Abstract: A golf training system generally includes a photoluminescent light-reactive surface and a light source that is placed on a golf club. During a training stroke performed over the photoluminescent surface, the light source excites phosphors in the light-reactive surface during a stroke and in doing so creates a transient visible “record” of the precise track the club head makes during the stroke. In some embodiments, the system can include a training ball having a phosphorescent material affixed to or integrated into the surface of the ball so that a light source placed on the golf club excites the phosphorescent material and indicates the point of contact between the golf club and the training ball.

Abstract: Certain embodiments of the invention provide a polypeptide comprising: (a) an amino acid sequence encoding a first chromophore; (b) a first linker; (c) an amino acid sequence having at least about 80% sequence identity to an amino acid sequence encoding a troponin C; (d) a second linker; and (e) an amino acid sequence encoding a second chromophore; wherein the first and second chromophores are a Förster resonance energy transfer (FRET) donor-acceptor pair; wherein the first chromophore is a donor chromophore and the second chromophore is an acceptor chromophore, or wherein the first chromophore is an acceptor chromophore and the second chromophore is a donor chromophore; and wherein the polypeptide is capable of integrating into a sarcomere. Certain embodiments of the invention also provide methods of using such polypeptides.

Abstract: This disclosure describes, in one aspect, a composition that generally includes an xNA molecule comprising at least six nucleotides, in an amount effective to improve at least one indicator of myocyte function and a pharmaceutically acceptable carrier. In another aspect, this disclosure describes a method of treating cardiac disease. Generally, the method includes administering to a subject a composition that includes an xNA molecule having at least six nucleotides, in an amount effective to improve at least one indicator of myocyte function, and a pharmaceutically acceptable carrier. In another aspect, this disclosure describes a method for evaluating the efficacy of treatment of cardiac disease. Generally, the method includes administering to a subject a composition that includes a first xNA molecule comprising a predetermined length in an amount effective to increase myocyte relaxation, then selecting a predetermined length of a second xNA molecule for at least one subsequent treatment.

Abstract: Peptide analogs of oxyntomodulin (OXM, glucagon-37), which have been modified to be resistant to cleavage and inactivation by dipeptidyl peptidase IV (DPP-IV) and to increase in vivo half-life of the peptide analog while enabling the peptide analog to act as a dual GLP-1/glucagon receptor (GCGR) agonist are described. The peptide analogs are useful for treatment of metabolic disorders such as diabetes and obesity.

Abstract: This disclosure describes, in one aspect, a composition that generally includes an xNA molecule comprising at least six nucleotides, in an amount effective to improve at least one indicator of myocyte function and a pharmaceutically acceptable carrier. In another aspect, this disclosure describes a method of treating cardiac disease. Generally, the method includes administering to a subject a composition that includes an xNA molecule having at least six nucleotides, in an amount effective to improve at least one indicator of myocyte function, and a pharmaceutically acceptable carrier. In another aspect, this disclosure describes a method for evaluating the efficacy of treatment of cardiac disease. Generally, the method includes administering to a subject a composition that includes a first xNA molecule comprising a predetermined length in an amount effective to increase myocyte relaxation, then selecting a predetermined length of a second xNA molecule for at least one subsequent treatment.

Abstract: Peptide analogs of oxyntomodulin (OXM, glucagon-37), which have been modified to be resistant to cleavage and inactivation by dipeptidyl peptidase IV (DPP-IV) and to increase in vivo half-life of the peptide analog while enabling the peptide analog to act as a dual GLP-1/glucagon receptor (GCGR) agonist are described. The peptide analogs are useful for treatment of metabolic disorders such as diabetes and obesity.

Abstract: The present invention relates to compositions and methods for treating and preventing skeletal muscle deficiencies. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188-P188) and methods of using the same for treating and preventing skeletal muscle deficiencies and injuries (e.g., dystrophin-deficient skeletal muscle; skeletal muscle having a contraction force deficit; skeletal muscle having a Ca2+ imbalance; skeletal muscle having microtears).

Abstract: The present invention relates to compositions and methods for treating and preventing skeletal muscle deficiencies. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188-P188) and methods of using the same for treating and preventing skeletal muscle deficiencies and injuries (e.g., dystrophin-deficient skeletal muscle; skeletal muscle having a contraction force deficit; skeletal muscle having a Ca2+ imbalance; skeletal muscle having microtears).

Abstract: The present invention relates to compositions and methods for treating and preventing skeletal muscle deficiencies. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188-P188) and methods of using the same for treating and preventing skeletal muscle deficiencies and injuries (e.g., dystrophin-deficient skeletal muscle; skeletal muscle having a contraction force deficit; skeletal muscle having a Ca2+ imbalance; skeletal muscle having microtears).

Abstract: This disclosure describes, in one aspect, a composition that generally includes an xNA molecule comprising at least six nucleotides, in an amount effective to improve at least one indicator of myocyte function and a pharmaceutically acceptable carrier. In another aspect, this disclosure describes a method of treating cardiac disease. Generally, the method includes administering to a subject a composition that includes an xNA molecule having at least six nucleotides, in an amount effective to improve at least one indicator of myocyte function, and a pharmaceutically acceptable carrier. In another aspect, this disclosure describes a method for evaluating the efficacy of treatment of cardiac disease. Generally, the method includes administering to a subject a composition that includes a first xNA molecule comprising a predetermined length in an amount effective to increase myocyte relaxation, then selecting a predetermined length of a second xNA molecule for at least one subsequent treatment.

Abstract: The present invention relates to compositions and methods for treating and preventing heart disease. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188-P188) and methods of using the same for treating and preventing heart disease (e.g., in subjects with muscular dystrophy) and for treating cells and tissue damage caused by ischemia and cell death (e.g., for treating dystrophin-deficient cells (e.g., myocytes)).

Abstract: The present invention relates to compositions and methods for treating and preventing heart disease. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188-P188) and methods of using the same for treating and preventing heart disease (e.g., in subjects with muscular dystrophy) and for treating cells and tissue damage caused by ischemia and cell death (e.g., for treating dystrophin-deficient cells (e.g., myocytes)).

Abstract: The present invention relates to compositions and methods for treating and preventing skeletal muscle deficiencies. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188-P188) and methods of using the same for treating and preventing skeletal muscle deficiencies and injuries (e.g., dystrophin-deficient skeletal muscle; skeletal muscle having a contraction force deficit; skeletal muscle having a Ca2+ imbalance; skeletal muscle having microtears).

Abstract: The present invention relates to compositions and methods for treating and preventing heart disease. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188—P188) and methods of using the same for treating and preventing heart disease (e.g., in subjects with muscular dystrophy) and for treating cells and tissue damage caused by ischemia and cell death (e.g., for treating dystrophin-deficient cells (e.g., myocytes)).

Abstract: The present invention relates to compositions and methods for treating and preventing heart disease. In particular, the present invention provides compositions comprising poloxamers (e.g., poloxamer 188-P1 88) and methods of using the same for treating and preventing heart disease (e.g., in subjects with muscular dystrophy) and for treating cells and tissue damage caused by ischemia and cell death (e.g., for treating dystrophin-deficient cells (e.g., myocytes)).

Abstract: The present invention relates to the overexpression of a calcium binding protein in cardiac myocytes in vivo and in vitro, and in particular, to the correction of diastolic dysfunction. Expression of the calcium binding protein parvalbumin in cardiac myocytes results in an increase in the rate of relaxation of the cardiac myocyte, in vivo and in vitro. The parvalbumin is expressed from an adenovirus vector, adeno-associated virus vector, or gutted adenovirus vector. The transfected in vivo and in vitro cardiac myocytes are also useful in drug screens.