[A pilot assessment of the FloTrac cardiac output monitoring system comparing with pulmonary artery catheter method by three versions].

BACKGROUND: Clinical significance of PA catheter is controversial. FloTrac sensor bases its calculations on arterial waveform characteristics. We conducted a pilot assessment of the FloTrac sensor by three versions comparing with pulmonary artery catheter (PCA) methodology. METHODS: Five patients undergoing cardiac surgery and four patients undergoing renal transplantation were enrolled. A PAC was inserted and radial arterial access was used for semi-invasive determination of CO (APCO) with the Vigileo. CO was measured simultaneously by bolus thermodilution and the Vigileo technique, and CCO was measured simultaneously. RESULTS: The correlation with output obtained by FloTrac and obtained by PCA is better with the newer version. Bland Altman analyses demonstrated better agreement between FloTrac and PCA methodology of the newer version. CONCLUSIONS: CO measured by a new semi-invasive arterial pressure waveform analysis device showed better agreement with pulmonary artery thermodilution measurement of the newer version.

5'-long terminal repeat-selective CpG methylation of latent human T-cell leukemia virus type 1 provirus in vitro and in vivo.

CpG methylation of the human T-cell leukemia virus type 1 (HTLV-1) long terminal repeat (LTR) has been implicated in proviral latency, but there is presently little information available regarding the pattern of LTR methylation and its effect on viral gene expression. To gain insight into the mechanisms of HTLV-1 latency, we have studied methylation of individual CpG sites in the U3-R region of the integrated proviral LTR by using bisulfite genomic sequencing methods. Surprisingly, our results reveal selective hypermethylation of the 5' LTR and accompanying hypomethylation of the 3' LTR in both latently infected cell lines and adult T-cell leukemia (ATL) cells having a complete provirus. Moreover, we observed a lack of CpG methylation in the LTRs of 5'-defective proviruses recovered from ATL samples, which is consistent with the selective hypomethylation of the 3' LTR. Thus, the integrated HTLV-1 provirus in these carriers appears to be hypermethylated in the 5' LTR and hypomethylated in the 3' LTR. These results, together with the observation that proviral gene expression is reactivated by 5-azacytidine in latently infected cell lines, indicate that selective hypermethylation of the HTLV-1 5' LTR is common both in vivo and in vitro. Thus, hypermethylation of the 5' LTR appears to be an important mechanism by which HTLV-1 gene expression is repressed during viral latency.