Alfred Ramirez Email & Phone Number

In addition to my previous responsibilities, I now led the development of the Finch’s data science computational platform which entailed: • Evaluate published and proprietary methods as potential additions to our platform. For example, the value of metagenome-assembled genomes (MAGs), alternatives to popular tools such as the biobakery suite, and metabolic modeling for predicting microbial community bioreactor behavior. • Formalize the development process of computational tools among the data science team to maximize reproducibility and ease-of-use. • Jointly integrate computational tools with our data engineering team to ensure robust and cost-efficient implementations.

Performed several functions as needed to fulfill project goals including: • Analyze microbial omics datasets to find signals in diseases such as C. diff, inflammatory bowel disease, and autism. • Develop and implement state-of-the-art computational methods for various data types including shotgun metagenomics, transcriptomics, and metabolomics. • Collaborate with laboratory scientists in experimental assay design and interpretation. For example, experimental assays to characterize a library of microbes in terms of inflammatory response, secreted metabolites, and functional capabilities of interest.

Integrated computational and experimental approaches to: 1) decipher cellular heterogeneity of adipose tissue, 2) uncover a novel regulator of the insulin signaling pathway, and 3) predict and validate metabolic flux differences between different types of adipocytes. In brief detail:Integrating Extracellular Flux Measurements and Genome-Scale Modeling Reveals Differences between Brown and White AdipocytesIn this manuscript, I designed a computational flux balance analysis framework to compare the metabolic fluxes between brown and white adipocytes. The software we created integrates commonly measured extracellular fluxes (e.g. Seahorse XF Extracellular Fluxes) to predict differences in every reaction in the metabolic network. We predicted and validated a difference in urea secretion between white and brown adipocytes. Membrane Metallo-Endopeptidase (Neprilysin) Regulates Inflammatory Response and Insulin Signaling in White PreadipocytesI performed RNA seq of subcutaneous and visceral human preadipocytes to search for molecular mechanisms underlying the observed phenotypic differences between the two types of adipose progenitors. I analyzed the data to reveal Neprilysin, a membrane-bound protease, as a potential regulator of insulin sensitivity and inflammatory response. I performed the insulin signaling and inflammation experiments to confirm the impact of MME perturbations in white preadipocytes.Network Analysis of Single-Cell RNA Seq Reveals Metabolic Heterogeneity of Human White AdipocytesI analyzed single-cell RNA seq of human preadipocytes undergoing adipogenesis. I applied PAGODA (Pathway and Gene Set Overdispersion Analysis) and t-SNE to reveal at least two types of metabolically-distinct white adipocytes. I collaborated with a computer science group at BU to jointly create a novel network-based approached to analyze single-cell RNA seq. We discovered a module of Zinc Finger Proteins potentially involved in regulating adipogenesis.

BE568 Systems Biology of Human Disease. Taught students fundamental analysis techniques and tools used in systems biology in the context of cancer and diabetes.

BE605 Molecular Bio-engineering. Taught first-year graduate students advanced principles in molecular bio-engineering and fundamental wet lab technique.

Lauffenburger Lab

Sought to determine the role of particular miRNAs in IFN-γ and TRAIL mediated cell death and assessing whether targeting these miRNAs offered new therapeutic strategies for hepatocellular carcinoma.

Analyzed the TNF-α induced activation of NF-κB, a transcription factor commonly deregulated in cancer. Designed and performed a study to determine the contributions of the TNFR/TAK1 and PI3K/Akt pathways to NF-κB activation and assess the therapeutic potential of each pathway.

Hopkins Lab

Analyzed aneuploidy and polyploidy in retinoblastoma, melanoma, and other cancer-prone Zebrafish lines. Working with a postdoc in the Hopkins lab, sought to determine whether aneuploidy and polyploidy contributed to carcinogenesis or whether these genetic aberrations were a result of cancer.

Doctor Of Philosophy (Phd), Biomedical Engineering

Bachelor Of Science (Bs), Biology And Physics