Tracing the Pathway from Drift-Wave Turbulence with Broken Symmetry to the Generation of Sheared Axial Mean Flow

This study traces the emergence of sheared axial flow from collisional drift wave turbulence with broken symmetry in a linear plasma device---CSDX. As the density profile steepens, the axial Reynolds stress develops and drives a radially sheared axial flow that is parallel to the magnetic field. Results show that the non-diffusive piece of the Reynolds stress is driven by the density gradient and results from the spectral asymmetry of the turbulence and thus is dynamical in origin. Taken together, these findings constitute the first simultaneous demonstration of the causal link between the density gradient, turbulence and stress with broken spectral symmetry, and the mean axial flow

[Ca2+]i in human heart failure: a review and discussion of current areas of controversy.

Multiple abnormalities have been reported in the setting of human heart failure. It is unclear whether detected changes reflect adaptive alterations in myocardium subjected to increased and sustained hemodynamic overload or are pathogenic to the disease process. As a result of the observation that the primary defect in heart failure is decreased pump function, investigators have concentrated their efforts on determining systolic [Ca2+]i as a logical corollary and a causative mechanism for contractile dysfunction. A simple cause and effect relationship has therefore been proposed with regard to contractile dysfunction and [Ca2+]i. Yet some investigators have found no difference in peak systolic [Ca2+]i between failing and non-failing human myocardium, whereas others have found peak [Ca2+]i to be significantly reduced in failing hearts. Resting calcium concentrations have been reported either to be elevated in failing human myocardium or not different from non-failing human myocardium. Investigators should now appreciate that the force-calcium relationship is not a simple relationship. One must take into account the prolonged time course and slowed mobilization of [Ca2+]i as opposed to simply peak [Ca2+]i. When put in perspective of mechanisms and determinants of the Ca(2+)-force relationship, we begin to realize that failing human myocardium has the "potential" to generate normal levels of force. Only when stressed by [Ca2+]i overload and/or frequency perturbation does myocardium from patients with end-stage heart disease demonstrate contractile failure. Although [Ca2+]i availability and mobilization are likely to play a role in the systolic as well as diastolic dysfunction reported in human heart failure, it is likely that other mechanisms are involved as well (e.g., myocardial energetics). Myocardial energetics is directly related to [Ca2+]i and mobilization in failing human myocardium, because metabolites, e.g., ADP, inhibit pumps, such as sarcoplasmic reticulum Ca2+ ATPase activity. We therefore conclude that there is a role for intracellular calcium mobilization and myocardial energetics for systolic and diastolic dysfunction seen in human heart failure

[Ca2+]i in Human Heart Failure: A Review and Discussion of Current Areas of Controversy.

Multiple abnormalities have been reported in the setting of human heart failure. It is unclear whether detected changes reflect adaptive alterations in myocardium subjected to increased and sustained hemodynamic overload or are pathogenic to the disease process. As a result of the observation that the primary defect in heart failure is decreased pump function, investigators have concentrated their efforts on determining systolic [Ca2+]i as a logical corollary and a causative mechanism for contractile dysfunction. A simple cause and effect relationship has therefore been proposed with regard to contractile dysfunction and [Ca2+]i. Yet some investigators have found no difference in peak systolic [Ca2+]i between failing and non-failing human myocardium, whereas others have found peak [Ca2+]i to be significantly reduced in failing hearts. Resting calcium concentrations have been reported either to be elevated in failing human myocardium or not different from non-failing human myocardium. Investigators should now appreciate that the force-calcium relationship is not a simple relationship. One must take into account the prolonged time course and slowed mobilization of [Ca2+]i as opposed to simply peak [Ca2+]i. When put in perspective of mechanisms and determinants of the Ca(2+)-force relationship, we begin to realize that failing human myocardium has the "potential" to generate normal levels of force. Only when stressed by [Ca2+]i overload and/or frequency perturbation does myocardium from patients with end-stage heart disease demonstrate contractile failure. Although [Ca2+]i availability and mobilization are likely to play a role in the systolic as well as diastolic dysfunction reported in human heart failure, it is likely that other mechanisms are involved as well (e.g., myocardial energetics). Myocardial energetics is directly related to [Ca2+]i and mobilization in failing human myocardium, because metabolites, e.g., ADP, inhibit pumps, such as sarcoplasmic reticulum Ca2+ ATPase activity. We therefore conclude that there is a role for intracellular calcium mobilization and myocardial energetics for systolic and diastolic dysfunction seen in human heart failure

Towards the Design of Cold-formed Steel Foam Sandwich Columns

In this paper a design method for the compressive capacity of sandwich panels comprised of steel face sheets and foamed steel cores is derived and verified. Foamed steel, literally steel with internal voids, provides the potential to mitigate many local stability issues through increasing the effective width-to thickness of the component for the same amount of material. Winter’s classical effective width expression was generalized to the case of steel foam sandwich panels. The provided analytical expressions are verified with finite element simulations employing brick elements that explicitly model the steel face sheets and steel foam cores. The closed-form design expressions are employed to conduct parametric studies of steel foam sandwich panels with various face sheet and steel foamed core configurations. The studies show the significant strength improvements possible with steel foam sandwich panels when compared with plain steel sheet/plate