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High-probability grants
According to our matching algorithm, Robert Fern is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 1997 — 2001 |
Fern, Robert E |
R29Activity Code Description:
Undocumented code - click on the grant title for more information. |
Ischemic Injury of Neonatal Cns White Matter Glia @ University of Washington
DESCRIPTION: (Adapted from Applicant's Abstract): The proposed research will examine mechanisms of CNS white matter injury following anoxia- ischemia, which is of causal relevance to periventricular leukomalacia (PL), the most common neurological lesion associated with cerebral palsy. Whole white matter structures from perinatal rats will be subjected to anoxic-aglycemic insults in vitro under conditions that allow fluorescent imaging of intracellular free Ca and membrane integrity. Stated Aims are: to develop an appropriate model; to develop techniques for in situ measurements of Ca and membrane integrity; to use these methods to determine the responses to anoxic-aglycemic insults; to assess the importance of Ca influx versus release from intracellular stores; to assess the relative importance of voltage-gated Ca channels, ligand-gated Ca channels and Na/Ca exchange in mediating the observed changes; to assess the role of extracellular K and glutamate in these processes; and to apply the results of these experiments to the functional loss experienced by CNS white matter during anoxia-ischemia.
|
0.919 |
| 2002 — 2006 |
Fern, Robert E |
R01Activity Code Description:
To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Ischemic Injury of Cns White Matter Glia @ University of Leicester
DESCRIPTION (Adapted from applicant's abstract): Immature white matter is subject to ischemic injury during the development of the lesion called periventricular leukomalacia, which is the major pathology, associated with cerebral palsy. The goal of this research is to understand the mechanisms that underlie acute ischemic cell death in immature white matter glial cells. Fluorescent ion-sensitive dyes will be loaded into glial cells in the neonatal rat optic nerve and used to measure changes in intracellular [Ca2+], [Na+] and pH during ischemia in situ. These ionic changes will be correlated to the occurrence of cell death and any casual relationships will be determined. Ionic substitution and drug application will be used to probe mechanisms that underlie ionic derangements that occur in neonatal white matter glia during ischemia. Glial cell types within neonatal white matter are likely to show acute changes in intracellular ions during ischemia due to quite different mechanisms. Live staining of glia in situ will be applied to distinguish astrocytes from oligodendrocytes, allowing both the characteristics of cell death and ionic distribution during ischemia to be analyzed in the two major types of marcoglia present in the CNS. Experiments will test three hypotheses: 1) Acute ischemic astrocyte death at the point in development most at risk (P10nRON), results from Na+ -influx and cell swelling. 2) Na+ -influx/cell swelling also accounts for a significant proportion of acute death of oligodendrocytes and of less mature astrocytes. 3) Non-NMDA glutamate receptors mediate only a proportion of toxic Ca2+ -influx into oligodendroglial during ischemia.
|
0.919 |