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, Jack Rosenbluth is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1985 — 1992 |
Rosenbluth, Jack |
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. |
Comparative Cytology of Nerve and Muscle Tissues
The proposed project is a continuation of studies of normal and abnormal myelinated nerve fibers in the peripheral and central nervous systems. The primary emphasis will be on two specialized regions, the node of Ranvier and the paranodal region, at both of which the axon forms specialized junctions with glial cells. The axoglial interrelationships at these sites will be examined by means of freeze-etching methods to clarify details of the membrane surfaces and of the structural connections between them and with cytoplasmic elements. The purpose of this analysis is to clarify: 1. the role the respective axoglial junctions in axolemmal differentiation, particularly with respect to the mechanism by which sodium channels accumulate and are retained in the nodal axolemma, and 2. the structural basis for attachment of the myelin sheath to the axon in the paranodal region. In addition, models of both peripheral and central axonopathy will be studied in order to determine the nature and sequence of changes in nodal and paranodal regions of the axolemma and in the axoglial interactions resulting from primary axon damage in comparison with the changes resulting from primary pathology of the myelin-forming cells. The emphasis here will be on changes that may affect the distribution of sodium channels, which may in turn underlie the pathophysiology of the respective types of neuropathy. Finally the development of axoglial junctions will be studied in a myelin-deficient mutant in order to assess the role of aberrant junctions in the development of the structural and functional abnormalities in these animals. The long term goal of all of these studies is to clarify the structural basis for pathophysiology in a variety of congenital and acquired diseases affecting myelinated nerve fibers.
|
1 |
1998 — 2000 |
Rosenbluth, Jack |
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. |
Abnormalities in Cns Myelinated Fibers @ New York University School of Medicine
DESCRIPTION (Applicant's Abstract): The proposed project consists of an analysis of lesions induced by implantation of antiglycolipid IgM antibody-secreting hybridoma cells into adult rat spinal cord dorsal columns. This procedure results in development of a focal demyelination with sparing of axons, similar to the plaques of demyelination seen in MS. The model will be used to examine the role of surviving oligodendrocyte precursors within the lesion and the role of glial cell migration from remote sources in bringing about remyelination. The principal investigator will examine the immunopathology of the lesions in correlation with electrophysiological findings and with changes in axolemmal sodium channel distribution as the lesion evolves in order to assess the functional consequences of "subtle" structural damage in myelinated nerve fibers. Implantation of the same hybridomas into neonatal animals produces characteristic dysmyelination resulting from intercalation of IgM between myelin lamellae as they develop, resulting in wide-spaced myelin with a period 2X or 3X normal. Sheaths of this kind occur in MS and in paraproteinemias. The principal investigator will follow changes in these "expanded" sheaths with time in order to obtain additional information about the stability of this abnormal form of myelin, about regulation of myelin sheath thickness and about the site of growth of CNS myelin sheaths.
|
1 |
2003 — 2013 |
Rosenbluth, Jack |
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. |
Pathology of Dysmyelination and Demyelination @ New York University School of Medicine
[unreadable] DESCRIPTION (provided by applicant): The myelin sheath/axon complex in the vicinity of the node of Ranvier of myelinated fibers is a precisely organized structural unit believed to have evolved to optimize rapid and efficient nerve conduction. The principal components are a very large and uniquely structured axoglial junction, which separates nodal sodium channels from internodal potassium channels. Minor damage to this intricate nodal/paranodal complex could significantly affect nerve conduction and cause functional losses, even with changes subtle enough to escape detection by routine methods. In view of the potential functional significance of "subtle" pathological changes in this complex, we wish to define them more fully in experimental models in which the pathogenetic elements can be controlled and in which we can analyze the pathology using not only classical light microscopic and ultrastructural techniques but also ultrastructural immunocytochemistry in conjunction with freeze-fracture methodology. We will make use of mutations affecting myelinated nerve fibers to assess the effects of specific deficiencies on the integrity of the axoglial junction, on the density and distribution of the nodal and internodal ion channel aggregates, on nerve conduction and on axon damage. We will also use the in vivo model of focal antibody-mediated dysmyelination and demyelination, which we have been working with, to determine whether equivalent abnormalities can be identified in this model of multiple sclerosis. [unreadable] [unreadable]
|
1 |