The objectives for this study were to determine 1) if there was a trend in stillbirths for the U.S. Holstein population, 2) if stillbirths are the same trait in primiparous and multiparous cows, and 3) what was the role of dystocia in stillbirths. A sample of 666,341 births from the MidStates Dairy Records Processing Center and the National Association of Animal Breeders was used to examine the influence of sire, herd, year, season, sex of calf, parity of dam, calving ease, and gestation length on the survival of the calf. Parity was scored as an ordered variable (1, 2, 3+). Calving ease was scored on a scale of 1 (no assistance) to 3+ (needed assistance). An increasing trend in stillbirths was found in primiparous and multiparous cows. The percentage of stillborn calves in primiparous cows increased from 9.5 in 1985 to 13.2 in 1996. Stillbirths in multiparous cows increased from 5.0 to 6.6% from 1985 to 1996. Variation about the trend was greater in primiparous cows than in multiparous cows. Dystocia was a major determinant of stillbirth incidence, but the association was stronger in primiparous cows. Sex of calf had different associations with stillbirth incidence in primiparous and multiparous cows. Gestation length and season of birth also had significant associations with stillbirth incidence. Logistic regression models with fixed and random effects were fit to the data to preserve the binary nature of the stillbirth response. The expected probability of stillbirths for an average herd and sire was 10% for primiparous cows and 5% for multiparous cows. Replacement of stillborn calves is a substantial cost to the dairy industry at more than $125.3 million per year. Because of the increasing incidence of stillbirths, these costs have increased by $75.9 million from 1985 to 1996.

Bronchopulmonary dysplasia (BPD) is a common lung disease of premature infants, with devastating short-and long-term consequences. The pathogenesis of BPD is multifactorial, but all triggers cause pulmonary inflammation. No therapy exists; therefore, we investigated whether the anti-inflammatory interleukin-1 receptor antagonist (IL-1Ra) prevents murine BPD. We precipitated BPD by perinatal inflammation (lipopolysaccharide injection to pregnant dams) and rearing pups in hyperoxia (65% or 85% O 2 ). Pups were treated daily with IL-1Ra or vehicle for up to 28 d. Vehicle-injected animals in both levels of hyperoxia developed a severe BPD-like lung disease (alveolar number and gas exchange area decreased by up to 60%, alveolar size increased up to fourfold). IL-1Ra prevented this structural disintegration at 65%, but not 85% O 2 . Hyperoxia depleted pulmonary immune cells by 67%; however, extant macrophages and dendritic cells were hyperactivated, with CD11b and GR1 (Ly6G/C) highly expressed. IL-1Ra partially rescued the immune cell population in hyperoxia (doubling the viable cells), reduced the percentage that were activated by up to 63%, and abolished the unexpected persistence of IL-1α and IL-1β on day 28 in hyperoxia/vehicle-treated lungs. On day 3, perinatal inflammation and hyperoxia each triggered a distinct pulmonary immune response, with some proinflammatory mediators increasing up to 20-fold and some amenable to partial or complete reversal with IL-1Ra. In summary, our analysis reveals a pivotal role for IL-1α/β in murine BPD and an involvement for MIP (macrophage inflammatory protein)-1α and TREM (triggering receptor expressed on myeloid cells)-1. Because it effectively shields newborn mice from BPD, IL-1Ra emerges as a promising treatment for a currently irremediable disease that may potentially brighten the prognosis of the tiny preterm patients.anti-inflammatory therapy | cytokines | receptor blockade | neonatal immunity

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Our novel LG estimate enables quantification of the severity of ventilatory instability underlying PB, making possible a priori selection of patients whose PB is immediately treatable with CPAP therapy.