Abstract: The disclosure provides compositions and methods for preventing, ameliorating a sign or symptom of, or treating peripheral nerve injury.

Abstract: The invention relates to treatment of heart failure in a mammal. Accordingly, the invention is directed to establishing a dosing regimen whereby the therapeutic benefits conferred by administration of a neuregulin such as glial growth factor 2 (GGF2) or a subsequence thereof are maintained and/or enhanced, while concomitantly minimizing any potential side effects.

Abstract: A method for modifying access of cells to extravascular spaces and regions comprising administering to a patient an enzyme that cleaves chondroitin sulfate proteoglycans is provided. It has been found that administration of an enzyme that cleaves chondroitin sulfate proteoglycans to a patient disrupts extravasation of cells from the blood stream into tissue. The present invention provides methods of reducing penetration of cells associated with inflammation into tissue of a patient. Several methods are also provided for the regulation and suppression of inflammation comprising administering enzymes that digest chondroitin sulfates. Also provided are methods of treating and preventing inflammation associated with infection, injury and disease.

Abstract: The present invention relates to a method for detecting heart damage in a patient. The invention also relates to methods for treatment of patients identified as having heart damage. The invention further pertains to methods for evaluating the efficacy of an ongoing therapeutic regimen designated to treat a damaged heart in a patient.

Abstract: The present invention relates to administering glial growth factor 2 (GGF2) to a patient in need thereof, to achieve serum levels of GGF2 within a desired therapeutic window determined based on the disease or disorder afflicting the patient. In a particular embodiment, the patient is suffering from a disease or disorder associated with reduced levels of myelination and the GGF2 is administered to promote myelination in the patient.

Abstract: The invention relates to treatment and prevention of heart failure in a mammal. The invention provides a dosing regimen whereby the therapeutic benefits conferred by administration of peptide comprising an epidermal growth factor-like domain, e.g., a neuregulin such as glial growth factor 2 (GGF2) or a functional fragment thereof, are maintained and/or enhanced, while concomitantly minimizing any potential side effects.

Abstract: The present invention relates to administering glial growth factor 2 (GGF2) to a patient in need thereof, to achieve serum levels of GGF2 within a desired therapeutic window determined based on the disease or disorder afflicting the patient. In a particular embodiment, the patient is suffering from a disease or disorder associated with reduced levels of myelination and the GGF2 is administered to promote myelination in the patient.

Abstract: The present invention is directed to a method of improving functional recovery following a central nervous system contusion injury. The method includes administering a therapeutically effective amount of glycosaminoglycan degrading enzyme. The glycosaminoglycan degrading enzyme may be dermatan sulfate or chondroitin sulfate degrading enzymes. The central nervous system contusion injury may include a traumatic brain injury or a spinal cord injury. The functional recovery may include autonomic functions, sensory functions, motor functions or the like.

Abstract: The invention relates to treatment of heart failure in a mammal. Accordingly, the invention is directed to establishing a dosing regimen whereby the therapeutic benefits conferred by administration of a neuregulin such as glial growth factor 2 (GGF2) or a subsequence thereof are maintained and/or enhanced, while concomitantly minimizing any potential side effects.

Abstract: The present invention relates to a method for detecting heart damage in a patient. The invention also relates to methods for treatment of patients identified as having heart damage. The invention further pertains to methods for evaluating the efficacy of an ongoing therapeutic regimen designated to treat a damaged heart in a patient.

Abstract: One aspect of the present invention relates to mutants of chondroitinase ABCI. Such chondroitinase ABCI mutants exhibit altered chondroitin lyase activity or increased resistance to inactivation from stressors including exposure to UV light or heat. Methods of using chondroitinase ABCI mutant enzymes are also provided.

Abstract: The present mention relates to a method for detecting heart damage in a patient. The invention also relates to methods for treatment of patients identified as having heart damage. The invention further pertains to methods for evaluating the efficacy of an ongoing therapeutic regimen designated to treat a damaged heart in a patient.

Abstract: Embodiments of the invention are directed to use of neuregulins to prevent or treat peripheral nerve injury, to attenuate, ameliorate or avoid the loss of peripheral nerve function.

Abstract: The invention relates to treatment and prevention of heart failure in a mammal. The invention provides a dosing regimen whereby the therapeutic benefits conferred by administration of peptide comprising an epidermal growth factor-like domain, e.g., a neuregulin such as glial growth factor 2 (GGF2) or a functional fragment thereof, are maintained and/or enhanced, while concomitantly minimizing any potential side effects.

Abstract: The invention relates to treatment of heart failure in a mammal. Accordingly, the invention is directed to establishing a dosing regimen whereby the therapeutic benefits conferred by administration of a neuregulin such as glial growth factor 2 (GGF2) or a subsequence thereof are maintained and/or enhanced, while concomitantly minimizing any potential side effects.

Abstract: A method for modifying access of cells to extravascular spaces and regions comprising administering to a patient an enzyme that cleaves chondroitin sulfate proteoglycans is provided. It has been found that administration of an enzyme that cleaves chondroitin sulfate proteoglycans to a patient disrupts extravasation of cells from the blood stream into tissue. The present invention provides methods of reducing penetration of cells associated with inflammation into tissue of a patient. Several methods are also provided for the regulation and suppression of inflammation comprising administering enzymes that digest chondroitin sulfates. Also provided are methods of treating and preventing inflammation associated with infection, injury and disease.

Abstract: The present disclosure relates to protein and nucleic acid mutants of chondroitinase ABCI. Such nucleic acid mutants encode for chondroitinase ABCI mutant enzymes exhibiting altered chondroitin lyase activity or increased resistance to inactivation from stressors including UV light or heat. Methods of using such nucleic acid mutants encoding chondroitinase ABCI mutant enzymes is also provided.

Abstract: The invention relates to treatment of heart failure in a mammal. Accordingly, the invention is directed to establishing a dosing regimen whereby the therapeutic benefits conferred by administration of a neuregulin such as glial growth factor 2 (GGF2) or a subsequence thereof are maintained and/or enhanced, while concomitantly minimizing any potential side effects.

Abstract: This disclosure relates to compositions capable of use in the treatment of spinal cord injuries and related disorders of the central nervous system (CNS), and in particular, compositions including proteoglycan degrading molecules and compositions capable of blocking and/or over coming the activity of neuronal growth inhibitory molecules, as well as fusion proteins which includes a proteoglycan degrading domain and a domain capable of blocking and or over coming the activity of neuronal growth inhibitory molecules.

Abstract: One aspect of the present invention relates to mutants of chondroitinase ABCI. Such chondroitinase ABCI mutants exhibit altered chondroitin lyase activity or increased resistance to inactivation from stressors including exposure to UV light or heat. Methods of using chondroitinase ABCI mutant enzymes are also provided.