all debris. Increasing volumes of supernatant (10-2000 microL) were added to the omental artery rings at baseline tone or after contraction with U46619 (10(-7) mol/L) or potassium chloride (60 mmol/L) to detect contractile and relaxant effects, respectively. Time-solvent control preparations were also run in parallel. RESULTS: Amniotic fluid had no effect on the basal tone of omental artery rings. Amniotic fluid had no effect on the tension in rings previously contracted with either U46619 or potassium chloride. CONCLUSIONS: Amniotic fluid has no direct effect on isolated human omental artery. The catastrophic hemodynamic changes associated with the syndrome of amniotic fluid embolism are not due to a direct effect of circulating amniotic fluid on vascular tone but rather may be due to secondary responses

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

The natural interleukin-1 receptor antagonist in the fetal, maternal, and amniotic fluid compartments: the effect of gestational age, fetal gender, and intrauterine infection.

OBJECTIVES: The interleukin-1 receptor antagonist is a newly discovered cytokine that blocks the biologic effects of interleukin-1 in vitro and in vivo. This cytokine is a physiologic component of amniotic fluid and is considered to be of critical importance in the homeostasis of the cytokine network. This study was undertaken to systematically examine the bioavailability of interleukin-1 receptor antagonist in the maternal, fetal, and amniotic fluid compartments during term and preterm parturition in women with and without microbial invasion of the amniotic cavity. STUDY DESIGN: The patient population consisted of (1) pregnant women in the midtrimester (n = 42), (2) patients who underwent cordocentesis for diagnostic purposes (n = 39), (3) patients with preterm labor (n = 126), (4) women with term gestation (n = 102), and (5) healthy nonpregnant women (n = 8). Amniotic fluid was cultured for aerobic and anaerobic bacteria, as well as Mycoplasma sp. Interleukin-1 receptor antagonist concentrations were determined by enzyme-linked immunoassay in maternal and fetal plasma, amniotic fluid, and neonatal urine. Microbial invasion of the amniotic cavity was defined as the presence of a positive amniotic fluid culture for microorganisms. RESULTS: (1) Interleukin-1 receptor antagonist was normally present in fetal plasma samples obtained by cordocentesis, and its concentration increased with advancing gestational age (n = 39; r = 0.61, p < 0.001). (2) Patients at term not in labor had higher amniotic fluid interleukin-1 receptor antagonist concentrations than patients in the midtrimester (median 40.1 ng/ml, range 5.7 to 213.1 vs median 16.2 ng/ml, range 3.2 to 62.2, respectively, p < 0.001). (3) Amniotic fluid and cord plasma interleukin-1 receptor antagonist concentrations were significantly higher in patients with preterm labor and microbial invasion of the amniotic cavity than in those without microbial invasion of the amniotic cavity (amniotic fluid: median 219.9 ng/ml, range 35.4 to 504 vs median 80.6 ng/ml, range 24.3 to 399, respectively, p < 0.001; umbilical cord plasma: median 4.8 ng/ml, range 0.3 to 167.0 vs median 1.0 ng/ml, range 0 to 276.0, respectively, p < 0.05). In contrast, these differences were not found in patients with term labor either with or without microbial invasion of the amniotic cavity. (4) In both term and preterm patients the amniotic fluid and neonatal urine concentrations of interleukin-1 receptor antagonist were significantly higher in female fetuses than in male fetuses (amniotic fluid, preterm: median 191.9 ng/ml, range 51.6 to 504.0 vs median 61.1 ng/ml, range 11.5 to 284.9, respectively, p < 0.001; amniotic fluid, term: median 58.7 ng/ml, range 25.5 to 264.0 vs median 33.9 ng/ml, range 3.4 to 132.4, respectively, p < 0.001; neonatal urine: median 317 ng/ml, range 59.0 to 440.8 vs median 12.2 ng/ml, range 2.5 to 61.6, respectively, p < 0.005). CONCLUSIONS: (1) Interleukin-1 receptor antagonist is physiologically present in the fetal, maternal, and amniotic fluid compartments; (2) microbial invasion of the amniotic cavity in the preterm gestation is associated with a significant increase in the concentrations of this cytokine in the fetal and amniotic fluid compartments but not in maternal plasma; (3) fetal urine is a source of amniotic fluid interleukin-1 receptor antagonist; (4) fetal plasma interleukin-1 receptor antagonist concentrations increase with gestational age; (5) there is a significant effect of fetal gender in amniotic fluid and neonatal urine concentrations of interleukin-1 receptor antagonist.

Amnion↗
PubMedDate not supplied

Reduction of sera requirements in amniotic fluid cell culture.

Reduction in serum requirement for culture of primary human amniotic fluid cells can be achieved by the addition of 10 growth-promoting factors to the nutrient medium. This supplemented medium preserves cell types normally found in amniotic fluid cell cultures supplemented with 20-30 per cent fetal bovine serum. The volume of amniotic fluid required to initiate culture can be as little as 1 ml. Amniotic fluid samples contaminated with red blood cells with no visible clot also grow well in the low serum medium. Cell-free amniotic fluid combined with equal parts of supplemented medium is useful in initiating cell culture.

Amniocentesis↗