Assessing the potential of using telecommunication microwave links in urban drainage modelling.

The ability to predict the runoff response of an urban catchment to rainfall is crucial for managing drainage systems effectively and controlling discharges from urban areas. In this paper we assess the potential of commercial microwave links (MWL) to capture the spatio-temporal rainfall dynamics and thus improve urban rainfall-runoff modelling. Specifically, we perform numerical experiments with virtual rainfall fields and compare the results of MWL rainfall reconstructions to those of rain gauge (RG) observations. In a case study, we are able to show that MWL networks in urban areas are sufficiently dense to provide good information on spatio-temporal rainfall variability and can thus considerably improve pipe flow prediction, even in small subcatchments. In addition, the better spatial coverage also improves the control of discharges from urban areas. This is especially beneficial for heavy rainfall, which usually has a high spatial variability that cannot be accurately captured by RG point measurements.

The use of health risk assessment to estimate desirable sampling detection limits.

The inclusion of non-detected chemicals in a health risk assessment may lead, in some cases, to estimated risks that exceed regulatory thresholds, because one must use the detection limit or half of the detection limit. This study presents a methodology which will allow one to estimate appropriate detection limits by conducting a health risk assessment prior to the source sampling program. The advantages and shortcomings of various levels of detail in the risk assessment to determine those detection limits are discussed. The application of the methodology is demonstrated with a case study of the potential health effects of power plant stack emissions.

Variations in estrone sulfatase activity in human leukocytes.

Peripheral blood leukocytes isolated from men and women were studied for their capacity to metabolize estrone (E1) sulfate. Fresh human leukocytes (granulocytes and mononuclear cells) were incubated in phosphate buffer, pH 7.4, containing [3H]E1S for 1 h at 37 C. The samples were extracted with chloroform for measurement of the [3H]E1 formed, and the results were corrected for nonenzymatic hydrolysis. The mean E1 sulfatase activity in leukocytes isolated from normal women in the follicular phase of their cycle was 75% higher than that during the luteal [1840 +/- 179 (+/- SE) vs. 1048 +/- 101 fmol E1 micrograms protein-1 h-1; P less than 0.004] and higher than that in normal men (875 +/- 123; P less than 0.002), but was not different from that in menopausal (1349 +/- 151) or hirsute women (1700 +/- 222). In pregnant women, the mean leukocyte E1 sulfatase activity was significantly lower (861 +/- 147) than that in nonpregnant women in the follicular phase (P less than 0.003). These results suggest that progesterone may modulate E1 sulfatase activity, whereas estrogens do not.

Adrenal steroids in maternal and cord blood after dexamethasone administration at midterm.

We undertook a study designed to evaluate whether it is feasible to suppress fetal adrenal secretion of androgens at mid-pregnancy by giving dexamethasone (DX) to the mother. Levels of DX and adrenal steroids were measured in maternal and cord plasma of 13 DX-treated and 16 untreated mothers undergoing abortion at 18-20 weeks of pregnancy. Maternal adrenal suppression was evidenced by a sharp fall of plasma cortisol (F), cortisone (E), corticosterone (B), and dehydroepiandrosterone sulfate (DHEA-S). However, in cord blood no fall of DHEA-S or corticosterone sulfate (BS) was found up to 20 hours after DX administration, and cord plasma ACTH remained detectable. The failure of DX to suppress the fetal adrenal at mid-pregnancy suggests that this drug would not be effective in the intrauterine treatment of congenital adrenal hyperplasia (C.A.H.).

Comparison of human chorionic gonadotropin measurements by radioimmunoassay and in vitro bioassay.

A sensitive, accurate, and reproducible in vitro bioassay was developed for measuring human chorionic gonadotropin (hCG), based on testosterone production by collagenase-dispersed interstitial cells of rat testes in response to hCG. The results were compared to those obtained by established beta hCG radioimmunoassay. The assay sensitivity was 25 pg hCG-CR119/ml (65 microIU second IRP/ml). The intra-assay coefficient of variation (CV) was 8.8%, and the interassay CV was 13% and 33% in the high and low ranges of the standard curve, respectively. hCG recoveries were 89.6 +/- 3.12% (SE, n = 12). The pattern of serum bio-hCG followed established patterns of immuno-hCG, with the highest level measured during the first trimester (mean, 52,600 +/- 7,250 SE (mIU/ml, n = 11), decreasing thereafter to a mean value of 7,400 +/- 1,500 mIU/ml at term. The mean ratio of the bio/immunoactivity was consistently greater than one and did not significantly change at the various stages of pregnancy, or between normal and molar pregnancies (first trimester, 1.75 +/- 0.12 SE; midtrimester, 1.46 +/- 0.12; term, 1.50 +/- 0.09; molar, 1.55 +/- 0.2). When serum bioactive and immunoactive hCG were measured in a woman at five weeks of pregnancy, an episodic secretion of hCG was obtained by both assays.

Estrone sulfatase activity in the human brain and estrone sulfate levels in the normal menstrual cycle.

When the plasma concentrations of estrone sulfate (E1S) were measured in five menstrual cycles, the highest concentrations were found on the day of LH peak (14.25 nmol/l +/- 2.94 [SE]). Peak levels of E1S were 20 times higher than the highest E2 levels measured (0.769 +/- 0.276 nmol/l). To determine whether E1S can be metabolized by adult and fetal tissues we examined estrone (E1) sulfatase activity in brain and other tissues. E1 Sulfatase activity was present in all tissues studied including adult endometrium, fat and skin. When the rate of sulfatase activity was measured in homogenates of fetal hypothalamus, frontal cortex and pituitary (n = 4), the hypothalamic activity (306.0 +/- 39.1 [SE] pmol/min/mg protein) was significantly higher than that of the frontal cortex (127.4 +/- 19.4, P less than 0.002) or pituitary (193.7 +/- 43.3, P less than 0.03). This was not apparent in the adult (n = 2) where the enzyme activity was similar in the hypothalamus (413.9 +/- 27.3) and frontal cortex (446.3 +/- 82.2) and lower in the pituitary (98.2 +/- 19.2). The Km for E1 sulfatase in the fetal frontal cortex was 28.9 microM. The high E1 sulfatase activity in estrogen responsive target tissues, particularly fetal hypothalamus, accompanied by a large circulating reservoir of E1S, suggest that this enzyme could possibly have a regulatory role in controlling the level of intracellular estrogens and in modulating their intracellular function.

Endurance training effects on plasma hormonal responsiveness and sex hormone excretion.

A prospective study of the hormonal effects of a moderate exercise training program (4-wk control, 8-wk training) was conducted in seven young women. Sixty-minutes continuous bicycle ergometer tests of fixed relative intensity were performed at the beginning, middle, and end of the training period. The capacity of these acute bouts of exercise to affect circulating levels of stress markers, reproductive hormones, and hormones with possible antireproductive potential was measured. In addition, the urinary excretion of reproductive hormones was monitored continuously via serial overnight urine collections. Within testing sessions, plasma concentrations of all stress markers and antireproductive hormones rose significantly. Across testing sessions, only beta-endorphin + beta-lipotropin and cortisol exhibited an increment in peak responses as training progressed. Plasma reproductive hormone levels showed insignificant acute changes, and cyclic menstruation and preovulatory gonadotropin surges continued in all subjects. However, ovarian function was disturbed in four subjects as evidenced by a decreased excretion of estriol, free progesterone, or both. Transient infertility is a known clinical accompaniment of hormonal changes of comparable subtlety.

Conversion of progesterone to corticosteroids by the midterm fetal adrenal and kidney.

Midterm fetal adrenal and kidney tissue homogenates were incubated with 3H-progesterone (1 microM) and its conversion to te 3H-corticosteroids metabolites studied. Cortisol (36.3%) and corticosterone (4.7%) were isolated from the adrenal, and 11-deoxycortisol (32.5%) and deoxycorticosterone (21.1%) from the kidney. The results of these incubations confirmed the presence of 17- and 21-hydroxylase activities in both fetal tissues, and that of 11 beta-hydroxylase activity only in fetal adrenal tissue. We conclude that during pregnancy when progesterone levels are high, biosynthesis by the fetal kidney of 11-deoxycortisol, the most abundant corticosteroid formed by this tissue in this investigation, might provide to the fetal adrenal an important precursor for cortisol biosynthesis within the fetal compartment.

Sex differences in fetal lung maturation.

It has been recognized that male infants are at greater risk of respiratory distress syndrome than are female infants. Amniotic fluid was obtained from 73 male and 76 female fetuses between 28 and 40 wk of gestation. To assess fetal pulmonary maturity, we determined the lecithin-sphingomyelin ratio and concentrations of saturated phosphatidyl choline and cortisol in all of these fluids. Analysis of covariance showed that female infants had higher indexes of pulmonary maturity than did male infants. The difference in degree of fetal pulmonary maturity was 1.2 to 2.5 wk, on the basis of these measurements, with females ahead of males. We conclude that there is a biochemical basis for the increased risk of respiratory distress syndrome in male infants.

Direct evidence of sudden rise in fetal corticoids late in human gestation.

Glucocorticoids accelerate fetal lung maturation in all mammals studied, and in some species, such as goat and sheep, concentrations of fetal cortisol increase sharply before term, bringing about a train of events leading to parturition. Studies of cortisol in the umbilical cord blood have revealed no such increase at the end of human pregnancy. But information obtained in that way is difficult to interpret because much of the fetal cortisol is of maternal origin and its concentration, if sampled at delivery, is affected by maternal stress. These problems can be avoided to some extent by studying other fetal corticoids. Corticosterone sulphate (once called compound B, and abbreviated to BS) is produced by fetal adrenal glands and is present in greater concentrations in human fetal plasma than in maternal plasma. It is hydrolysed by the placental sulphatases and is a poor substrate for for placental 11 beta- hydroxysteroid dehydrogenase. We report here confirmation that the bulk of maternal BS originates from the fetus, and that its concentration increases suddenly at term.

Estriol determinations in diabetic pregnancies complicated by nephropathy.

In order to study the effect of renal disease on urinary estriol clearance rate, we have measured the concentrations of plasma and urinary estriol (E3) in pregnancies of 69 diabetic patients, 25 of whom had nephropathy. No correlation was found between endogenous creatinine clearance (CCr) and estriol clearance (CE3) rates (r = 0.07), and mean CE3 of diabetic patients with diminished CCr (less than 100 ml/min) was not significantly different from that of patients with normal CCr (greater than or equal to 100 ml/min). The ratios between total, unconjugated estriol and urinary estriol concentrations in patients with diminished CCr were not different from those patients with normal CCr. Cases where high plasma estriol and low urinary estriol concentrations coexisted were not found. It is concluded that in this group of diabetic patients, diminished CCr had no discernible effect on urinary CE3 possibly because renal tubular function remained intact. In patients with diabetic nephropathy either urinary or plasma E3 could be used to assess fetoplacental function.

Amniotic fluid testosterone and follicle-stimulating hormone in the determination of fetal sex.

To determine whether hormone analysis could be used for accurate determination of fetal sex, we measured testosterone (T) and follicle-stimulating hormone (FSH) in 130 amniotic fluid samples at midgestation. The mean unconjugated T in amniotic fluid of 73 patients carrying male fetuses was 202 pg. per milliliter (95 per cent confidence limits [CL]: 70 to 580) and all but three had levels higher than 90 pg. per milliliter. The mean amniotic fluid unconjugated T for 49 patients carrying female fetuses of 41 pg. per milliliter (95 per cent CL: 11 TO 125) was fivefold lower than that for the male fetuses and all but three patients carrying female fetuses had amniotic fluid T levels of 90 pg. per milliliter or lower. The mean amniotic fluid FSH of 0.7 ml. U. per milliliter (95 per cent CL: less than 0.5 to 3.4) for subjects with male fetuses was tenfold lower than that for patients with female fetuses. Amniotic fluid FSH levels less than 2.0 ml. U. per milliliter were found in 88 per cent of patients carrying male fetuses and in only one patient with a female fetus, and levels greater than 10 ml. U. per milliliter were found in those with female fetuses only. In eight patients (7 per cent of cases), neither amniotic fluid T nor FSH determinations were indicative of fetal sex. Measurement of unconjugated T and FSH in amniotic fluid may be an adjunct to other methods of determining fetal sex.

PIP: An investigation was undertaken to determine whether hormone analysis of amniotic fluid could be used to accurately predict fetal sex. Testosterone (T) and follicle-stimulating hormone (FSH) were measured in 130 patients with male fetuses and 49 were from patients with female fetuses. The mean concentration of unconjugated T for male fetuses was 202 pg/ml (95% confidence limits - CL: 70-580), and all but 3 had levels higher than 90 pg/ml. The mean amniotic fluid T concentration of patients carrying female fetuses of 41 pg/ml (95% CL: 11-125) was 5-fold lower than that for the male fetuses and all but 3 with female fetuses had amniotic fluid T levels of 90 pg/ml or lower. The mean amniotic fluid FSH of .7 ml U/ml (95% CL: less than .5-3.4) for patients with male fetuses was 10-fold lower than that for patients with female fetuses. 88% of the patients carrying male fetuses had amniotic fluid levels of less than 2 ml U/ml. Levels greater than 10 ml U/ml were only found in those with female fetuses.

Dexamethasone levels in treated pregnant women and newborn infants.

Dexamethasone concentration was measured in plasma and amniotic fluid by radioimmunoassay using a rabbit antiserum raised against DX-hemisuccinate-albumin. Recoveries of added tracers averaged 70% after paper chromatography. The within- and between-assay coefficients of variation averaged 10%. The lower limit of detection was 0.2 mug/dl when 0.4 ml of plasma was assayed. Ten healthy pregnant women at term had cesarean sections 8 to 11 hours following administration of 8 mg of DX orally. DX levels in maternal vein, in umbilical vein and artery, and in amniotic fluid averaged 2.2, 2.9, 2.6, and 2.5 mug/dl, respectively. Although cortisol levels were markedly suppressed, the total relative glucocorticoid activity in blood of fetuses treated with DX far exceeded that of the untreated group.

Plasma cortisol and cortisone in pregnancies with normal and anencephalic fetuses.

Plasma cortisol (F), cortisone (E), and progesterone (P), were measured in the umbilical vein (UV), umiblical artery (UA), and maternal peripheral vein (MPV) of 17 normal patients, and of 8 patients carying anencephalic fetuses. The plasma F in MPV of patients undergoing vaginal delivery after labor of spontaneous onset was significantly higher than that of patients delivered by elective cesarean section, whereas the plasma F concentrations in the UA or UV of the 2 groups were not statistically different from each other. The anencephalic fetuses had UA plasma F and E concentrations which were significantly lower than those of normal fetuses, suggesting that a main portion of UA cortisol and cortisone originates in the fetal adrenal. The UV and MPV plasma F and E concentrations of patients carrying anencephalic fetuses did not differ, however, from those of normal patients, suggesting that these UV corticoids are derived mainly from maternal sources. The amniotic fluid cortisol levels of the patients carying anencephalic fetuses were lower than those observed in the normal pregnancies, suggesting that amniotic fluid cortisol is derived mainly from fetal sources.

Amniotic fluid cortisol after premature rupture of membranes.

Total amniotic fluid cortisol concentration was studied in 12 patients at 24 to 34 weeks of gestation after premature rupture of membranes of one to eight days duration. Rupture of the membranes of less than 24 hours duration was associated with normal amniotic fluid cortisol concentrations. Rupture of membranes for more than 24 hours was associated in 10 of 12 patients with higher than normal amniotic fluid cortisol levels. The rise in amniotic fluid cortisol concentrations following premature rupture of the membranes may reflect increased fetal or maternal cortisol production or both, and could explain enhanced lung maturation in such infants.