Doctor of Philosophy / Department of Sociology, Anthropology, and Social Work / Gerad D. Middendorf / For over two decades the people of northern Uganda endured horrific atrocities during Africa’s forgotten war in the form of attacks and child abductions by the Lord’s Resistance Army, animal rustling by neighboring ethnic groups, and internal displacement of an unimaginable 90 percent of the northern parts of the country. With the majority of internally displaced persons spending over a decade in IDP camps, an entire generation of Acholi was socialized and acculturated in a non-traditional environment. A decade after the last LRA attack, I ask, what are the cultural impacts of the conflict and how has the culture recovered from the trauma. Using ethnographic analysis, this dissertation is rooted in over 150 interviews. While it has been presented to the world at large that Joseph Kony’s LRA is the one of the biggest problems facing the region, I found it is not the case. Interviewees discussed serious inadequacies in education, land conflict, culture loss, climate change, drought, famine, a perceived generational divide, and a strong distrust of the Ugandan government. Additionally this research examines the case of Uganda through the lens of, and attempts to build upon, Jeffrey Alexander’s cultural trauma process. I argue the increasing reach and instantaneous nature of social media can interact with, alter, and prolong the trauma process. The externalization of defining a problem and solutions for that problem while the trauma process is occurring, or shortly after the trauma has subsided, can lead to retraumatization.

Ageing and obesogenic diets are two prominent problems in the developed world, as both lead to an increase in body mass and insulin resistance, which can then result in further pathophysiologies, such as type 2 diabetes, cancer and cardiovascular disease. Protein tyrosine phosphatase 1B (PTP1B) contributes to development of body weight gain and insulin resistance through negatively regulating leptin and insulin signalling, respectively. Liver-specific ptp1b deletion from birth improves insulin sensitivity, lipid metabolism and decreases endoplasmic reticulum (ER) stress. However, as a therapy in humans, PTP1B inhibition would target pre-diabetic and diabetic adults; therefore, we investigated the effects of liver-specific inhibition of PTP1B in adult, insulin resistant, obese mice. Restricting the amount of the essential amino acid, methionine, five-fold in the diet, decreases body weight, adiposity and improves insulin sensitivity in young mice. In order to delineate if this would be a feasible treatment in adulthood, we administered the diet to 12-month-old mice with age-induced obesity and insulin resistance and compared its effects to those in 2-month-old mice. As hepatic ptp1b deletion and methionine restriction (MR) both improve hepatic insulin signalling, we investigated if the combined treatment could have additive effects compared to MR alone on whole-body glucose homeostasis. To examine if the effects of MR are methionine-specific or if they would occur with restriction of other EAAs, we compared leucine restriction (LR) to MR in adult mice. Overall, hepatic PTP1B inhibition in adult mice reversed high-fat diet (HFD) -induced glucose intolerance, hepatic lipid accumulation and ER stress. MR administered to 12-month-old adult mice reversed the metabolic effects of ageing back to levels measured in healthy, young, 2-month-old mice. The combination of MR and hepatic ptp1b deletion from birth had no further beneficial effect in male mice, but possibly an additional effect in female mice. MR produced stronger beneficial metabolic effects than LR in mice, suggesting methionine-specific mechanisms may play a role.

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In the present study, the corrosion behaviour of several magnesia-chrome (MC) and magnesia-alumina spinel (MA) bricks against fayalite type slags was investigated and the role of the spinel phases was highlighted . The experimental results revealed that the corrosion resistance of the MC bricks was superior to the MA bricks against KIVCET slags in static and dynamic conditions . As a result of the interaction between MgO from MC bricks and the slag, a modified forsterite phase (Mg, Fe, Zn, Ca)₂SiO₄ was formed, which destroyed the precipitated complex spinel bonds at the grain boundaries of periclase and magnesia-chromia spinel . Furthermore, both MgO and MgO-MgAl₂O₄ spinel in the MA brick dissolved into the slag, which resulted in modified forsterite phases of (Mg, Fe, Zn, Ca)₂SiO₄ and (Mg, Fe, Zn)(Fe, Al)₂O₄ complex spinels, respectively. In addition, the accretion formation in the KIVCET furnace was investigated through solubility experiments of Cr₂0₃ in the KIVCET slag with various amounts of lead, which revealed that the net contribution of Cr₂0₃ to the spinel formation is the highest in the barren (no Pb) slag, followed by high-lead (11% Pb) and it is the lowest for the low-lead (6% Pb) slag. The amount of spinel solid solution increased consistently with increasing Cr₂0₃ dissolved and the PbO existent in the slag. From examinations of several used bricks from the tuyere area of a Peirce Smith nickel converter, it was found that the corrosion is due to the interaction of the partially oxidized matte penetrating deep into the brick and the magnesia grains forming (Mg, Fe, Ni, Co) xOy spinels . Analyses of brick samples used in the KIVCET Electric Furnace roof identified deep reaching sulphation, which weakened the bonding phase between coarse magnesia grains. In the Bottom Blown Oxygen Converter, a highly aggressive lead and bismuth oxide rich slag penetrated deep into the brick, which destroyed the grain boundaries, causing the refractory to be easily eroded at the refractory-slag interface. Our studies concluded that the spinel phases, either as magnesium chromate, magnesium aluminate or complex spinel [(Mg, Fe)(Cr, Al, Fe)₂O₄], enhanced the corrosion resistance of a basic refractory to fayalite type slags from the non-ferrous smelting and converting furnaces. / Applied Science, Faculty of / Materials Engineering, Department of / Graduate

Type 2 diabetes mellitus results from a combination of insulin resistance and impaired insulin secretion. The aim of this study is to investigate the effect of endogenous and exogenous cannabinoids on insulin resistant cell lines, viz skeletal muscle (C2C12) and fat (3T3-L1), and to investigate the effects of these cannabinoids on insulin secretion in pancreatic β-cells (INS 1). Insulin resistance was induced in the cells using 20 ng/mL TNF-α (3T3-L1) and 100 nM insulin (C2C12). Insulin resistant cells were exposed to cannabinoids for 48 hours after which glucose uptake, RT-PCR and Western blot analysis was performed. Additionally, adipokine assays were performed on the 3T3-L1 cells. The insulin resistant 3T3-L1 and C2C12 cells had reduced glucose uptake, decreased IRS-1 and Glut-4 expression indicative of an insulin resistant state. The extract and THC significantly enhanced glucose uptake, IRS-1 and Glut-4 in 3T3-L1 and C2C12 cells. The extract and THC thus have the potential to be an insulin sensitizing agent. Interleukin-6 was significantly decreased by THC. INS 1 cells, cultured under normoglycemic conditions, were exposed to cannabinoids for 48 hours after which glucose-stimulated insulin secretion, radioimmunoassay, oxygen consumption, RT-PCR and Western blot analysis was performed. Insulin stimulatory index was not significantly affected after cannabinoid exposure, except by THC. The cannabinoids decreased insulin content, in a concentration dependent manner, but the inhibition mechanism remains elusive. The cannabinoid Treated cells showed insulin gene expression levels similar to the control, while only THC proved effective in significantly stimulating Glut-2 gene expression. Oxygen consumption studies showed levels lower than the control cells. Most of the cannabinoids inhibited insulin secretion under normoglycemia except THC, while the cannabinoids exhibited the potential to improve insulin resistant adipocyte and myocytes response to glucose and gene regulation.

Type 2 diabetes mellitus (T2DM) is rapidly emerging as one of the greatest global health issues of the 21st century. Insulin-resistance is a condition associated with T2DM and in the cell it is defined as the inadequate strength of insulin signalling from the insulin receptor downstream to the final substrates of insulin action involved in multiple metabolic, gene expression, and mitogenic aspects of cellular function. To investigate the potential mechanisms involved in the development of insulin-resistance, two in vitro liver cell models were established using palmitate or a combination of insulin and fructose as inducers. The development of insulin-resistance was determined via the capacity of the hepatocytes to maintain normal glucose metabolism functionality by measuring hepatic gluconeogenesis and glycogenolysis. It was established that the treatments induced the development of insulinresistance after 24 hours chronic exposure. Previous studies have investigated the potential of Sutherlandia frutescens extracts as therapeutic agents for insulin-resistance. The aim of this study was thus to investigate the ability of a hot aqueous extract of S. frutescens to reverse the insulin-resistant state, via measuring gluconeogenesis and glycogenolysis, the associated changes in cellular physiology (lipid accumulation, oxidative stress, and acetyl- CoA levels), and changes in mRNA expression. The results showed that S. frutescens had a significant effect on reversing the insulin-resistant state in both models of insulin-resistance. Furthermore, S. frutescens was capable of reducing lipid accumulation in the form of triacylglycerol in the high insulin/fructose model, while this was unaffected in the palmitate model. However, S. frutescens did reduce the accumulation of diacylglycerol in the palmitate model. Oxidative stress, seen to be associated with the insulin-resistant state, was successfully treated using the extract, as indicated by a reduction in reactive oxygen species. However no change was seen in the nitric oxide levels, in either model. Interestingly, although S. frutescens had no effect on the level of acetyl-CoA in the insulin/fructose model, it was found to increase this in the palmitate model. It is suggested that this may be due to increased β-oxidation and metabolic activity induced by the extract. The analysis of mRNA expression gave some insight into possible mechanisms by which insulin-resistance develops, although the results were inconclusive due to high variability in samples and the possibility of the RNA being compromised. Future studies will address this issue. The results of this study reflect different proposed clinical causes of insulin-resistance through the responses seen in the two cell models. These indicate that liver steatosis and insulin-resistance are induced by high palmitate as well as high insulin and fructose levels, and reversed by S. frutescens. Therefore the potential of S. frutescens to be used as a therapeutic agent in the treatment of insulin-resistance is indicated by this study.

In this study, 400 presumptive Enterococcus isolates previously recovered from Kat River and Fort Beaufort Abstraction water dam were subjected to molecular confirmation and pathotyping. Two hundred and seventy-four (68%) of these isolates were confirmed to be enterococci species. Confirmations studies were polymerase chain reaction (PCR) based, using enterococci specific primers targeting the tuf gene. The confirmed enterococci isolates were further differentiated into their pathotypes, the targets of which were: E. faecalis, E. avium, E. hirae, E. casseliflavarus and E. gallinarum using well documented species specific primer sequences. E. faecalis accounted for 20% of the isolates, followed by E. avium (16%), E. hirae (13%), E. casseliflavarus (5%) and E. gallinarum (3%). Furthermore, all the confirmed isolates were analysed for antibiotic susceptibilities using a panel of nine different antibiotics, namely vancomycin, linezolid, ciprofloxacin, ampicillin, gentamicin, chloramphenicol, tetracycline, erythromycin, penicillin, and those that were resistant were assayed for the presence of relevant antibiotic resistance genes. All the 274 isolates were found to harbour vanA resistance gene confirming their phenotypic resistance to the vancomycin. Similarly, 60% (109/180) of the isolates showed phenotypic resistance to erythromycin which was further confirmed by the presence of ermA genes in these isolates. The presence of antibiotic resistant bacteria in surface waters poses a risk to public health.

The effect of varying concentrations of glucose or the gastrointestinal hormones, gastric inhibitory polypeptide (GIP) and somatostatin (SS-14), on the in vitro immunoreactive insulin (IRI) response to the parasympathetic neurotransmitter, acetylcholine (ACh) was investigated. The isolated, vascularly perfused rat pancreas was used in all experiments. Acetylcholine (1.0 µM) did not stimulate IRI secretion in the presence of 2.2 mM glucose. However, in the presence of 4.4, 6.6, or 8.9 mM glucose, ACh (1.0 µM) potently stimulated IRI secretion (approximately fourfold). At a higher glucose concentration (17.8 mM), the IRI response to ACh was reduced. GIP also potentiated the IRI response to 1.0 µM ACh. This potentiation was most marked in the presence of 1.0 nM GIP, whereas the effect of concomitant infusion of 0.2 nM GIP and 1.0 µM ACh was only slightly greater than additive. SS-14 potently inhibited ACh-stimulated IRI secretion. These results demonstrated the glucose dependency of cholinergically stimulated IRI secretion, and that physiological levels of glucose and GIP increased B-cell sensitivity to cholinergic stimulation. It was suggested that the parasympathetic stimulation of IRI secretion associated with food intake could be affected by postprandial increases in glucose, GIP, and SS-14. The idea that endogenously released somatostatin may have influenced glucose or GIP-stimulated IRI secretion was not supported by the present experiments, since neither glucose (8.9 mM) nor GIP (2.0 nM) were found to have a significant effect on the release of pancreatic somatostatin-like immunoreactivity (SLI). Both atropine (1.0 µM) and hexamethonlum (100 µM) inhibited the IRI response to ACh. This suggested that the parasympathetic stimulation of IRI secretion was mediated not only by muscarinic receptors on the B-cell, but also by nicotinic receptors on intrapancreatic ganglia. Neither atropine nor hexamethonlum had a significant effect on glucose- or GIP-stimulated IRI secretion, indicating that the IRI response to these stimuli was not mediated by cholinergic receptors. Both SS-14 and the synthetic somatostatin analog SMS 201-995 (SMS; Sandostatin®) inhibited IRI secretion stimulated by 8.9 mM glucose, 2.0 nM GIP, or 1;.0 µM ACh, but not 17.8 mM glucose. The most potent inhibition by both SS-14 and SMS was observed in the presence of the weakest IRI stimuli (8.9 mM glucose and 1.0 µM ACh). These results suggested that the inhibitory effects of somatostatin on the B-cell could be overcome by the presence of strong stimuli. In addition, the inhibitory effects of the native hormone and the analog were found to be approximately equipotent (weight basis), indicating that the increased potency of SMS previously observed in vivo was due to its longer half-life in plasma, and not due to a more potent direct effect on the B-cell. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

This study examined the acute and chronic responses of brain-derived neurotrophic factor (BDNF), cathepsin B (CatB), insulin-like growth factor-1 (IGF-1), and interleukin-6 (IL-6) and if changes in these biomarkers were correlated during resistance training. Fourteen resistance trained men performed resistance training 3 days per week for 6 weeks in two groups. The only difference between groups was the proximity to failure of each set (4-6 repetitions in reserve or 1-3 repetitions in reserve). Serum was collected immediately before and after training on day 1 of weeks 1 and 6. There were no significant group interactions for any of the biomarkers assessed, there were no main effects for time (p>0.05), and no significant correlations were observed between any of the biomarkers. However, a significant main effect for exercise for BDNF (p=0.03) and IL-6 (p=0.003) was observed. For CatB, a significant exercise × time (p=0.002) interaction was observed, indicating differences in the acute change of CatB in week 6 (+15.78%; g=0.25) vs. week 1 (-7.46%; g=0.13). In summary, these results suggest that multi-joint resistance exercise far from failure can confer a BDNF response. This investigation is the first to demonstrate the potential for acute resistance exercise to elicit a transient increase in CatB. / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2021. / FAU Electronic Theses and Dissertations Collection

This study examined the effect of resistance training proximity to failure on strength, muscle hypertrophy, and fatigue. Fourteen men were randomized into two groups (4-6 rating of perceived exertion-RPE per set or 7-9 RPE per set) and completed an eight-week program. Squat and bench press strength, muscle thickness, subjective fatigue, muscle soreness, and biomarkers (creatine kinase-CK and lactate dehydrogenase-LDH) were assessed. There were no significant differences (p>0.05) in the rate of strength gains and equivalence testing revealed hypertrophy was not statistically similar nor different. All results for indirect markers of muscle damage and fatigue indicated similar recovery between groups within 48 hours; however, a small between group effect size (g=0.39) existed indicating higher session RPE in the 7-9 RPE group across the entire training program. These results suggest that strength and possibly hypertrophy outcomes are similar when training each set to 4-6 RPE or 7-9 RPE in trained men. / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2021. / FAU Electronic Theses and Dissertations Collection