Criticism of the testamentary undue influence doctrine in the United States: lessons for South Africa?

This article analyzes undue influence in the South African law of wills in light of scholarly criticism of the testamentary undue influence doctrine in the United States. The Article assesses particularly whether the so-called “undue influence paradox”, identified in American scholarship, is manifest in the South African law of wills: is testamentary undue influence’s role as protector of testamentary freedom undermined in order to realize economic family protectionism? The Article proceeds, with due recognition of the differences between the American and South African legal traditions, from American scholars’ conceptualization of the paradox and their views on other complexities associated with the doctrine, to an exposition on the conceptualization, the statutory regulation, and the judicial utilization of testamentary undue influence in South Africa. The Article determines whether or not the South African legal position conforms to some or all of the assertions made in regard to the undue influence paradox and further complexities associated with the testamentary undue influence doctrine in the American context. The Article provides a mixed jurisdiction’s response to the call for the abolition of the testamentary undue influence doctrine in recent scholarship from the United States.National Research Foundation (NRF

Dry and back again: characterization of desiccation-associated differentiation of leaf tissues in Craterostigma pumilum Hochst

Resurrection plants are a polyphyletic group of angiosperms which display true desiccation tolerance - the ability to survive near complete loss of cellular water for extended periods, while recovering metabolic competence upon watering. This is achieved by employing tailored protection behaviours depending on the relative state of (de)hydration. Recent work has raised interest in desiccation associated changes related to tissue destiny in desiccation tolerant vegetative tissues. In this thesis, physiological and transcriptomic techniques were used to characterize such a phenomenon in the homoiochlorophyllous dicot resurrection plant Craterostigma pumilum. Detailed phenotypic observation and pulse-amplitude-modulation fluorometry were used to identify the critical water contents at which key physiological changes occur in leaves of C. pumilum and how this relates to desiccation-associated differentiation between leaf Tip and Base tissues. This was followed by transcriptomic analyses and comparison between these two tissues, to identify potentially key processes involved in desiccation associated tissue differentiation. All findings were then synthesised with existing information reported on for other resurrection plant species to create a theoretical model of desiccation-associated tissue differentiation. This differentiation phenomenon is shown to be transcriptionally initiated during the desiccation commitment stage of the C. pumilum dehydration cycle but is only realised phenotypically during early rehydration and after initial water movement through the leaf tissues. This work provides strong evidence for the existence of desiccation-associated tissue differentiation in C. pumilum and highlights the potential involvement of the phytohormone auxin in the determination of leaf tissue responses to progressive dehydration and anhydrobiosis in resurrection plants

The pharmacological modification of reperfusion injury with particular reference to calcium fluxes in the isolated rat heart

Myocardial reperfusion injury is thought to be caused by reperfusion induced i) cytosolic Ca²⁺ overload and/or, ii) the formation of oxygen derived freeradicals. At the start of this study, data implicating cytosolic Ca²⁺ overload in the genesis of reversible reperfusion injury were inconclusive. Although several workers have approached this problem by measurements of cytosolic calcium ions, it was my aim to examine the potential sources of such calcium overload. The experiments reported in this thesis were therefore designed to examine the role of altered intracellular and transsarcolemmal Ca²⁺ fluxes in the genesis of reperfusion stunning and arrhythmias. The study was also aimed at elucidating the possible sources and entry pathways contributing to this proposed cytosolic Ca²⁺ overload. In order to investigate the possible role of altered reperfusion Ca²⁺ fluxes in reperfusion injury, we exposed the isolated working, and Langendorff perfused rat heart model to ischaemia and reperfusion to induce reperfusion stunning and arrhythmias. Hearts were pre-treated (before ischaemia) or reperfused with pharmacological compounds, or by interventions known to enhance or inhibit intracellular or transsarcolemmal Ca²⁺ fluxes. The severity of reperfusion stunning (mechanical dysfunction) was measured by reperfusion aortic output, coronary flow and left ventricular pressure. The incidence of reperfusion ventricular arrhythmias was measured by the incidence of ventricular tachycardia and/ or fibrillation. In selected studies, the metabolic status of hearts was evaluated using biochemical assays performed on myocardial tissue samples. Data obtained in these studies indicate that increased Ca²⁺ fluxes through sarcolemmal L-type Ca²⁺ channels during early reperfusion exacerbate stunning, while inhibition of these fluxes with the Ca²⁺ antagonist drug nisoldipine or by Mg²⁺ or Mn²⁺ improve reperfusion function. These data also suggest that although interventions increasing Ca²⁺ fluxes early in reperfusion exacerbate reperfusion stunning, these same interventions improve reperfusion function when performed later. The data also indicate that Ca²⁺ may enter the myocyte indirectly via activation of the Na⁺/H⁺ and Na⁺/Ca²⁺ exchanger during reperfusion. Inhibition of Na⁺/H⁺ exchange activity by HOE 694 during reperfusion attenuated reperfusion stunning and arrhythmias. Both activation of the Na⁺/H⁺ (and Na⁺/Ca²⁺) exchanger and Ca²⁺ influx via the Ca²⁺ channel could contribute to reperfusion induced Ca²⁺ overload and subsequent injury. The study also showed that altered intracellular Ca²⁺ oscillations play a role in reperfusion stunning and arrhythmias as shown by the use of the SR Ca²⁺ release channel blocker, ryanodine. Inhibition of the sarcoplasmic reticulum Ca²⁺ A TP-ase pump by two novel inhibitors, thapsigargin and cyclopiazonic acid, during ischaemia and early reperfusion improved reperfusion function and reduced the incidence of ventricular arrhythmias. function when unphysiologically high concentrations of the peptide were infused into the heart during reperfusion. Taken together, these data suggest that: 1) Ca²⁺ fluxes during early reperfusion (intracellular and transsarcolemmal) play a role in reperfusion injury, 2) that both the Ca²⁺ channel and Na⁺/H⁺ exchange activity contribute to reperfusion injury by possibly contributing to cytosolic Ca²⁺ overload and that, 3) altered intracellular Ca²⁺ oscillations through the SR play a role in both stunning and arrhythmias. Thus the proposal is that modulation of Ca²⁺ fluxes through either the sarcolemma or the sarcoplasmic reticulum, lessen reperfusion injury (stunning and arrhythmias). Although these data do not provide direct evidence of reperfusion Ca²⁺ overload, they support the concept that calcium ions play a role in the genesis of reversible reperfusion injury

A general solution to optimising the DC-bus energy storage requirements in single phase inverers

Thesis is submitted in fulfilment of the requirements for the degree of Master of Science in Engineering to the Faculty of Engineering and Built Environment, University of the Witwatersrand, Johannesburg 2018Power electronic converters that convert DC to AC, or vice versa, require an energy buffer between the AC and DC ports of the converter to compensate for the instantaneous power mismatch. Electrolytic capacitors are mostly used for these buffering applications because of the high energy density when compared to other capacitors, but unfortunately this type of capacitor also has low reliability. This dissertation proposes a general solution from a fundamental approach to solve the required capacitor power requirements on the DC-bus of an inverter. From the resulting model, an alternative active filter design technique to reduce the required capacitance of the DC-bus capacitor of a single phase inverter is presented. In this model, the minimum and maximum voltages of the capacitor can be chosen and the corresponding waveforms are calculated. An optimum region for the choice of capacitor voltage is shown to visually illustrate the trade-offs between the capacitor voltage, capacitance and converter losses. In this optimum area the reduction in capacitance is enough to allow the elimination of electrolytic capacitors, while maintaining comparable volume. In this technique, the DC-bus capacitor is decoupled from the DC-bus to allow wide voltage variation and the power processed by the capacitor is directly controlled, instead of the bus voltage. The allowable voltage variation of the capacitor can also be selected to fit the application or traded off in favour of capacitance as chosen by the designer. This general solution is applicable to any bi-directional converter used to decouple the capacitor from the DC-BusXL201

A.N. Pelzer, 1915-1981

Waar ek teenwoordig was toe prof Pelzer op sy eie voortreflike wyse die lewe en betekenis van sy voorganger as professor in Geskiedenis, prof. I D Bosman, in oenskou geneem bet, daar is dit met huiwering dat ek hier oor hom, my voorganger as professor in Geskiedenis, probeer skryf