National Institutes of Health, Public Health Service, DHHS.
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 companies and may also be available for licensing.
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.
Methods and Compositions for Analysis of M3 Muscarinic Acetylcholine Receptors
Jurgen Wess, Masahisa Yamada (NIDDK), DHHS Reference No. E-291-00/0 filed 30 Oct 2000, Licensing Contact: John Rambosek; 301/496-7056 ext. 270; e-mail: email@example.com
This invention discloses transgenic mice that have the M3 Muscarinic Acetylcholine Receptor deleted by gene knockout technology. These mice were developed in order to better understand the physiological relevance of the M3 receptor. Unexpectedly, these knockout mice have a phenotype that includes significant reduction in food intake, weight loss, peripheral fat deposits, as well as very low serum leptin and insulin levels. It was also found that the M3 receptor is highly expressed in the hypothalamus, a region of the brain known to be critically involved in regulation of food uptake. The mice also show physiological changes (increased levels of hypothalmic agouti-related peptide mRNA and decreased expression of propiomelanocortin mRNA) consistent with those observed in fasted animals. However, the knockout mice also have changes Start Printed Page 17721(reduced levels of melanin concentrating hypothalmic mRNA) inconsistent with fasted animals. These data point to the existence of a novel cholinergic pathway involving M3 cholinergic receptor mediated stimulation of food intake. This technology strongly suggests that agents which can specifically and selectively act as antagonists of the M3 subtype receptors may be useful in the treatment of obesity.
Methods for Preventing Strokes by Inducing Tolerance to E-selectin
John M. Hallenbeck, et al. (NINDS), Serial No. 60/206,693 filed 24 May 2000, Licensing Contact: Norbert Pontzer; 301/496-7736 ext. 284; e-mail: firstname.lastname@example.org
This invention provides methods of treating or preventing brain damage in stroke through administration of E-selectin, an inducible adhesion molecule on endothelial cells. The expression of E-selectin is induced on human endothelium in response to activation by cytokines IL-1 and TNF. E-selectin mediates the adhesion of various leukocytes, including neutrophils, monocytes, eosinophils, natural killer cells, and a subset of T cells to activated endothelium. Activation of vascular endothelial cells by proinflammatory cytokines is believed to be involved in conversion of the luminal surface of endothelium from anticoagulant and anti-inflammatory to procoagulant and pro-inflammatory leading to thrombosis. Segmental vascular activation and thrombosis are involved in the development of strokes.
Recently, a new method and pharmaceutical formulation have been found that induce tolerance mucosally, such as by intranasal administration. The potential of mucosally administered antigens to inhibit immune responses in an antigen specific fashion has encouraged attempts to apply these routes to counteract immune dysfunctions such as allergies and in particular, autoimmune disease. Intranasal administration of E-selectin induces tolerance to E-selectin and leads to immune-deviation of a subset of lymphocytes such that they can suppress activation of vessel segments that are beginning to express E-selectin. Thus the ability of intranasal E-selectin treatment to decrease stroke lesions and delay the onset of stroke in stroke-prone spontaneously hypertensive rats suggests that the initial vessel activation and damage in stroke may be immunologically mediated. Production of immunosuppression via antigen-specific modulation of the immune response (mucosal tolerance) should have no systemic immunosuppressive effects.Start Signature
Dated: March 23, 2001.
Director, Division of Technology Development and Transfer, Office of Technology Transfer, National Institutes of Health.
[FR Doc. 01-8086 Filed 4-2-01; 8:45 am]
BILLING CODE 4140-01-P