Differential control of eNOS by multiple agonists: Ca and non-Ca dependant eNOS activation in UA endothelial cells (UAEC)

Jacqueline Cale Use of micro array membranes to characterize differential gene expression in cultured and freshly isolated uterine artery endothelial cells. Don Neff Effects of aspirin and tylenol on the release of luteinizing hormone-releasing hornione in cultured rat hypothalami. Michael Byers Estrogen receptor expression and steroid regulation in ovine uterine arteries. Francisco Diaz PGF 2 a d~erentially regulates LHr mR/VA, but not cfos/cjun mRNA in porcine CL after acquisition of luteolytic capacity. Michael Wolfgang Nonsurgical transfer of in vivo and in vitro produced blastocysts in the rhesus monkey. Jim Haughing Effect of estradiol cypionate in early postpartum dairy cattle. Sheirlie Vella Use of a novel cell per~fusion system for the study of hypothalmnic and pituitary hormone release In natural pregnancies, the embryo/fetus is genetically different from the mother because of carrying a complement of paternal genes. This situation comprises one of the major paradoxes of contemporary immunology, raising the question of how the genetically different embryo/fetus and mother co-exist during gestation. Human pregnancy, where cells from the implanted blastocyst migrate in massive numbers into the decidualized maternal endometrium, presents the greatest challenge. Over the course of the past two decades, many conditions providing protection to the human fetal semiallograft have been identified. These are provided by both the mother and by the extraembryonic tissues of the embryo/fetus. They include soluble substances such as prostaglandins, progesterone and anti-inflammatory cytokines that include transforming growth factor-p and interleukin-l 0. All of these are produced in the female reproductive tract during pregnancy and are present in the uterus and placenta. Remarkably, the placenta and extraplacental membranes themselves have evolved an array of powerful protective mechanisms. To prevent destruction by maternal complement-fixing antibodies to paternally-derived and fetal antigens, the placenta exhibits high levels of the cell surface regulatory proteins that interrupt the complement cascade. Recent experiments in knockout mice show clearly that in the absence of appropriate complement regulatory proteins, complement is activated at the implantation site and pregnancy is prevented. To protect against maternal cytotoxic immune cells directed against paternally-derived major histocompatibility antigens, known in humans as the HLA antigens, the placenta exerts strict control over their expression. Unlike other organs, placentas do not express HLA class II antigens, and the major placental HLA class I antigens, HLA-E and HLA-G, have few alleles and are unlikely to be recognized as foreign by the mother. HLA-E expressed on migrating trophoblast cells appears to prevent cytotoxic …