Institute for Medicine and Engineering

The mission of the Institute for Medicine and Engineering (IME) is to stimulate fundamental research at the interface between biomedicine and engineering/physical/computational sciences leading to innovative applications in biomedical research and clinical practice. The IME was created in 1996 by the Schools of Medicine (SOM) and Engineering and Applied Science (SEAS) to pursue opportunities for collaborative research. The IME has been successful in obtaining over $80 million in extramural grants, and funded programs. These include a research center in Cell Studies of Pulmonary Artery Hypertension, and a Penn Center for Molecular Discovery.

Membership: The Institute houses 11 core faculty, 6 from the School of Medicine and 5 from SEAS, who were recruited to form the basis for the IME; however, the Institute extends beyond the core group to include 106 members from various schools including School of Medicine, SEAS and Arts and Sciences faculty. The Institute interacts with 24 other Centers or departments.

Multi-disciplinary Research: The IME mission to foster research at the interface of medicine and engineering is met (i) through 8 central investigators who span these disciplines in both schools, (ii) through the core facilities, pilot grant programs, research training, and educational events involving its very wide membership (of 106). The research conducted by central investigators is quite broad, ranging from cell and molecular biology to tissue engineering, biophysics and nanobiology/medicine. Having established a strong basic research foundation the Institute is now expanding translational programs in medicine and engineering.

Strategic Importance: The IME relates directly to 3 major themes of the SOM Research Strategic Plan: Cancer, Neurosciences and Cardiovascular Biology. The University Strategic Plan identifies the link between engineering and medicine as one of the key drivers of success and recommends "fostering advances in engineering, computing, chemistry, mathematics and behavioral sciences that can be applied to life sciences." Because of the multi-disciplinary nature of the Institute, it is well positioned to take advantage of the new NIH roadmap. Because of its unique interface with SEAS, the IME is a strong force in faculty retention by providing unique directions and connections for research among faculty.

 

 

 

 

School of Engineering and Applied Science

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  • Publication
    Contrast Adaptation in Subthreshold and Spiking Responses of Mammalian Y-Type Retinal Ganglion Cells
    (2005-01-26) Zaghloul, Kareem A; Boahen, Kwabena A; Zaghloul, Kareem A; Boahen, Kwabena A; Demb, Jonathan B
    Retinal ganglion cells adapt their responses to the amplitude of fluctuations around the mean light level, or the "contrast." But, in mammalian retina, it is not known whether adaptation arises exclusively at the level of synaptic inputs or whether there is also adaptation in the process of ganglion cell spike generation. Here, we made intracellular recordings from guinea pig Y-type ganglion cells and quantified changes in contrast sensitivity (gain) using a linear-nonlinear analysis. This analysis allowed us to measure adaptation in the presence of nonlinearities, such as the spike threshold, and to compare adaptation in subthreshold and spiking responses. At high contrast (0.30), relative to low contrast (0.10), gain reduced to 0.82 ± 0.016 (mean ± SEM) for the subthreshold response and to 0.61 ± 0.011 for the spiking response. Thus, there was an apparent reduction in gain between the subthreshold and spiking response of 0.74 ± 0.013. Control experiments suggested that the above effects could not be explained by an artifact of the intracellular recording conditions: extracellular recordings showed a gain change of 0.58 ± 0.022. For intracellular recordings, negative current reduced the spike output but did not affect the gain change in the subthreshold response: 0.80 ± 0.051. Thus, adaptation in the subthreshold response did not require spike-dependent conductances. We conclude that the contrast-dependent gain change in the spiking response can be explained by both a synaptic mechanism, as reflected by responses in the subthreshold potential, and an intrinsic mechanism in the ganglion cell related to spike generation.