The Michael E. DeBakey M.D. for research excellence recognizes the exceptional faculty members of the Baylor College of Medicine for their published scientific contributions to clinical or basic science research in the last three years.
The recipients of the DeBakey Research Awards 2019 are Dr. Carl Allen, assistant professor of pediatrics – hematology / oncology; Dr. Christie Ballantyne, professor, head of the cardiology section and vice president of research in the Department of Medicine; Dr. Robert Britton; professor of molecular virology and microbiology; Dr. Aleksandar Milosavljevic, professor of molecular and human genetics; and the dott. Marco Sardiello, assistant professor of molecular and human genetics.
"These five awards are representative of the quality and scope of research at the College. Their work has made a significant contribution to their fields of study and to improving human health," said Dr. Adam Kuspa, senior vice president and dean of the search for Baylor.
The awards, named in honor of the pioneering heart surgeon Dr. Michael DeBakey, the first president of Baylor College of Medicine, were presented at a ceremony and scientific symposium on May 15th. Sponsored by the DeBakey Medical Foundation, the award includes medallion and memorial funds to support further research.
Kuspa delivered the awards along with Dr. George Noon, a professor of surgery and president of the DeBakey Medical Foundation, who was a colleague of DeBakey.
Dr. Carl Allen is an assistant professor of pediatrics – hematology / oncology and a member of Dan L Duncan's Center for Global Cancer. Allen's work focused on defining the pathogenesis mechanisms of Langerhans cell histiocytosis (LCH). The uncertain classification of LCH as a disorder of immune dysregulation with respect to neoplastic disease has blocked access to research support from organizations supported by the National Cancer Institute, limiting opportunities to improve outcomes for patients through clinical trials. The work that changes Dr. Allen's and colleagues' paradigm has redefined LCH as a myeloproliferative disorder. Not only has this work uncovered new therapeutic opportunities, but it has also contributed to the NCI, including LCH, in its portfolio of diseases that could benefit from translational research and clinical trial support.
Dr. Christie Ballantyne is professor of medicine, head of the cardiology section, vice president of research for the Department of Medicine, director of the Center for the prevention of cardiometabolic diseases and director of Maria and Alando J. Ballantyne, MD, Atherosclerosis Clinical Research Laboratory . He also holds the J. S. Abercrombie chair in atherosclerotic and lipoproteic research. Ballantyne is one of the leading experts on the subject of lipids, atherosclerosis and prevention of heart disease. Conducts Cardiovascular Event Reduction with Icosapent Ethyl-Intervention Trial or REDUCE-IT, which recently found that patients with high triglyceride levels, despite statin therapy, had a lower risk of cardiovascular events during intake of icosapent ethyl, a type of omega-3 fatty acid, compared to placebo. His recent work also found that troponin I, a protein that is commonly used to diagnose a heart attack, can be detected in adults without previous cardiovascular disease or heart failure and by adding this protein to a commonly used risk prediction model. led to prediction of the most accurate risk for hospitalization of heart attack, stroke and heart failure.
The dott. Robert Britton is a professor of molecular virology and microbiology and a member of the Center for Global Cancer of Dan L Duncan and the Center for Metagenomics Research and the Baylor Microbiome. His research and that of his laboratory are focused on the study of C. difficile, a bacterium that can cause serious infections in humans. The impact of C. diff, as it is commonly called, is staggering: some 14,000 deaths per year derive from C. diff infection in the United States alone and 200,000 worldwide. What is particularly worrying is that antibiotics used to treat infections are actually a risk factor for C. diff infection by eliminating the beneficial bacteria and allowing C. diff to obtain a fortress in the gastrointestinal tract. His recent work focused on how changes in food additives can lead to the emergence of pandemic strains of pathogenic bacteria such as C. diff in the human gastrointestinal tract and are likely to inform FDA policy on the approval of such additives.
The dott. Aleksandar Milosavljevic is a professor of molecular and human genetics, director of the quantitative and computational bioscience program, co-director of the computational and integrative biomedical research center and a member of Dan L Duncan's Center for Global Cancer. His laboratory develops bioinformatics methods and advanced data platforms while contributing to the fields of genomics, clinical genomics, epigenomics and the communication of extracellular RNA. Milosavljevic's laboratory guides the development of the FDA-approved ClinGen database to inform the clinical interpretation of genetic variation, and the lab currently serves as a data coordination center for the NIH Extracellular RNA Communications project, which produced the ExRNA Atlas and developed the first complete map of extracellular RNA in human biofluids. Developments in his work have recently been published in Science, Genome Medicine and the American Journal of Human Genetics.
Dr. Marco Sardiello is an assistant in molecular and human genetics at Baylor and a member of the Jan and Dan Duncan Neurological Research Institute of Texas Children & # 39; s Hospital. The Sardiello laboratory has quickly become a leader in the field of lysosome-autophagy biology which studies the cell waste disposal system and how its malfunction leads to the accumulation of cellular waste and lysosomal storage disorders, including Batten disease and other neurodegenerative conditions. More recently, in 2019, the Sardiello laboratory laid the foundations for a better understanding and treatment of tuberous sclerosis, a disease characterized by the formation of tumors in multiple organs and glycogen accumulation. mTORC1, a protein complex that regulates cellular metabolism, has long been considered the main driving force of tuberous sclerosis, but the Sardiello laboratory has discovered a second mechanism independent of mTORC1. This work could guide new approaches to treat the disease.
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