A major obstacle to the wide application of implantable glucose sensors is that the progressively lose function after a relatively short period of time in vivo. This is a result of tissue responses such as inflammation and fibrosis with resulting loss of vasculature as well as degradation of the sensor. Although our current Nafion-based glucose sensor displayed excellent stability in vitro, it rapidly calcified and degraded in vivo. The investigator hypothesizes that in vivo sensor performance can be enhanced by developing new membranes and by controlling the tissue interface by suppressing inflammation and fibrosis as well as increasing neovascularization.
Aim 1 will develop new membranes to replace Nafion, and also to develop novel surface hydrogels with tissue response modifiers (TRM's) to control fibrosis, inflammation, and neovascularization.
Aim 2 will develop biodegradable TRM delivery systems to control inflammation, fibrosis and neovascularization.
Aim 3 will evaluate in vitro and in vivo (rats), the developed sensors and components to determine performance, including life span.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Research Project (R01)
Project #
1R01RR014171-01
Application #
2870410
Study Section
Special Emphasis Panel (ZRG7-SSS-8 (45))
Project Start
1998-09-30
Project End
2001-09-29
Budget Start
1998-09-30
Budget End
1999-09-29
Support Year
1
Fiscal Year
1998
Total Cost
Indirect Cost
Name
University of Connecticut
Department
Type
Schools of Medicine
DUNS #
City
Farmington
State
CT
Country
United States
Zip Code
06030
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