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Investigators at the NIH have discovered a potential means for preventing or treating a herpes virus infection by inhibiting the activity of the host cell’s histone demethylases. When herpesviruses enter a cell, they are inactivated by cellular defense mechanisms that wrap the viral genome in repressive chromatin structures. In order for viral replication to progress, the host’s own histone demethylases are recruited to the viral genome to reverse this repression.

Malaria is the single leading cause of death, especially among children, in the developing world. Malaria is caused by infection with parasites of the genus Plasmodium, transmitted by mosquitos. In addition to transmission, vital steps in the parasite lifecycle occur in the mosquito host. The invention offered for licensing relates to therapeutic compounds and related pharmaceutical compositions that can be used in the prevention and treatment of malaria infection.

The invention offered for licensing is a computer program called "NHLBI AbDesigner" that allows the user to input a unique identifier for an individual mammalian protein to be analyzed in order to find out what short peptides in its amino sequence would most likely result in a strong immunogenic response when injected into a research animal. The software displays standard predictors of immunogenicity and antigenicity in easy-to-view heat maps and also allows users to choose peptides most likely to elicit antibodies that are specific to said protein.

NIH investigators have discovered a series of small compounds with the potential to treat a variety of cancers as well as hemolytic anemia. Contrary to most cancer medications, these molecules can be non-toxic to normal cells because they target a protein specific to the metabolic pathways in tumors, thus representing a significant clinical advantage over less-specific chemotherapeutics.

The invention offered for licensing and commercial development is in the field of Interventional Magnetic Resonance Imaging (“iMRI”). More specifically the invention discloses interventional devices in which the heat generated at the device during the imaging process can be controlled to not exceed acceptable levels.

The invention offered for licensing and commercial development is in the field of Interventional Magnetic Resonance Imaging (“iMRI”). More specifically the invention discloses a guidewire for magnetic resonance imaging with a single channel design to reduce complexity and to provide conspicuous tip visibility under MRI. In the design of the present device, the guidewire body includes an antenna formed from a rod and a helical coil coupled together. The helical coil can have multiple windings without a gap between the windings.

This invention discloses methods for treating neurodegenerative diseases by administering cyclin dependent kinase 5 (Cdk5) inhibitory peptides derived from P35, the activator of Cdk5. Abnormally hyperactive Cdk5 has been shown to be associated with a variety of neurodegenerative disorders. Disclosed in this invention are isolated peptide fragments, pharmaceutical compositions and methods for use of such for treating subjects with a neurodegenerative disease, such as Alzheimer’s disease (AD), Amyotrophic Lateral Sclerosis (ALS) and Parkinson’s disease (PD).

NIH Inventors have recently discovered a novel Leucine-rich repeat and calponin homology domain-containing protein 4 (Lrch4) in a proteomic screen of the plasma membrane of lipopolysaccharide (LPS)-exposed macrophages. Expression data by RT-PCR revealed that all Lrch family members (1-4) are expressed in macrophages, but only Lrch4 was recruited into lipid rafts (signaling microdomains of the plasma membrane) by LPS. Lrch4 is the most highly expressed Lrch family member in mouse tissues. It is a predicted single-spanning transmembrane protein that is encoded by the Lrch4 gene in humans.

The nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1) encodes a protein that has anti-inflammatory, proapoptotic, and antitumor properties. It plays a pivotal role in antitumorigenesis induced by chemopreventive compounds. Transgenic mice expressing human NAG-1 have been developed by the NIH investigator and collaborator.

The invention relates to techniques and devices for cardiovascular valve repair, particularly annuloplasty techniques and devices in which tensioning elements are positioned to treat regurgitation of the mitral valve or tricuspid valve. More specifically, the technology pertains to a new device for myocardial septal traversal ("cerclage reentry") that also serves to capture (ensnare) and externalize the traversing guidewire.