
Scientist with a proven track record of R & D experience in the field of infectious and systemic disease with more than two years of working experience in the pharmaceutical industry as an Analytical Development Scientist. Proven track record of scientific accomplishments and innovations in epithelial-linked (i.e., GI, renal, respiratory) systemic disease (i.e. hyperuricemia, sterile and non-sterile inflammation) and complexity of disease progression utilizing animal models correlating with hypotheses generated from cloud-based multi-omics discovery platforms (i.e. ROSALIND for nanoString, BASEPAIR for RNA Ses, DAVID bioinformatic esources). My MS in Regulatory Science (Pharma) and the METRUM Research Institute course on ADME, DMPK, and the identification of predictive disease models in non-clinical settings have equipped me with valuable knowledge. I have considerable knowledge in Metabolic clearance assay, drug metabolism pathways, and inhibition/activation of the metabolic assay.
Demonstrate a high drive and initiative, logic and decision-making abilities, and critical thinking skills. Multiple research publications in quality journals include Nature Communication. I possess supervisory capabilities for subordinate staff in the research laboratory and have a proven track record of mentoring Ph.D. students.
OUTSTANDING ACCOMPLISHMENT: Contribute to effective methods, assay validation, robustness study, and scientific discussion to keep the analytical department and Catalent at the state of the art to produce positive outcomes for clients by generating key data packages and scientific strategies. I have recently introduced a new workflow of AAV capsid lysis to boost accurate, reliable method of AAV titration that is superior to current practice of AAV capsid lysis
OUTSTANDING ACCOMPLISHMENTS: (1) I am the first scientist to discover how genetic causes of intestinal urate transport failure produce chronic hyperuricemia. In contrast, an acute increase in soluble urate, on the other hand, regulates the anti-inflammatory response and protects the host against infection when an infection occurs. [10.1038/s41467-020-16525-w] (2) First demonstrated that SARSCoV2 infection caused intestinal enterochromaffin cell hyperplasia, which could elevate 5HT. 5HT may be a crucial determinant of COVID19 associated diarrhea, alveolar flooding/Acute Respiratory Distress Syndrome, which has significant implications for COVID19 treatment [https://doi.org/10.1096/fasebj.2022.36.S1.0R556].
OUTSTANDING ACCOMPLISHMENTS: (1) We have established that zinc could be an alternative strategy to reduce Shigella-induced inflammatory responses and epithelial barrier dysfunction [https://doi.org/10.1152/ajpgi.00092.2018]. We found a substance similar to cucurbitacin in cucumbers that activates TMEM16A chloride channels and could help treat cystic fibrosis and problems with slow-moving intestines.