Trauma during pregnancy is uncommon, but with increasing trauma severity leads to increased fetal loss. Preventive strategies exist and when admitted monitoring standards should be followed.
Clinical concern about maternal fever during labor has largely been related to the possibility of infection. Although it has been assumed that fever during labor is usually secondary to infection, a recent study suggested that for women with low-risk fullterm pregnancies, much of the fever that develops during labor may not be infectious in origin but rather a consequence of the use of epidural analgesia. associated with an increased risk of preterm or cesarean delivery (such as multiple pregnancy, diabetes, cervical incompetence, or pregnancy-induced hypertension) were ineligible. Overall, 64% of eligible women were enrolled in the study. Women enrolling were randomly assigned to have their labor managed under a protocol of active management of labor or were assigned to usual care. The active management of labor protocol specified the criteria for the diagnosis of labor, the timing and dose of oxytocin, and use of oneto-one nursing throughout the course of labor. Epidural analgesia was not part of the trial protocol but was administered to women in both groups upon request. Active management of labor did not alter the rate of cesarean delivery. A complete description of the study methodology and results has been published elsewhere.'6The current analysis included women from both the active management and usual care groups but was limited to women with
SUMMARY
Tuberous sclerosis complex (TSC) is associated with neurodevelopmental abnormalities, including defects in neuronal migration. However, the alterations in cell signaling mechanisms critical for migration and final positioning of neurons in TSC remain unclear. Our detailed cellular analyses reveal that reduced Tsc2 in newborn neurons causes abnormalities in leading processes of migrating neurons, accompanied by significantly delayed migration. Importantly, we demonstrate that Reelin-Dab1 signaling is aberrantly regulated in TSC mouse models and in cortical tubers from TSC patients owing to enhanced expression of the E3 ubiquitin ligase, Cul5, a known mediator of pDab1 ubiquitination. Likewise, mTORC1 activation by Rheb overexpression generates similar neuronal and Reelin-Dab1 signaling defects, and directly upregulates Cul5 expression. Inhibition of mTORC1 by rapamycin treatment or by reducing Cul5 largely restores normal leading processes and positioning of migrating neurons. Thus, disrupted Reelin-Dab1 signaling is critically involved in the neuronal migration defects of TSC.
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