Abstract: The present invention is related to methods and compositions for the therapeutic and diagnostic use in the treatment of diseases and disorders which are caused by or associated with amyloid or amyloid-like proteins including amyloidosis, a group of disorders and abnormalities associated with amyloid protein such as Alzheimer's disease. The present invention provides novel methods and compositions comprising highly specific and highly effective antibodies having the ability to specifically recognize and bind to specific epitopes from a range of ?-amyloid proteins.

Abstract: Methods of suppressing a humoral immune response to a thymus-dependent (TD) antigen are disclosed. The methods involve administering to a subject a TD antigen with an antagonist of a molecule which mediates contact-dependent helper effector functions. In a preferred embodiment, the antagonist is an antagonist of gp39. Primary and secondary humoral immune responses can be suppressed and suppression is prolonged.

Abstract: The present invention is directed to novel methods of treating a subject with a bone deficit disorder. The methods generally include administering to a subject in need thereof a pharmaceutically acceptable formulation comprising a parathyroid hormone (PTH) peptide analogue in a daily dose sufficient to result in an effective pharmacokinetic profile and maintained adenylate cyclase activity, while simultaneously reducing undesirable side effects.

Abstract: A method for analyzing extracellular body fluids as to the presence of the Y-box protein YB-1 and fragments thereof, which are secreted by the cell, in order to determine inflammatory processes and malignant diseases in mammals. Also, it relates to the use of YB-1 as a marker and a kit for detecting YB-1, polypeptide fragments of YB-1, and combinations thereof. Also disclosed is a pharmaceutical composition which is used for treating inflammatory processes and malignant diseases and which contains the YB-1 protein, fragments of protein YB-1, and antibodies against the YB-1 protein and/or fragments of protein YB-1.

Abstract: The invention provides a vector encoding a derivative of EBNA-1 that is not cytotoxic when expressed efficiently in cells, which supports extrachromosomal replication, maintenance and transcription from extrachromosomal oriP containing vectors but does not substantially activate transcription from host cell genes. Also provided is a vector having oriP and encoding a derivative of EBNA-1. The vectors of the invention may be employed in vitro and in gene therapy.

Abstract: Isolated mammalian nucleic acid molecules encoding receptor protein tyrosine kinases expressed in primitive hematopoietic cells and not expressed in mature hematopoietic cells are provided. Also included are the receptors encoded by such nucleic acid molecules; the nucleic acid molecules encoding receptor protein tyrosine kinases having the sequences shown in FIG. 1a (murine flk-2), FIG. 1b (human flk-2) and FIG. 2 (murine flk-1); the receptor protein tyrosine kinases having the amino acid sequences shown in FIG. 1a, FIG. 1b and FIG. 2; ligands for the receptors; nucleic acid sequences that encode the ligands; and methods of stimulating the proliferation and/or differentiation of primitive mammalian hematopoietic stem cells comprising contacting the stem cells with a ligand that binds to a receptor protein tyrosine kinase expressed in primitive mammalian hematopoietic cells and not expressed in mature hematopoietic cells.

Abstract: This invention relates to the staging, diagnosis and treatment of cancerous diseases (both primary tumors and tumor metastases), particularly to the mediation of cytotoxicity of tumor cells; and most particularly to the use of cancerous disease modifying antibodies (CDMAB), optionally in combination with one or more CDMAB/chemotherapeutic agents, as a means for initiating the cytotoxic response. The invention further relates to binding assays, which utilize the CDMAB of the instant invention. The anti-cancer antibodies can be conjugated to toxins, enzymes, radioactive compounds, cytokines, interferons, target or reporter moieties and hematogenous cells.

Abstract: The present invention relates to the use of synthetic double-stranded nucleic acid or nucleic acid analogue molecules with a bent shape structure for the prevention and treatment of pathologies induced directly or indirectly by the HMGB1 protein.

Abstract: The present invention provides humanized, chimeric and human anti-CD19 antibodies, anti-CD19 antibody fusion proteins, and fragments thereof that bind to a human B cell marker. Such antibodies, fusion proteins and fragments thereof are useful for the treatment and diagnosis of various B-cell disorders, including B-cell malignancies and autoimmune diseases.

Abstract: A method for the treatment of inflammatory disorders is disclosed, particularly the treatment of arthritis. The method comprises the administration of a function blocking antibody which is capable of binding an epitope of VLA-1.

Abstract: Methods and compositions for use in modulating the activity(s) of WISP-1 polypeptide are provided. WISP-1 antagonists include anti-WISP-1 antibodies, WISP-1 immunoadhesins and WISP-1 variants (and fusion proteins thereof) which inhibit or neutralize induction or secretion of HAS2, HA, CD44 or RHAMM by native human WISP-1 polypeptide in at least one type of mammalian cell. The invention also provides methods for in vitro, in situ, and/or in vivo diagnosis and/or treatment of mammalian cells or pathological conditions associated with native WISP-1 polypeptides.

Abstract: Methods and compositions for use in modulating the activity(s) of WISP-1 polypeptide are provided. WISP-1 antagonists include anti-WISP-1 antibodies, WISP-1 immunoadhesins and WISP-1 variants (and fusion proteins thereof) which inhibit or neutralize induction or secretion of IIAS2, IIA, CD44 or RIIAMM by native human WISP-1 polypeptide in at least one type of cells or pathological conditions associated with native WISP-1 polypeptides.

Abstract: A therapeutic method of modulating the immune response, by administering to a patient an amount of IL-4 effective to promote peripheral blood lymphocyte adhesion to microvascular endothelial cells in lymphoid organs. The IL-4 is preferably coadministered with IL-1?. An improved method of screening a cell line for the production of a binding partner that binds with a cell adhesion molecule, by contacting the binding partner with IL4-activated and nonactivated microvascular endothelial cells, and selecting binding partners that bind to the IL4-activated microvascular endothelial cells but not to the nonactivated microvascular endothelial cells. The selected binding partners may thereafter be tested for the ability to block lymphocyte binding to cytokine-activated endothelial cells. The binding partners are preferably also characterized by binding to human VCAM-1 and to IL4- or TNF?-activated bone marrow stromal cells. A representative embodiment is mAb 6G10 produced by hybridoma ATTC No. HB10519.

Abstract: Isolated mammalian nucleic acid molecules encoding receptor protein tyrosine kinases expressed in primitive hematopoietic cells and not expressed in mature hematopoietic cells are provided. Also included are the receptors encoded by such nucleic acid molecules; the nucleic acid molecules encoding receptor protein tyrosine kinases having the sequences shown in FIG. 1a (murine flk-2), FIG. 1b (human flk-2) and FIG. 2 (murine flk-1); the receptor protein tyrosine kinases having the amino acid sequences shown in FIG. 1a, FIG. 1b and FIG. 2; ligands for the receptors; nucleic acid sequences that encode the ligands; and methods of stimulating the proliferation and/or differentiation of primitive mammalian hematopoietic stem cells comprising contacting the stem cells with a ligand that binds to a receptor protein tyrosine kinase expressed in primitive mammalian hematopoietic cells and not expressed in mature hematopoietic cells.

Abstract: Methods of treating, preventing and/or managing cancer as well as and diseases and disorders associated with, or characterized by, undesired angiogenesis are disclosed. Specific methods encompass the administration of a selective cytokine inhibitory drug alone or in combination with a second active ingredient. The invention further relates to methods of reducing or avoiding adverse side effects associated with chemotherapy, radiation therapy, hormonal therapy, biological therapy or immunotherapy which comprise the administration of a selective cytokine inhibitory drug. Pharmaceutical compositions, single unit dosage forms, and kits suitable for use in methods of the invention are also disclosed.

Abstract: The present invention relates generally to the treatment of cancer using donor lymphocyte infusions of T cells. Further, the present invention relates generally to methods for stimulating and activating allogeneic and/or xenogeneic cells which can then be used in a DLI setting.

Abstract: The present invention relates to methods and compositions for treating or preventing autoimmune and/or inflammatory disease. In particular, the present invention provides therapeutics for impairing the expansion and function of autoreactive T cells and/or NK cells, by modulating NKG2D.

Abstract: The present invention relates to a method for treating recurrent tumor metastases following liver resection that includes administration of an effective amount of an agonist of A2A adenosine receptors (ARs).

Abstract: The present invention relates to a bi-specific antibody or antibody fragment having at least one arm that is reactive against a targeted tissue and at least one other arm that is reactive against a linker moiety. The linker moiety encompasses a hapten to which antibodies have been prepared. The antigenic linker is conjugated to one or more therapeutic or diagnostic agents or enzymes. The invention provides constructs and methods for producing the bispecific antibodies or antibody fragments, as well as methods for using them.

Abstract: The present invention relates to compositions and methods for detecting and inhibiting squamous cell carcinoma using agents that target the laminin 5 alpha 3 G4-G5 domain.

Abstract: Methods of using M-CSF antibodies to treat macrophage-associated diseases including atherosclerosis and HIV are provided.

Abstract: The present invention relates generally to the field of hyperglycemia-induced complications. More particularly, it concerns methods and compositions for the treatment and prevention of microvascular complications associated with diabetes. In one embodiment, the present invention provides a method of inhibiting hyperglycemia-induced platelet activation in a subject by administering to the subject an effective amount of a TRPC6 inhibitor.

Abstract: The present invention provides antibodies capable of binding to human tissue factor, which do not inhibit tissue factor mediated blood coagulation compared to a normal plasma control. Further described are methods of making and methods of using the antibodies of the invention.

Abstract: Disclosed are the surprising discoveries that aminophospholipids, such as phosphatidylserine and phosphatidylethanolamine, are stable and specific markers accessible on the luminal surface of tumor blood vessels, and that the administration of an anti-aminophospholipid antibody alone is sufficient to induce thrombosis, tumor necrosis and tumor regression in vivo. This invention therefore provides anti-aminophospholipid antibody-based methods and compositions for use in the specific destruction of tumor blood vessels and in the treatment of solid tumors. Although various antibody conjugates and combinations are thus provided, the use of naked, or unconjugated, anti-phosphatidylserine antibodies is a particularly important aspect of the invention, due to simplicity and effectiveness of the approach.

Abstract: The present invention provides methods and compositions for modulating transendothelial migration (TEM) of leukocytes. In particular, inhibition of TEM can provide a potent therapeutic approach to treating inflammatory conditions. The invention specifically relates to the discovery that the adhesion molecule CD99L2 mediates TEM of leukocytes. CD99L2 is present on endothelial cells and leukocytes and mediates leukocyte-endothelial cell adhesion. Blockade of CD99L2 by use of a specific antibody blocks migration of leukocytes into a site of inflammation. CD99L2 shows functional analogy to the structurally-related molecule, CD99, inhibition of which, in conjunction with inhibition of PECAM, causes near total blockade of TEM. Thus, blocking CD99L2 on either endothelial cells or monocytes can block migration 80-90%. In conjunction with PECAM inhibitors, TEM blockade can approach 100%. Therapeutic treatments involving inhibition of CD99L2 show significant promise in remediation of inflammatory conditions.

Abstract: The present application describes therapy with antagonists which bind to B cell surface markers, such as CD20. In particular, the application describes the use of such antagonists to treat autoimmune disease in a mammal who experiences an inadequate response to a TNF?-inhibitor.

Abstract: Antibodies, or antigen-binding portions thereof, to aspartyl (asparaginyl) ?-hydroxylase are provided. The anti-aspartyl (asparaginyl) ?-hydroxylase antibodies, or antigen-binding portions thereof, can modulate activity of aspartyl (asparaginyl) ?-hydroxylase.

Abstract: Compositions and methods for preventing, reducing or inhibiting immunologic disorders are provided. Suitable compositions include one or more LIGHT-HVEM antagonists. LIGHT-HVEM antagonists include compounds that inhibit, reduce, or block the biological activity or expression of LIGHT and/or HVEM. LIGHT-HVEM antagonists can reduce or inhibit the binding of LIGHT to HVEM, but do not significantly modulate the binding of LT? to LT?R. Suitable compositions include antibodies and antibody fragments, decoy polypeptides, small molecule inhibitors and inhibitory nucleic acids. Methods for using LIGHT-HVEM antagonists to reduce or inhibit T cell activation and survival are also provided. Therapeutic uses for LIGHT-HVEM antagonists to prevent or treat immunologic diseases and disorders including graft rejection, graft-versus-host disease, inflammatory immune responses, and autoimmune disorders are provided.

Abstract: The present invention provides methods and compositions useful in the treatment or prevention of Chlamydia infections. The methods and compositions inhibit the entry of Chlamydia into a host cell expressing EMP2 by interfering with the interaction between the Chlamydia and EMP2. The compositions include EMP2 nucleic acids and polypeptides as well as anti-EMP2 antibodies.

Abstract: A method of preparing a human recipient for a graft from a human which includes: administering donor peripheral blood progenitor cells to the recipient, and providing a minimally ablative.

Abstract: Polypeptides capable of forming antigen binding structures specific for Rhesus D antigens include the sequences indicated in the FIGS. 1a to 16b. The obtained polypeptides, being Fab fragments, MAY be used directly as an active ingredient in pharmaceutical and diagnostic compositions. The Fab and their DNA sequences can also be used for the preparation of complete recombinant Anti-Rhesus D antibodies. Useful in pharmaceutical and diagnostic compositions.

Abstract: There are provided uses of an antibody directed to CX3CR1 and fractalkine. Killer lymphocytes can be readily identified, eliminated and separated by using an anti-CX3CR1 antibody. Further, there can be provided an antibody drug for suppressing chemotaxis and cytotoxic activity of killer lymphocytes by suppressing an interaction between CX3CR1 and fractalkine.

Abstract: The invention involves methods of regulating cell growth and division to control disease processes by manipulating mitochondrial metabolism and the expression of cell surface immune proteins. The invention also involves related compositions and screening assays.

Abstract: A method is provided for reducing the occurrence of fever, headache, nausea and/or vomiting associated with administration of a therapeutic compound to a mammal in need thereof, comprising administering to the mammal a first conditioning dose of a non-target cell depleting compound which binds to a cell surface receptor on a target mammalian cell; and administering a second therapeutic dose of the compound, wherein the second dose is higher than the first dose.

Abstract: Methods for preventing or treating an antibody-mediated disease in a patient are presented, the methods comprising administration of a monoclonal antibody capable of binding to a human CD40 antigen located on the surface of a human B cell, wherein the binding of the antibody to the CD40 antigen prevents the growth or differentiation of the B cell. Monoclonal antibodies useful in these methods, and epitopes immunoreactive with such monoclonal antibodies are also presented.

Abstract: The present invention describes methods for inhibition angiogenesis in tissues using vitronectin ?v?3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing ?v?3 antagonists.

Abstract: A method for the decrease of fat absorption in a mammal, wherein the animal is orally fed an antibody produced against lipase, an enzyme which is required for fat absorption.

Abstract: The invention provides for SPARC polypeptides with a mutation corresponding to a deletion of the third glutamine in the mature form of the human SPARC protein, nucleic acids encoding such polypeptides, antibodies against such polypeptides, and methods of the use of such polypeptides, nucleic acids, and antibodies.

Abstract: The present invention describes methods for inhibition angiogenesis in tissues using vitronectin ?v?3 antagonists, and particularly for inhibiting angiogenesis in inflamed tissues and in tumor tissues and metastases using therapeutic compositions containing ?v?3 antagonists.

Abstract: An antibody capable of recognizing amyloid ? while not recognizing amyloid ? precursor proteins, and a method for using the same. A monoclonal antibody characterized by being capable of recognizing the N-terminus peptide of amyloid ? while not recognizing amyloid ? precursor proteins, an amyloid ? assay kit, a therapeutic agent of Alzheimer's disease, and a method for treating Alzheimer's disease using the monoclonal antibody.

Abstract: Methods of using inhibitors of the CD2/LFA-3 interaction in treating skin conditions characterized by increased T cell activation and abnormal antigen presentation in the dermis and epidermis in mammals, including humans. Such conditions include psoriasis, UV damage, e.g., photoaging, atopic dermatitis, cutaneous T cell lymphoma such as mycosis fungoides, allergic and irritant contact dermatitis, lichen planus, alopecia areata, pyoderma gangrenosum, vitiligo, ocular cicatricial pemphigoid, and urticaria.

Abstract: The present invention provides methods for reducing or inhibiting angiogenesis in a tissue, by contacting ?5?1 integrin in the tissue with an agent that interferes with the specific binding of ?5?1 integrin to a ligand expressed in the tissue; and methods of identifying angiogenesis in a tissue, by contacting the tissue with an agent that specifically binds ?5?1 integrin, and detecting specific binding of the agent to ?5?1 integrin associated with a blood vessel in the tissue. Also provided are methods of diagnosing a pathological condition characterized by angiogenesis in a tissue in an individual; methods of reducing or inhibiting angio genesis in a tissue in an individual; and methods of reducing the severity of a pathological condition associated with angiogenesis in an individual, by administering to the individual an agent that interferes with specific binding of ?5?1 integrin to a ligand in a tissue associated with the pathological condition.

Abstract: A method of inhibiting microvascular bleeding is provided. Antibody to protein C administered to a patient in a pharmaceutically acceptable carrier prevents anticoagulation by greater than 90% of activated protein C in human plasma.

Abstract: Fully human antibodies and antigen-binding portions thereof that bind to human 4-1BB and that allow binding of human 4-1BB to a human 4-1BB ligand. In one aspect, the antibody is an IgG4 antibody. Also provided is a method for treating a disease in a subject comprising administering a therapeutically effective amount of the antibody to said subject.

Abstract: The use of compounds that block complement component C5 or its active fragments C5a and/or C5b (such compounds collectively referred to as “C5 blockers”) to treat established joint inflammation (arthritis) is disclosed. Administration of such C5 blockers has been found to: 1) arrest and/or reduce inflammation in joints which are already inflamed, and 2) inhibit the spread of inflammation to unaffected joints.

Abstract: Methods of treating and/or prophylaxis Alzheimer's disease by preventing the formation of cerebral amyloid due to the growth and disruption of dense microspheres (DMS) are disclosed utilizing medicaments that are effective in preventing or inhibiting the growth and disruption of DMS.

Abstract: The present invention is directed to methods and means for making and using Angptl3 polypeptides. The invention specifically concerns the use of Angptl3 polypeptides in inducing liver regeneration and angiogenesis. Further methods include the use of Angptl3 polypeptides in the diagnosis and treatment of liver disease. Also provided herein are antibodies which bind to the polypeptides of the present invention.

Abstract: This invention pertains to a method for treating ulcerative colitis. Specifically, the method comprises orally or rectally administering to a human having ulcerative colitis a therapeutically effective amount of an antibody which binds to a tropomyosin isoform associated with ulcerative colitis. In another embodiment, the invention pertains to a method for treating ulcerative colitis in a human which comprises the steps of (a) obtaining from a human a colon epithelial cell extract containing a tropomyosin isoform associated with ulcerative colitis; (b) purifying the tropomyosin isoform until the tropomyosin isoform is substantially homogeneous; (c) developing an antibody which binds to the tropomyosin isoform; and (d) orally or rectally administering to a human having ulcerative colitis a therapeutically effective amount of the antibody to bind to the tropomyosin isoform associated with ulcerative colitis.

Abstract: A polypeptide (8F4 molecule) with a T-cell costimulating biological activity is disclosed, as well as monoclonal antibodies against said 8F4 molecule and hybridoma cells which produce the monoclonal antibodies, the use as medicaments of substances which inhibit the biological activity of the disclosed 8F4 polypeptide, in particular monoclonal antibodies, natural or synthetic ligands, agonists or antagonists, in particular for preventing or treating diseases which involve the immune system, the use of said 8F4 molecule or cells containing said 8F4 molecule as medicaments, in particular for preventing or treating diseases which involve the immune system, and the use of substances which specifically recognize the disclosed polypeptide, in particular monoclonal antibodies, natural or synthetic ligands, agonists or antagonists, for diagnosing diseases which involve the immune system.

Abstract: Novel anti-IL-23p40 specific human Ig derived proteins, including, without limitation, antibodies, fusion proteins, and mimetibodies, isolated nucleic acids that encode the anti-IL-23p40 Ig derived proteins, vectors, host cells, transgenic animals or plants, and methods of making and using thereof, are useful for therapeutic compositions, methods and devices. Preferably, the anti-IL-23p40 specific human Ig derived proteins do not bind the p40 subunit of IL-12 and, thus, do not neutralize IL-12-related activity.