Making a Difference for the Future
The mission of our Institute for Clinical and Translational Research is to enhance the discipline of clinical and translational research by promoting multidisciplinary collaboration, addressing translational 'blocks' in research, providing infrastructure and collaborative support, and enhancing training, education, and career development, as part of the CTSA consortium.
The Institute for Clinical and Translational Research (ICTR) is jointly sponsored by the Albert Einstein College of Medicine and Montefiore Medical Center. The ICTR will re-engineer clinical and translational research, reorganize research facilities, transform training and educational programs, and expand the cadre of young investigators. As Dean Spiegel enunciated in Einstein's Strategic Research Plan, “Translational research poses a great challenge to institutions everywhere seeking closer integration between basic and clinical research. The public expects that just as research over the past decades has improved human health and led to such ‘medical miracles’ as organ transplantation, so translational research in the genome era will fundamentally change the way medicine is practiced.”
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To access the available ICTR resources CLICK HERE.
Featured Investigators
Michael Brownlee, MD, the Anita and Jack Saltz Professor of Diabetes Research, has been studying hyperglycemia-induced damage in type 1 diabetes. “Diabetes selectively damages cells, like endothelial cells and mesangial cells. This is important, because it tells us that the explanation for what causes complications must involve mechanisms going on inside these cells, rather than outside,” Brownlee stated. In a series of ground-breaking papers, Dr. Brownlee found that all four pathways causing diabetic complications were linked, “we discovered that all of these different pathogenic mechanisms do reflect a single hyperglycemia-induced process and that this single unifying process is the overproduction of superoxide by the mitochondrial electron transport chain.” The process is initiated by an increased production of reactive oxygen species (ROS), produced by the cells' mitochondria. The ROS inhibits the pathways through which cell damage occurs. More...