[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