Researchers have developed synthetic platelets that can be used to stop bleeding and enhance healing at the site of an injury. The researchers have demonstrated that the synthetic platelets work well in animal models but have not yet begun … Read more
Post-doctoral Fellowship, Biology and Biological Engineering, California Institute of Technology
Dr. Polacheck’s laboratory investigates the physical interactions between cells and their environment and how forces at the cellular scale contribute to tissue development, homeostasis, and disease. To study how cells sense and generate forces in living tissue, the Polacheck lab develops microfluidic technology to build microtissues in the laboratory that mimic the architecture and multicellular function of human tissues in vivo. By integrating these organ-on-chip models with genome editing, induced-pluripotent stem cell technology, and other cell and molecular biology techniques, the Polacheck lab has developed a novel approach for understanding the molecular machinery employed by cells to generate force sand to transduce forces from their environment into biological responses. The lab seeks to leverage these biological insights to inform novel drug targets for diseases in which misregulation of cellular forces contribute to pathogenesis, such vascular disease, cancer, and fibrosis. Furthermore, the lab works to translate the technology and techniques developed to build microtissues into tissue engineered therapies for organ replacement and regenerative medicine.
Dr. Magness’ research is focused on the basic biology of intestinal stem cells, the genes that control their behavior, and translational approaches to stem cell based therapies for human disease and injury of the intestine. Furthermore his research focuses on elucidating genetic mechanisms underlying stemness and developing translational models to establish a finer understanding of stem cell-driven regeneration dynamics in homeostasis and injury. Using a combination of genetic mouse models and micro-frabricated bioengineered platforms, Dr. Magness’ team is exploiting the self-renewal capacity and multi-potency of ISCs to develop long-term ex vivo models of the intestine and colon with primary tissues. These biomimetic models offer new solutions for compound screening and cell-based therapies.
2011-2013 Post-doctoral Fellowship, Department of Orthopaedic Surgery, University of Pennsylvania
My current and future research in tissue engineering will focus on the following topics:
– Automated cell culture systems (for applying controlled interventions and monitoring the resulting function)
– Control of expression of adult muscle phenotype (adult myosin isoforms: fast twitch & slow twitch)
– Compliant tendons (for mechanical impedance matching and the reduction of stress concentrations)
– Motor unit level control of engineered skeletal muscle constructs (a collaboration with CNCT in EECS)
– Nerve-muscle interface (to provide nerve-derived trophic factors and to aid in expression of adult phenotype)
– Angiogenesis and perfusion (to allow large tissue cross sections).
The overall goal of Dr. Cole’s Orthopaedic Mechanobiology Lab is to determine mechanisms underlying the prevalent bone deficits and deformities with various clinical conditions, including stroke, nerve injury at birth, and pediatric scoliosis.
Ke Cheng’s laboratory studies regenerative medicine by using patient-derived stem cells, biomaterials, micro-RNAs and bioengineering approaches. Translational research is a major focus of the lab. Prior to the launch of Cheng Lab at North Carolina, Dr. Cheng directed the stem cell lab for multiple human trials, including the world’s first clinical trial using cardiac stem cells to treat heart attach. Currently, we are testing the following strategies to treat cardiovascular diseases: 1) purified and more potent stem cell products derived from the natural mixture of cardiac stem cells; 2) biomaterials derived from patient’s own tissues; 3) micro-RNAs involved in tissue regeneration; 4) nano theranostic agents that can augment endogenous repair; 5) novel mechanisms of cell extravasation, namely angiopellosis.
