The focus of this special issue of Molecular and Cellular Biochemistry is underlying mechanisms that regulate cardiac growth. The new information provided 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.
The focus of this special issue of Molecular and Cellular Biochemistry is underlying mechanisms that regulate cardiac growth. The new information provided 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.Hinweis: Dieser Artikel kann nur an eine deutsche Lieferadresse ausgeliefert werden.
Produktdetails
Produktdetails
Developments in Molecular and Cellular Biochemistry 43
Preface. 1. Lysophospholipids do not directly modulate Na+-H+ exchange; D.P. Goel, et al. 2. Antioxidant enzyme gene expression in congestive heart failure following myocardial infarction; N. Khaper, et al. 3. Modulation of cardiac remodeling by adenosine: In vitro and in vivo effects; F. Villareal, et al. 4. Right ventricular collagen and fibronectin levels in patients with pulmonary atresia and ventricular septal defect; T.H.F. Peters, et al. 5. A mouse model of familial hypertrophic cardiomyopathy caused by an alpha-tropomyosin mutation; R. Prabhakar, et al. 6. Analysis of postextrasystolic relaxation response in the human heart; K. Kato, et al. 7. Differential effects of calpain inhibitors on hypertrophy of cardiomyocytes; J.R. Pollack, et al. 8. Cardiac adaptation to endurance exercise in rats; A. Fenning, et al. 9. Matrix metalloproteinase inhibitors attenuate endotoxemia induced cardiac dysfunction: a potential role for MMP-9; M.M. Lalu, et al. 10. Functional and structural characterization of anti-beta1-adrenoceptor autoantibodies of spontaneously hypertensive rats; G. Wallukat, et al. 11. Quinapril inhibits progression of heart failure and fibrosis in rats with dilated cardiomyopathy after myocarditis; W. Juan, et al. 12. Calpain-1 dependent degradation of troponin 1 mutants in familial hypertrophic cardiomyopathy; J. Barta, et al. 13. Gender mediated cardiac protection from adverse ventricular remodeling is abolished by ovariectomy; G.L. Brower, et al. 14. Protein kinase C isoform selective signals that lead to cardiac hypertrophy and the progression of heart failure; A. Sa
Preface. 1. Lysophospholipids do not directly modulate Na+-H+ exchange; D.P. Goel, et al. 2. Antioxidant enzyme gene expression in congestive heart failure following myocardial infarction; N. Khaper, et al. 3. Modulation of cardiac remodeling by adenosine: In vitro and in vivo effects; F. Villareal, et al. 4. Right ventricular collagen and fibronectin levels in patients with pulmonary atresia and ventricular septal defect; T.H.F. Peters, et al. 5. A mouse model of familial hypertrophic cardiomyopathy caused by an alpha-tropomyosin mutation; R. Prabhakar, et al. 6. Analysis of postextrasystolic relaxation response in the human heart; K. Kato, et al. 7. Differential effects of calpain inhibitors on hypertrophy of cardiomyocytes; J.R. Pollack, et al. 8. Cardiac adaptation to endurance exercise in rats; A. Fenning, et al. 9. Matrix metalloproteinase inhibitors attenuate endotoxemia induced cardiac dysfunction: a potential role for MMP-9; M.M. Lalu, et al. 10. Functional and structural characterization of anti-beta1-adrenoceptor autoantibodies of spontaneously hypertensive rats; G. Wallukat, et al. 11. Quinapril inhibits progression of heart failure and fibrosis in rats with dilated cardiomyopathy after myocarditis; W. Juan, et al. 12. Calpain-1 dependent degradation of troponin 1 mutants in familial hypertrophic cardiomyopathy; J. Barta, et al. 13. Gender mediated cardiac protection from adverse ventricular remodeling is abolished by ovariectomy; G.L. Brower, et al. 14. Protein kinase C isoform selective signals that lead to cardiac hypertrophy and the progression of heart failure; A. Sa
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