Jeffrey R. Millman

The paper develops a predictive digital model of human pancreatic cell differentiation using single-cell multiomic data to identify regulators and validate their roles in islet fate specification.

This study evaluates dithizone staining for localizing subcutaneously transplanted islets in mice, showing it reliably identifies insulin-producing β-cells and enables consistent dosing.

This study compares the hypoxia response of stem cell-derived and primary human islets using single-cell transcriptomics, revealing divergent metabolic and apoptotic responses.

The paper shows that depolymerizing F-actin with latrunculin A during early differentiation improves hPSC-derived islet maturation and function by altering signaling pathways and lineage specification.

This study shows that the IFIH1 E627* variant protects human pancreatic islets from stress-induced dysfunction by reducing immune responses and apoptosis.

This study investigates how Coxsackievirus B (CVB) infection affects different cell types in human pancreatic islets using single-cell RNA sequencing, revealing cell-specific transcriptional and functional responses.

This study uses magnetic sorting to enrich human stem cell-derived islets for CD49a, improving β-cell identity and function for diabetes therapy.

This study develops CRISPR-engineered glioblastoma organoids to model tumor progression, revealing transcriptional and spatial changes in neurodevelopmental gene networks.

This study compares SC-β cells with fetal and adult β cells using single-cell sequencing, finding they share a core β-cell identity but have unique transcriptional profiles with neural-biased gene networks.

This study uses a patient-derived stem cell model to show that a specific WFS1 variant causes mild Wolfram syndrome, which can be treated with chemical chaperones.

This study assesses the in vitro function of human stem cell-derived β cells, finding they exhibit increased insulin secretion, cellular respiration, and cytoplasmic calcium ion concentration in response to high glucose.