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This thesis is aimed at the study of high angular momentum states in neutron deficient nuclei in the mass 60 region, with approximately equal numbers of protons and neutrons, (N~Z). The main motivations of this work are to provide an insight into the mechanisms for generation of high angular momentum states in a limited particle valence space above the N=Z=28 doubly magic core, and to investigate the role of the isospin quantum number in heavy N=Z nuclei. The decay scheme for the odd-odd N=Z nucleus 6231Ga has been deduced for the first time, and the decay schemes for 61Zn and 61Cu have been extended. The data came from two experiments, the first using the reaction 24Mg + 40Ca at a beam energy of 65 MeV, performed at the Argonne National Laboratory, Chicago, US, using the germanium gamma-ray detector array 'AYEBALL' in conjunction with the Argonne Fragment Mass Analyzer and a gas filled ionisation chamber. The second experiment using the reaction 28Si + 40Ca at a beam energy of 88 MeV was performed at the Niels Bohr Institute, Riso, Copenhagen, Denmark using the 'PEX' gamma-ray detector array with a charged particle detector ball and an array of liquid scintillator neutron detectors. The data analysis techniques and results of the experimental analysis are presented. Gamma-ray energy spectra for different nuclei are shown according to the mass, neutron number and proton number of the nucleus. The proposed decay schemes are justified by coincidence and DCO arguments, and are compared to shell model calculations using a restricted pf5/2 g9/2basis. In the case of 62Ga, these are then compared with the latest IBM-4 calculation, which explicitly includes T=0 and T=1 bosons. Suggestions are also made for future work to complement this data.

No description available.

The experiments in this thesis tested <i>in vitro</i> and <i>in vivo</i> the proposal that zinc-deficient superoxide dismutase, resulting from mutations or oxidative damage to the enzyme, gains ascorbate oxidase activity that contributes to the pathology of amyotrophic lateral sclerosis (ALS). They also tested whether flavonoids can help protect against this activity.<p>The <i>in vitro</i> experiments showed that zinc-extracted Cu/Zn-SOD (Cu-SOD) as well as SOD treated with H2O2 or H2O2 plus ascorbate accelerated ascorbate oxidation 100 to 300 %, while native SOD had no effect. With Cu-SOD, the activity was unaffected by EDTA, EGTA, or catalase, showing that the catalytic copper was firmly bound and that the H2O2 product of SOD activity was not responsible. Catechin and uric acid slowed ascorbate oxidation by Cu-SOD by 72% and 67%, respectively.<p>The <i>in vivo</i> study investigated tissue levels of ascorbate and biomarkers of oxidative stress in a transgenic mice bearing a mutation in Cu/Zn-SOD as a model of familial ALS (FALS mice), and the effects of dietary ascorbate and quercetin. In FALS mice on control modified AIN93G diet for 10 weeks compared to the wild-type, liver thiobarbituric acid reactive substances (TBARS) were 47% higher and liver oxidized vitamin C was 2800% higher. These results support, in liver, that mutant SOD acquired ascorbate oxidase activity and increased oxidative stress. The only difference in other tissues was a 136% increase in GSH/GSSG ratio in thigh muscle of FALS mice.<p>In dietary treatments of FALS mice, spinal cord TBARS was 93 % higher with ascorbate-supplemented diet compared to control diet, suggesting that dietary ascorbate increased oxidative stress. Also in spinal cord, oxidized-vitamin C was 250% higher in ascorbate + quercetin-fed FALS mice, which suggests there is no protection by quercetin against ascorbate oxidation. In brain, protein thiols were 56% and 58% lower in quercetin-fed and ascorbate + quercetin-fed FALS mice, suggesting that quercetin worsened oxidative damage. In liver, quercetin feeding produced a 40% decrease in vitamin C, total vitamin C and oxidized-vitamin C, perhaps by down-regulating ascorbate biosynthesis. Overall the results support a gain of ascorbate oxidase activity of mutant SOD in ALS, but do not support protection by dietary treatment with ascorbate or quercetin.

The experiments in this thesis tested <i>in vitro</i> and <i>in vivo</i> the proposal that zinc-deficient superoxide dismutase, resulting from mutations or oxidative damage to the enzyme, gains ascorbate oxidase activity that contributes to the pathology of amyotrophic lateral sclerosis (ALS). They also tested whether flavonoids can help protect against this activity.<p>The <i>in vitro</i> experiments showed that zinc-extracted Cu/Zn-SOD (Cu-SOD) as well as SOD treated with H2O2 or H2O2 plus ascorbate accelerated ascorbate oxidation 100 to 300 %, while native SOD had no effect. With Cu-SOD, the activity was unaffected by EDTA, EGTA, or catalase, showing that the catalytic copper was firmly bound and that the H2O2 product of SOD activity was not responsible. Catechin and uric acid slowed ascorbate oxidation by Cu-SOD by 72% and 67%, respectively.<p>The <i>in vivo</i> study investigated tissue levels of ascorbate and biomarkers of oxidative stress in a transgenic mice bearing a mutation in Cu/Zn-SOD as a model of familial ALS (FALS mice), and the effects of dietary ascorbate and quercetin. In FALS mice on control modified AIN93G diet for 10 weeks compared to the wild-type, liver thiobarbituric acid reactive substances (TBARS) were 47% higher and liver oxidized vitamin C was 2800% higher. These results support, in liver, that mutant SOD acquired ascorbate oxidase activity and increased oxidative stress. The only difference in other tissues was a 136% increase in GSH/GSSG ratio in thigh muscle of FALS mice.<p>In dietary treatments of FALS mice, spinal cord TBARS was 93 % higher with ascorbate-supplemented diet compared to control diet, suggesting that dietary ascorbate increased oxidative stress. Also in spinal cord, oxidized-vitamin C was 250% higher in ascorbate + quercetin-fed FALS mice, which suggests there is no protection by quercetin against ascorbate oxidation. In brain, protein thiols were 56% and 58% lower in quercetin-fed and ascorbate + quercetin-fed FALS mice, suggesting that quercetin worsened oxidative damage. In liver, quercetin feeding produced a 40% decrease in vitamin C, total vitamin C and oxidized-vitamin C, perhaps by down-regulating ascorbate biosynthesis. Overall the results support a gain of ascorbate oxidase activity of mutant SOD in ALS, but do not support protection by dietary treatment with ascorbate or quercetin.

This thesis is addressed to the theoretical controversy which revolves around the explanation of the higher unemployment rates that prevailed after 1957 . The debate that has been generated concerning the causes of this unemployment problem is usually referred to as the "structural" versus "deficient-demand" debate. An attempt is made to present a representative view of both sides of the debate as well as a critical evaluation of both positions. Care is taken to keep both positions separated for each leads to entirely different policy recommendations. A more general theoretical structure is presented which will be useful in analyzing the relevance of structural unemployment. Finally, the controversy is analyzed in terms of current economic development.

<p> Oxygen deficient SrTiO3-x with x = 0.28(2) was prepared in single crystal form and found to have a perovskite structure with a small tetragonal distortion. The structure was studied by powder and single crystal X-ray diffraction and electron diffraction. No long range order of the oxygen vacancies could be detected. The transport studies show that SrTiO2.72 is a metallic conductor. </p> <p> Some new K2NiF4 - type compounds, PrSrVO4, SmSrVO4, EuSrVO4 and PrSrGaO4, were prepared and studied by powder diffraction methods. The crystal structures of LaSrVO4, CeSrVO4, PrSrVO4 and NdSrVO4 were refined from powder neutron diffraction data. Powder X-ray diffraction data for all the new compounds above and for EuSrAlO4 are presented here. </p> <p> Magnetic susceptibilities are reported for SrTiO2.72 which exhibits metal-like Pauli-paramagnetism, PrSrGaO4, NdSrGaO4, EuSrAlO4 and LnSrVO4 where Ln = La, Ce, Pr and Nd. </p> / Thesis / Master of Science (MSc)

Thesis (MSc)--Stellenbosch University, 2015. / ENGLISH ABSTRACT: Reverse total shoulder arthroplasty is used as the treatment for arthritic rotator cuff deficient shoulders. Some of the most common complications of a reverse shoulder arthroplasty are scapular notching, glenoid dissociations, glenohumeral dislocation, loosening or dissociation of the humeral component and nerve injury. Clinical outcomes are dependent on the preoperative diagnosis, the function of the deltoid and remaining rotator cuff muscles, biomechanical design of the prosthesis, and the orientation and placement of the reverse shoulder component. This study aims to optimize the patient-specific placement of a reverse shoulder component. A simulation software package was developed that can be used to determine the optimal placement of the reverse shoulder prosthesis for a specific patient. This is achieved by maximizing the humerothoracic range of motion and minimizing the adduction deficit. The motion of the simulation model is driven by shoulder complex motion equations adjusted for each patient. This data was obtained from literature with the motion of the arm fixed to the coronal, scapular and sagittal elevation planes. The influence of the various components of the Tornier Aequalis® - Reversed II system, together with changing the glenoid component inclination and humeral component retroversion, was investigated. This allowed the simulation software to be verified and validated, as well as applying the insight and knowledge gained to a case study. Further simulations evaluated a design change of the humeral component neck-shaft angle from the standard 155 ° to 145 ° or 165 °. The reverse shoulder simulation software provides accurate patient-specific Three Dimensional (3D) pre-operative planning and shoulder complex motion simulation. / AFRIKAANSE OPSOMMING: Omgekeerde volledige skouerartoplastie word as behandeling van ontsteking in gewrigsomhulsel-aangetaste skouers gebruik. Onder die algemeenste komplikasies van 'n omgekeerde skouergewrig-operasie is kepe in die skouerblad (skapulier), lostrekkings of onthegting van die gewrigskom (glenoïede), ontwrigting van die boarm/skouergewrig, die loskom of onthegting van die boarmbeen en beskadiging van senuwees. Mediese resultate is afhanklik van diagnose voor die operasie, die werking van die driehoekspier (deltoïede) en oorblywende draaispiere, die biomeganiese ontwerp van die prostese en die oriëntasie en plasing van die omgekeerde skouerkomponent. Hierdie studie is gemik op die beste pasiënt-spesifieke plasing van die omgekeerde skouerkomponent. Die simulasie-sagtewarepakket wat ontwikkel is, kan gebruik word om die optimale plasing van die omgekeerde skouerprostese in die geval van 'n spesifieke pasiënt te bepaal. Dit word gedoen deur die bewegingsvermoë van die bo-armbeen te maksimaliseer en die gebrekkige werking van die trekspiere te minimaliseer. Die werking van die simulasiemodel word gedryf deur die beweging van skouerkomponente te vergelyk, aangepas vir elke pasiënt. Hierdie data is verkry uit literatuur en die koppeling van die arm se beweging aan die belangrikste, skouerblad- en sagittale elevasievlakke. Die invloed van die onderskeie komponente van die Tornier Aequalis® - Reversed II-stelsel is saam met die verandering van die gewrigskom-komponent se helling en bo-armkomponent se terugstoting ondersoek. Sodoende kon die simulasie-sagteware nagegaan, bevestig en geldig verklaar word; en die insig en kennis wat verkry is op 'n gevallestudie toegepas word. Met verdere simulasies is 'n ontwerpwysiging ge- ëvalueer waar die skouerkomponent se beenpyphoek vanaf die standaard van 155° na 145° of 165° verander is. Die omgekeerde skouersimulasiesagteware maak akkurate pasiëntspesifieke driedimensionele (3D) beplanning voor 'n operasie en simulasie van die bewegings skouerdele moontlik.

Biochemical consequences of ascorbate deficiency were studied in the leaf tissue of Arabidopsis thaliana ascorbate-deficient vtc mutants with a view of understanding the relationship between ascorbate, stress response and metabolism. Ascorbate is an important antioxidant and is also a cofactor for 2-oxoglutarate-dependent dioxygenases, which are involved in the biosynthesis of a number of metabolites. The response of wild type (Col-0) and vtc1, vtc2-1, vtc2-2 and vtc3-1 mutants to high light intensity, wounding and salinity was investigated using a metabolomics and proteomics approach. Metabolite profiling and comparative proteomics were performed by liquid chromatography-quadrupole time of flight mass spectrometry (LC-QToF MS) and targeted analysis of plant hormones and flavonoids by liquid chromatography triple-quadrupole mass spectrometry (LC-QQQ-MS). These combined analyses revealed the effect of ascorbate deficiency and stress on metabolites and cell wall proteins. LC-QToF-MS based untargeted metabolite profiling methodologies were developed for analysis of metabolites on a large scale. Using this method about 3000-5000 metabolites (mass-retention time pairs) could be reproducibly detected in A. thaliana leaf extract and aligned between samples. Approximately 1000 metabolites were differentially expressed between WT and vtc mutants in different experiments. Of these, twenty eight compounds were confirmed to be differentially expressed by LC-QQQ-MS between WT and vtc mutants, and eight of these compounds were positively identified and validated with standards. The plant hormones abscisic acid (ABA), salicylic acid (SA) and jasmonic acid (JA) have all been implicated in plant stress responses and differences in their accumulation in some of the vtc mutants have been reported. A systematic study of the response to stress of these hormones in several vtc mutants was carried out using LC- QQQ- MS. While some of the mutants showed increased SA and SA-glycoside accumulation, stress-induced ABA and JA accumulation was generally unaffected. Methods for identifying the metabolites in a targeted manner by LC- QQQ-MS was developed and were shown that all vtc mutants were impaired in the accumulation of anthocyanin in response to HL treatment. In strong contrast to anthocyanin, flavonol glycosides were not affected by ascorbate deficiency. Therefore, ascorbate deficiency has a specific effect on the anthocyanin biosynthesis. Ascorbate occurs in the plant cell wall and isolation of apoplastic fluid showed that all vtc mutants have decreased apoplastic ascorbate compared to WT. Ionically-bound proteins were from the cell wall of A. thaliana leaves. Peroxidase specific activity in this fraction tended to be higher in vtc mutants than WT. High light intensity also increased peroxidase activity in WT and vtc mutants. To determine which peroxidase isoenzyme caused increased peroxidase activity, ionically-bound cell wall N-glycosylated proteins were isolated by Concanavalin A chromatography and analysed by LC-QToF-MS. Comparison of WT and vtc2-2 grown in low light and high light identified 937 peptides significantly different between WT and vtc2-2 and some are also affected by light intensity. Specifically, peroxidases 33 and 34 had increased abundance in vtc2-2. The results show that ascorbate deficiency causes a detectable change in the metabolome of A. thaliana leaves, with specific effects on anthocyanin accumulation being detected. Ascorbate deficiency also influences the expression of cell wall proteins. Peroxidase activity is increased, and this response could be related to the increased pathogen resistance reported in vtc mutants.

Nonalcoholic steatohepatitis (NASH) has been identified as a source of significant inter individual variation in drug metabolism. A previous ex vivo study demonstrated significant changes in hepatic Cytochrome P450 (CYP) activity in human NASH. This study evaluated the in vivo activities of multiple CYP isoforms simultaneously in prominent diabetic NASH mouse models. The pharmacokinetics of CYP selective substrates: caffeine, losartan, and omeprazole changed significantly in a diabetic NASH mouse model, indicating attenuation of the activity of Cyp1a2 and Cyp2c29, respectively. Decreased mRNA expression of Cyp1a2 and Cyp2c29, as well as an overall decrease in CYP protein expression, was found in the diabetic NASH mice. Overall, these data suggest that the diabetic NASH model only partially recapitulates the human ex vivo CYP alteration pattern. Therefore, in vivo determination of the effects of NASH on CYP activity should be conducted in human, and more appropriate models are required for future drug metabolism studies in NASH.