Preterm delivery occurs in approximately 10% of pregnancies, with marked impact on perinatal/neonatal morbidity and mortality. Premature babies account for greater than 80% of neonatal mortalities and greater than 90% of neonatal morbidities in the U.S. A circadian rhythm of uterine contractions has been observed in primates and humans. Notably, a basal number of contractions seems to increase as gestational age inceases, with a particular predisposition to nighttime uterine contractility. Increased nighttime oxytocin levels, with uterine contractions, have been demonstrated in rhesus monkeys. Unbound activin A, inactivated by follistatin--its natural binding protein--is not demonstrated in the nonpregnant female. However, it is detected in the first trimester of pregnancy with marked elevation at term, particularly at parturition. In gestations with preterm labor and delivery, the activin A levels also increase dramatically. After delivery, the activin A level falls quickly and is essentially not detectable after 6 hours postpartum. Activin A has also been shown to increase oxytocin peripherally after direct administration into the paraventricular nucleus of the hypothalamus, as well as binding to oxytocin-containing dendrites. When amnion cells are incubated with Activin A, prostaglandin E2a is induced. PGE2a is a well-know uterotonic. Given these conditions, activin A may play and important role in the cascade that initiates true delivery, pathological or otherwise. This study will focus on the circadian pattern of uterine contractions, activin A, follistatin, and oxytocin levels over a 24 hour period in women of various gestational ages, primarily 25-27 weeks, 30-32 weeks, 35-37 weeks, 40-42 weeks. Blood will be collected at serial intervals over a 24 hour period, controlling exposure to light and amount of activity/stress experiences. The levels of Activin A, Follistatin, and Oxytocin, and uterine contractions will be compared in the different gestational ages.