Awardee OrganizationUNIV OF MASSACHUSETTS MED SCH WORCESTER
Description
Abstract Text
Past and proposed work in this laboratory have included the
following major areas of clinical and basic research:
metabolism, protein binding and peripheral effects of the thyroid
hormones (TH); regulation of TSH secretion; effects of iodine on
thyroid function in man and rodents; and immunological aspects of
thyroid pathophysiology. A synthetic flavonoid, EMD 21388 (F),
which inhibits the serum protein binding (TBPA) of the TH and 5'-
deiodinase activity (5'-D) in vitro will be utilized to study, in
the rat, the in vivo effects of rapid displacement of the TH from
their major serum binding protein (TBPA) in peripheral tissues,
the possible thyromimetic effects of F in vivo and in vitro
(using GH producing tumor cell lines), and the possible in vivo
and in vitro inhibitory effects of F on 5'-D. Starvation and
other experimental conditions in the rat are associated with the
appearance of serum TBG (rTBG), and preliminary studies suggest
an enhanced response in females compared to males. This will be
further investigated to determine the possible etiology of this
finding. The prevalence of Familial Dysalbuminemic
Hyperthyroximenia (FDH), which appears to be relatively common,
especially in Puerto Rican families, will be determined by
studying families of newborns whose serum T4 concentration is at
least 2SD above the mean. The role of iodine intake on the
prevalence of thyroid dysfunction in the elderly and in the
pathogenesis of autoimmune thyroid diseases in man and in the
diabetes prone BB/Wor rat will continue to be addressed. New
immunosuppressant drugs (thalidomide and ciamexone) will be used
in an attempt to prevent the occurrence of spontaneous and iodine
induced lymphocytic thyroiditis (LT) in the BB/Wor rat. This
model will also be used to determine whether, as in humans,
transient LT is common during the post partum period. Finally,
preliminary retrospective studies suggest that chronic
levothyroxine therapy for hypothyroidism and for TSH suppression
in premenopausal women enhances bone loss. A prospective study
is now planned to confirm these observations. The overall aims
of this proposal is to provide further information on the binding
and peripheral metabolism and effects of the TH and to further
delineate the role of iodine and class II (Ia) antigen in the
etiology of autoimmune thyroid disease in man and rat.
National Institute of Diabetes and Digestive and Kidney Diseases
CFDA Code
DUNS Number
603847393
UEI
MQE2JHHJW9Q8
Project Start Date
01-December-1978
Project End Date
30-November-1993
Budget Start Date
01-December-1988
Budget End Date
30-November-1989
Project Funding Information for 1989
Total Funding
$269,739
Direct Costs
$166,505
Indirect Costs
$103,234
Year
Funding IC
FY Total Cost by IC
1989
National Institute of Diabetes and Digestive and Kidney Diseases
$269,739
Year
Funding IC
FY Total Cost by IC
Sub Projects
No Sub Projects information available for 2R01DK018919-15
Publications
Publications are associated with projects, but cannot be identified with any particular year of the project or fiscal year of funding. This is due to the continuous and cumulative nature of knowledge generation across the life of a project and the sometimes long and variable publishing timeline. Similarly, for multi-component projects, publications are associated with the parent core project and not with individual sub-projects.
No Publications available for 2R01DK018919-15
Patents
No Patents information available for 2R01DK018919-15
Outcomes
The Project Outcomes shown here are displayed verbatim as submitted by the Principal Investigator (PI) for this award. Any opinions, findings, and conclusions or recommendations expressed are those of the PI and do not necessarily reflect the views of the National Institutes of Health. NIH has not endorsed the content below.
No Outcomes available for 2R01DK018919-15
Clinical Studies
No Clinical Studies information available for 2R01DK018919-15
News and More
Related News Releases
No news release information available for 2R01DK018919-15
History
No Historical information available for 2R01DK018919-15
Similar Projects
No Similar Projects information available for 2R01DK018919-15