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Error-driven upregulation of memory representations
Learning an association does not always succeed on the first attempt. Previous studies associated increased error signals in posterior medial frontal cortex with improved memory formation. However, the neurophysiological mechanisms that facilitate post-error learning remain poorly understood. To address this gap, participants performed a feedback-based association learning task and a 1-back localizer task. Increased hemodynamic responses in posterior medial frontal cortex were found for internal and external origins of memory error evidence, and during post-error encoding success as quantified by subsequent recall of face-associated memories. A localizer-based machine learning model displayed a network of cognitive control regions, including posterior medial frontal and dorsolateral prefrontal cortices, whose activity was related to face-processing evidence in the fusiform face area. Representation strength was higher during failed recall and increased during encoding when subsequent recall succeeded. These data enhance our understanding of the neurophysiological mechanisms of adaptive learning by linking the need for learning with increased processing of the relevant stimulus category.
Severity of neonatal influenza infection is driven by type I interferon and oxidative stress
Neonates exhibit increased susceptibility to respiratory viral infections, attributed to inflammation at the developing pulmonary air-blood interface. IFN I are antiviral cytokines critical to control viral replication, but also promote inflammation. Previously, we established a neonatal murine influenza virus (IV) model, which demonstrates increased mortality. Here, we sought to determine the role of IFN I in this increased mortality. We found that three-day-old IFNAR-deficient mice are highly protected from IV-induced mortality. In addition, exposure to IFNβ 24 h post IV infection accelerated death in WT neonatal animals but did not impact adult mortality. In contrast, IFN IIIs are protective to neonatal mice. IFNβ induced an oxidative stress imbalance specifically in primary neonatal IV-infected pulmonary type II epithelial cells (TIIEC), not in adult TIIECs. Moreover, neonates did not have an infection-induced increase in antioxidants, including a key antioxidant, superoxide dismutase 3, as compared to adults. Importantly, antioxidant treatment rescued IV-infected neonatal mice, but had no impact on adult morbidity. We propose that IFN I exacerbate an oxidative stress imbalance in the neonate because of IFN I-induced pulmonary TIIEC ROS production coupled with developmentally regulated, defective antioxidant production in response to IV infection. This age-specific imbalance contributes to mortality after respiratory infections in this vulnerable population.
Golden hour management of infants with congenital diaphragmatic hernia: 15 year experience at a high-volume center
To review the evolution of golden hour management and outcomes for infants with congenital diaphragmatic hernia (CDH).
General movement assessments in neonates born with congenital gastrointestinal anomalies: a single site, retrospective study
We aimed to characterize general movements in neonates with congenital gastrointestinal anomalies and to compare them to general movements in extremely low birth weight (ELBW) infants.
Young infants’ exposure to parabens: lotion use as a potential source of exposure
Parabens are widely used as antimicrobials in personal care products and pharmaceuticals. While previous studies demonstrate paraben exposure is ubiquitous, data investigating infants’ exposure is limited.
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