Advanced Bulk Processing of Lightweight Materials for Utilization in the Transportation Sector

The overall objective of this research is to develop the microstructure of metallic lightweight materials via multiple advanced processing techniques with potentials for industrial utilization on a large scale to meet the demands of the aerospace and automotive sectors. This work focused on (i) refining the grain structure to increase the strength, (ii) controlling the texture to increase formability and (iii) directly reducing processing/production cost of lightweight material components. Advanced processing is conducted on a bulk scale by several severe plastic deformation techniques including: accumulative roll bonding, isolated shear rolling and friction stir processing to achieve the multiple targets of this research. Development and validation of the processing techniques is achieved through wide-ranging experiments along with detailed mechanical and microstructural examination of the processed material. On a broad level, this research will make advancements in processing of bulk lightweight materials facilitating industrial-scale implementation. Where accumulative roll bonding and isolated shear rolling, currently feasible on an industrial scale, processes bulk sheet materials capable of replacing more expensive grades of alloys and enabling low-temperature and high-strain-rate formability. Furthermore, friction stir processing to manufacture lightweight tubes, made from magnesium alloys, has the potential to increase the utilization of these materials in the automotive and aerospace sectors for high strength - high formability applications. With the increased utilization of these advanced processing techniques will significantly reduce the cost associated with lightweight materials for many applications in the transportation sectors

Critical success factors of Jewish entrepreneurs : a South African perspective

This study aims to explore the critical success factors of Jewish entrepreneurs in South Africa. The primary purpose of this study was to determine what elements contribute to the success of Jewish entrepreneurs and what causes these elements.In doing so, these entrepreneurs were classified into two groups, namely successful and less successful.For the purpose of this study success was measured using two variables:1. Turnover 2. GrowthTurnover - for the purpose of this study an annual turnover of R2 000 000 was used as an indicator to classify the different companies into successful and less successful. If a company turned over more than R 2 000 000 then it fell into the successful category and vice versa.Growth - growth was measured by the increase/decrease of three employees from the companies’ inception until its current state.It was evident that culture plays an extremely important role in this study which was confirmed by the literature. The co-ethnic ties within the Jewish community are extremely strong and are a major contributing factor.Information was gathered via the means of a questionnaire consisting of 28 questions. 50 questionnaires were sent out and 32 were received back. From these 32 responses, the author extracted the relevant information.The author discovered that Jewish people in South Africa are an ethnic minority and was unable to pinpoint an exact reason for the success of Jewish entrepreneurs in South Africa.Dissertation (MBA)--University of Pretoria, 2012.Gordon Institute of Business Science (GIBS)unrestricte

The immunological consequences of obesity on primary and secondary immune defenses to the 2009 pandemic H1N1 influenza virus

Obese individuals are more susceptible to hospitalization and death from infection with the 2009 pandemic H1N1 influenza virus (pH1N1). Greater pH1N1 severity in the obese is a global public health concern given the persistent threat of influenza outbreaks and the current obesity epidemic. In this dissertation, the consequences of obesity on pH1N1 immunity were investigated in mice to uncover mechanisms by which obesity enhances pH1N1 illness. During a primary pH1N1 infection, 80% of obese mice died compared with 40% of lean, low fat diet fed mice and no mortality in lean, chow fed mice. Further, a genetic model of obesity was generated in which leptin signaling was conditionally disrupted in hypothalamic neurons to confirm that obesity, independent of diet, enhances pH1N1 mortality. Both diet- and genetic-induced obese mice exhibited greater lung damage during infection, likely due to fewer lung regulatory T cells and impaired regulatory T cell function. We extended our analysis to include a secondary heterologous pH1N1 infection model. Obese mice had fewer cross-reactive, non-neutralizing pH1N1 antibodies, overactive CD8+ effector memory T cell responses and greater lung damage in this model. During the primary pH1N1 infection, obese mice had greater serum and bronchoalveolar lavage leptin concentrations compared with lean mice. Given that leptin regulates T cell function, we then determined if conditional disruption of leptin signaling in T cells ameliorates obesity-induced pH1N1 mortality. However, obese mice lacking leptin signaling in T cells were not protected from pH1N1 mortality compared with control, obese mice. The pathophysiological complications of obesity are diverse and complex. Therefore, we also extended our analysis to include 1H NMR-based metabolic profiling of urine, feces, serum, lungs, bronchoalveolar lavage fluid, mesenteric white adipose tissue, and livers to obtain a more comprehensive examination of infection responses in obese mice. We uncovered a number of metabolites and metabolic signatures uniquely altered in obese mice that, ultimately, may facilitate early prediction of influenza infection outcomes and help to identify mechanisms for impaired. In summary, novel immunologic and metabolic techniques were integrated in this dissertation to establish that obesity enhances greater lung damage during primary and secondary pH1N1 infections in mice.Doctor of Philosoph

Sustained Id2 regulation of E proteins is required for terminal differentiation of effector CD8+ T cells.

CD8+ T cells responding to infection differentiate into a heterogeneous population composed of progeny that are short-lived and participate in the immediate, acute response and those that provide long-lasting host protection. Although it is appreciated that distinct functional and phenotypic CD8+ T cell subsets persist, it is unclear whether there is plasticity among subsets and what mechanisms maintain subset-specific differences. Here, we show that continued Id2 regulation of E-protein activity is required to maintain the KLRG1hi CD8+ T cell population after lymphocytic choriomeningitis virus infection. Induced deletion of Id2 phenotypically and transcriptionally transformed the KLRG1hi "terminal" effector/effector-memory CD8+ T cell population into a KLRG1lo memory-like population, promoting a gene-expression program that resembled that of central memory T cells. Our results question the idea that KLRG1hi CD8+ T cells are necessarily terminally programmed and suggest that sustained regulation is required to maintain distinct CD8+ T cell states

The impact of obesity on the immune response to infection

There is strong evidence indicating that excess adiposity negatively impacts immune function and host defence in obese individuals. This is a review of research findings concerning the impact of obesity on the immune response to infection, including a discussion of possible mechanisms. Obesity is characterised by a state of low-grade, chronic inflammation in addition to disturbed levels of circulating nutrients and metabolic hormones. The impact of these metabolic abnormalities on obesity-related comorbidities has undergone intense scrutiny over the past decade. However, relatively little is known of how the immune system and host defence are influenced by the pro-inflammatory and excess energy milieu of the obese. Epidemiological data suggest obese human subjects are at greater risk for nosocomial infections, especially following surgery. Additionally, the significance of altered immunity in obese human subjects is emphasised by recent studies reporting obesity to be an independent risk factor for increased morbidity and mortality following infection with the 2009 pandemic influenza A (H1N1) virus. Rodent models offer important insight into how metabolic abnormalities associated with excess body weight can impair immunity. However, more research is necessary to understand the specific aspects of immunity that are impaired and what factors are contributing to reduced immunocompetence in the obese. Additionally, special consideration of how infection in this at-risk population is managed is required, given that this population may not respond optimally to antimicrobial drugs and vaccination. Obesity impacts millions globally, and greater understanding of its associated physiological disturbances is a key public health concern

The inflammation highway: metabolism accelerates inflammatory traffic in obesity

As humans evolved, perhaps the two strongest selection determinants of survival were a robust immune response able to clear bacterial, viral, and parasitic infection and an ability to efficiently store nutrients to survive times when food sources were scarce. These traits are not mutually exclusive. It is now apparent that critical proteins necessary for regulating energy metabolism such as peroxisome proliferator-activated receptors (PPARs), Toll-like receptors (TLRs), and fatty acid-binding proteins (FABPs) also act as links between nutrient metabolism and inflammatory pathway activation in immune cells. Obesity in humans is a symptom of energy imbalance: the scale has been tipped such that energy intake exceeds energy output and may be a result, in part, of evolutionary selection toward a phenotype characterized by efficient energy storage. As discussed in this review, obesity is a state of low-grade, chronic inflammation that promotes the development of insulin resistance and diabetes. Ironically, the formation of systemic and/or local, tissue-specific insulin resistance upon inflammatory cell activation may actually be a protective mechanism that co-evolved to repartition energy sources within the body during times of stress during infection. However, the point has been reached where a once beneficial adaptive trait has become detrimental to the health of the individual and an immense public health and economic burden. This article reviews the complex relationship between obesity, insulin resistance/diabetes, and inflammation, and while the liver, brain, pancreas, muscle, and other tissues are relevant, we focus specifically on how the obese adipose microenvironment can promote immune cell influx and sustain damaging inflammation that can lead to the onset of insulin resistance and diabetes. Finally, we address how substrate metabolism may regulate the immune response and discuss how fuel uptake and metabolism may be a targetable approach to limit or abrogate obesity-induced inflammation

Creation of Two Valid Scales: Willingness to Fly in an Aircraft and Willingness to Pilot an Aircraft

The purpose of the current study was to develop two scales that could be used concurrently or independently to measure passenger willingness to fly (WTF), and aviator willingness to pilot (WTP), respectively. This is especially useful to determine challenges involving acceptance of new aviation technology for both pilots and passengers. There were five stages in developing the WTF scale for passengers, following Hinkin’s scale development process. Cronbach’s Alpha and Guttmann’s Split Half tests were used to confirm high internal consistency and reliability, while factor analysis was used to confirm construct validity. The scale was tested in order to confirm sensitivity to differences in actual participant willingness to fly. After developing the WTF scale for passengers, researchers made minor lexical adjustments and created the WTP scale, calculating Cronbach’s Alpha, Guttmann’s Split Half test, and factor analysis; thus, ensuring high internal consistency, reliability and validity. These two scales may help provide researchers with a better applied understanding of applications within the aviation and consumer perceptions literature and also assist with pilot training and acceptance of new aviation technology

Diffusion of Macromolecules across the Nuclear Pore Complex

Nuclear pore complexes (NPCs) are very selective filters that monitor the transport between the cytoplasm and the nucleoplasm. Two models have been suggested for the plug of the NPC. They are (i) it is a reversible hydrogel or (ii) it is a polymer brush. We propose a mesoscopic model for the transport of a protein through the plug, that is general enough to cover both. The protein stretches the plug and creates a local deformation. The bubble so created (prtoein+deformation) executes random walk in the plug. We find that for faster relaxation of the gel, the diffusion of the bubble is greater. Further, on using parameters appropriate for the brush, we find that the diffusion coefficient is much lower. Hence the gel model seems to be more likely explanation for the workings of the plug