Abstract: The invention is based on the discovery that compounds of Formula I are unexpectedly highly potent and selective inhibitors of the adenosine A1 receptor. Adenosine A1 antagonists can be useful in the prevention and/or treatment of numerous diseases, including cardiac and circulatory disorders, degenerative disorders of the central nervous system, respiratory disorders, and many diseases for which diuretic treatment is suitable.

Abstract: The invention provides Cripto-specific antibodies, or biologically functional fragments thereof, and uses thereof. Antibodies which bind Cripto and inhibit Cripto activity are provided. Antibodies which bind Cripto and inhibit the interaction between Cripto and ALK4 and/or between Cripto and Activin B are provided. Antibodies which bind Cripto and inhibit tumor growth are also provided. Antibodies which bind Cripto, inhibit Cripto activity, and inhibit tumor growth are also provided. The invention also provides methods of using these antibodies in therapeutic, diagnostic, and research applications.

Abstract: Disclosed are immunogenic Nogo receptor-1 polypeptides, Nogo receptor-1 antibodies, antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof and nucleic acids encoding the same. Also disclosed are compositions comprising, and methods for making and using, such Nogo receptor antibodies, antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof and nucleic acids encoding the same.

Abstract: The present invention relates to reagents which modify the activity of TWEAK and their use as therapeutic agents for the treatment of immunological disorders.

Abstract: Antibodies and antibody fragments that bind to the receptor GFRalpha3 and inhibit formation of a Neublastin-GFRalpha3-Ret ternary complex are disclosed. Also disclosed are methods of using the antibodies and antibody fragments to inhibit phosphorylation of Ret in a cell and treat disorders and in a subject.

Abstract: Methods of treating multiple sclerosis and other disorders are disclosed.

Abstract: The invention provides a method of producing multiple polypeptides, such as antibodies or antibody fragments, in a eukaryotic cell using a single expression vector. The expression vector is engineered to comprise two or more expression cassettes under the control of a single promoter wherein the expression cassettes have splice sites which allow for their alternative splicing and expression as two or more independent gene products at a desired ratio. Use of the vector for the efficient expression of recombinant antibodies in eukaryotic host cells is disclosed as well as the use of such antibodies in diagnostic and therapeutic applications.

Abstract: Tumor Necrosis Factor Related Ligand (TRELL) polypeptides, a novel member of the tumor necrosis factor family (TNF) and compositions comprising them are disclosed.

Abstract: Monoclonal antibodies that specifically bind to M.96. Also included are methods of using these antibodies to treat mammals having or at risk of having O06-mediated diseases, or to diagnose % Qmediated diseases.

Abstract: This invention features combination therapies that include a composition that activates lymphotoxin-beta receptor signaling in combination with one or more other biologic agents, as well as therapeutic methods.

Abstract: The present invention is based on the discovery that oligodendrocyte-myelin glycoprotein (OMgp), which is ex-pressed by oligodendrocytes and CNS myelin, negatively regulates oligodendrocyte and neuronal differentiation and survival. Based on these discoveries, the invention relates generally to methods of promoting neuronal and oligodendrocyte survival and differentiation by administration of an OMgp anatagonist. Additionally, the invention generally relates to methods of treating various diseases, disorders or injuries associated with demyelination, dysmyelination, oligodendrocyte/neuronal cell death, axonal injury and/or differentiation by the administration of an OMgp antagonist.

Abstract: The invention is based, at least in part, on the development of multivalent and stabilized forms of CD23 binding molecules and methods of use thereof for the treatment of immune cell disorders, including leukemias or lymphomas such as CLL.

Abstract: A lighting control console for controlling a lighting control system including a digital processor and a digital storage unit. The lighting control console can comprise several control elements, in particular keys, linear regulators and/or induction regulators, which are arranged on the top of the casing and can be used to enter operating commands. The lighting control console encompasses a display device with at least one screen that is arranged on the top of the casing. The data for the user can be graphically displayed on the screen. The lighting control console can include a casing provided with at least one cover, which can be adjusted between a closed position and an open position, wherein the cover covers at least one extra control element arranged in or on the casing in its closed position, thereby protecting the extra control element against external influences in its closed position.

Abstract: The instant invention is based, at least in part on the finding that binding molecules which bind to different epitopes within IGF-1R result in improved IGF-1 and/or IGF-2 blocking capabilities when compared to binding molecules that bind to a single IGF-1R epitope. The instant invention provides compositions that bind to multiple epitopes of IGF-1R, for example, combinations of monospecific binding molecules or multispecific binding molecules (e.g., bispecific molecules). Methods of making the subject binding molecules and methods of using the binding molecules of the invention to antagonize IGF-1R signaling are also provided.

Abstract: The invention provides methods and compositions for increasing the delivery of nucleic acids into a host by administering a nucleic acid encoding a therapeutic nucleic acid along with an agent that modulates Kupffer cell function in the host.

Abstract: This invention relates to compositions and methods useful for activating LT-? receptor signaling, which in turn elicits potent anti-proliferative effects on tumor cells. More particularly, this invention relates to lymphotoxin heteromeric complexes formed between lymphotoxin-a and multiple subunits of lymphotoxin-?, which induce cytotoxic effects on tumor cells in the presence of lymphotoxin-? receptor activating agents. Also within the scope of this invention are antibodies directed against the lymphotoxin-? receptor which act as lymphotoxin-? receptor activating agents alone or in combination with other lymphotoxin-? receptor activating agents either in the presence or absence of lymphotoxin-a/? complexes. A screening method for selecting such antibodies is provided. This invention also relates to compositions and methods using cross-linked anti-lymphotoxin-? receptor antibodies either alone or in the presence of other lymphotoxin-? receptor activating agents to potentiate tumor cell cytotoxicity.

Abstract: The invention provides Cripto blocking antibodies, or biologically functional fragments thereof, and uses thereof. Antibodies which bind Cripto and modulate Cripto signaling are provided. Antibodies which bind Cripto and block the interaction between Cripto and ALK4 are provided. Antibodies which bind Cripto and modulate tumor growth are also provided. Antibodies which bind Cripto, modulate signaling, and modulate tumor growth are also provided. Antibodies which bind Cripto, block the interaction between Cripto and ALK4 and modulate tumor growth are provided. The invention also provides methods of using these antibodies in therapeutic, diagnostic, and research applications.

Abstract: A fusion polypeptide is described having the amino acid sequence X-Y-Z, or portion thereof, comprising the amino acid sequence of a glycosylated interferon-beta (X); Y is an optional linker moiety; and Z is a polypeptide comprising at least a portion of a polypeptide other than glycosylated interferon-beta. It is preferred that X is human interferon-beta-1a. Mutants of interferon-beta-1a are also described.