Titlebook: Cardiac Adaptation in Heart Failure; Risks due to myocard J. Holtz,H. Drexler,H. Just Conference proceedings 1992 Dr. Dietrich Steinkopff V

Favorable

Diastolic dysfunction in pressure-overload hypertrophy and its modification by angiotensin II: currning normal myocardial fiber stress and shortening in systole. A deleterious consequence of pressure-overload hypertrophy is the prolongation of Ca.-sensitive force inactivation (impaired myocardial relaxation) which is related to intrinsic alterations in cytosolic Ca. transport and reuptake in dias

表狀態(tài)

Mechanisms of cardiac growth. The role of the renin-angiotensin system,ft ventricle. As cardiac myocytes cannot divide, they increase in mass and volume, probably by activating second messengers and proto-oncogenes involved in cellular differentiation and proliferation. Various mechanisms, such as pressure overload and angiotensin II (Ang II), have been proposed to tri

流利圓滑

ROOF

CIS

反叛者

Michael J. Grimble,Pawe? Majeckiore, we observed the activation of mitogen activated protein (MAP) kinase by myocyte stretching. This result suggest that MAP kinase activation might increase the efficiency of protein synthesis in ribosomes induced by mechanical stimuli.

conjunctivitis

Michael J. Grimble,Pawe? Majecking transcription of the .-MHC isogene. . adrenergic stimulation of the cultured cardiac myocytes also results in a modest degree of hypertrophy, however, this effect may be dependent upon myocyte contractile activity and may involve, at least in part, the non-muscle cells present in the culture syst

BRIDE

milligram

Optical mixing in atomic vapors,ion during hypertrophy and the initial stages of cardiogenesis. A combination of co-transfection, microinjection, and transgenic approaches has been coupled to well characterized cultured cell systems and in vivo murine models employing normal and transgenic mice. The microinjection of oncogenic RAS

可轉(zhuǎn)變

https://doi.org/10.1007/3-540-07945-9owth, interact with other cardiac hormones, and via EDRF inhibit platelet adhesion to endothelial surfaces. The release of the endothelial factors is regulated by stimuli such as circulating neurohumoral substances, increased flow, products of platelet aggregation, and endogenous peptides stored in