Daniel Baugh Institute, founded in 1911 and endowed by Daniel Baugh, a prominent Philadelphia businessman and very active board member of Thomas Jefferson University. The Institute began as an anatomy research organization, as new methods were driving great progress in that field at the time.
About the Institute & History
The Daniel Baugh Institute was reformulated when new faculty joined TJU in March, 2000, moving from a Computational Biology Group in the DuPont Company (led by Dr. James Schwaber, pictured below in June, 1999) in order to join collaborators already in the Department of Pathology, Anatomy and Cell Biology, including Drs. Hoek, Knudsen and Kholodenko.
From the beginning we have envisioned the DBI as a part of a partnership with the University of Delaware Engineering School. Jefferson is the medical school for the state of Delaware and this partnership brings together the needed cross-disciplinary faculty and environments. As one of a very few of academic groups working in bioinformatics, the new Institute aims to blend medical and engineering faculties to support research, educational and business initiatives. Collaborating investigators/Institute members include Drs. Gao, Edwards, Robinson, Tunde and Elias at the University of Delaware Engineering School (UDel).
Below, this picture shows some Institute members on the 5th floor of Jefferson Alumni Hall in front of the plaque honoring the bequest from Daniel Baugh that supports the Institute and the picture of the original building, part of the gift, which initially housed the Institute. The building is located at the corner of 11th Street and Clinton. Some Institute faculty and their labs are missing from the picture: those of Profs. Jan Hoek and Boris Kholodenko.
Daniel Baugh Institute
- Amygdalar neuronal plasticity and the interactions of alcohol, sex, and stress
- Pharmacological ceramide reduction alleviates alcohol-induced steatosis and hepatomegaly in adiponectin knockout mice
- Decorin induces mitophagy in breast carcinoma cells via peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and mitostatin
- Inputs drive cell phenotype variability
- Molecular modeling of ErbB4/HER4 kinase in the context of the HER4 signaling network helps rationalize the effects of clinically identified HER4 somatic mutations on the cell phenotype