Abstract: The inventive technology is directed to the generation of a novel transgenic mammalian model for the study of Laing distal myopathy. The novel animal model of the invention may include a transgenic animal, and preferably a transgenic mouse, expressing the ?-myosin R1500P mutation transgene that produces one or more phenotypes associated with MPD1. The ?-myosin R1500P mutation transgene may further be selectively expressed in fast muscle tissue of the transgenic animal.

Abstract: Methods and compositions are provided for inducing physiologic hypertrophy in a cell for treatment or prevention of a cardiovascular disease or condition. In certain embodiments methods and compositions involve an aquaporin 7 inducer.

Abstract: Methods and compositions are provided for inducing physiologic hypertrophy in a cell for treatment or prevention of a cardiovascular disease or condition.

Abstract: Methods and compositions are provided for inducing physiologic hypertrophy in a cell for treatment or prevention of a cardiovascular disease or condition.

Abstract: Methods and compositions are provided for inducing physiologic hypertrophy in a cell for treatment or prevention of a cardiovascular disease or condition. In certain embodiments methods and compositions involve an aquaporin 7inducer.

Abstract: Disclosed herein are a collection of miRNAs and genes whose expression is altered in hypertrophic cardiomyopathy. Accordingly, these miRNAs and genes, singly or in combination, are useful as molecular markers for diagnosis or prognosis of hypertrophic cardiomyopathy. The miRNAs and genes disclosed can also be therapeutic targets for cardiac hypertrophy. For example, agents such as miRNA mimics, miRNA inhibitors or siRNAs for a given miRNA or gene can be used to modulate the level of these molecules thereby inhibiting or preventing hypertrophic cardiomyopathy.

Abstract: The invention provides a method of treating myocardial failure in a human. The method comprises administering an effective amount of transgene encoding ?-MHC that directly causes an increase in the quantity of ?-MHC in the myocardial tissue of the heart.

Abstract: The present invention provides for methods of treating and preventing cardiovascular diseases, in particular pathological cardiac hypertrophy and chronic heart failure, by applying an inhibitor of Ku. The present invention also provides for methods of screening to find inhibitors of Ku and inhibitors of cardiac hypertrophy and heart failure.

Abstract: The present invention provides methods of diagnosing myocardial failure in a human. The methods comprise obtaining a sample of myocardial tissue from a ventricle of the heart. In one embodiment, the expression of ?-myosin heavy chain, ?-myosin heavy chain, or both, are quantitated and their expression levels compared to that seen normal human ventricular myocardial tissues. In another embodiment, the expression of ?1-thyroid hormone receptor, ?2-thyroid hormone receptor, a ?1-thyroid hormone receptor+?1-thyroid hormone receptor, or combinations thereof, are quantitated, and their expression levels compared to that seen normal human ventricular myocardial tissues. Therapeutic interventions based on altering the expression of the aforementioned genes also are provide.

Abstract: The invention provides methods of diagnosing myocardial failure in a human. The methods comprise obtaining a sample of myocardial tissue from a ventricle of the heart of the human. In one method, the expression of ?-myosin heavy chain (?-MHC), ?-myosin heavy chain (?-MHC), or both in the sample is quantitated, and it is determined by statistical analysis if the expression of ?-MHC, ?-MHC, or both in the sample is significantly different than their expression in normal human ventricular myocardial tissue. A second method comprises quantitating the expression of ?1-thyroid hormone receptor (?1-THR), ?2-THR, ?1-THR+?1-THR, or combinations thereof in the sample, and determining by statistical analysis if the expression of ?1-THR, ?2-THR, or ?1-THR+?1-THR in the sample is significantly different than their expression in normal human ventricular myocardial tissue. The invention also provides kits for diagnosing myocardial failure by these methods.

Abstract: The invention provides methods of diagnosing myocardial failure in a human. The methods comprise obtaining a sample of myocardial tissue from a ventricle of the heart of the human. In one method, the expression of &agr;-myosin heavy chain ((&agr;-MHC), &bgr;-myosin heavy chain (&bgr;-MHC), or both in the sample is quantitated, and it is determined by statistical analysis if the expression of &agr;-MHC, &bgr;-MHC, or both in the sample is significantly different than their expression in normal human ventricular myocardial tissue. A second method comprises quantitating the expression of &agr;1-thyroid hormone receptor (&agr;1-THR), &agr;2-THR, &agr;1-THR+&bgr;1-THR, or combinations thereof in the sample, and determining by statistical analysis if the expression of &agr;1-THR, &agr;2-THR, or &agr;1-THR+&bgr;1-THR in the sample is significantly different than their expression in normal human ventricular myocardial tissue.

Abstract: The present invention discloses a transgenic mouse that is a model for congestive heart failure. The disclosed mouse is a subset of a transgenic mouse line that is a model for hypertrophic cardiomyopathy. Also disclosed are a recombinant nucleic acid molecule encoding a transgene, and methods of using the transgenic mouse model to study congestive heart failure and conditions and treatments related thereto.

Abstract: This invention relates to two methods for solubilizing proteins which are rendered insoluble by bacterial expression. One method comprises directly lysing the host bacterial cells with the detergent Sarkosyl. The other method comprises conventional lysing of the bacteria followed by an extraction process using Sarkosyl and fractionation. These methods render the proteins soluble. They do not entail harsh denaturation of the proteins, and therefore do not require renaturation of the proteins in many cases. Rather, they render the proteins soluble, in their native form.