BACKGROUND: Preeclampsia is a pregnancy-induced multiorganic disease. The incidence is 5 - 7 % in all pregnant women. To assess the value of circadian blood pressure rhythm in preeclamptic women, 24-hour blood pressure monitoring might be useful. The purpose of this study was to determine the predictive value of circadian blood pressure rhythm for the maternal and obstetrical outcome in patients with mild preeclampsia. PATIENTS AND METHODS: Sixty-six patients with mild preeclampsia underwent 24-hour blood pressure monitoring between 29 and 39 weeks gestation. Twenty-eight patients with normal circadian blood pressure rhythm were compared with thirty-eight patients with suspended circadian blood rhythm. RESULTS: There was no difference in age, body mass index, gravidity, parity, miscarriage, or fetal outcome between the two groups. The rate of secondary caesarean section was 39.5 % in the suspended circadian blood pressure group and 21.4 % in the normal circadian blood pressure group, respectively (P = 0.03). CONCLUSIONS: In patients with mild preeclampsia, the circadian blood pressure rhythm appears to be unsuitable as a screening test. Further research is required for more etiological and pathophysiological insights into the development of clinically useful tools with predictive value.

Adolescent↗

PubMedDate not supplied

Purification and properties of the soluble 17 beta-hydroxysteroid dehydrogenase of rabbit uterus.

17 beta-Hydroxysteroid dehydrogenase activity towards estradiol-17 beta has been demonstrated in the 105,000 x g supernatant of rabbit uterus. Hydroxylapatite chromatography of the enzyme activity isolated by ammonium sulfate precipitation, gel filtration and DEAE-cellulose chromatography yielded a single 17 beta-hydroxysteroid dehydrogenase activity. Further purification of the enzyme preparation by isoelectric focusing resulted in multiple peaks of activity. The molecular weight of the enzyme, caculated from mobility data on Sephadex gel, is approximately 64,000. Some properties of partially purified 17 beta-hydroxysteroid dehydrogenase activity have been studied. Estradiol-17 beta reacts at a faster rate than testosterone. The Km for estradiol is 4.16 x 10(-5) mol/l for the NAD-linked enzyme activity and 4.37 x 10(-5) mol/l when NADP as cofactor was used. The ratio of the maximal velocity for NADP to that for NAD was 1.42. The pH-optimum for estradiol appears between 9.5 and 10.5 and for estrone between 5.5 and 6.5. The enzyme appears to be of the sulfhydryl type.

17-Hydroxysteroid Dehydrogenases↗

PubMedDate not supplied

[Microsome-associated 17 beta-hydroxysteroid dehydrogenases of human placenta, i solubilization, enrichment and separation of two 17 beta-hsd-activities after phospholipase-Treatment].

Treatment of human placenta microsomes with phospholipase A or D inhibits the 17beta-hydroxysteroid dehydrogenase (17beta-HSD) activity, parallel with the hydrolysis of membrane phospholipids. The 17beta-HSD activity of phospholipase treated microsomes is reactivated by synthetic phospholipids. The distribution of 17beta-HSD activity in subfractions of original microsomes and of phospholipase treated microsomes obtained by zonal centrifugation was studied. Solubilization of the microsomal 17beta-HSD was achieved by phospholipase A treatment. Two 17beta-HSD were solubilized from human placenta microsomes by phospholipase A treatment and were further purified by ammonium sulphate precipitation, gel filtration on BioGel A-0.5 m, DEAE-Sephadex chromatography and by isoelectric focusing. The enzymes were purified 25.8 and 17.4 times. The isoelectric points and molecular weights of the two 17beta-HSD were determined. Both enzymes are of a 17beta-HSD type. One of the 17beta-HSD, however, was sensitive to estradiol-17beta, the other to testosterone. The question of whether the two enzymes constitute a monomer and a dimer of the same 17beta-HSD or are completely different enzymes, is discussed.

Centrifugation, Zonal↗

PubMedDate not supplied

[Microsome-associated 17beta-hydroxysteroid dehydrogenases of human placenta, ii kinetic studies and characterization of the solubilized estradiol-and testosterone-"sensitive" 17beta-HSD-Activities].

Detailed enzyme kinetic parameters of the reactions catalyzed by the two 17beta-hydroxysteroid dehydrogenases (17beta-HSD), which were solubilized from the microsomes of human placenta by treatment with phospholipase A, followed by enrichment and separation were determined. Both enzymes are strictly substrate specific. The most active substrate of one of the 17beta-HSD (fraction A) is estradiol-17beta, the other 17beta-HSD (fraction B) is sensitive to testosterone. Both NAD and NADP can serve as hydrogen transferring coenzymes, the latter giving about one-third of the initial rate of the former. With respect to the influence of temperature, different buffers and pH values, Michaelis constants (Km) with estradiol-17beta and testosterone as substrates, the solubilized and separated microsomal 17beta-HSD behave like those isolated from the cytoplasmic fraction. The two 17beta-HSD, after solubilization from the microsomal fraction of human placenta, enrichment and separation from each other, show only a little activity for the transfer of hydrogen between C17 of estradiol-17beta and C17 of androstenedione. On the other hand, intact microsomes and an integrated system prepared by recombination of the 17beta-enzymes by preincubation in phosphate buffer are able to catalyse very actively the transfer of hydrogen between estradiol-17beta and androstenedione. The effect of temperature and time on the recombination of the two enriched and separated microsomal enzyme activities and the determination of the pH-optimum of the hydrogen transfer reaction are described. Finally it is proposed that the hydrogen transfer between steroid hormones represents an aspect of the true reaction mechanism of steroid hormones: Steroid hormones function as hydrogen transferring coenzymes by forming part of a chain of hydrogen carriers.

Androstenedione↗

PubMedDate not supplied

Effects of TNF-alpha and retinoic acid on the proliferation of the clear cell and chromophilic types of human renal cell carcinoma in vitro.

Since no effective therapeutic approach is known so far for metastatic renal cell carcinoma (RCC), we analyzed the anti-proliferative effects of TNF-alpha and retinoic acid (RA), applied either alone or in combination on 7 different RCC cell lines in vitro. In 5 out of 7 cell lines, a significant (p < 0.05) dose-dependent inhibition of tumor cell proliferation became evident after exposure to TNF-alpha, the response being of modest magnitude in 5 cell lines. In 2 cell lines the effects were more pronounced with a reduction of cell viability to 55 +/- 11% of the control. Northern blot analysis revealed no expression of TNF-alpha and p75 TNF-receptor in any cell line. All the cell lines showed p55 TNF-receptor mRNA. Scatchard analysis revealed no correlation between TNF-alpha receptor status and growth inhibitory response to TNF-alpha, the number of TNF-receptors per cell ranging from 0 to 3,976, and the affinity values from Kd = 0.621 nmol/l to Kd = 4.28 nmol/l. Exposure to RA alone resulted in significant (p < 0.05), but modest growth inhibition in 2 out of 7 cell lines with a reduction of cell viability to 83 +/- 1% of the control. In 2 out of 7 cell lines, combination of RA and TNF-alpha was significantly (p < 0.05) more effective than the single application of each compound. Northern blot analysis revealed no transcripts of CRABP I and retinoic acid receptor (RAR)-beta. All the cell lines expressed RAR-alpha mRNA and one cell line additionally expressed RAR-gamma mRNA. A correlation between RAR status and RA response was not seen.

Adenocarcinoma, Clear Cell↗