Outer Continental Shelf; oil, gas, and sulphur operations: Documents incorporated by reference; update,

[Federal Register: October 25, 2000 (Volume 65, Number 207)]

[Notices]

[Page 63874-63875]

From the Federal Register Online via GPO Access [wais.access.gpo.gov]

[DOCID:fr25oc00-96]

DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health

Government-Owned Inventions; Availability for Licensing

AGENCY: National Institutes of Health, Public Health Service, DHHS.

ACTION: Notice.

SUMMARY: 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 filedon selected inventions to extend market coverage for companies and may also be available for licensing.

ADDRESSES: 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 will be required to receive copies of the patent applications.

A Cultured Cell Line which Expresses the GLU4 Glucose Transporter Isoform Labeled with a Short Hemaglutinin Peptide and a Modified Green Fluorescence Protein

Samuel W. Cushman (NIDDK), DHHS Reference No. E-264-00/0 filed26Jul 2000; Licensing Contact: Marlene Shinn; 301/496-7056 ext. 285; email: shinnm@od.nih.gov.

The aforementioned invention is currently available through a Biological Materials License as a research tool. Insulin regulates glucose uptake by inducing the translocation of GLUT4, a glucose transporter isoform expressed in fat and muscle, from intracellular components to the plasma membrane. The NIH announces the discovery of a cell line that expresses the GLUT4 glucose transporter isoform with a short hemaglutin peptide (HA) and a modified green fluorescent protein (GFP). The HA peptide is recognized by a specific antibody when GLUT4 is in the plasma membrane but not when GLUT4 is sequestered inside the cell. The modified GFP can be detected by its fluorescence whether it is inside the cell or on the cell surface. This allows the HA label to quantitate the GLUT4 subcellular distribution and the GFP label, the total GLUT4 expression. Therefore, this invention can be used in high through-put screening, as an assay reagent, and it may aid specifically in ascertaining compounds that have the insulin-like effect of stimulating GLU4 translocation from an intracellular compartment to the cell surface.

Dmt-tic Di- and Tri-Peptidic Derivatives and Related Compositions and Methods of Use

Lawrence H. Lazarus (NIEHS), DHHS Reference No. E-103-00/0 filed24 Mar 2000; Licensing Contact: Marlene Shinn; 301/496-7056 ext. 285; e-mail: shinnm@od.nih.gov.

A major obstacle in the treatment of many cancers involves the clinical manifestation of drug resistance. Currently, toxic substances are used in clinical and therapeutic settings to inhibit glycoproteins in the cell membrane of some cancer cells that have the ability to pump out of the cell drugs that would be potentially lethal. The most common of these glycoproteins is the 170-kd ATP-dependent transmembrane efflux pump. The multidrug resistance (MDR1) phenotype, however, is not the sole source of drug resistance since MDR1 is a member of a superfamily of proteins structurally related to the transmembrane P-glycoproteins.

NIH scientists have prepared a series of -opiod analogs of Dmt-tic (2',6'-dimethyl-L-tyrosine-1,2,3,4-tetrahydroisoquinoline-3- carboxylic acid). At least one of the analogs, which is biologically stable and exerts no known side effects, has been observed to inhibit the ability of MDR1 to pump out a fluorescent probe from the cell membrane. Thus, these analogs might represent novel chemosensitizing agents to treat both hematologic malignancies (lymphomas) and solid tumors (e.g. breast and colon) without toxic effects in patients.

In addition, this invention provides more potent -opioid antagonists and -opiod antagonists with duel binding

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affinity and biological activity toward -opiod and - opiod receptors. These compounds therefore, have the potential to treat opiate and alcohol abuse, neurological diseases, neuropeptide or neurotransmitter imbalances, neurological and immune dysfunction, graft rejections through immunosuppression with antagonists, pain control through short half-life agonists, and shock and brain injuries.

Scratch Wound Assay Device

Katherine Malinda et al. (NINR), Serial No. 09/496,134 filed01 Feb 2000; Licensing Contact: Dale Berkley; 301/496-7735 ext. 223; e-mail: berkleyd@od.nih.gov.

Tissue wounds undergo a complex and ordered series of events to repair tissue. These events may include infiltration of inflammatory immune cells as part of the process to remove and destroy necrotic tissue, increased vascularization by angiogenic factors, and increased cell proliferation and extracellular matrix deposition. Although the basic process of tissue repair has been characterized, the individual steps and factors necessary to carry out this complex series of events are not yet well understood or fully identified. Accordingly, there is a need to develop a way of reproducibly injuring a layer of cells to study the effects of different compounds of treatments on the ability of the remaining cells to repair the damaged area.

The present invention provides a device that reproducibly makes a wound of a desired size in a cell layer grown on a cell culture material. The device allows researchers to use small volumes of cells and test materials suggesting its use as a tool in high throughput screening of compounds. This provides researchers with a faster, more accurate way of screening large numbers of factors and determining the effects of cell growth and migration agents in model wounds produced in the cell, organ, or tissue layer.

Method of in vitro T cell Differentiation of CD34+ Progenitor Cells

Ruiz et al. (NIAID), DHHS Reference No. E-206-98/0 filed29 Oct 1999; Licensing Contact: J. P. Kim; 301/496-7056 ext. 264; e-mail: kimj@od.nih.gov.

The present invention relates to a human in vitro system for inducing the growth and de novo differentiation of T cells from CD34+ progenitor cells in the presence of various cytokine cocktails and lymph node stroma. The mature T cells which are generated may be used to treat individuals with primary or acquired T cell immunodeficiencies, including HIV infection.

Dated: October 13, 2000. Jack Spiegel, Director, Division of Technology, Development and Transfer, Office of Technology Transfer, National Institutes of Health.

[FR Doc. 00-27356 Filed10-24-00; 8:45 am]

BILLING CODE 4140-01-P