Titlebook: Biochemistry of Hypertrophy and Heart Failure; Lorrie A. Kirshenbaum,Ian M. C. Dixon,Pawan K. Sin Book 2003 Springer Science+Business Medi

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Book 2003ovided in this special issue can be utilized to design new treatment modalities that will reduce the incidence of cardiac failure which will improve quality of life in patients with chronic heart disease.

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,Functional and structural characterization of anti-β1-adrenoceptor autoantibodies of spontaneously . The antibodies recognized an epitope of the second extracellular loop of the β.-adrenoceptor identical to that epitope identified in Chagas’ disease. In conclusion, our assumption is supported that old SHR-rat are an useful animal model for investigating the role of anti-β.-adrenoceptor anti-bodies in the induction of human cardiomyopathy.

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Kostengünstig Entwickeln und Konstruierenphic response at two points, promoting hypertrophy at the first and limiting it at the second. Calpain appears to be the protease involved at the first point, and there may be another cysteine protease acting at the second site.

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Modulation of cardiac remodeling by adenosine: , and , effects,tors and beneficial actions on the cardiovascular system are reviewed. In addition new, . and . data will be presented supporting the concept that adenosine exerts actions that may ameliorate adverse cardiac remodeling.

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Differential effects of calpain inhibitors on hypertrophy of cardiomyocytes,phic response at two points, promoting hypertrophy at the first and limiting it at the second. Calpain appears to be the protease involved at the first point, and there may be another cysteine protease acting at the second site.

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Protein kinase C isoform-selective signals that lead to cardiac hypertrophy and the progression of the actions of the conventional PKC isoforms, and suggest that these proteins may play a particularly significant role in pathways leading to cardiac growth and/or cardioprotection also are considered.