5% vs 68.4% preintervention (P value .80). Most mothers (81.3%; 1339) watched all 4 videos, and 308 mothers (18.7%) watched none. The mothers who watched all 4 videos were more likely to breastfeed exclusively (72.7% vs 55.3%) and less likely to exclusively formula feed than the mothers who watched none (1.1% vs 19.8%; P less then .0001).  https://www.selleckchem.com/products/incb28060.html  CONCLUSIONS There was no change in exclusive breastfeeding rates pre- versus post-video education intervention. However, most mothers watched all 4 videos, and those who did were significantly more likely to engage in any breastfeeding (98.9%) compared with those who watched none (80.2%) during the postpartum hospitalization. Copyright © 2020 by the American Academy of Pediatrics.Recurrent seizures, which define epilepsy, are transient abnormalities in the electrical activity of the brain. The mechanistic basis of seizure initiation, and the contribution of defined neuronal subtypes to seizure pathophysiology, remains poorly understood. We performed in vivo two-photon calcium imaging in neocortex during temperature-induced seizures in male and female Dravet syndrome (Scn1a+/-) mice, a neurodevelopmental disorder with prominent temperature-sensitive epilepsy. Mean activity of both putative principal cells and parvalbumin-positive interneurons (PV-INs) was higher in Scn1a+/- relative to wild-type controls during quiet wakefulness at baseline and at elevated core body temperature. However, wild-type PV-INs showed a progressive synchronization in response to temperature elevation that was absent in PV-INs from Scn1a+/- mice. Hence, PV-IN activity remains intact interictally in Scn1a+/- mice, yet exhibits decreased synchrony immediately prior to seizure onset. We suggest that impaired PV-Iion may contribute to transition to seizure in Dravet syndrome. Copyright © 2020 the authors.The spatiotemporal dynamics of excitatory neurotransmission must be tightly regulated to achieve efficient synaptic communication. By limiting spillover, glutamate transporters are believed to prevent excessive activation of extrasynaptically-located receptors that can impair synaptic plasticity. While glutamate transporter expression is reduced in numerous neurodegenerative diseases, the contributions of transporter dysfunction to disease pathophysiology remains ambiguous as the fundamental relationship between glutamate dynamics and plasticity, and the mechanisms linking these two phenomena, remain poorly understood. Here, we combined electrophysiology and real-time high-speed imaging of extracellular glutamate transients during long-term potentiation (LTP) induction and characterized the sensitivity of the relationship between glutamate dynamics during theta burst stimulation (TBS) and the resulting magnitude of LTP consolidation, both in control conditions and following selective and non-selective glutamahe strength of synaptic connections through a phenomenon known as synaptic plasticity. Synaptic plasticity is well-accepted to represent the cellular mechanisms underlying learning and memory, and many forms of plasticity are initiated by the excitatory neurotransmitter glutamate. While essential for rapid cellular communication in the brain, excessive levels of extracellular glutamate can negatively impact brain function. In this study, we demonstrate that pharmacological manipulations that increase the availability of extracellular glutamate during neural activity can have profoundly negative consequences on synaptic plasticity. We identify mechanisms through which excess glutamate can negatively influence synaptic plasticity and discuss the relevance of these findings to neurodegenerative diseases and in the aging brain. Copyright © 2020 the authors.In Drosophila, dopamine signaling to the mushroom body intrinsic neurons, Kenyon cells (KCs), is critical to stabilize olfactory memory. Little is known about the downstream intracellular molecular signaling underlying memory stabilization. Here we address this question in the context of sugar-rewarded olfactory long-term memory (LTM). We show that associative conditioning increases the phosphorylation of MAPK in KCs, via Dop1R2 signaling. Consistently, the attenuation of Dop1R2, Raf or MAPK expression in KCs selectively impairs LTM but not short-term memory. Moreover, we show that the LTM deficit caused by the knockdown of Dop1R2 can be rescued by expressing active Raf in KCs. Thus, the Dop1R2/Raf/MAPK pathway is a pivotal downstream effector of dopamine signaling for stabilizing appetitive olfactory memory.SIGNIFICANCE STATEMENTDopaminergic input to the Kenyon cells (KCs) is pivotal to stabilize memory in Drosophila This process is mediated by dopamine receptors like Dop1R2. Nevertheless, little is known for its underlying molecular mechanism. Here we show that the Raf/MAPK pathway is specifically engaged in appetitive long term memory in KCs. With combined biochemical and behavioral experiments, we reveal that activation of the Raf/MAPK pathway is regulated through Dop1R2, shedding light on how dopamine modulates intracellular signaling for memory stabilization. Copyright © 2020 the authors.BACKGROUND Coil occlusion has become the standard treatment for many ruptured aneurysms. However, specific aneurysm structures pose technical difficulties and may require the use of adjunctive neck-bridging devices, which necessitate the use of dual antiplatelet therapy. The hydrophilic polymer coating (pHPC, phenox) is a surface modification that inhibits platelet adhesion. OBJECTIVE To present initial experience with the pCONUS HPC device as an adjunct to coil embolization for ruptured aneurysms using single antiplatelet therapy (SAPT). METHODS All patients who were treated with the pCONUS HPC for ruptured aneurysms using SAPT were retrospectively identified. The occurrence of thromboembolic and hemorrhagic complications was recorded together with the angiographic and clinical follow-up details. RESULTS Fifteen patients were identified (nine female) with a median age of 54 years (range 27-81). Six aneurysms were located at the anterior communicating artery, five at the middle cerebral artery bifurcation, two at the basilar artery bifurcation, one at the posterior communicating artery, and one involving the intradural internal carotid artery.