This invention relates to a method for repairing and reconstructing a damaged or non-functional muscle, in particular to a method and a tool kit using in vitro primed motor endplate-expressing muscle progenitor cells (MPCs) to promote innervation of the damaged or non-functional muscle using an agent without any genetic manipulation. This method is particularly useful for repairing or reconstructing damaged or non-functional head and neck muscles, and urinary detrusor bladder muscle.

The present invention features methods of treating patients with chronic heart failure by administering a neuregulin polypeptide within a dosage range which is both effective and safe.

Disclosed herein are compositions and methods for the treatment of otic disorders with immunomodulating agents and auris pressure modulators. In these methods, the auris compositions and formulations are administered locally to an individual afflicted with an otic disorder, through direct application of the immunomodulating and/or auris pressure modulating compositions and formulations onto the auris media and/or auris interna target areas, or via perfusion into the auris media and/or auris interna structures.

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.

This invention relates to treatment of neuroinjury in a post-acute window or in a chronic period following neuroinjury.

A method and kit for treating a neurodegenerative disease or central nervous system disorder in a subject using a GlyB4 fusion protein is provided, as is a kit containing the same.

Provided herein are methods for promoting differentiation of cardiac progenitor cells toward myocytes and suppressing the conversion of cardiac progenitor cells into fibroblasts and myofibroblasts cells in a subject determined to have cardiac progenitor cells in or around the heart, by administering a therapeutically effective amount of an NRG-1 peptide or functional variant or fragment thereof. The methods disclosed herein can be used to treat, prevent, or delay the progression of cardiac injury, for example heart failure or myocardial infarction.

Provided herein are methods for promoting differentiation of cardiac progenitor cells toward myocytes and suppressing the conversion of cardiac progenitor cells into fibroblasts and myofibroblasts cells in a subject determined to have cardiac progenitor cells in or around the heart, by administering a therapeutically effective amount of an NRG-1 peptide or functional variant or fragment thereof. The methods disclosed herein can be used to treat, prevent, or delay the progression of cardiac injury, for example heart failure or myocardial infarction.

This disclosure relates to mRNA therapy for (i) the promotion and/or improvement of wound healing, (ii) the prevention and/or reduction of scar formation at a wound, (iii) the reduction of the visibility of a scar, and/or (iv) the treatment of epidermolysis bullosa. mRNAs for use in the invention, when intradermally (e.g., using microneedles) or topically administered in vivo, encode a wound healing polypeptide (e.g., a growth factor, a cytokine, a chemokine, a protease inhibitor, or a collagen).

The present invention relates to a targeting module comprising a chemically synthesized peptide binding moiety specific for a human cell surface protein or protein complex, a kit comprising the targeting module and a vector or a cell comprising a nucleic acid encoding a universal chimeric antigen receptor and the use for the treatment of cancer, infections and autoimmune disorders.