[Federal Register: February 1, 1999 (Volume 64, Number 20)] [Notices] [Page 4885-4886] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr01fe99-87] ----------------------------------------------------------------------- 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 [[Page 4886]] federally-funded research and development. Foreign patent applications are filed on 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. Broad Spectrum Chemokine Antagonist and Uses Thereof B Moss, I Damon-Armstrong (NIAID) DHHS Reference No. E-065-98/1 filed 08 Jan 99 (based on Provisional U.S. Patent Application No. 60/070,945 filed 10 Jan 98) Licensing Contact: Leopold Luberecki, Jr.; 301/496-7735 ext. 223; e- mail: 1187a@nih.gov Chemokines are the small proteins involved in recruitment of leukocytes (white blood cells) to areas of tissue injury or infection, so they are also in part responsible for inflammation. There are two major classes of chemokines: CXC () and CC (). Chemokines elicit leukocyte movement by binding to a receptor on the cell surface. Typically, CXC chemokines direct the movement of neutrophils and CC chemokines direct the movement of other types of leukocytes. Previously, the open reading frame of the recently sequenced molluscum contagiosum viral genome was predicted to encode a protein that would function as a CC chemokine antagonist by mimicking the chemokine and thus diverting it from its receptor. The inventors have cloned, expressed, purified, and demonstrated the broad-spectrum ability of this viral protein to inhibit chemotaxis of multiple different leukocyte classes to different chemokines in both the CXC and CC classes. Thus, the protein has potential use as an anti-inflammatory agent and as an antiviral agent to treat HIV. Cell Expansion System for Use in Neural Transplantation L Studer, V Tabar, J Yan, R McKay (NINDS) Serial No. 60/093,991 filed 24 Jul 98 Licensing Contact: Leopold Luberecki, Jr.; 301/496-7735 ext. 223; e- mail: 1187a@nih.gov Cell transplantation therapy typically involves transplanting primary cells or immortalized cells into patients. The promising but still inconsistent data stemming from those clinical trials using primary cells in Parkinson's disease are believed to be due to an insufficient number, function and uniformity of the transplanted cells. In an effort to overcome these problems an improved method for isolating, growing and differentiating precursor cells into dopaminergic neurons has been developed. The process described provides for an expansion of the cell number of primary cells by up to 1000 fold. This technique could assist in solving the problem of obtaining sufficient cells for a reliable, effective cell transplantation therapy. The process consists essentially in the isolation and in vitro numerical expansion of an early mesencephalic precursor population, the use of serum, cAMP, dopamine and ascorbic acid during differentiation and the development of an aggregation technique during cell differentiation that allows convenient grafting of dopaminergic neurons. Real-Time Interactive Functional Magnetic Resonance Imaging JA Frank, J Ostuni, JH Duyn (CC) Serial No. 09/090,166 filed 04 Jun 98 Licensing Contact: John Fahner-Vihtelic; 301/496-7735 ext. 270; e-mail: jf35z@nih.gov The present disclosure describes a device and methods for capturing whole brain raw data image files as they are being produced from a magnetic resonance (MR) system. The invention performs reconstruction of the data, registration, statistical analysis, and then displays the results within seconds after completion of the MR image acquisition. This invention provides the ability to have a quick look at the image maps produced of brain activity or brain perfusion. It gives the clinician or researcher performing the diagnosis or study, the flexibility to modify the procedure ``on the fly'' to produce a more meaningful image or data set. Method of Reducing Perivascular Lesions Using Insulin-Like Growth Factor I HD Webster, S Komoly, D Yao, X Liu, LD Hudson (NINDS) Serial No. 08/705,820 filed 30 Aug 96 (based on Provisional U.S. Patent Application No. 60/003,055 filed 31 Aug 95) Licensing Contact: Leopold Luberecki, Jr.; 301/496-7735 ext. 223; e- mail: 1187a@nih.gov A perivascular lesion is a site near or surrounding a lesion in the blood vessel system that is accompanied by an accumulation of inflammatory leukocytes and/or damage to perivascular tissue. Although it is unclear how a perivascular lesion originates, the sequence of events leading to such lesions induce increased vascular endothelial permeability and induce toxic effects on the nervous system, which may lead to myelin injury. Myelin is a protein-lipid composite that insulates axons, which are the cellular processes by which electrical impulses travel through the nervous system. When myelin sheaths sustain injury, entire segments of myelin degenerate, thus affecting the ability of impulses to travel. Typically, perivascular lesions occur after or during: brain or spinal cord trauma, ischemic injury or insult; certain inflammatory diseases affecting the musculo-skeletal system, central nervous system, and peripheral nervous system; and certain autoimmune disorders. The application claims a method to reduce perivascular lesions by administering an effective amount of insulin- like growth factor I to treat diseases or disorders associated with demyelination, such as multiple sclerosis, experimental autoimmune encephalomyelitis, neuromyelitis optica, optic neuritis, acute encephalomyelitis, cervical myelopathy, and spinal cord injury. Dated: January 25, 1999. Jack Spiegel, Director, Division of Technology Development and Transfer, Office of Technology Transfer. [FR Doc. 99-2246 Filed 1-29-99; 8:45 am] BILLING CODE 4140-01-M