Translational Research: Translating Bench Science into Practical Applications for Medicine
To the UBRP student who is not sure whether to pursue research or medicine, the integration of the two fields was exemplified in the translational research lecture given by John Bloom MD, Specialist in Pulmonology, and Roger Miesfeld PhD, Department of Biochemistry and Molecular Biophysics. The unique and important quality about translational research, as Drs. Bloom and Meisfeld stated, “is to translate knowledge derived from basic science and bench research in the laboratory into practical applications to the patient leading to identifying new targets in disease pathways (genes or proteins) that can be exploited for the development of novel drugs.” On Wednesday, July 20, the two shared with students their past research collaboration on the effects of glucocorticoids in airway inflammation.
While on sabbatical, Dr. Bloom observed (from a physician’s viewpoint) an increase in the frequency of asthma in children. Asthma is defined as inflammation of the bronchi that lead to the lungs, and as a result can cause difficulty in a person’s ability to breathe. A common treatment for asthma is inhaled corticosteroids (ICS). Corticosteroids target the presence of white blood cells called eosinophils, which cause the inflammation. Dr. Bloom found that the presence of eosinophils affected the severity of asthma and the use of corticosteroid therapy exhibited a reduction in eosinophil production. However, it was observed that the complexity of steroid signaling created variable responses among patients during corticosteroid therapy.
By collaborating with Dr. Miesfeld, who had already been working with glucocorticoids, they began to study how glucocorticoids regulated eosinophil apoptosis or “cell suicide.” Their study included specific targets required to initiate apoptosis and whether or not glucocorticoid sensitivity of human eosinophils was an allergic or asthmatic reaction. At the end of their investigation, they found that there was a possibility that differences in expression of signaling genes may indicate glucocorticoid sensitivity and further studies would be needed to state whether or not differences in eosinophil transcriptome indicated glucocorticoid sensitivity.
At the end of the lecture, Dr. Miesfeld suggested that students ask themselves if they are interested in the medical application of research or the mechanistic view of the disease pathway. For undergraduates interested in medical school or graduate school or considering an MD/PhD, the opportunity to participate in cross-disciplinary research is always available.
To the UBRP student who is not sure whether to pursue research or medicine, the integration of the two fields was exemplified in the translational research lecture given by John Bloom MD, Specialist in Pulmonology, and Roger Miesfeld PhD, Department of Biochemistry and Molecular Biophysics. The unique and important quality about translational research, as Drs. Bloom and Meisfeld stated, “is to translate knowledge derived from basic science and bench research in the laboratory into practical applications to the patient leading to identifying new targets in disease pathways (genes or proteins) that can be exploited for the development of novel drugs.” On Wednesday, July 20, the two shared with students their past research collaboration on the effects of glucocorticoids in airway inflammation. 
While on sabbatical, Dr. Bloom observed (from a physician’s viewpoint) an increase in the frequency of asthma in children. Asthma is defined as inflammation of the bronchi that lead to the lungs, and as a result can cause difficulty in a person’s ability to breathe. A common treatment for asthma is inhaled corticosteroids (ICS). Corticosteroids target the presence of white blood cells called eosinophils, which cause the inflammation. Dr. Bloom found that the presence of eosinophils affected the severity of asthma and the use of corticosteroid therapy exhibited a reduction in eosinophil production. However, it was observed that the complexity of steroid signaling created variable responses among patients during corticosteroid therapy.