ABSTRACT
To compare the peak global longitudinal myocardial strain (PGLS) and peak segmental longitudinal myocardial strain (PSLS) values by speckle-tracking echocardiography (STE) obtained using two different echocardiography devices. STE is an emerging quantitative ultrasound technique that allows an accurate evaluation of global and segmental myocardial function. However, there is a lack of standardization of the acquired data among different manufacturers. Sixty-three subjects, mean age 56.2±10.4 years, underwent complete echocardiographic studies with two different devices (Philips IE33 and General Electric VIVID E9) performed by the same operator. Thirty-one of them had known cardiac disease, with estimated left ventricular ejection fraction <50%, while 32 were free of any cardiovascular disease (control subjects). All images were digitally stored and analyzed using off-line post processing with QLAB 9 and EchoPAC 11 Software packages. PSLS and PGLS were calculated. A strong relationship between QLAB and EchoPAC was found for PGLS (r=0.91, P<0.001), PSLS-4 chamber (CH; r=0.79, P<0.001), PSLS-2CH (r=0.73, P<0.001), and PSLS-3CH (r=0.78, P<0.001) QLAB. Bland-Altman analysis showed absolute differences vs average of -0.16, -0.37, -0.21, and -0.16 for PGLS, PSLS-4CH, PSLS-2CH, and PSLS-apical long-axis views respectively. Segmental analysis showed a good agreement between the apical segments, whereas poor correlations were found for the basal segments. Receiver operating characteristic curve analysis showed that cutoff values for PGLS of -17.5 and -17.75% with Philips or GE systems gave a sensitivity and specificity of 93.5 and 87.5%, and 90 and 87.5%, respectively, in the discrimination of the patients from the controls. Both Philips and GE echo stations were found to give comparable results for PGLS, with approximately the same cutoff values, suggesting that their PGLS results may be interchangeable.
Subject(s)
Aortic Valve/abnormalities , Calcinosis/complications , Coronary Occlusion/etiology , Coronary Vessel Anomalies/complications , Aortic Valve Insufficiency/diagnostic imaging , Aortic Valve Insufficiency/etiology , Calcinosis/diagnostic imaging , Chest Pain/etiology , Collateral Circulation , Coronary Occlusion/diagnostic imaging , Coronary Vessel Anomalies/diagnostic imaging , Female , Humans , Middle Aged , Sinus of Valsalva , Tomography, X-Ray ComputedABSTRACT
The serine-threonine protein kinase encoded by the tumor progression locus 2 (Tpl2) proto-oncogene transduces Toll-like receptor and death receptor signals in a variety of cell types. Here we show that Tpl2 undergoes phosphorylation at Thr(290) both in cells overexpressing Tpl2 and in cells stimulated with lipopolysaccharide (LPS) or tumor necrosis factor-alpha and that phosphorylation on this site parallels Tpl2 activation. Reconstitution of Tpl2(-/-) macrophages with wild type Tpl2 or Tpl2 T290D restored ERK activation by LPS, whereas reconstitution of the same cells with Tpl2 T290A did not, suggesting that phosphorylation at Thr(290) is required for the physiological activation of Tpl2 by external signals. Both the wild type Tpl2 and the kinase-inactive mutant Tpl2 K167M undergo Thr(290) phosphorylation, suggesting that Thr(290) may be a site of trans-phosphorylation rather than auto-phosphorylation. Pretreatment of 293 cells and primary macrophages with the Ikappa-B kinase-beta (IKKbeta) inhibitor PS-1145 blocked Tpl2 phosphorylation at Thr(290), suggesting that phosphorylation depends on IKKbeta, an obligatory positive regulator of Tpl2. We conclude that Tpl2 phosphorylation at Thr(290) is induced by LPS, depends on IKKbeta, and is required for the physiological activation of Tpl2 by external signals.
