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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书目名称Biochemistry of Hypertrophy and Heart Failure影响因子(影响力)




书目名称Biochemistry of Hypertrophy and Heart Failure影响因子(影响力)学科排名




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书目名称Biochemistry of Hypertrophy and Heart Failure网络公开度学科排名




书目名称Biochemistry of Hypertrophy and Heart Failure被引频次




书目名称Biochemistry of Hypertrophy and Heart Failure被引频次学科排名




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书目名称Biochemistry of Hypertrophy and Heart Failure年度引用学科排名




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书目名称Biochemistry of Hypertrophy and Heart Failure读者反馈学科排名

泰然自若

Lysophospholipids do not directly modulate NA+-H+ exchange,phosphatidylinositol (LPI) and lysoplasmenylcholine (LP.C) also did not alter Na.-H. exchange at all concentrations and reaction times examined. We conclude that any stimulatory effects of lysolipids on Na.-H. exchange do not occur through a direct action on the exchanger or its membrane lipid envir

Serenity

Antioxidant enzyme gene expression in congestive heart failure following myocardial infarction, remained unchanged at all time points. The mRNA levels for catalase remained unchanged at 1 and 4 weeks PMI and were significantly reduced by about 44% at 16 weeks PMI as compared to the controls. The protein levels for MnSOD, CuZnSOD, GSHPx at 1 and 16 weeks remained unchanged in treated and untre

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GOUGE

Analysis of postextrasystolic relaxation response in the human heart,uding patients and controls, correlation analysis between (EDVI, ESVI, and EF) and PRR yielded the following: (a) EDVI vs. PRR: R = 0.273, p = 0.036; (b) ESVI vs. PRR: R = 0.446, p < 0.001; and (c) EF vs. PRR: R = -0.520, p < 0.001. Thus, normal or non-failing human hearts showed a decline of -dP/dt

COWER

Cardiac adaptation to endurance exercise in rats,myocardial stiffness (22 ± 1.1 to 19.1 ± 0.3) and reduced purine efflux during pacing-induced workload increases. .P-NMR spectroscopy in isolated hearts from trained rats showed decreased PCr and PCr/ATP ratios with increased creatine, AMP and ADP concentrations. Thus, this endurance exercise protoc

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公理

Calpain-1-dependent degradation of troponin I mutants found in familial hypertrophic cardiomyopathyh the use of Western immunoblotting and densitometry. The results indicated that both the wild-type and the mutant cTnI molecules were susceptible to Calpain-1. However, the degradation of the cTnI molecules in the troponin complex was less intense than that of the non-complexed forms. Moreover, pho