scholarly article | Q13442814 |
P50 | author | Steven Colan | Q57424879 |
P2093 | author name string | Douglas B Cowan | |
Pedro J del Nido | |||
Francis X McGowan | |||
Koh Takeuchi | |||
Yeong-Hoon Choi | |||
Ingeborg Friehs | |||
Christof Stamm | |||
Adrian M Moran | |||
P2860 | cites work | Functional consequences of caspase activation in cardiac myocytes | Q28215640 |
Apoptosis in the pathogenesis and treatment of disease | Q28235731 | ||
Apoptosis in isolated adult cardiomyocytes exposed to adriamycin | Q33178685 | ||
Genetic dissection of cardiac growth control pathways | Q33938724 | ||
Left ventricular hypertrophy: pathogenesis, detection, and prognosis | Q33977917 | ||
Cytoplasmic signaling pathways that regulate cardiac hypertrophy | Q34142151 | ||
Reperfusion injury induces apoptosis in rabbit cardiomyocytes | Q34190792 | ||
Wall stress and patterns of hypertrophy in the human left ventricle | Q35194096 | ||
Death begets failure in the heart | Q36070078 | ||
Apoptosis in pressure overload-induced heart hypertrophy in the rat. | Q37356640 | ||
Calculation of left ventricular wall stress | Q37943408 | ||
Myocyte cell death and ventricular remodeling | Q40901815 | ||
The cellular and molecular response of cardiac myocytes to mechanical stress. | Q41388060 | ||
End-systolic regional wall stress-length and stress-shortening relations in an experimental model of normal, ischemic and reperfused myocardium | Q43602512 | ||
Still stressed out but doing fine: normalization of wall stress is superfluous to maintaining cardiac function in chronic pressure overload. | Q43843205 | ||
Genetic alterations that inhibit in vivo pressure-overload hypertrophy prevent cardiac dysfunction despite increased wall stress. | Q43843213 | ||
Role of alpha 1-adrenoceptor activity in progression of cardiac hypertrophy in guinea pig hearts with pressure overload | Q44512673 | ||
Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats | Q47341587 | ||
Use of the indirect axillary pulse tracing for noninvasive determination of ejection time, upstroke time, and left ventricular wall stress throughout ejection in infants and young children | Q48553868 | ||
Blockade of MyD88 attenuates cardiac hypertrophy and decreases cardiac myocyte apoptosis in pressure overload-induced cardiac hypertrophy in vivo. | Q50752354 | ||
Left ventricular hypertrophy in ascending aortic stenosis mice: anoikis and the progression to early failure. | Q52539656 | ||
Downregulation of Apoptosis-Inducing Factor in Harlequin Mutant Mice Sensitizes the Myocardium to Oxidative Stress–Related Cell Death and Pressure Overload–Induced Decompensation | Q63412946 | ||
Left ventricular chamber filling and midwall fiber lengthening in patients with left ventricular hypertrophy: overestimation of fiber velocities by conventional midwall measurements | Q67274127 | ||
Left ventricular mechanics and contractile state in children and young adults with end-stage renal disease: effect of dialysis and renal transplantation | Q68196177 | ||
Myocardial performance after arterial switch operation for transposition of the great arteries with intact ventricular septum | Q68409689 | ||
Apoptosis in myocytes in end-stage heart failure | Q71554187 | ||
Necrotic and apoptotic myocyte cell death in the aging heart of Fischer 344 rats | Q71645793 | ||
The cellular basis of pacing-induced dilated cardiomyopathy. Myocyte cell loss and myocyte cellular reactive hypertrophy | Q71730434 | ||
Acute myocardial infarction in humans is associated with activation of programmed myocyte cell death in the surviving portion of the heart | Q71741492 | ||
Hypothesis: apoptosis may be a mechanism for the transition to heart failure with chronic pressure overload | Q72355233 | ||
Left ventricular end-systolic wall stress-velocity of fiber shortening relation: a load-independent index of myocardial contractility | Q72745852 | ||
Apoptosis in the failing human heart | Q73215232 | ||
Increased cardiomyocyte apoptosis during the transition to heart failure in the spontaneously hypertensive rat | Q73399760 | ||
Increased cardiomyocyte apoptosis and changes in proapoptotic and antiapoptotic genes bax and bcl-2 during left ventricular adaptations to chronic pressure overload in the rat | Q77879730 | ||
Activation of apoptotic caspase cascade during the transition to pressure overload-induced heart failure | Q79162337 | ||
P433 | issue | 6 | |
P407 | language of work or name | English | Q1860 |
P304 | page(s) | 1356-62, 1362.e1-3 | |
P577 | publication date | 2009-03-17 | |
P1433 | published in | The Journal of Thoracic and Cardiovascular Surgery | Q2795598 |
P1476 | title | Myocyte apoptosis occurs early during the development of pressure-overload hypertrophy in infant myocardium | |
P478 | volume | 137 |
Q35825883 | Apoptosis in severe, compensated pressure overload predominates in nonmyocytes and is related to the hypertrophy but not function |
Q91939758 | Association of Endonuclease G Gene Variants with Cardiovascular Disease Risk Factors |
Q35705411 | Combination Treatment With Antihypertensive Agents Enhances the Effect of Qiliqiangxin on Chronic Pressure Overload-induced Cardiac Hypertrophy and Remodeling in Male Mice |
Q59794806 | Computational analysis of the hemodynamic characteristics under interaction influence of β-blocker and LVAD |
Q33872265 | Electron transport chain dysfunction in neonatal pressure-overload hypertrophy precedes cardiomyocyte apoptosis independent of oxidative stress |
Q92238007 | Exploration of Multiple Signaling Pathways Through Which Sodium Tanshinone IIA Sulfonate Attenuates Pathologic Remodeling Experimental Infarction |
Q51660669 | Expression of Bax Protein and Morphological Changes in the Myocardium in Experimental Acute Pressure Overload of the Left Ventricle. |
Q41832606 | Hemodynamic stability during biventricular pacing after cardiopulmonary bypass |
Q46307244 | Hydroxysafflor yellow A attenuates left ventricular remodeling after pressure overload-induced cardiac hypertrophy in rats |
Q30867239 | Left ventricular hypertrophy: The relationship between the electrocardiogram and cardiovascular magnetic resonance imaging. |
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