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Biomedical subjects

C D Wolfe

Publications and source records attributed to C D Wolfe.

84 records · Page 5Linked to original sources
PubMed1990

A longitudinal study of maternal digoxin-like immunoreactive substances in normotensive pregnancy and pregnancy-induced hypertension.

The serum of women in the third trimester of pregnancy demonstrates cross-reactivity with some commercially available antibodies to digoxin. A number of studies have suggested that levels of this digoxin-like immunoreactive substance(s) are further increased in patients with pregnancy-induced hypertension, and some have proposed that the digoxin-like immunoreactive substance could be useful as a predictor of pregnancy-induced hypertension. We measured digoxin-like immunoreactive substance levels every 2 weeks throughout the third trimester in 170 women; of these, 20 developed hypertension. Digoxin-like immunoreactive substance levels rose with gestational age. A graph of the slope of digoxin-like immunoreactive substance plotted against gestational age was fitted for the results obtained from each woman. There was no significant difference in the mean rate of increase of digoxin-like immunoreactive substance level per week between pregnancy-induced hypertension and normotensive pregnancy, nor was there any difference between these two groups at any gestational age studied. These results suggest that measuring digoxin-like immunoreactive substance levels is not useful as a predictor of pregnancy-induced hypertension.

Blood Pressure↗
PubMed1990

The rate of rise of corticotrophin releasing factor and endogenous digoxin-like immunoreactivity in normal and abnormal pregnancy.

Maternal plasma concentrations of corticotrophin releasing factor (CRF) and endogenous digoxin-like immunoreactivity (EDLI) were estimated in 80 normal and 88 abnormal pregnancies which were sampled sequentially from 24 weeks gestation to delivery. A slope was fitted for each woman's antenatal EDLI and CRF values, both of which rose significantly during gestation, and the mean of the slopes for the normal and abnormal groups for each value compared. There was no evidence of significant mean differences between groups for EDLI but there was evidence of a significant mean difference for CRF (P less than 0.05). After adjustment for other variables which may affect pregnancy outcome, the slopes for CRF were found not to be significantly related to outcome.

Corticotropin-Releasing Hormone↗
PubMed1989

Serum digoxin-like substances in pregnancy-induced hypertension.

1. Endogenous digoxin-like immunoreactivity (EDLI) was measured in the serum of 85 normotensive pregnant (NTP) women and 77 women with pregnancy-induced hypertension (PIH) by a radioimmunoassay (New England Nuclear). All women were in the third trimester. 2. EDLI, which was undetectable in serum from non-pregnant women, was present in NTP and PIH and was significantly higher in PIH. EDLI correlated with gestational age in NTP, but not in PIH. 3. Ouabain-sensitive Na+ transport was estimated in normal peripheral blood leucocytes after incubation with sera from 50 NTP and 42 PIH women. Significant inhibition of active Na+ transport occurred only with the serum of hypertensive patients without proteinuria. 4. EDLI did not correlate with the effect of the sera on active Na+ transport. The radioimmunoassay therefore provides a poor index of Na+ transport inhibitory activity in PIH.

Biological Transport, Active↗
PubMed1988

A comparison of endogenous digoxin-like immunoreactivity and sodium transport inhibitory activity in umbilical arterial and venous serum.

1. Endogenous digoxin-like immunoreactivity (EDLI) was measured by radioimmunoassay for digoxin in 13 paired samples of arterial and venous umbilical cord serum. EDLI was present in vein and artery, but was higher in the venous samples (P less than 0.025). 2. The venous cord serum inhibited the ouabain-sensitive sodium efflux rate constant of a normal mixed leucocyte population when compared with the effect of arterial cord serum (P less than 0.005). 3. It is suggested that the placenta may be involved in the production or metabolism of neonatal EDLI and of the inhibitor of sodium transport.

Biological Transport, Active↗
PubMed1988

A specific carrier substance for human corticotrophin releasing factor in late gestational maternal plasma which could mask the ACTH-releasing activity.

Late gestational maternal plasma contains a carrier substance for corticotrophin releasing factor (CRF-41) with a molecular weight in the region of 40,000. Using gel chromatography and CRF-41 immunoradiometric assay (IRMA), we show that binding of the peptide to its plasma carrier can be disrupted by treatment with urea. The binding capacity of the carrier substance is not saturated, since time-dependent incorporation of synthetic CRF-41 occurs at 4 degrees C. The carrier substance is also present in normal male plasma. It is specific for human CRF-41, not binding to ACTH, GnRH, vasopressin or ovine CRF-41. Most of the high concentration of CRF-41 in late gestational maternal plasma is bound to the carrier. Dilutions of pooled fractions containing carrier-bound CRF-41 after chromatography of maternal plasma had ACTH-releasing activity as did the synthetic peptide. However, the more concentrated chromatographic fractions at the apex of the carrier-bound CRF-41 peak showed reduced bioactivity, indicating that the higher concentrations of carrier in the original maternal plasma could mask the ACTH-releasing activity of CRF-41.

Adrenocorticotropic Hormone↗
PubMed1988

Plasma corticotrophin-releasing factor (CRF) in normal pregnancy.

Corticotrophin-releasing factor (CRF) was measured directly in maternal plasma using an immunoradiometric assay (IRMA). In the first and second trimester CRF levels were within the non-pregnant range (mean 15 pg/ml). A total of 72 women was followed sequentially from 28 weeks until delivery and CRF levels rose from a median of 20 pg/ml at 28 weeks to 1320 pg/ml at 40 weeks and 1732 pg/ml during labour. There was a strong correlation (rs = 0.81, P less than 0.001) between gestational age and CRF levels. The rate of rise of CRF (pg/ml) per week was associated with weight gain (rs = 0.36, P less than 0.05) but with no other obstetric variable. There was an association between umbilical cord and maternal plasma CRF levels (rs = 0.54, P less than 0.01).

Corticotropin-Releasing Hormone↗
PubMed1988

Plasma corticotrophin-releasing factor (CRF) in abnormal pregnancy.

Maternal plasma levels of cortiocotrophin-releasing factor (CRF) have been measured in abnormal pregnancy states to assess their potential as biochemical markers for at-risk pregnancies. CRF levels were not significantly altered in patients with hydatidiform mole, polyhydramnios or diabetes. CRF levels were elevated in pregnancies complicated by accidental antepartum haemorrhage at 28 weeks (P less than 0.03) but not for the rest of the third trimester. In twin pregnancies CRF levels were significantly raised throughout the third trimester (28-32 weeks, P less than 0.01; 34-36 weeks, P less than 0.001). In patients with pregnancy-induced hypertension (28 weeks, P less than 0.001; 32-36 weeks, P less than 0.001; and 38-40 weeks, P less than 0.01), preterm labour and premature rupture of the membranes (28 weeks, P less than 0.004; 30-32 weeks, P less than 0.002; and 34-36 weeks, P less than 0.001), CRF levels were significantly raised and in some patients levels were elevated 11 weeks before the onset of signs or symptoms. These observations raise the possibility that maternal CRF measurement may be of use as a predictive indicator of certain at-risk pregnancies.

Corticotropin-Releasing Hormone↗
PubMed1987

Plasma corticotropin-releasing hormone concentrations during pregnancy and parturition.

Plasma CRH was measured in maternal plasma throughout the third trimester of pregnancy, during labor, and postpartum. CRH levels were also measured in arterial and venous umbilical cord plasma samples. In normal pregnant women, plasma CRH increased from 50 +/- 15 (+/- SEM) pg/mL at 28 weeks gestation (n = 41) to 1462 +/- 182 pg/mL at 40 weeks (n = 55) and 1680 +/- 101 pg/mL (n = 65) in labor. Women with pregnancy-induced hypertension (n = 49) had plasma CRH levels significantly elevated above this normal range. Similarly, women who subsequently went into premature labor had raised levels several weeks before the onset of labor. After delivery, plasma CRH returned to normal within 15 h. Total plasma cortisol levels varied little throughout the third trimester, but increased during labor and remained elevated 2-3 days postpartum. There was, therefore, no correlation between plasma cortisol and CRH, implying that this placental CRH is not primarily involved in the control of the maternal hypothalamo-pituitary adrenal axis during pregnancy. The concentrations of CRH in umbilical cord plasma samples were considerably lower than those in the maternal circulation and were close to those in normal nonpregnant adults.

Adolescent↗