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, Phillip C. Jobe is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1985 |
Jobe, Phillip Carl |
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. |
Neurotransmitter Abnormalitites in Epilipsy @ College of Medicine At Peoria
A number of animal models of human epilepsy have been developed and are used in attempts to determine the neurophysiological and neurochemical basis of the human disease. We believe that our model, the genetically derived epilepsy-prone rat, can serve as an excellent model for study of the neurochemical basis of epilepsy (see Appendix A for relevant reviews). These animals represent a unique and valuable resource. They are not commercially available and there are only three existing colonies. One is our own and it is maintained in Shreveport, LA in our facilities. The second is housed at the University of Arizona, while the third is housed at the University of Moscow. The present proposal is designed to provide a detailed neurochemical evaluation of monoaminergic neuronal tracts in the central nervous system of this model. The evaluation will be carried out in an attempt to correlate sound-induced seizure susceptibility and intensity with neurochemical abnormalities. Epilepsy-prone animals and control animals will be obtained from the Principal Investigator's colonies. In initial studies, six areas of the central nervous system will be evaluated. These are: the spinal cord, pons-medulla, cerebellum, midbrain, hypothalamus-thalamus and telencephalon. Any differences found in these large areas will be traced to more specific structures by further dissection. In these structures, we intend to estimate the functional integrity of noradrenergic, serotonergic and dopaminergic nerve tracts by measuring: (1) neurotransmitter turnover; (2) activities of enzymes involved in synthesis of the amines; and (3) tissue levels of neurotransmitter metabolites.
|
0.969 |
1989 — 1991 |
Jobe, Phillip Carl |
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. |
Noradrenergic Seizure Regulation @ University of Illinois At Chicago
The proposed research project is component of a broadly based effort to elucidate abnormalities responsible for the epilepsies. More specifically, the project is designed to determine the role of central nervous system noradrenergic transmission in the regulation of seizure predisposition in the genetically epilepsy-prone rat (GEPR). These animals have been chosen for this investigation partially because extensive data derived from their use provide an intriguing neurochemical foundation for our proposed studies. Also, the existing body of data suggests a high probability for a positive experimental outcome. Another major consideration persuaded us to select GEPRs as experimental outcome. Another major consideration persuaded us to select GEPRs as experimental subjects. These animals are attractive as a model of human epilepsy. The accumulating body of neurochemical evidence strongly supports the concept that brain noradrenergic deficits in the GEPR are partially responsible for the marked degree of seizure predisposition characteristic of these animals. Importantly, we now have data which provides clues for anatomically localizing the etiologically important noradrenergic terminal fields within the brain. The current project is designed to capitalize on this information. Discrete intracerebral neurotoxic lesions or pharmacologic treatments will be used to produce specific noradrenergic deficits or increments in terminal fields which are candidates for regulation of seizure predisposition in the GEPR. Once a noradrenergic alteration has been made, we will determine whether it causes changes in selected indices of seizure predisposition. The approaches to be utilized will enable us to identify the noradrenergic terminal fields which are responsible for epileptogenesis.
|
0.97 |