[Federal Register Volume 61, Number 214 (Monday, November 4, 1996)]
[Notices]
[Pages 56697-56698]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 96-28274]
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DEPARTMENT OF HEALTH AND HUMAN SERVICES
Government-Owned Inventions; Availability for Licensing
AGENCY: National Institutes of Health, Public Health Service, DHHS.
ACTION: Notice.
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SUMMARY: The inventions listed below are owned by an agency 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.
ADDRESSES: Licensing information and a copy of the U.S. patent
applications referenced below may be obtained by
[[Page 56698]]
contacting Stephen Finley, Ph.D., at the Office of Technology Transfer,
National Institutes of Health, 6011 Executive Boulevard, Suite 325,
Rockville, MD 20852-3804 (telephone 301/496-7735, ext. 215; fax 301/
402-0220). A signed Confidential Disclosure Agreement will be required
to receive a copy of the patent applications.
A Method for Imaging Nicotinic Acetylcholinergic Receptors in the Brain
Using Radiolabeled Pyridyl 7-Azabicycloheptanes
ED London, AS Kimes, A Horti, RF Dannals, M Kassiou (NIDA) Serial No.
08/642,636 filed 06 May 96
The current invention embodies the use of radiolabeled analogs of
epibatidine to noninvasively image and quantify levels of nicotinic
acetylcholine receptors in a living mammalian brain, using Positron
Emission Tomography or other nuclear medicine methods. As nicotinic
acetylcholine receptors have been implicated in various
neuropathological and physiological disorders, including Alzheimer's
disease, the invention may represent a powerful new method for the
noninvasive diagnosis of Alzheimer's disease and other disorders. In
addition, the method embodied in the invention may prove valuable for
use in monitoring the progression of various disorders and in
determining the efficacy of drug therapy protocols used in the
treatment of these disorders. (portfolio: Central Nervous System--
Diagnostics, in vivo)
Identification of an Allelic Ser857-Asn857 Variation of the
Human Delayed Rectifier Potassium Channel DRK1 (KCNB1 locus)
D Goldman, AW Bergen, CM Mazzanti, S Michelini (NIAAA) Serial No. 60/
020,348 filed 24 Jun 96
The DRK1 potassium channel is voltage sensitive such that as
phosphorylation of the protein is increased the current is reduced,
thereby increasing the cell's excitability. The amino- and carboxyl-
terminal regions of DRK1 are located in the cytoplasm. A new, but
naturally occurring substitution of the human delayed rectifier
potassium channel DRK1 (KCNB1 locus) was mapped to chromosome 20q13.2.
The nonconservative substitution occurs at position 857 in the carboxy
terminal region of the protein. Transmembrane sequences of the rat and
human DRK1 have been shown elsewhere to be identical, but have
different pharmacological and conductance differences. The substitution
of cytoplasmic serine to asparagine may effectively remove a possible
phosphorylation site which could result in increased excitability of
the cell or effect the function of the protein by altering the
conformation, thereby accounting for the pharmacological and
conductance changes. The DRK1 was mapped to the same locus as the
dominantly inherited EEG trait difference, a low voltage alpha trait
difference (20q13.3-13.3), but no correlation could be found between
the substitution and the low voltage alpha trait. (portfolios: Central
Nervous System--Therapeutics, psychotherapeutics; Central Nervous
System--Diagnostics; Central Nervous System--Research Materials).
Dated: October 28, 1996.
Barbara M. McGarey,
Deputy Director, Office of Technology Transfer.
[FR Doc. 96-28274 Filed 11-1-96; 8:45 am]
BILLING CODE 4140-01-M
