Physical determinants of left ventricular isovolumic pressure decline: model prediction with in vivo validation.

Point: Left ventricular volume during diastasis is the physiological in vivo equilibrium volume and is related to diastolic suction.

Point: Left ventricular volume during diastasis is the physiological in vivo equilibrium volume and is related to diastolic suction.

[Anonymous].  2010.  Point: Left ventricular volume during diastasis is the physiological in vivo equilibrium volume and is related to diastolic suction.. Journal of applied physiology (Bethesda, Md. : 1985). 109(2):606-8.

Titin-isoform dependence of titin-actin interaction and its regulation by S100A1/Ca2+ in skinned myocardium.

Last word on point: Counterpoint: Left ventricular volume during diastasis is the physiological in vivo equilibrium volume and is related to diastolic suction.

Last word on point: Counterpoint: Left ventricular volume during diastasis is the physiological in vivo equilibrium volume and is related to diastolic suction.

[Anonymous].  2010.  Last word on point: Counterpoint: Left ventricular volume during diastasis is the physiological in vivo equilibrium volume and is related to diastolic suction.. Journal of applied physiology (Bethesda, Md. : 1985). 109(2):615.

Mouse intact cardiac myocyte mechanics: cross-bridge and titin-based stress in unactivated cells.

Contribution of titin and extracellular matrix to passive pressure and measurement of sarcomere length in the mouse left ventricle.

Contribution of titin and extracellular matrix to passive pressure and measurement of sarcomere length in the mouse left ventricle.

[Anonymous].  2011.  Contribution of titin and extracellular matrix to passive pressure and measurement of sarcomere length in the mouse left ventricle.. Journal of molecular and cellular cardiology. 50(4):731-9.

Titin based viscosity in ventricular physiology: an integrative investigation of PEVK-actin interactions.

Titin-actin interaction: PEVK-actin-based viscosity in a large animal.

Mouse and computational models link Mlc2v dephosphorylation to altered myosin kinetics in early cardiac disease.

The multifunctional Ca(2+)/calmodulin-dependent protein kinase II delta (CaMKIIδ) phosphorylates cardiac titin's spring elements.

The multifunctional Ca(2+)/calmodulin-dependent protein kinase II delta (CaMKIIδ) phosphorylates cardiac titin's spring elements.

[Anonymous].  2013.  The multifunctional Ca(2+)/calmodulin-dependent protein kinase II delta (CaMKIIδ) phosphorylates cardiac titin's spring elements.. Journal of molecular and cellular cardiology. 54:90-7.