Cardiology Archives

Probenecid Improves Cardiac Function in Patients With Heart Failure With Reduced Ejection Fraction In Vivo and Cardiomyocyte Calcium Sensitivity In Vitro.

Probenecid Improves Cardiac Function in Patients With Heart Failure With Reduced Ejection Fraction In Vivo and Cardiomyocyte Calcium Sensitivity In Vitro.

A model of cardiac contraction based on novel measurements of tension development in human cardiomyocytes.

Timing and magnitude of systolic stretch affect myofilament activation and mechanical work.

Investigation into the cardiotoxic effects of doxorubicin on contractile function and the protection afforded by cyclosporin A using the work-loop assay.

Human myocytes are protected from titin aggregation-induced stiffening by small heat shock proteins

S-glutathionylation of cryptic cysteines enhances titin elasticity by blocking protein folding.

Large-Scale Modulation of Titin Elasticity by S-Glutathionylation of Cryptic Cysteines.

Automated analysis of contractile force and Ca2+ transients in engineered heart tissue.

Myofilament dysfunction contributes to impaired myocardial contraction in the infarct border zone.

Timing and magnitude of systolic stretch affect myofilament activation and mechanical work.”

Investigation into the cardiotoxic effects of doxorubicin on contractile function and the protection afforded by cyclosporin A using the work-loop assay.

Human myocytes are protected from titin aggregation-induced stiffening by small heat shock proteins.

S-glutathionylation of cryptic cysteines enhances titin elasticity by blocking protein folding.

E258K HCM-causing mutation in cardiac MyBP-C reduces contractile force and accelerates twitch kinetics by disrupting the cMyBP-C and myosin S2 interaction.

Ablation of cardiac myosin-binding protein-C accelerates contractile kinetics in engineered cardiac tissue.

Doxorubicin induced myocardial injury is exacerbated following ischaemic stress via opening of the mitochondrial permeability transition pore.

Deranged myofilament phosphorylation and function in experimental heart failure with preserved ejection fraction.

Deranged myofilament phosphorylation and function in experimental heart failure with preserved ejection fraction.

Effects of alterations in sarcomere structure and prestretch timing on cardiac muscle mechanics.

A gain-of-function mutation in the M-domain of cardiac myosin-binding protein-C increases binding to actin.

Ablation of cardiac myosin-binding protein-C accelerates contractile kinetics in engineered cardiac tissue.

Effect of aging on power output properties in rat skinned cardiac myocytes.

Fabrication and evaluation of reconstructed cardiac tissue and its application to bio-actuated microdevices.

Calcium sensitivity and the Frank-Starling mechanism of the heart are increased in titin N2B region-deficient mice.

Probenecid Improves Cardiac Function in Patients With Heart Failure With Reduced Ejection Fraction In Vivo and Cardiomyocyte Calcium Sensitivity In Vitro.

Probenecid Improves Cardiac Function in Patients With Heart Failure With Reduced Ejection Fraction In Vivo and Cardiomyocyte Calcium Sensitivity In Vitro.

A model of cardiac contraction based on novel measurements of tension development in human cardiomyocytes.

Timing and magnitude of systolic stretch affect myofilament activation and mechanical work.

Investigation into the cardiotoxic effects of doxorubicin on contractile function and the protection afforded by cyclosporin A using the work-loop assay.

Human myocytes are protected from titin aggregation-induced stiffening by small heat shock proteins

S-glutathionylation of cryptic cysteines enhances titin elasticity by blocking protein folding.

Large-Scale Modulation of Titin Elasticity by S-Glutathionylation of Cryptic Cysteines.

Automated analysis of contractile force and Ca2+ transients in engineered heart tissue.

Myofilament dysfunction contributes to impaired myocardial contraction in the infarct border zone.

Timing and magnitude of systolic stretch affect myofilament activation and mechanical work.”

Investigation into the cardiotoxic effects of doxorubicin on contractile function and the protection afforded by cyclosporin A using the work-loop assay.

Human myocytes are protected from titin aggregation-induced stiffening by small heat shock proteins.

S-glutathionylation of cryptic cysteines enhances titin elasticity by blocking protein folding.

E258K HCM-causing mutation in cardiac MyBP-C reduces contractile force and accelerates twitch kinetics by disrupting the cMyBP-C and myosin S2 interaction.

Ablation of cardiac myosin-binding protein-C accelerates contractile kinetics in engineered cardiac tissue.

Doxorubicin induced myocardial injury is exacerbated following ischaemic stress via opening of the mitochondrial permeability transition pore.

Deranged myofilament phosphorylation and function in experimental heart failure with preserved ejection fraction.

Deranged myofilament phosphorylation and function in experimental heart failure with preserved ejection fraction.

Effects of alterations in sarcomere structure and prestretch timing on cardiac muscle mechanics.

A gain-of-function mutation in the M-domain of cardiac myosin-binding protein-C increases binding to actin.

Ablation of cardiac myosin-binding protein-C accelerates contractile kinetics in engineered cardiac tissue.

Effect of aging on power output properties in rat skinned cardiac myocytes.

Fabrication and evaluation of reconstructed cardiac tissue and its application to bio-actuated microdevices.

Calcium sensitivity and the Frank-Starling mechanism of the heart are increased in titin N2B region-deficient mice.

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