SUMMARY The neural substrates and pathophysiological mechanisms underlying the onset of cognitive and motor deficits in autism spectrum disorders (ASDs) remain unclear. Mutations in ASD-associated SHANK3 in mice (Shank3B−/−) result in the accelerated maturation of corticostriatal circuits during the second and third postnatal weeks. Here, we show that during this period, there is extensive remodeling of the striatal synaptic proteome and a developmental switch in glutamatergic synaptic plasticity induced by cortical hyperactivity in striatal spiny projection neurons (SPNs). Behavioral abnormalities in Shank3B−/− mice emerge during this stage and are ameliorated by normalizing excitatory synapse connectivity in medial striatal regions by the downregulation of PKA activity. These results suggest that the abnormal postnatal development of striatal circuits is implicated in the onset of behavioral deficits in Shank3B−/− mice and that modulation of postsynaptic PKA activity can be used to regulate corticostriatal drive in developing SPNs of mouse models of ASDs and other neurodevelopmental disorders.

Left ventricular assist devices have emerged as a safe and effective therapy for end‐stage heart failure patients. However, little is known about the safety of these devices during pregnancy. We describe a 23‐year‐old woman who received a left ventricular device for nonischemic cardiomyopathy of uncertain origin. She became pregnant approximately 1 year later. With close monitoring of her hemodynamic parameters, she was able to achieve a gestational age of 34 weeks, at which time she delivered a healthy male infant by cesarean delivery. Pregnancies in women with left ventricular assist devices may be successful, but remain medically challenging and complex pregnancies. Close multidisciplinary involvement and frequent assessment of device parameters during pregnancy is warranted.

Introduction: Mothers with a short cervix have been shown to have increased risk of spontaneous preterm delivery (PTD) and newborn morbidity. Those who require an ultrasound-indicated cerclage experience the highest rates of morbidity. Inflammation has been linked to a short cervix, and it has been linked to pregnancies affected by small for gestational age (SGA) newborns. To date, there are no studies that have investigated an association between a short cervix, with or without an ultrasound-indicated cerclage, and a SGA newborn. Methods: This was a case-control study examining all pregnancies with a transvaginal cervical length <25 mm found at their second trimester anatomy scan. Cases were subdivided into those who received an ultrasound-indicated cerclage (Group 1, n ¼ 52) and those who did not (Group 2, n ¼ 139). Controls were defined as pregnancies with a transvaginal cervical length >25 mm with no cerclage (Group 3, n ¼ 186) whose due date was within 2 months of the case pregnancy. Each short cervix case was matched with a control from group 3 in a 1:1 ratio. The primary outcome was birthweight <10% (SGA). Unadjusted data was analyzed with simple odds ratios. A logistic regression was used to control for confounding variables and provide an adjusted odds ratios (aOR). Results: The incidence of SGA among cases overall (group 1 þ group 2) was 13.6% (26/191). In group 3, the SGA incidence was 4.3% (8/186). The adjusted odds ratio (aOR) for a SGA infant was significant, 2.8 (95% CI 1.2, 6.6). Subgroup analysis showed that Group 1 had an increased risk for an SGA infant [aOR 4.9 (95% CI 1.8, 13.7)], but Group 2 did not show a significant finding [aOR 2.3 (95% CI 0.9, 5.7)]. Conclusion: Pregnancies complicated by a short cervical length <25mm, with or without a cerclage, were associated with an increased risk for a SGA newborn. Most of this significance was due to the pregnancies which received an ultrasound-indicated cerclage for a mid-trimester short cervix.