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Global longitudinal strain aids the detection of non-obstructive coronary artery disease in the resting echocardiogram

European heart journal cardiovascular imaging, 2012-07, Vol.13 (7), p.579-587

2012

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Cardiac troponin T mutations: correlation between the type of mutation and the nature of myofilament dysfunction in transgenic mice

The Journal of physiology, 2001-10, Vol.536 (2), p.583-592

2001

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Protein Kinase Cε Overexpression Alters Myofilament Properties and Composition During the Progression of Heart Failure

Circulation research, 2004-08, Vol.95 (4), p.424-432

2004

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LONGITUDINAL TWO-DIMENSIONAL SPECKLE TRACKING INDICES ON REST ECHOCARDIOGRAPHIC IMAGES PREDICTS SIGNIFICANT CORONARY DISEASE

Journal of the American College of Cardiology, 2010-03, Vol.55 (10), p.A86.E818-A86.E818

2010

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alpha -Adrenergic response and myofilament activity in mouse hearts lacking PKC phosphorylation sites on cardiac TnI

American journal of physiology. Heart and circulatory physiology, 2002-06, Vol.282 (6), p.H2397-H2405

2002

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Protein kinase C epsilon induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism

American journal of physiology. Heart and circulatory physiology, 2005-11, Vol.289 (5), p.H1881-H1888

2005

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Transgenic incorporation of skeletal TnT into cardiac myofilaments blunts PKC-mediated depression of force

American journal of physiology. Heart and circulatory physiology, 2001-03, Vol.280 (3), p.H1011-H1018

2001

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Three-dimensional experimental spatial dynamics modelling of a reciprocating Freon compressor housing

Optics and lasers in engineering, 1996-01, Vol.25 (4), p.265-288

1996

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Acoustic radiation prediction of a compressor housing from three-dimensional experimental spatial dynamics modeling

Applied acoustics, 1996, Vol.47 (2), p.165-185

1996

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The N-terminal Region of Troponin T is Essential for the Maximal Activation of Rat Cardiac Myofilaments

Journal of molecular and cellular cardiology, 1999-04, Vol.31 (4), p.867-880

1999

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Protein kinase Cepsilon induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism

American journal of physiology. Heart and circulatory physiology, 2005-11, Vol.58 (5), p.H1881

2005

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Protein kinase C{varepsilon} induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism

American journal of physiology. Heart and circulatory physiology, 2005-11, Vol.289 (5), p.H1881

2005

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Protein kinase Cε induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism

American journal of physiology. Heart and circulatory physiology, 2005, Vol.58 (5), p.H1881-H1888

2005

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Protein kinase C∈ overexpression alters myofilament properties and composition during the progression of heart failure

Circulation research, 2004, Vol.95 (4), p.424-432

2004

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Increased contractility and altered Ca2+ transients of mouse heart myocytes conditionally expressing PKCbeta

American Journal of Physiology: Cell Physiology, 2001-05, Vol.49 (5), p.C1114

2001

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Increased contractility and altered Ca 2+ transients of mouse heart myocytes conditionally expressing PKCβ

American Journal of Physiology: Cell Physiology, 2001-05, Vol.280 (5), p.C1114-C1120

2001

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Increased contractility and altered Ca2+ transients of mouse heart myocytes conditionally expressing PKC{beta}

American Journal of Physiology: Cell Physiology, 2001-05, Vol.280 (5), p.C1114

2001

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Increased contractility and altered Ca2+ transients of mouse heart myocytes conditionally expressing PKCβ

American Journal of Physiology: Cell Physiology, 2001, Vol.49 (5), p.C1114-C1120

2001

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α-Adrenergic response and myofilament activity in mouse hearts lacking PKC phosphorylation sites on cardiac TnI

American journal of physiology. Heart and circulatory physiology, 2002-06, Vol.51 (6), p.H2397-H2405

2002

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Visual statistical analysis of three-dimensional structural dynamics data

Mechanical systems and signal processing, 1995-05, Vol.9 (3), p.299-316

1995

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Transgenic incorporation of skeletal TnT into cardiac myofilaments blunts PKC-mediated depression of force

American journal of physiology. Heart and circulatory physiology, 2001-03, Vol.49 (3), p.H1011-H1018

2001

Volltextzugriff (PDF)

PKC -mediated phosphorylation and altered primary structure of troponin modulate cardiac myofilament activation

Montgomery, David E

2001

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A WEIGHTED LEAST-SQUARES DISCRETE FINITE ELEMENT FORMULATION FOR MODELING THREE-DIMENSIONAL VELOCITY RESPONSE FIELDS MEASURED BY A LASER DOPPLER VIBROMETER

Mechanical systems and signal processing, 1996-07, Vol.10 (4), p.471-495

1996

Volltextzugriff (PDF)

Protein kinase Cepsilon overexpression alters myofilament properties and composition during the progression of heart failure

Circulation research, 2004-08, Vol.95 (4), p.424-432

2004

Volltextzugriff (PDF)

Von Willebrand Disease: Basic and Clinical Aspects

1. Aufl., 2011

Volltextzugriff (PDF)

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Global longitudinal strain aids the detection of non-obstructive coronary artery disease in the resting echocardiogram

Cardiac troponin T mutations: correlation between the type of mutation and the nature of myofilament dysfunction in transgenic mice

Protein Kinase Cε Overexpression Alters Myofilament Properties and Composition During the Progression of Heart Failure

LONGITUDINAL TWO-DIMENSIONAL SPECKLE TRACKING INDICES ON REST ECHOCARDIOGRAPHIC IMAGES PREDICTS SIGNIFICANT CORONARY DISEASE

alpha -Adrenergic response and myofilament activity in mouse hearts lacking PKC phosphorylation sites on cardiac TnI

Protein kinase C epsilon induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism

Transgenic incorporation of skeletal TnT into cardiac myofilaments blunts PKC-mediated depression of force

Three-dimensional experimental spatial dynamics modelling of a reciprocating Freon compressor housing

Acoustic radiation prediction of a compressor housing from three-dimensional experimental spatial dynamics modeling

The N-terminal Region of Troponin T is Essential for the Maximal Activation of Rat Cardiac Myofilaments

Protein kinase Cepsilon induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism

Protein kinase C{varepsilon} induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism

Protein kinase Cε induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism

Protein kinase C∈ overexpression alters myofilament properties and composition during the progression of heart failure

Increased contractility and altered Ca2+ transients of mouse heart myocytes conditionally expressing PKCbeta

Increased contractility and altered Ca 2+ transients of mouse heart myocytes conditionally expressing PKCβ

Increased contractility and altered Ca2+ transients of mouse heart myocytes conditionally expressing PKC{beta}

Increased contractility and altered Ca2+ transients of mouse heart myocytes conditionally expressing PKCβ

α-Adrenergic response and myofilament activity in mouse hearts lacking PKC phosphorylation sites on cardiac TnI

Visual statistical analysis of three-dimensional structural dynamics data

Transgenic incorporation of skeletal TnT into cardiac myofilaments blunts PKC-mediated depression of force

PKC -mediated phosphorylation and altered primary structure of troponin modulate cardiac myofilament activation

A WEIGHTED LEAST-SQUARES DISCRETE FINITE ELEMENT FORMULATION FOR MODELING THREE-DIMENSIONAL VELOCITY RESPONSE FIELDS MEASURED BY A LASER DOPPLER VIBROMETER

Protein kinase Cepsilon overexpression alters myofilament properties and composition during the progression of heart failure

Von Willebrand Disease: Basic and Clinical Aspects

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