Development of a computationally efficient bubble column simulation approach by way of statistical bubble micro-flow modelling

Includes abstract.Includes bibliographical references.The intimate contact achieved between the gas and liquid phases in bubble columns, coupled with the inherent efficient mixing these reactors offer, yield excellent heat and mass transfer characteristics. These attributes have been exploited commercially for decades, however, due to the complexity of the underlying hydrodynamics, the prediction of bubble columns based on empirical models can be unreliable outside of the operating ranges used to fit these models. Computational Fluid Dynamics (CFD) has emerged as an attractive tool for simulating these reactors and is based on numerically approximating the fundamentally based Navier-Stokes equations on a discretized domain. The application of CFD has become more practical as the cost of computational resources has declined and has lead to the establishment of three distinct modelling approaches which have been evaluated for the purpose of bubble column simulation in a number of research papers over the past two decades. Here the Euler-Euler approach has been recommended for the simulation of large scale columns, however, this approach is based on the most assumptions and yields the least amount of flow field information. The Euler-Lagrange approach treats bubbles as discrete particles which allows for the incorporation of a deterministic bubble size distribution and the direct consideration of heat and mass transfer effects. The most fundamental approach, Direct Numerical Simulation (DNS), predicts flow properties at the bubble scale, however, is extremely computationally expensive and is therefore only practically applicable to the investigation of a very small number of bubbles. The objective of this study is to contribute to the simulation of gasliquid flow interaction occurring in bubble columns by proposing a novel technique for simulating bubble scale flow information at a significantly reduced computational expense. For this purpose, it is proposed to predict the micro-flow fields around individual bubbles, within an Euler-Lagrange framework, with an algebraic model termed the Bubble Cell Model (BCM). The high gradient regions around individual bubbles are thereby accounted for with an algebraic flow model that can be rapidly evaluated as opposed to the two-phase partial differential Navier-Stokes equations, thereby reducing the numerical complexity of the problem. Since no such flow models currently exist and accuracy and fast evaluation are imperative, a statistical approach to the construction of the BCM is justified

Left regional cardiac perfusion in vitro with platelet-activating factor, norepinephrine and K+ reveals that ischaemic arrhythmias are caused by independent effects of endogenous 'mediators' facilitated by interactions, and moderated by paradoxical antagonism

1. Various putative drug targets for suppression of ischaemia-induced ventricular fibrillation (VF) have been proposed, but therapeutic success in the suppression of sudden cardiac death (SCD) has been disappointing. Platelet-activating factor (PAF) is a known component of the ischaemic milieu. We examined its arrhythmogenic activity, and its interaction with two other putative mediators, norepinephrine and K(+), using an ischaemia-free in vitro heart bioassay, and a specific PAF antagonist (BN-50739). 2. PAF (0.1–100 nmol) was administered selectively to the left coronary bed of rat isolated hearts using a specially designed catheter. In some hearts, PAF was administered to the left coronary bed during concomitant regional perfusion with norepinephrine and/or K(+). In separate studies, PAF accumulation in the perfused cardiac tissue was evaluated using (3)H-PAF. 3. PAF evoked ventricular arrhythmias concentration-dependently (P<0.05). It also widened QT interval and reduced coronary flow selectively in the PAF-exposed left coronary bed (both P<0.05). Two exposures of hearts to PAF were necessary to evoke the QT and rhythm effects. 4. The PAF-induced arrhythmias and coronary vasoconstriction were partially suppressed by the PAF antagonist BN-50739 (10 μM), although BN-50739 itself widened QT interval. 5. K(+) (8 and 15 mM) unexpectedly antagonised the arrhythmogenic effects of PAF without itself eliciting arrhythmias (P<0.05). Norepinephrine (0.1 μM) had little or no effect on the actions of PAF, while failing to evoke arrhythmias itself. Nevertheless, the combination of 15 mM K(+) and 0.1 μM norepinephrine evoked arrhythmias of a severity similar to arrhythmias evoked by PAF alone, without adding to or diminishing the arrhythmogenic effects of PAF. 6. (3)H-PAF accumulated in the cardiac tissue, with 43±5% still present 5 min after bolus administration, accounting for the need for two exposures of the heart to PAF for evocation of arrhythmias. 7. Thus, PAF, by activating specific receptors in the ventricle, can be expected to contribute to arrhythmogenesis during ischaemia. However, its interaction with other components of the ischaemic milieu is complex, and selective block of its actions (or its accumulation) in the ischaemic milieu is alone unlikely to reduce VF/SCD

Ezetimibe added to statin therapy after acute coronary syndromes

BACKGROUND: Statin therapy reduces low-density lipoprotein (LDL) cholesterol levels and the risk of cardiovascular events, but whether the addition of ezetimibe, a nonstatin drug that reduces intestinal cholesterol absorption, can reduce the rate of cardiovascular events further is not known. METHODS: We conducted a double-blind, randomized trial involving 18,144 patients who had been hospitalized for an acute coronary syndrome within the preceding 10 days and had LDL cholesterol levels of 50 to 100 mg per deciliter (1.3 to 2.6 mmol per liter) if they were receiving lipid-lowering therapy or 50 to 125 mg per deciliter (1.3 to 3.2 mmol per liter) if they were not receiving lipid-lowering therapy. The combination of simvastatin (40 mg) and ezetimibe (10 mg) (simvastatin-ezetimibe) was compared with simvastatin (40 mg) and placebo (simvastatin monotherapy). The primary end point was a composite of cardiovascular death, nonfatal myocardial infarction, unstable angina requiring rehospitalization, coronary revascularization ( 6530 days after randomization), or nonfatal stroke. The median follow-up was 6 years. RESULTS: The median time-weighted average LDL cholesterol level during the study was 53.7 mg per deciliter (1.4 mmol per liter) in the simvastatin-ezetimibe group, as compared with 69.5 mg per deciliter (1.8 mmol per liter) in the simvastatin-monotherapy group (P<0.001). The Kaplan-Meier event rate for the primary end point at 7 years was 32.7% in the simvastatin-ezetimibe group, as compared with 34.7% in the simvastatin-monotherapy group (absolute risk difference, 2.0 percentage points; hazard ratio, 0.936; 95% confidence interval, 0.89 to 0.99; P = 0.016). Rates of pre-specified muscle, gallbladder, and hepatic adverse effects and cancer were similar in the two groups. CONCLUSIONS: When added to statin therapy, ezetimibe resulted in incremental lowering of LDL cholesterol levels and improved cardiovascular outcomes. Moreover, lowering LDL cholesterol to levels below previous targets provided additional benefit