Download Biophysics of the Failing Heart: Physics and Biology of by R. John Solaro, Jil C. Tardiff PDF

By R. John Solaro, Jil C. Tardiff

Subjects within the monograph “Biophysics of the Failing middle” comprise state-of-the-art chapters contemplating significant biophysical mechanisms for why hearts responding to received or inherited stressors input into maladaptive methods ultimately resulting in an lack of ability of the guts to reply successfully to hemodynamic quite a bit particularly in the course of workout. The chapters describe biophysical strategies which were utilized to figure out the triggers for the center failure technique in addition to the mechanisms for maintaining the issues. those options comprise measurements of lively and passive mechanical houses and hemodynamics at degrees of association starting from molecules to hearts beating in situ. Biophysical recommendations and ways also are utilized to choice of signaling and sign transduction, energetics, ionic currents, delivery strategies, electro-chemical and chemo-mechanical coupling. by means of its emphasis on biophysical points of a established scientific situation, the monograph is exclusive in its viewpoint and concentration. The breadth of knowledge within the chapters multi function position might be of price to clinicians and researchers in any respect degrees. glossy learn methods and scientific figuring out of center failure calls for integration of a number of facets of the problems. in general, combos of clinician scientists and researchers writer the chapters. a prime advantage of the booklet is couched in its didactic procedure including its emphasis on how biophysical thoughts and strategies relief in analysis and improvement of recent therapies.

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Extra resources for Biophysics of the Failing Heart: Physics and Biology of Heart Muscle

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2007). Beta-adrenergic enhancement of sarcoplasmic reticulum calcium leak in cardiac myocytes is mediated by calcium/calmodulin-dependent protein kinase. Circulation Research, 100, 391–398. 47. , et al. (2007). Ca2+/ calmodulin kinase II increases ryanodine binding and Ca2+-induced sarcoplasmic reticulum Ca2+ release kinetics during beta-adrenergic stimulation. Journal of Molecular and Cellular Cardiology, 43, 281–291. V. Zima and D. Terentyev 48. Bassani, J. , Bassani, R. , & Bers, D. M. (1994).

This effect was explained by a decrease in SERCA activity and an enhancement of NCX extrusion of Ca [189, 190, 194]. Furthermore, the same mechanism was attributed to a decreased response to inotropic agents of human failing heart at the end stage [195]. Alternatively, it has been proposed that defective regulation of the RyR by CaMKII plays a critical role in the blunted FFR of the failing heart [44]. , via changes in ATP hydrolysis products) (for review see [1, 171]). The dependence of cardiac SR Ca uptake on energy supply has been demonstrated in different experimental conditions [196–198].

In the following chapter we will focus on the voltage-dependent Ca entry mechanisms (LTCC, TTCC, and NCX) that contribute current to the cardiac AP. Their molecular structure and voltage-dependent properties will be reviewed and the contribution of these proteins to the electrophysiological phenotype observed in HF will be discussed. Consideration will be given to the role that subcellular remodeling has for the plasma membrane Ca flux and which Ca-fluxes further the activation of transcription factors that enhance the remodeling process.

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