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Biomedical subjects

J G Quirk

Publications and source records attributed to J G Quirk.

At least 55 records · Page 3Linked to original sources
PubMed1986

CA 125 antigen in human amniotic fluid and fetal membranes.

The cancer antigen CA 125 is manifest by serous cystadenocarcinoma of the ovary and to a lesser extent by other gynecologic and nongynecologic tumors. Its presence was screened for in normal human fetal tissues and fluids. Appreciable quantities of CA 125 were discovered in amniotic fluid by both a dot blot assay and the commercially available immunoradiometric assay kit. The most likely source of this antigen was found not to be the developing fetus, since antigen was absent from cord blood and fetal urine, but rather the chorionic membrane, which contained significant quantities of the antigen. CA 125 was found in extracts of maternal decidua, but none was found in extracts of placenta or amnion. The CA 125 antigen was determined by gel filtration experiments to be in excess of 700,000 daltons and probably in the range of 2 to 3 X 10(6) daltons. Size heterogeneity based on gel filtration and anion heterogeneity based on anion exchange chromatography have both been demonstrated for the CA 125 molecule. The amniotic fluid antigen is composed of two subunits of approximately 240,000 and 180,000 daltons as detected by iodine 125-labeled OC 125 monoclonal antibody. The antigen may contain additional subunits not detected by the monoclonal antibody. Size and change heterogeneity as well as the poor definition of the subunit bands on polyacrylamide gels also suggest this molecule contains an appreciable carbohydrate component.

Amnion↗
PubMed1984

Prolonged pregnancy. I. Observations concerning the causes of fetal distress.

During a 2-year prospective investigation of prolonged pregnancy in 727 women, 59 (8%) were delivered by cesarean section for fetal distress. This condition was diagnosed by means of electronic fetal heart rate monitoring in 47 of the women, and the patterns were unexpectedly characteristic of umbilical cord compression rather than uteroplacental insufficiency. Blinded sonar examinations were performed in 213 women, and the incidence of cesarean section for fetal distress as now described was significantly increased in those with oligohydramnios (two or fewer 1 cm pockets of amniotic fluid). We conclude that the pathophysiology of fetal distress in prolonged pregnancy is typically oligohydramnios that leads to compromised umbilical cord perfusion, rather than uteroplacental insufficiency.

Amniotic Fluid↗
PubMed1984

Fetal lung maturation in twin gestation.

Clear amnionic fluid was collected at cesarean section and the lecithin/sphingomyelin (L/S) ratio was used to evaluate fetal lung maturation in 42 twin gestations. The L/S ratios of twin pairs were usually similar in both numerical value and predictive accuracy except when the greater L/S ratio from one member of a pair indicated borderline lung maturity. Twin fetal lung maturation was found to be independent of sex, zygosity, and birth weight discordance. Comparison of mean L/S ratios in twins to those of uncomplicated singleton pregnancies revealed that fetal lung maturation occurred several weeks earlier in twins.

Amniotic Fluid↗
PubMed1984

Ureteral obstruction during pregnancy.

We report on a woman with recurrent renal failure due to bilateral ureteral obstruction during the mid trimester of pregnancy. The first pregnancy was terminated due to obstructive renal failure. In the second pregnancy renal function again deteriorated due to bilateral ureteral obstruction. After successful placement of a right ureteral catheter and a left percutaneous nephrostomy, renal function normalized and the gestation was continued through 37 weeks. Recurrent ureteral obstruction during pregnancy was attributed to changes following bilateral ureteral reimplantation. Patients with a history of urologic surgery warrant surveillance for renal failure secondary to mechanical obstruction. Those with a history of proved obstruction during pregnancy might benefit from the prophylactic placement of ureteral catheters and chronic antimicrobial therapy during subsequent gestations.

Adolescent↗
PubMed1984

Sinusoidal fetal heart rate pattern after intrauterine transfusion.

Two pregnancies complicated by severe Rh-isoimmunization and the development of sinusoidal fetal heart rate patterns immediately after intrauterine transfusions are presented. An intermittent sinusoidal pattern resolved, in one fetus, with sonographic evidence of delayed but complete absorption of transfused red blood cells. In contrast, the second fetus exhibited a continuous sinusoidal pattern coincident with cardiac decompensation detected by echocardiography, severe anemia, and failure to absorb transfused red blood cells. Possible pathophysiologic mechanisms for the development of sinusoidal patterns after fetal transfusions are discussed. It is concluded that a sinusoidal fetal heart rate pattern may occur after fetal transfusion and that the subsequent course of this pattern provides meaningful information about fetal condition as well as the success of intrauterine transfusion.

Adolescent↗
PubMed1984

Effect of myo-inositol on the glycerophospholipid composition of adult and fetal rat lung tissue.

In many species including man, the second most abundant lipid in lung surfactant is phosphatidylglycerol (PG) which may comprise 10% of the total lipid in surfactant from mature lungs. Infants delivered before their surfactant contained a large amount of PG are at greater risk of succumbing to hyaline membrane disease. Regulation of the PG content of lung surfactant is not understood completely, but the reciprocal changes in the amount of phosphatidylinositol (PI) and PG in surfactant as the lung mature are suggestive of regulation at the level of a common precursor. The immediate common precursor of PI and PG is CDP-diacylglycerol which is found in only small amounts in most mammalian cells and likely restricts the biosynthesis of both PI and PG. It has been observed in several species that the enzymes that synthesize PI and PG compete for the limited amount of CPD-diacylglycerol and this competition is influenced by the availability of myo-inositol. We and others have presented evidence that myo-inositol availability in the developing lung may be an important factor in the regulation of lung surfactant composition. In the present investigation, myo-inositol was administered chronically to nonpregnant and to pregnant rats and the effect of this treatment on the glycerophospholipid composition of lung tissue and lung lavage was measured. In addition, the influence of myo-inositol administration to pregnant rats on the glycerophospholipid composition of lung tissue of their fetuses was investigated. The concentration of myo-inositol in adult and fetal blood was measured by gas-liquid chromatography of its trimethylsilyl derivative. For determination of glycerophospholipid composition, the total lipid extracts of lung tissues and lung lavage were separated by 2-dimensional thin-layer chromatography and quantified by lipid phosphorus assay of individual spots. The concentration of myo-inositol in the serum of pregnant rats was significantly higher than in nonpregnant rats (Tab. I, Fig. 1). Treatment of the rats with myo-inositol resulted in a significant elevation of serum concentrations of myo-inositol throughout the experimental period. Between day 18 and day 21 of the gestation there was a significant decrease in serum myo-inositol concentrations in fetuses of saline treated rats. Treatment of the pregnant dams with myo-inositol resulted in a significant elevation in fetal serum concentrations of myo-inositol on both day 18 and day 21 of gestation (Tab. I).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Significance of brown and/or green amniotic fluid at the time of second trimester genetic amniocentesis.

During a two-year period, 83 discolored fluids (77 green, six brown) were obtained during genetic amniocenteses of 1227 patients. When compared with case-matched control subjects, those patients with discolored fluid had no differences in the incidence of spontaneous abortions, abnormal fetal karyotypes, infant abnormalities, occurrence of preterm labor, or requirement for delivery by cesarean section. The only statistically significant difference between control and test patients was that one in 83 versus 32 of 83 reported bleeding before amniocentesis (P less than .001). Both green and brown fluids had spectrophotometric peaks at 400 to 408 nm, similar to that reported for meconium. However, discolored fluid had measurable free hemoglobin, whereas meconium-stained fluid from term gestations did not, suggestive of an in utero hemorrhage. Further, when fetal blood, in concentrations calculated to yield a hemoglobin content similar to those measured in the discolored fluids, was incubated in amniotic fluid the spectrophotometric peak and absorbance units at 400 to 408 nm were similar to those for the discolored fluids. These observations are supportive of the hypothesis that blood breakdown products from an episode of intrauterine bleeding are responsible for the discolored fluid. Discolored amniotic fluid during second trimester, as an isolated finding, does not prognosticate a poor pregnancy outcome.

Amniocentesis↗
PubMed1983

The influence of myo-inositol on phosphatidylglycerol synthesis by rat type II pneumonocytes.

Type II pneumonocytes isolated from adult rat lung were incubated in a serum-free medium containing [14C]glycerol and the incorporation of 14C into glycerophospholipids was measured. After 24 h, more than 80% of the 14C incorporated into total lipids or into phosphatidylcholine and approx. 90% of the 14C incorporated into phosphatidylglycerol after 24 h was recovered in the glycerophosphoester moieties of these molecules. Supplementation of the incubation medium with foetal-bovine serum (10%, v/v) did not alter the incorporation of [14C]glycerol by type II pneumonocytes after 24 h into either a total lipid extract or phosphatidylcholine. In the presence of foetal-bovine serum, however, the incorporation of 14C into phosphatidylglycerol was decreased and the incorporation of 14C into phosphatidylinositol was increased. In the absence of foetal-bovine serum, the incorporation of 14C into phosphatidylglycerol was decreased progressively as the concentration of myo-inositol in the incubation medium was increased. The range of concentration (0.04-0.50 mM) over which myo-inositol had the greatest influence on [14C]glycerol incorporation into phosphatidylglycerol by type II pneumonocytes in vitro encompassed the concentration range measured in foetal-rat serum late in gestation. At 4 days before birth, the concentration of myo-inositol in foetal-rat serum was 0.36 mM and decreased to 0.23 mM 1 day before birth. The concentration of myo-inositol in adult rat serum increased from 0.03 mM to 0.06 mM during pregnancy. Isolated rat type II pneumonocytes were found to take up myo-inositol by a saturable process. A half-maximal rate of myo-inositol uptake occurred at a concentration of myo-inositol of 0.29 mM. The results of this investigation are consistent with the hypothesis that late in gestation there is a decreasing availability of myo-inositol to the foetal lungs and that this favours the biosynthesis of phosphatidylglycerol for surfactant at the expense of phosphatidylinositol biosynthesis.

Animals↗
PubMed1983

A rapid and specific enzymatic method for the quantification of phosphatidylcholine, disaturated phosphatidylcholine, and phosphatidylglycerol in amniotic fluid.

An enzymatic procedure for the quantification of phosphatidylcholine, disaturated phosphatidylcholine, and phosphatidylglycerol in amniotic fluid is described. By use of this method, choline and glycerol are released enzymatically from phosphatidylcholine and phosphatidylglycerol, respectively, in reactions catalyzed by phospholipase D. The hydrogen peroxide generated from choline (by the action of choline oxidase) and from glycerol (by the combined action of glycerokinase and glycerol-3-phosphate oxidase) is quantified spectrophotometrically after the addition of horseradish peroxidase, aminoantipyrine, and phenol. The phosphatidylcholine concentration in amniotic fluid was found to be approximately 10 to 30 nmol/ml between the twenty-third and thirty-sixth week of gestation and increased sevenfold to eightfold between the thirty-seventh week and term. The procedure can be modified for the quantification of disaturated phosphatidylcholine. The concentration of phosphatidylglycerol was approximately 2 nmol/ml between the twenty-third and thirty-sixth week and increased to 10 to 20 nmol/ml between the thirty-seventh and forty-first week of pregnancy. Since contamination of amniotic fluid with bile pigments does not interfere with either assay, the phosphatidylcholine and phosphatidylglycerol concentrations in amniotic fluid can be determined in samples that are contaminated with meconium.

Amniotic Fluid↗
PubMed1983

myo-Inositol homeostasis in the human fetus.

The concentration of myo-inositol in the serum of pregnant women (21.4 microM) remained unchanged throughout pregnancy and was not significantly different from that in the serum of nonpregnant women (24.5 microM). myo-Inositol concentrations in mixed cord serum averaged 125 microM at midgestation. At term, the concentration of myo-inositol was 60.2 microM in the umbilical artery and 45.4 microM in the umbilical vein. In every umbilical cord examined, the ratio of myo-inositol concentration in umbilical artery to that in umbilical vein exceeded 1.0. Activity of a putative regulatory enzyme in the biosynthesis of myo-inositol from glucose, ie, glucose 6-P:inositol 1-P cyclase (cyclase), was measured in placenta, fetal lung, and fetal liver. In placenta at midgestation and at term, cyclase activity was 87.8 and 90.7 nmol X g-1 tissue X h-1, respectively. Cyclase activity in fetal lung and liver at midgestation was 54.6 and 54.4 nmol X g-1 tissue X h-1, respectively. The gestational decline in the concentration of myo-inositol in fetal serum may represent a decreasing availability of myo-inositol to the fetal lungs and could be important in the mechanism whereby the amounts of phosphatidylglycerol and phosphatidylinositol in lung surfactant are regulated during fetal lung development.

Female↗
PubMed1982

Maternal and fetal pharmacokinetics of moxalactam given intrapartum.

Two grams of moxalactam was given intravenously to 28 women at high risk for infection following cesarean delivery. After a mean time of 48 minutes from infusion, maternal sera, cord sera, and uterine tissue obtained at delivery had concentrations of moxalactam of 62 micrograms/ml, 22.2 micrograms/ml, and 9.6 micrograms/gm, respectively. The maternal serum half-time was calculated to b e 2.1 hours. R and S epimeric distribution was determined in these sera and tissues, and the mean R/S ratios were 0.95, 0.93, and 1.22 for the three groups, respectively. The significance of these observations is discussed. A new method in which a high-pressure liquid chromatographic assay is used is described, and results are compared to those obtained with the microbiological assay. The high-pressure liquid chromatographic method was found to be quick, accurate, an reproducible.

Bacteriological Techniques↗
PubMed1982

Regulation of lamellar body acidic glycerophospholipid biosynthesis in fetal rabbit lung in organ culture.

To study the regulation of lamellar body acidic glycerophospholipid biosynthesis, fetal rabbit lung tissue obtained on day 23 of gestation was maintained in vitro. Tissues were cultured in serum-free medium with and without the addition of cortisol, thyroxine or a combination of both hormones. The addition of cortisol plus thyroxine to the medium resulted in the formation of lamellar bodies containing increased amounts of phosphatidylglycerol and decreased amounts of phosphatidylinositol. The addition of myo-inositol to culture medium containing cortisol plus thyroxine suppressed the incorporation of [14C]glycerol into both phosphatidylglycerol and bis(monoacylglycero)phosphate and enhanced the incorporation of [14C]glycerol into phosphatidylinositol. The effect of myo-inositol on the radioactive labeling of these lamellar body acidic glycerophospholipids was rapid, and was half-maximal at myo-inositol concentrations of approximately 0.10 mM.

Animals↗
PubMed1982

Myo-inositol homeostasis in foetal rabbit lung.

In several species, lung maturation is accompanied by a decline in the phosphatidylinositol content of lung surfactant and a concomitant increase in its phosphatidylglycerol content. To examine the possibility that this developmental change is influenced by the availability of myo-inositol, potential sources of myo-inositol for the developing rabbit lung were investigated. On day 28 of gestation the myo-inositol content of foetal rabbit lung tissue (2.3+/-0.5mumol/g of tissue) was not significantly different from that of adult lung tissue but the activity of d-glucose 6-phosphate:1l-myo-inositol 1-phosphate cyclase (cyclase) in foetal lung tissue (81.0+/-9.0nmol.h(-1).g of tissue(-1)) was higher than that found in adult lung tissue (23.2+/-1.0nmol.h(-1).g of tissue(-1)). Day 28 foetal rabbit lung tissue was found also to take up myo-inositol by a specific, energy-dependent, Na(+)-requiring mechanism. Half-maximal uptake of myo-inositol by foetal rabbit lung slices was observed when the concentration of myo-inositol in the incubation medium was 85mum. When the myo-inositol concentration was 1mm (but not 100mum) the addition of glucose (5.5mm) stimulated myo-inositol uptake. myo-Inositol uptake was observed also in adult rabbit lung and was found to be sub-maximal at the concentration of myo-inositol found in adult rabbit serum. The concentration of myo-inositol in the serum of pregnant adult rabbits (47.5+/-5.5mum) was significantly lower than that of non-pregnant adult female rabbits (77.9+/-9.2mum). On day 28 of gestation the concentration of myo-inositol in foetal serum (175.1+/-12.0mum) was much less than on day 25, but more than that found on day 30. A transient post-partum increase in the concentration of myo-inositol in serum was followed by a rapid decline. Much of the myo-inositol in foetal rabbit serum probably originates from the placenta, where on day 28 of gestation a high cyclase activity (527+/-64nmol.h(-1).g of tissue(-1)) was measured. The gestational decline in serum myo-inositol concentration, together with the decreasing cyclase activity of the lungs, is consistent with the view that maturation of the lungs is accompanied by decreased availability of myo-inositol to this tissue.

Animals↗
PubMed1982

Intrapartum monitoring and management of the low birth weight fetus.

All physicians responsible for the care of gravidae at high risk for preterm labor and delivery must be expert in the management of these pregnancies. Only a fraction of women who present in labor remote from term are candidates for long-term tocolysis. Whatever treatment regimen is utilized, the clinician must be familiar with their risks as well as their benefits. The majority of women who present with preterm labor will require delivery or will deliver despite efforts to the contrary. If delivery is imminent or indicated, intensive intrapartum monitoring of these fetuses, especially those weighing less than 1500 gm, is mandatory. The mother should be transferred to a facility that contains both expert obstetric care and a neonatal intensive care unit staffed with individuals experienced in the management of these very low birth weight infants. Attempts at pharmacologic induction of lung maturation should be reserved for those situations in which: (1) the fetal membranes are intact, (2) the fetal lungs are likely to be immature, (3) delivery of the infant may be delayed without undue risk for 48 hours following initiation of therapy, and finally, (4) the informed consent of the parents has been obtained. (By the same token, the probable efficacy of glucocorticoids should not serve as license to deliver the preterm infant.) Preterm infants are viable, even at 25 to 26 weeks of gestation, provided that labor and delivery are managed expertly. When vaginal delivery is contemplated, labor, if induced, should not be forceful. Fetal heart rate and uterine contractions should be monitored continuously. Evidence of fetal jeopardy must be dealt with expeditiously. Nontraumatic delivery, including the liberal use of cesarean section, into the hands of an experienced neonatologist will reduce the number of asphyxiated premature infants and, therefore, the risk of hyaline membrane disease. For the very low birth weight infant presenting as a breech, abdominal delivery is recommended. It is important that the uterine incision, regardless of type, be large enough to allow for nontraumatic delivery of the infant. If greater improvements in the survival and outcome of low birth weight infants are to continue, it is mandatory that there be close collaboration not only between obstetrician and pediatrician, but also between all physicians and nursing staff who care for this group of high-risk patients.

Analgesia↗