Administering Intravenous Fluid in the Immediate Postpartum Period Minimizes Ultimate Formula Feeding.

Background: Human milk is the optimal form of nutrition for infants. Interventions associated with a decreased rate of exposure to infant formula are of benefit. We hypothesized that intravenous (IV) fluids could be associated with a reduction of infant formula when infants are separated from their mother. Methods: Retrospective chart review of term infants admitted to Rady Children's Neonatal Intensive Care Units (NICUs) for possible sepsis who received antibiotic treatment but did not develop sepsis. IV fluid use and formula exposure were analyzed. Results: Six hundred twenty-eight infants met the inclusion criteria. Around 25.6% received IV fluids and 74.4% did not. IV fluid administration was associated with a significantly reduced chance of formula exposure while in the NICU (odds ratio: 0.694, 95% confidence interval: 0.484-0.993; *p = 0.046). Conclusion: This retrospective chart review found that infants transferred to the NICU and separated from their mothers due to chorioamnionitis exposure who received IV fluids were significantly less likely to receive any infant formula than infants who were not administered IV fluids.

Human tau mutations in cerebral organoids induce a progressive dyshomeostasis of cholesterol.

Mutations in the MAPT gene that encodes tau lead to frontotemporal dementia (FTD) with pathology evident in both cerebral neurons and glia. Human cerebral organoids (hCOs) from individuals harboring pathogenic tau mutations can reveal the earliest downstream effects on molecular pathways within a developmental context, generating interacting neurons and glia. We found that in hCOs carrying the V337M and R406W tau mutations, the cholesterol biosynthesis pathway in astrocytes was the top upregulated gene set compared with isogenic controls by single-cell RNA sequencing (scRNA-seq). The 15 upregulated genes included HMGCR, ACAT2, STARD4, LDLR, and SREBF2. This result was confirmed in a homozygous R406W mutant cell line by immunostaining and sterol measurements. Cholesterol abundance in the brain is tightly regulated by efflux and cholesterol biosynthetic enzyme levels in astrocytes, and dysregulation can cause aberrant phosphorylation of tau. Our findings suggest that cholesterol dyshomeostasis is an early event in the etiology of neurodegeneration caused by tau mutations.