We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Donna M. Geddes is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2004 — 2005 |
Geddes, Donna M |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Role of (Cl-)I Alterations On Gaba Function After Tbi @ University of Pennsylvania
DESCRIPTION (provided by applicant): Traumatic brain injury (TBI) is initiated by a physical deformation to the brain tissue and often results in dysfunction or death. Previously, researchers have devoted substantial attention to the initial disruption in [Ca2+]i homeostasis. However, recent data from ischemic and excitotoxic injury models suggest that alterations in [CI-]i may also profoundly impact neuronal function. Neuronal [CI-]i is regulated by cation-chloride transporters that either accumulate (NKCC1) or extrude (KCC2) chloride. Alterations in [CI-]i can cause reduced inhibition, due to excitatory function of the primary inhibitory neurotransmitter, GABA. I hypothesize that TBI causes an immediate influx of [CI-]i through altered membrane permeability, resulting in GABA excitation. The enhanced [CI-]i will result in reduced KCC2 and enhanced NKCC1 expression in the post-acute phase (12-24 hrs) of TBI, resulting in long-term loss of inhibition. I propose to evaluate this hypothesis using an in vitro model of TBI where neurons are cultured on a flexible silicone membrane and subjected a rapid pressure pulse. Understanding the mechanism of injury induced [CI-]I alterations will aid in the development of better treatments for post-traumatic seizures.
|
0.913 |