Perturb-multiome
CRISPR perturbation × single-cell gene expression and chromatin accessibility.
Research
My research connects technology development, cardiovascular biology, and predictive computation.
Research logic
Build causal measurements. Discover regulatory mechanisms. Predict the next intervention.
Perturbation Omics Technologies
Experimental platforms that pair programmed perturbations with transcriptomic, epigenomic, and spatial phenotypes.
Single-cell atlases reveal biological heterogeneity but are primarily observational. Perturbation omics moves from association to mechanism by measuring controlled interventions across thousands of individual cells.
The long-term goal is a unified platform that progresses from pooled discovery to multimodal mechanism and spatial validation.

Cardiovascular Functional Genomics
Causal maps of the programs that govern cardiac maturation, maladaptive remodeling, and regenerative potential.
Cardiovascular development and disease involve coordinated changes across cardiomyocytes, fibroblasts, vascular cells, immune cells, and other populations.
My future program will connect human genetics, physiological models, multi-omic measurements, and perturbation screens to experimentally testable mechanisms.

AI-enabled Biology
Interpretable computational systems that predict cellular responses and guide more informative experiments.
Perturbation datasets contain defined interventions and therefore provide an unusually strong foundation for biological prediction.
Models will be evaluated by whether they identify mechanisms, generalize across contexts, and prioritize experiments that produce new knowledge.
Current projects
Public descriptions remain deliberately concise while studies are ongoing.
CRISPR perturbation × single-cell gene expression and chromatin accessibility.
Spatial response fields and local tissue effects of perturbation.
Programmable gene regulation in cardiovascular models.
Chromatin dynamics across postnatal cardiac maturation.