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Five different algorithms for determining left ventricular (LV) ejection fraction (EF) and volumes from two-dimensional echocardiographic examination (TDE) were compared with standard methods for obtaining EF and volume from x-ray cineangiography (cine) and EF from radionuclide ventriculography (RVG) in 35 patients. Although all methods correlated positively, the degree of correlation varied with the algorithm used. For EF determination, TDE algorithms (especially those using multiple planes of section) were superior to unidimensional algorithms commonly used with M-mode echocardiography. The best algorithm (modified Simpson's rule) correlated well enough with cine EF (r = 0.78; SEE 0.097) and RVG EF (r = 0.75; SEE 0.087) to make clinically useful estimates. TDE volumes also correlated meaningfully with cine end-diastolic and end-systole volumes (r = 084; n = 70) but were associated with a large standard error of the estimate (43 ml) and offered less advantage over unidimensional volume estimates. Quantitative application of TDE appears to be a useful noninvasive method of evaluating LVEF, but is not as useful for estimating LV volumes.

Survivin, a unique antiapoptotic factor, plays an important role in cell cycle regulation. Numerous clinical studies have shown that survivin is markedly overexpressed in most common types of cancer, suggesting that transcriptional deregulation is a major mechanism involved in aberrant expression of survivin in cancers. In this study, we have identified several polymorphisms in the survivin gene promoter. One of these polymorphisms is located at CDE/CHR repressor elements, and appears to be a common mutation with high frequency among cancer cell lines compared to normal cell line controls. The presence of the mutation was correlated in these cell lines with increased survivin expression at the both mRNA and protein levels. Furthermore, gel mobility shift analysis and transcriptional analysis showed the mutation changed cell cycle-dependent transcription by modifying the binding motif of the CDE/CHR repressor. These results indicate that the high level of survivin in some cancers is, at least in part, due to a genetic defect in the promoter region of the human survivin gene, which causes derepression of survivin transcription apparently due to the mutated CDE/CHR repressor binding motifs.

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