Research

We aim to develop a context-aware data-driven functional genomics framework that can characterize tissue-specific gene representations, provide context-aware genotype to phenotype mapping, and enable network-based exploration of disease genetics.

We develop algorithms, systems and software architectures for automating reconstruction of accurate representations of neural tissue structures, such as nanometer-scale neurons' morphology and synaptic connections in the mammalian cortex.

Our goal is to develop better metagenomic binning by origin species of fragments of sequenced environmental DNA.

We develop, parameterize, and validate a model for tumor growth inhibition using in vivo mouse data and study the effects of modeling uncertainty and inter-individual variability on drug candidate efficacy predictions.

This project uses computational biology and chemistry tools to design a pharmaceutical to combat the Zika Virus.

We use computational models of biological pathways in disease to estimate the range of possible responses to various hypothetical drugs, given patient variability and limited pathway-relevant data.

Existing methods for cloning and recombination of DNA enable construction of arbitrary sequences. However, the sequential nature of these techniques makes them time-consuming and expensive. Furthermore, while the transformation of an existing plasmid into a host strain can be reliable when a selection marker is used, there are many current limitations: the number of different plasmids that can be co-transformed is limited by the choice of markers and compatible origins of replication; plasmids are less stable than chromosomal DNA and are difficult to maintain indefinitely without mutation; and cistronic interactions cannot be designed since each new nucleotide sequence added is on an unconnected DNA molecule. To overcome these limitations, we are designing reconfigurable chromosomes consisting of both fixed and variable regions. While the fixed region is carefully optimized and tuned ahead of time, the variable region can be modified in the field, at the point-of-use, leading to rapid and on-demand realization of novel biocircuits with many different phenotypes.

In order to be able to design synthetic organs that function autonomously, we will need to engineer artificial tissue homeostasis. To control the size of these artificial tissues, two major mechanisms will have to be engineered.

Using adversarial signals and a cycle-consistency based regularization, we can supplement paired regression tasks with unpaired data to improve regression performance.

Using medical knowledge to improve learned representations of patient health trajectories.

Integrating multi-modal clinical data and using recurrent and convolution neural networks to predict when patients will need important interventions.