This paper presents and proves an algorithm to calculate the isotopic composition of individual (nominal) isotopic peaks. From this information one can calculate the accurate masses of isotopic peaks. This opens the way to use accurate mass measurements to determine chemical compositions of compounds using non-mono-isotopic peaks. The algorithm is computationally efficient and rigorously correct in the absence of roundoff error. Highly effective error correction strategies are described to detect and correct computational errors arising in practical calculations. Results from theoretical calculations of isotopic masses for a krypton inclusion complex agreed well with experimental measurements. (J Am Soc Mass Spectrom 2004, 15, 12-21)

We previously reported that chick anterolateral endoderm (AL endoderm) induces cardiomyogenesis in mouse embryoid bodies. However, the requirement to micro-dissect AL endoderm from gastrulation-stage embryos precludes its use to identify novel cardiomyogenic factors, or to scale up cardiomyocyte numbers for therapeutic experiments. To circumvent this problem we have addressed whether human definitive endoderm (hDE) cells, which can be efficiently generated in large numbers from human embryonic stem cells (hESCs), can mimic the ability of AL endoderm to induce cardiac myogenesis. Results demonstrate that both hDE cells and medium conditioned by them induce cardiac myogenesis in pluripotent hESCs, as indicated by rhythmic beating and immunohistochemical/quantitative polymerase chain reaction monitoring of marker gene expression. The cardiomyogenic effect of hDE is enhanced when pluripotent hESCs are preinduced to the mes-endoderm state. Because this approach is tractable and scalable, it may facilitate identification of novel hDE-secreted factors for inclusion in defined cardiomyogenic cocktails.

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Pulmonary hypertension and associated vascular changes may frequently accompany left-sided heart disease in the adult cardiac surgical population. Perioperative assessment of right ventricular function using echocardiography is well established. In general, understanding the constraints upon which the right ventricle must work is mostly limited to invasive monitoring consisting of pulmonary artery pressures, cardiac output, and pulmonary vascular resistance. The latter 2 measurements assume constant (mean) flows and pressures. The systolic and diastolic pressures offer a limited understanding of the pulsatile constraints, which may become significant in disease. In normal physiology, pressure and flow waves display near-similar contours. When left atrial pressure and pulmonary vascular resistance are increased, changes in pulmonary arterial compliance will result in elevated impedance to right ventricular ejection. Pressure reflections, the result of strong reflectors, return more quickly in a noncompliant system. They augment pulmonary artery pressure causing a premature reduction in flow. As a result, pressure and flow waves will now be dissimilar. The impact of vascular changes on right ventricular ejection can be assessed using pulmonary artery Doppler spectral imaging. The normal flow velocity profile is rounded at its peak. Earlier peaks and premature reductions in flow will make it appear more triangular. In some cases, the flow pattern may appear notched. The measurement of acceleration time, the time from onset to peak flow velocity is an indicator of constraint to ejection; shortened times have been associated with increased pulmonary vascular resistance and pressure. Understanding the changes in the pulmonary arterial system in disease and the physics of the hemodynamic alterations are essential in interpreting pulmonary artery Doppler data. Analyzing pulmonary artery Doppler flow signals may assist in the evaluation of right ventricular function in patients with pulmonary vascular disease.