Suspected Chorioamnionitis and Myometrial Contractility: Mechanisms for Increased Risk of Cesarean Delivery and Postpartum Hemorrhage.

OBJECTIVE: Chorioamnionitis is associated with an increased risk of cesarean delivery and uterine atony. We hypothesized that the onset of maternal fever is temporally associated with decreased uterine contractility. STUDY DESIGN: Retrospective cohort. SETTING: Academic center. PATIENTS: Term participants who developed a fever in the setting of an intrauterine pressure catheter. MAIN OUTCOME MEASURE: Montevideo units (MVUs) and oxytocin dose at time 0 (first oral temperature ≥38°C) and in the five 1--hour blocks preceding and following T0. ANALYSIS: Montevideo units relative to the onset of fever. Results were adjusted for oxytocin dose and parity in a mixed-effects model. RESULTS: One hundred participants were included. Uterine contractility was maintained for 2 hours after the onset of maternal fever but thereafter significantly and steadily declined by an average of 6.9 ± 3.2 MVU/h ( P = .03), despite the absence of a parallel decline in oxytocin exposure. Multiparas and nulliparas showed a similar pattern of waning uterine contractility. Patients who delivered vaginally maintained contractility, while those who delivered via cesarean had diminishing contractility ( P = .01). The postpartum hemorrhage (PPH) rate (postpartum bleeding requiring treatment) was 32%. CONCLUSIONS: A decline in myometrial contractility occurs 2 hours following the onset of maternal fever. Increased risk of cesarean delivery appears to be directly associated with waning uterine contractility and decreased uterine responsiveness to oxytocin. Clinically, close attention should be given to maintaining adequate uterine contractions following a diagnosis of suspected chorioamnionitis. The likelihood of successful vaginal delivery may decrease over time, and the risk of PPH is clinically significant.

Pre- and perinatal risk factors for autism spectrum disorder in a New Jersey cohort.

This study evaluated the prevalence of pre- and perinatal risk factors in a cohort of children with autism spectrum disorders compared with the New Jersey population. Our cohort included 268 individuals with an autism spectrum disorder. Birth histories were obtained by a self-administered questionnaire. The autism spectrum disorders cohort rates of 7 perinatal risk factors were significantly higher than New Jersey state rates: mother's age 35 years or older, low birth weight, multiple gestation, prematurity, vaginal bleeding, prolonged labor, and hypoxia. Analysis of clustering of risk factors in the cohort showed no significant differences across maternal and paternal age groups. Older mothers in the cohort had a higher risk of infant hypoxia. Multiple risk factors during pregnancy appear to be associated with a higher risk of autism spectrum disorders in offspring, supporting the hypothesis that environmental influences in conjunction with genetics contribute to the causes of autism spectrum disorders.

A single brief burst induces GluR1-dependent associative short-term potentiation: a potential mechanism for short-term memory.

Recent work showed that short-term memory (STM) is selectively reduced in GluR1 knockout mice. This raises the possibility that a form of synaptic modification dependent on GluR1 might underlie STM. Studies of synaptic plasticity have shown that stimuli too weak to induce long-term potentiation induce short-term potentiation (STP), a phenomenon that has received little attention. Here we examined several properties of STP and tested the dependence of STP on GluR1. The minimal requirement for inducing STP was examined using a test pathway and a conditioning pathway. Several closely spaced stimuli in the test pathway, forming a single brief burst, were sufficient to induce STP. Thus, STP is likely to be induced by the similar bursts that occur in vivo. STP induction is associative in nature and dependent on the NMDAR. STP decays with two components, a fast component (1.6 +/- 0.26 min) and a slower one (19 +/- 6.6 min). To test the role of GluR1 in STP, experiments were conducted on GluR1 knockout mice. We found that STP was greatly reduced. These results, taken together with the behavioral work of D. Sanderson et al. [Sanderson, D., Good, M. A., Skelton, K., Sprengel, R., Seeburg, P. H., Nicholas, J., et al. Enhanced long-term and impaired short-term spatial memory in GluA1 AMPA receptor subunit knockout mice: Evidence for a dual-process memory model. Learning and Memory, 2009], provide genetic evidence that STP is a likely mechanism of STM.