[Federal Register Volume 62, Number 36 (Monday, February 24, 1997)]
[Notices]
[Pages 8252-8254]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 97-4369]
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DEPARTMENT OF HEALTH AND HUMAN SERVICES
National Institutes of Health
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, DHHS.
ACTION: Notice.
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The inventions listed below are owned by agencies of the U.S.
Government and are available for licensing in the U.S. in accordance
with 35 U.S.C. 207 to achieve expeditious commercialization of results
of federally-funded research and development. Foreign patent
applications are filed on selected inventions to extend market coverage
for U.S. companies and may also be available for licensing.
ADDRESS: Licensing information and copies of the U.S. patent
applications listed below may be obtained by writing to the indicated
licensing contact at the Office of Technology Transfer, National
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville,
Maryland 20852-3804 (telephone 301/496-7057; fax 301/402-0220). A
signed Confidential Disclosure Agreement (CDA) will be required to
receive copies of the patent applications.
Chromosomal Markers and Diagnostic Tests For Manic-Depressive
Illness
S Detera-Wadleigh (NIMH), E Gershon (NIMH), J Badner (NIMH), L Goldin
(NIMH), W Berrettini (Thomas Jefferson University), T Yoshikawa (NIMH),
A Sanders (NIMH), L Esterling (NIMH)
Serial No. 60/029,278 filed 28 Oct 96
Licensing Contact: Stephen Finley, 301/496-7735, ext. 215.
Bipolar disease, or manic-depressive illness, affects approximately
1% of the population and is generally controlled through medication.
Not all patients respond similarly to a given medication. A medication
that works well in one individual may be ineffective in another
individual. It is unclear why this is, but it has been theorized that
bipolar disease may involve multi-genes, possible on several
chromosomes. It is not known if one genetic locus dominates over
another, but if one does, then it may explain the variable
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medication effectiveness. One genetic locus has been identified on
chromosome 18 having allelic variations which may be used to determine
if an individual has an increased susceptibility to bipolar disease.
This method may be useful in determining if an individual has an
increased susceptibility to bipolar disease, or ultimately, it may
provide a means to predict which medication will provide the best
treatment. (portfolio: Central Nervous System--Diagnostics, in vitro)
The Use of Functional N-Methyl-D-Aspartate Antagonists to
Ameliorate or Prevent Aminoglycoside-induced Ototoxicity
A Basile and P Skolnick (NIDDK)
Serial No. 08/712,477 filed 11 Sep 96
Licensing Contact:: Stephen Finley, 301/496-7735, ext. 215.
Aminoglycoside (AGS) antibiotics are extremely effective at
treating bacterial infections such as sepsis, endocarditis, and
tuberculosis, but are currently used in only 3% of all clinical
admissions in the United States because of their tendency to induce
ototoxicity. Approximately 30-40% of all patients who receive an AGS
antibiotic will develop measurable and usually permanent hearing loss.
A guinea pig model was used to test whether N-Methyl-D-Aspartate (NMDA)
antagonists could prevent or reduce the severity of the hearing loss
when AGS antibiotics were administered. For example, the NMDA
antagonists, dizocilpine and ifenprodil, were tested with the AGS
antibiotics, neomycin and kanamycin, and were found to prevent or
lessen the hearing loss in over 98% of the animals tested. Over 75% of
the tested animals maintained normal hearing levels. It is believed
that the use of this method will allow physicians to readily administer
aminoglycoside antibiotics without the fear of causing permanent
hearing loss in the patient. (portfolio: Internal Medicine--
Therapeutics, other)
A Basal Cell Carcinoma Tumor Suppressor Gene
M Dean et al. (NCI)
Serial No. 60/017,906 filed 17 May 96
Licensing Contact: Ken Hemby, 301/496-7735 ext. 265.
Novel human nucleic acid sequences and polypeptides derived from
the tumor suppressor, PTC or patched gene which have been mapped to
human chromosome 9q22.3-q31, have been discovered for use in cancer
diagnosis and therapy. Mutations of this gene are associated with
Nevoid Basal Cell Carcinoma Syndrome (NBCCS) a disease associated with
skin cancer and human developmental defects such as Gorlin Syndrome
comprising skeletal defects, craniofacial and brain abnormalities.
Methods of detection of PTC in a tissue sample have been found as well
as recombinant cells, antibodies, and pharmacological compositions
useful in treatment of the disease. Methods of diagnosis of and therapy
for NBCCS have also been found.
The PTC gene is thought to encode a protein which selectively
switches off growth factor production in certain cells by interaction
with members of the family of proteins encoded by the ``hedgehog''
gene, which instructs cells during development and growth. NBCCS is the
result of abnormal PTC gene products that encode non-functional or
functionally reduced NBCCS polypeptides. This lack of function may be
caused by insertions, deletions, point mutations, splicing errors,
premature termination codons, missing initiators, etc. The tumors
caused by NBCCS are slow growing tumors that rarely metastasize, but
which can cause significant morbidity and occasional mortality from
local invasion. (portfolios: Cancer--Diagnostics; Cancer--Therapeutics;
Cancer--Research Materials)
Process for Detecting Alzheimer's Disease Using Cultured Cells
KK Sanford-Miffin, R Parshad, JH Robbins (NCI)
Serial No. 08/611,330 filed 08 Mar 96 (CIP of 08/225,825, CIP of 07/
957,315)
Licensing Contact: Leopold J. Luberecki, Jr., 301/496-7735 ext.
223.
A novel process has been developed for distinguishing between
clinically normal individuals and those who have Alzheimer's disease
(AD), a form of senile dementia that affects millions of Americans.
This invention should aid considerably in the diagnosis of sporadic AD
before signs and symptoms become fully apparent and will make it
possible in familiar AD to determine the presence or absence of AD
gene(s) years before the patient becomes symptomatic. Previous studies
of AD revealed that cells cultured from patients with familial or
sporadic AD were hypersensitive to the lethal effects of ionizing
radiation; however, none of these assays provided large enough
differences between normal and AD cells to be useful in reliably
distinguishing an AD patient from normal. The present invention
provides an improved assay that demonstrates very large differences
between AD cells and normal cells because it is based on the cytogenic
response of an individual's cultured cells to fluorescent light in the
presence and absence of a DNA repair inhibitor during the post-exposure
period. This greater difference makes it possible to distinguish a
single AD cell line (i.e., a cell line from one AD patient) from lines
from most, if not all, normal people. The test is conducted on either
skin fibroblasts or peripheral blood lymphocytes. (portfolio: Central
Nervous System--Diagnostics, in vitro, other)
Methods and Compositions for Monitoring DNA Binding Molecules in
Living Cells
H Htun and G Hager (NCI)
OTT Reference No. E-021-96/0 filed 08 Dec 95 and OTT Reference No. E-
021-96/1 (CIP); foreign rights are available
Licensing Contact: Stephen Finley, 301/496-7735, ext. 215.
This technology is directed to methods of detecting the binding of
fluorescently labeled compounds to DNA by a direct, real time, visual
detection and to the characterization/screening of ligands to ligand-
dependent DNA-binding proteins. Using cell lines harboring multiple
copies of a defined transcriptional regulatory unit, visualization
system and assay have been developed to determine the effect of ligand
in promoting binding of ligand-dependent DNA binding proteins to
nuclear targets, including to a define transcriptional regulatory DNA
sequence. Quantitative and qualitative analyses show that when this
technology is applied to study the effect of ligand, such as antagonist
RU486 and agonist dexamethasone, on the glucocorticoid receptor,
agonist ligand induces a nuclear accumulation of the receptor in a
dose-dependent manner that is strickingly different from an antagonist
ligand. Furthermore, by taking advantage of a unique cell line
designated 3134, which contains 200 copies of a promotor region each
containing 4 copies of a specific DNA-binding sequence for the receptor
in a tandem array thereby producing 1600 copies of the DNA binding
region, the agonist-induced binding of the receptor to this array can
be observed in living cells. This cell line and the related methods may
prove to be an important aid in monitoring steriod administration to
patients through the direct measurement of steroid activity from a
blood sample. This method is also applicable for high throughput visual
(quantitative and qualitative) screening of ligands to orphan receptors
either agonist or antagonist, determining the effective dosage levels
of agonist/antagonists on a real time basis, and to identify modifying
chemical or biological agents that alter DNA-binding specificity in
living cells. (portfolios:
[[Page 8254]]
Internal Medicine--Diagnostics, anti-inflammatory; Internal Medicine--
Diagnostics, imaging agents; Internal Medicine--Therapeutics)
Dated: February 12, 1997.
Barbara M. McGarey,
Deputy Director, Office of Technology Transfer.
[FR Doc. 97-4369 Filed 2-21-97; 8:45am]
BILLING CODE 4140-01-M
