Reducing Maternal Mortality Rates in Alabama Through Patient Education: A Scoping Review.

Maternal mortality continues to rise in the United States and disproportionately affects those in Alabama. Lack of patient education on warning signs is a preventable cause of maternal mortality. This article aims to systematically quantify existing research investigating the effect of patient education on maternal outcomes. The inclusion criteria required an article to be (a) original research, (b) conducted within the United States, (c) in English, and (d) published between January 2012 and September 2022. PubMed® and Embase® databases were searched using key words and filters. Rayyan®, a systematic review research tool, was utilized to assess articles in a blinded two-person review process. A blinded third researcher resolved conflicts. A total of 3,139 articles were compiled; 3,115 articles did not meet inclusion criteria, and 24 articles were retrieved after an abstract review. Ultimately, 11 articles were included after a full-text review. None of these articles were specific to Alabama. However, they did contain evidence for patient education improving maternal mortality. More research is required in Alabama to demonstrate the effect of educating patients on maternal mortality. These articles contain evidence for education as a tool to improve maternal outcomes.

Complex N-Linked Glycosylation: A Potential Modifier of Niemann-Pick Disease, Type C1 Pathology.

Complex asparagine-linked glycosylation plays key roles in cellular functions, including cellular signaling, protein stability, and immune response. Previously, we characterized the appearance of a complex asparagine-linked glycosylated form of lysosome-associated membrane protein 1 (LAMP1) in the cerebellum of Npc1-/- mice. This LAMP1 form was found on activated microglia, and its appearance correlated both spatially and temporally with cerebellar Purkinje neuron loss. To test the importance of complex asparagine-linked glycosylation in NPC1 pathology, we generated NPC1 knock-out mice deficient in MGAT5, a key Golgi-resident glycosyl transferase involved in complex asparagine-linked glycosylation. Our results show that Mgat5-/-:Npc1-/- mice were smaller than Mgat5+/+:Npc1-/- mice, and exhibited earlier NPC1 disease onset and reduced lifespan. Western blot and lectin binding analyses of cerebellar extracts confirmed the reduction in complex asparagine-linked glycosylation, and the absence of the hyper-glycosylated LAMP1 previously observed. Western blot analysis of cerebellar extracts demonstrated reduced calbindin staining in Mgat5-/-:Npc1-/- mice compared to Mgat5+/+:Npc1-/- mutant mice, and immunofluorescent staining of cerebellar sections indicated decreased levels of Purkinje neurons and increased astrogliosis in Mgat5-/-:Npc1-/- mice. Our results suggest that reduced asparagine-linked glycosylation increases NPC1 disease severity in mice, and leads to the hypothesis that mutations in genes involved in asparagine-linked glycosylation may contribute to disease severity progression in individuals with NPC1. To examine this with respect to MGAT5, we analyzed 111 NPC1 patients for two MGAT5 SNPs associated with multiple sclerosis; however, we did not identify an association with NPC1 phenotypic severity.