The General Hospital Corporation

Novartis Ag

Mark C Fishman

Stefanie Urlinger

Michael Otto Bardroff

Seth Alexander Ettenberg

Michael A Moskowitz

Paul L Huang

Feng Cong

Janine R Shulok

Mariel Donzeau

Tao P Zhong

Randall T Peterson

Tom Thuren

Shi Yin Foo

Craig Basson

Michihiro Igarashi

Stephen M Strittmatter

Janine Shulok

The present invention relates to a method for treating or alleviating the symptoms of peripheral arterial disease (PAD) in a subject, comprising administering about 25 mg to about 300 mg of an IL-1&#x3b2; binding antibody or functional fragment thereof.

Use of IL-1 &#x3b2; binding antibodies for treating peripheral arterial disease

Antibodies and fragments that bind to the protein target Dickkopf (DKK1) are provided, as are methods of use and kits, for treating a target cell, in particular, a cell associated with an osteolytic condition.

Compositions and methods of use for antibodies of Dickkopf-1

Compositions and methods of use for antibodies of dickkopf-1

The invention provides methods of diagnosing diseases and conditions associated with PKC&#x3bb;, methods for identifying compounds that can be used to treat or to prevent such diseases and conditions, and methods of using these compounds to treat or to prevent such diseases and conditions. Also provided in the invention are animal model systems that can be used in screening methods.

Methods for diagnosing and treating diseases and conditions associated with protein kinase C&#x3bb;

The invention provides a novel gene, gridlock, and its encoded protein. gridlock plays a role in vascular development and modeling, and a mutation in gridlock has been associated with an aortic arch disease, coarctation. Thus, gridlock nucleic acid molecules and polypeptides can be used in methods of diagnosing, treating, and preventing gridlock-related diseases and conditions, such as aortic arch diseases.

Gridlock nucleic acid molecules, polypeptides, and diagnostic and therapeutic methods

This invention relates to transgenic non-human animals comprising a disrupted endothelial nitric oxide synthase gene. These animals exhibit abnormal wound-healing properties and hypertension. This invention also relates to methods of using the transgenic animals to screen for compounds having a potential therapeutic utility for vascular endothelial disorders, such as hypertension, cerebral ischemia or stroke, atherosclerosis and wound-healing activities. Moreover, this invention also relates to methods of treating a patient suffering from hypertension and wound-healing abnormalities with the compounds identified using the transgenic animals, and methods of making the transgenic animals. A method of treating a wound using nitroglycerin is also provided.

Endothelial NOS transgenic animals and methods of use

Endothelial NOS knockout mice and methods of use

Inhibition of nerve growth normally helps to prevent aberrant pathway or target selection, but also prevents needed regeneration in the mammalian central nervous system. The responsible inhibitory ligands are unknown, but pertussis toxin-sensitive G proteins, which are enriched in growth cones, appear to be involved in causing the responding growth cones to collapse. GAP-43 is an intracellular protein that can amplify the response to the stimulation of G protein-coupled receptors. We have attempted to modify the sensitivity of nerves to inhibitory signals by the use of GAP-43 peptides. The peptide corresponding to the native amino terminus sequence stimulates G.sub.o and enhances the growth cone collapse induced by inhibitory ligands. Modification of two critical cysteines generates peptides which inhibit G.sub.o and which markedly reduce the degree of inhibitor-mediated growth cone collapse.

Peptides to overcome inhibition of nerve growth

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Newton Center, MA, United States of America

Mark C Fishman