Document Type

Abstract

Publication Date

2-11-2026

Academic Year

2025-2026

Comments

Presented at the 2026 Scholarly Inquiry (SI) Research Project Symposium.

Abstract

Hypoxic-ischemic encephalopathy (HIE) affects three million neonates every year, often leading to conditions including cerebral palsy, epilepsy, and motor or cognitive deficits. A risk factor for neonatal HIE is maternal inflammation; however, little is known about the mechanism behind this. Maternal inflammation may increase maternal microchimerism, maternal cells that enter the fetal compartment. Maternal microchimerism may change fetal inflammatory pathways, organ repair, and immune system development. We hypothesized that patients with HIE have a greater percentage of maternal cells in their cord blood or circulating postnatal blood than those without HIE. To test this hypothesis, fetal cord blood or early postnatal blood samples (< 14 days old) were collected from neonates with and without HIE. Genomic DNA from these samples underwent short tandem repeat (STR) analysis (Promega) to identify contaminating maternal DNA. STR investigations are conducted using polymerase chain reaction techniques at various genetic loci that are unique to individuals, making them useful in genetic distinction. Thirteen samples were included in this analysis. We found that all samples were diploid at each STR locus. We concluded that our samples either did not have maternal microchimerism or that STR analysis was not sufficiently sensitive to detect a small quantity of contaminating maternal DNA. We are currently piloting a technique to sensitively detect maternal microchimerism using digital PCR of the AMELX locus (X chromosome locus) given its increased sensitivity to copy number variation. This strategy is being validated using a mouse line that allows tracing of maternal cells (GFP+) in wildtype offspring.

Additional Files
Lakhiani_Saniya_poster.pdf (1780 kB)

Language

English

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