They found that twist was reduced as a result of pericardiotomy and increased again as a result of resuturing of the pericardium. This was attributed to changes in left ventricular shape that occurred as a result of pericardiotomy. Why Do We Need to Study Twist? Rotation and twist are concepts that first PDE inhibitor became familiar to echocardiographers with the appearance of speckle tracking echocardiography. In what ways this knowledge will Inhibitors,research,lifescience,medical be of use in clinical settings remains unclear. In addition, we feel there are several limitations in measuring rotation and twist in routine

clinical practice. For example, there may be an intervender variability of speckle tracking measurements. Three-dimensional speckle tracking echocardiography, not two-dimensional speckle tracking echocardiography, should be used to avoid the effect of the through plane motion. Nonetheless, as previously stated, there can be no doubt that measuring twist will further our understanding of cardiac mechanics. Inhibitors,research,lifescience,medical Also, identification of hyper-rotation probably implies Inhibitors,research,lifescience,medical subendocardial dysfunction that is caused by various reasons. I await the day when rotation and twist are recognized as new evaluations of cardiac function.
Doxorubicin is a widely-used anticancer agent and the major limitation of its use is dose-related cardiotoxicity.1) At present,

doxorubicin cardiotoxicity Inhibitors,research,lifescience,medical is routinely screened noninvasively by measurement of the left ventricular (LV) ejection fraction

(EF), but abnormal observations can be made only when cardiac damage already has reached significant proportions.2) Recently, myocardial apoptosis was suggested as a common mechanism of acute and chronic myocyte loss.3-5) In the pathophysiology of cardiovascular disease, programmed cell death of cardiomyocytes has been suggested to be an important contributor because apoptotic cardiomyocytes have been identified during hypoxia, ischemia, cardiac overload, acute myocardial infarction, end-stage heart failure in vivo, and anthracycline Inhibitors,research,lifescience,medical use.6),7) Doxorubicin induces apoptosis in several cell lines and, in a rat model, the kidneys, intestines, and cardiomyocytes.7-9) PD184352 (CI-1040) Therefore, the detection of apoptosis could be an opportunity for the noninvasive exploration of early cardiomyopathy. The detection methods used in most studies evaluating apoptosis of the heart are based on the occurrence of DNA fragmentation, such as the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay and DNA laddering. However, in vivo detection of cell death is not possible with TUNEL or DNA gel electrophoresis.10) One of the earliest events after triggering cell death is the externalization of phosphatidylserine (PS) to the outer leaflet of the plasma membrane of the cell. Detection of PS exposure can be easily achieved by the phospholipid binding protein annexin A5.