RESUMO
BACKGROUND: Urine sodium concentration has been suggested as a marker to guide enteral sodium supplementation in preterm infants; however, no previous data have demonstrated relationships between urine sodium concentration and postnatal growth. METHODS: We performed a single-center retrospective cohort study on 224 preterm infants admitted to the neonatal intensive care unit at the Children's Hospital of Georgia between January 2010 and July 2022. Spot urine sodium was measured in preterm infants (<34 weeks postmenstrual age [PMA]) between days of life (DOLs) 7 and 28. Our exposure of interest was spot urine sodium concentration (milliequivalents per liter) obtained between postnatal days 7 and 28, and our primary outcome was weight velocity (grams per kilograms per day) determined at DOL 28. Statistical relationships were assessed by multivariate analysis with subgroup comparisons by Student t test and analysis of variance. RESULTS: In 224 preterm infants (199 ± 17 days, 56% male, 71% Black), urine sodium concentration did not associate with weight velocity at DOL 28 and 36 weeks PMA. Urine sodium concentration was weakly associated with gestational age at birth, and Black preterm infants had higher urine sodium values when compared with "other," but not White preterm infants. CONCLUSION: Spot urine sodium during the first month of life does not associate with weight velocity at DOL 28 or 36 weeks PMA.
RESUMO
Fear expressed toward threat-associated stimuli is an adaptive behavioral response. In contrast, the generalization of fear responses toward nonthreatening cues is a maladaptive and debilitating dimension of trauma- and anxiety-related disorders. Expressing fear to appropriate stimuli and suppressing fear generalization require integration of relevant sensory information and motor output. While thalamic and subthalamic brain regions play important roles in sensorimotor integration, very little is known about the contribution of these regions to the phenomenon of fear generalization. In this study, we sought to determine whether fear generalization could be modulated by the zona incerta (ZI), a subthalamic brain region that influences sensory discrimination, defensive responses, and retrieval of fear memories. To do so, we combined differential intensity-based auditory fear conditioning protocols in mice with C-FOS immunohistochemistry and designer receptors exclusively activated by designer drugs (DREADDs)-based manipulation of neuronal activity in the ZI. C-FOS immunohistochemistry revealed an inverse relationship between ZI activation and fear generalization: The ZI was less active in animals that generalized fear. In agreement with this relationship, chemogenetic inhibition of the ZI resulted in fear generalization, while chemogenetic activation of the ZI suppressed fear generalization. Furthermore, targeted stimulation of GABAergic cells in the ZI reduced fear generalization. To conclude, our data suggest that stimulation of the ZI could be used to treat fear generalization in the context of trauma- and anxiety-related disorders.
