Last Friday, several members of the ENT-erest group attended the ENT Resident Research Day at the Methodist Hospital – Baylor Med Neurosensory Center. There were eight 10-15 minute presentations (4 basic science, 4 clinical) done by the residents followed up by a fantastic lecture on “outcomes research” by a distinguished guest speaker.
During the idle time, it was great to catch up with the two ENT residents I worked with in April who apparently found this site at some point after I left the lab — shout out to both of you. 😉 I also enjoyed meeting the other residents and faculty who were present.
Here are some things I learned from the presentations:
- Hematopoietic stem cells (HSC) are subdivided based on their regeneration capacity into short-term (ST) and long-term (LT). One would surmise that all the cells in a supposedly homogeneous group of either ST-HSCs or LT-HSCs would express similar transcriptional profiles, but they are indeed very different. Apparently, there’s more than one combination of gene levels which provides a cell with the aforementioned regeneration capacities.
- Head and neck squamous cell carcinoma (HNSCC) tumor cells with a loss of appropriate TP53 activity (the proverbial “guardian of the genome”) show a metabolic imbalance favoring glycolysis over oxidative phosphorylation (even in the presence of oxygen). We can sabotage this by using 2-deoxyglucose, a well known competitive inhibitor of glycoslysis, to essentially starve the tumor cells. HNSCC tumor cells with the “wild type” variant of TP53 can initially be treated with metformin (a well known oral hypoglycemic used to treat diabetes) to induce a metabolic imbalance in favor of glycolysis. Then, 2-deoxyglucose can be utilized for the same reasons outlined above.
- Prestin, an anion transporter motor protein located in the lateral membrane of the outer hair cell (OHC), is associated with the OHCs motility during auditory processing. Chloride anions typically flux across prestin, but when replaced with fluoride, there was a shift in the electric potential across the membrane towards depolarization while maintaining a similar peak capacitance.
- Interferon alpha (IFN-α) serves as one of the innate immune system’s first-line responses to a viral infection. IFN-α levels rise acutely, but fall precipitously well before the viral infection actually clears. Dr. Gelbard’s research shows that it’s the IFN-α itself, not the virus or transcription factors like IRF-7, which negatively feedback on the plasmacytoid dendritic cells to explain this fall in IFN-α levels. Of note, this transcriptional abrogation is rapid and reversible.