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Experiment 3 Results of this experiment are summarized in Table 3. Mifepristone appeared to have a biphasic effect. Conceptus diameter (P = 0.07) and uterine acid phosphatase secretion (P < 0.05) were both increased at the 100-mg dose. By contrast, conceptus diameter (P < 0.05) and total uterine protein secretion (P = 0.06) were decreased at the 400-mg dose. There was no effect of the four treatments on the number of conceptuses recovered on Day 11 of gestation. There was also no effect of the four treatments on variation in conceptus diameter, as measured by the average within-litter CV. Experiment 4 Pregnancy rate in this experiment was 79% and did not differ between treatments (Table 4). Mifepristone clearly decreased uterine capacity at 105 days of gestation. The number of dead fetuses (mummies) at 105 days of gestation was numerically but not significantly greater in the mifepristone-treated UHO gilts than in control UHO gilts. The decrease in uterine capacity coincided with an increase (P = 0.05) in fetal weight (after using placental weight as a covariate). In contrast to progesterone treatment, analysis of the number of large and small fetuses and placentas indicated that the numbers of small fetuses and placentas were lower (P < 0.01) in the mifepristone-treated gilts compared with control gilts. The numbers of large fetuses and placentas were not affected by treatment. There was no effect of mifepristone treatment on overall placental weights, fetal heart and brain weights, or fetal hematocrit. Fetal liver weights were higher in mifepristone-treated gilts (P < 0.05) compared with control gilts, but this effect disappeared after fetal weight was used as a covariate, suggesting that the increase in liver weight essentially reflected the increase in fetal weight after mifepristone treatment. Regression analysis of the fetal organ weight data indicated that heart and liver weights are linearly related to fetal weights: heart weight = 0.22 + 0.0082(fetal weight) (R2 = 0.88), and liver weight = -0.86 + 0.026(fetal weight) (R2 = 0.87). By contrast, the relationship between brain weights and fetal weights was curvilinear: brain weight = 16.74 + 0.017(fetal weight) - 0.0000061(fetal weight)2 (R2 = 0.42). A plot of this relationship (not shown) suggests that brain weights begin to decrease at <800 g fetal weight. TABLE 3. Least squares means (±SEM) for traits from gilts on Day 11 of gestation after treatment with 0-400 mg mifepristone on Day 2 of gestation. a Greater than control after log transformation (P = 0.07). b Less than control after log transformation (P < 0.05). c Less than control after log transformation (P = 0.06). d Greater than control after log transformation (P < 0.05). TABLE 4. Least squares means (±SEM) for traits from UHO gilts treated with either corn oil (control) or mifepristone on Day 2 of pregnancy. a Mifepristone group less than control (P < 0.01). b Mifepristone group greater than control after using placental weight as a covariate (P = 0.05). c Mifepristone group greater than control (P < 0.05). Effect disappears after using fetal weight as a covariate. FIG. 1. The frequency of stillborn piglets and piglets that did not survive until weaning within different birth-weight classes. The chances that a piglet would be stillborn (P < 0.05) or would die before weaning (P < 0.01) increased when birth weights were <1 kg compared with piglets weighing >1 kg at birth. All piglets weighing <0.5 kg at birth died before weaning.