Ultrasonographic growth measurements in triplet pregnancies.

The incidence of triplet pregnancies is increasing due to the widespread use of ovulation induction agents and assisted conception treatments. The aim of this study was to acertain the normal ultrasonographic measurements for fetal growth parameters in triplet pregnancies. The ultrasonographic measurements of all triplet pregnancies managed in two major hospital centres were reviewed retrospectively and those in which there was less than 25% discordance in birth weight were included in the study. Triplet 50th centile for fetal biparietal diameter, whilst falling through the normal singleton centile range from 27 weeks gestation, did not fall below the 10th centile value of singletons. Triplet 50th centile for head circumference was equivalent to the singleton 10th centile from 23 weeks gestation. Triplet 50th centile for abdominal curcumference was persistently below that of the singleton 50th centile, falling below the singleton 10th centile from 29 weeks gestation. Normal growth rate of triplet gestations in the third trimester of pregnancy varies from that of singletons. An awareness of this altered growth rate is necessary to avoid the inappropriate diagnosis of asymmetrical triplet fetal growth retardation. We suggest that the growth curves presented here may be used to monitor triplet fetal growth.

Outcome of inadvertent administration of a gonadotrophin-releasing hormone agonist (buserelin) in early pregnancy.

All women undergoing pituitary down-regulation before planned in-vitro fertilization (IVF) treatment in two IVF units were studied to assess the risks of and to pregnancies occurring inadvertently when gonadotropin-releasing hormone agonists (GnRHa) were used to achieve pituitary desensitization during the luteal phase prior to planned IVF treatment. In 2670 cycles, 25 women conceived (0.9% of cycles). Of these, three resulted in pre-clinical abortions (12%) but there were no clinical abortions, and 22 have ended with live births at term of apparently normal infants. Collation of these and other published data suggest that pregnancy outcome is not adversely affected by GnRHa administration in the luteal phase of the conception cycle.

Basic FGF activates phospholipase D in endothelial cells in the absence of inositol-lipid hydrolysis.

In the absence of inositol-lipid hydrolysis, mitogenic concentrations of basic fibroblast growth factor (bFGF) stimulated phosphatidylbutanol formation in the presence of butan-1-ol in [3H]myristate-labeled human umbilical vascular endothelial (HUVE) cells, indicating that the fibroblast growth factor receptor was able to couple to the activation of phospholipase D (PLD). The ability of bFGF and 12-O-tetradecanoylphorbol-13-acetate (TPA) to stimulate PLD activity was completely abolished in cells pretreated with 400 nM TPA for 48 h to downregulate protein kinase C (PKC). bFGF-stimulated PLD activity was inhibited by genistein (5 microM; P < 0.02) and the PKC inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7, 5 microM; P < 0.001) as well as by the removal of calcium from extracellular environment. bFGF induced DNA synthesis in a dose-dependent manner, and pretreatment of cells with H-7 inhibited the mitogenic activity of bFGF. These results indicate that activation of PKC is responsible for bFGF-induced PLD activation and the mitogenic activity of bFGF in HUVE cells. A coupled PLD/3-sn-phosphatidate phosphohydrolase pathway may play a role in the regulation of endothelial cell proliferation.

Identification and localization of alternately spliced mRNAs for vascular endothelial growth factor in human uterus and estrogen regulation in endometrial carcinoma cell lines.

Repair of human endometrium after menstruation and preparation of the endometrium for implantation involves profound angiogenic changes. Vascular endothelial cell growth factor (VEGF) is a recently identified growth factor with significant angiogenic properties. Four species of mRNA encoding VEGFs were identified in human endometrium and myometrium. All species were present throughout the menstrual cycle. Two species, VEGF165 and VEGF121, were present in peripheral leukocytes, indicating tissue-specific splicing of the two other VEGF transcripts. In situ hybridization of mRNA encoding VEGF was not restricted to vascular smooth muscle but was present in epithelial and stromal cells of endometrium throughout the cycle, and the distribution changed during the course of the cycle. All four species of VEGF were expressed by the endometrial carcinoma cell lines Ishikawa, HEC 1-A, and HEC 1-B. Estradiol increased steady-state levels of mRNA encoding VEGF in a dose- and time-dependent manner in HEC 1-A cells. Conditioned medium from these cells possessed angiogenic activity that was depleted by passage through a heparin affinity column. None of the cell lines demonstrated mRNA for acidic or basic fibroblast growth factor (FGF), despite previous reports of the identification of immunoreactive basic FGF in HEC 1-A and HEC 1-B cells. These findings show that VEGFs, not FGFs, are the principal angiogenic growth factors secreted by these cells and that human endometrium expresses a secreted angiogenic growth factor whose site of expression changes during the menstrual cycle.