by Lo Veng Cheong. / Parallel title in Chinese characters. / Thesis (Ph.D.) -- Chinese University of Hong Kong, 1991. / Bibliography: leaves 116-119. / ACKNOWLEDGEMENT --- p.i / ABSTRACT --- p.ii / LIST OF SYMBOLS --- p.iv / LIST OF FIGURES --- p.ix / LIST OF TABLES --- p.xii / Chapter CHAPTER ONE --- INTRODUCTION --- p.1 / Chapter CHAPTER TWO --- SURVEYS ON THEORETICAL MODELS --- p.7 / Chapter 2.1 --- Some Basic Concepts --- p.7 / Chapter 2.1.1 --- Vacancy Mechanism and Interstitial Mechanism --- p.7 / Chapter 2.1.2 --- Relative Contribution from Various Point Defects Species --- p.15 / Chapter 2.1.3 --- Impurity Point Defect Pairs or 'Centers' --- p.20 / Chapter 2.1.4 --- Anomalous Diffusion --- p.21 / Chapter 2.2 --- Historical Review on Theoretical Models --- p.22 / Chapter 2.3 --- Formulation of the General Model --- p.29 / Chapter 2.3.1 --- Effects to be and Not to be Considered --- p.30 / Chapter 2.3.2 --- Derivation of the Basic Equations --- p.31 / Chapter CHAPTER THREE --- MODELING OF THE DAMAGE ENHANCED DIFFUSION OF IMPLANTED BORONS IN SILICON --- p.35 / Chapter 3.1 --- Brief Description of Powell's Experiment --- p.35 / Chapter 3.2 --- Modeling --- p.38 / Chapter 3.3 --- Results and Discussion --- p.45 / Chapter CHAPTER FOUR --- EXPERIMENTAL INVESTIGATION OF BORON DIFFUSION DIFFUSION ASSISTED BY THE NON-UNIFORMITY OF POINT DEFECTS --- p.66 / Chapter 4.1 --- Introduction --- p.66 / Chapter 4.2 --- Experimental --- p.67 / Chapter 4.3 --- Results and Discussion --- p.88 / Chapter CHAPTER FIVE --- CONCLUSION AND FURTHER SUGGESTIONS --- p.103 / Chapter 5.1 --- Conclusion --- p.103 / Chapter 5.2 --- Further Suggestions --- p.104 / Chapter APPENDIX A --- DOPANT CONCENTRATION DEPENDENCE OF THE ENHANCED DIFFUSION --- p.107 / Chapter APPENDIX B --- FLOW CHART OF NUMERICAL SIMULATION --- p.111 / REFERENCE --- p.116

A ventricular septal defect occurring on its own is a congenital defect of the interventricular septum of the heart causing varying degrees of increased pulmonary blood flow and associated clinical symptoms. It may also occur in association with obstruction in the right ventricle resulting in diminished pulmonary blood flow. Very little is documented about the incidence of ventricular septal defects in South African children. The aim of this study was to briefly review the embryology and consider the normal anatomy of the interventricular septum. In addition, the clinical and surgical notes of all children that underwent surgical repair of ventricular septal defects (these included isolated ventricular septal defects, those with multiple ventricular septal defects, as well as those associated with tetralogy of Fallot and double chambered right ventricle) referred to the paediatric cardiothoracic unit at the Charlotte Maxeke Academic Hospital, from the Paediatric Cardiology units at the Charlotte Maxeke Academic Hospital, Chris Hani Baragwanath Academic Hospital and the Rahima Moosa Hospitals between 2001 and 2004, were analysed for the position, number of and size of ventricular septal defects. For this purpose, 11 cadaveric neonatal hearts were dissected while seven post-mortem specimens of the heart, four with isolated ventricular septal defects and three with tetralogy of Fallot were analysed. In addition, 50 cases of isolated ventricular septal defects, 42 cases with tetralogy of Fallot and eight cases with double chambered right ventricle were retrospectively reviewed. The membranous and the muscular septum made up the largest components of the interventricular septum in the normal neonatal hearts. A perimembranous ventricular septal defect was the most common type of defect diagnosed in these patients (the majority of the patients were Black children), 78% of cases with a single isolated ventricular septal defect, 90% in patients with tetralogy of Fallot, and 75% in the group with double chambered right ventricle. The average sizes of all perimembranous defects (from the echocardiogram) were classified as small, moderate or large. An additional interesting finding was prolapse of the right coronary cusp of the aortic valve into the isolated ventricular septal defect and occurred in 22% (11 out of 50) of patients. Aortic regurgitation occurred in association with prolapse of the right coronary cusp in 54.5% (5 out of 11) of cases. This prevalence in black patients is much higher than has been documented in White or Japanese children. Non-compaction of the left ventricle was seen in one post-mortem specimen in association with a perimembranous ventricular septal defect and dilated cardiomyopathy. This recently described abnormality is alluded to in the discussion. Attention is drawn to the abnormality known as double chambered right ventricle, where the size of the ventricular septal defect is variable and where the site of obstruction in the right ventricle is caused by muscle bundles lower than that seen in tetralogy of Fallot. Knowledge of ventricular septal defects found in South African children will help in the assessment and care of these patients with one of the most common congenital cardiac malformations.

Mitochondrial function is critical for the survival of eukaryotes. Hence, mitochondrial dysfunctions are involved in numerous human diseases. An essential process for a normal mitochondrial function is mitochondrial gene expression which is tightly regulated in response to various physiological changes. The accurate control of mitochondrial gene expression is essential in order to provide the appropriate oxidative phosphorylation capacity for diverse metabolic demands. Recent findings in the basic mitochondrial replication and transcription regulation helped advance our understanding of organelle function and basic pathogenetic mechanisms of mitochondrial DNA mutations associated with oxidative phosphorylation defects. Mitochondrial transcription is regulated by the mitochondrial transcription termination factor (mTERF) both at the initiation and termination levels. A protein family containing highly conserved mTERF motifs has been identified recently and its members named generically as "terfins." In this work, one of these factors, mTERFD3, has been characterized in vitro and in vivo. The mTERFD3 protein is highly conserved throughout evolution. It is a mitochondrial protein localized to the matrix and is abundantly expressed in high energy demand tissues. We found that it contains 4 putative leucine zippers and is able to form dimers in vitro. We showed that mTERFD3 binds mtDNA at the transcription initiation site in the mtDNA regulatory region. These findings suggest that mTERFD3 may be involved in regulating mitochondrial gene expression at the transcriptional initiation level. In order to study the functional significance of mTERFD3 in vivo we developed a mouse deficient in mTERFD3 using a gene trapping strategy. The KO mice had a normal lifespan but showed decreased weight gain and decreased fat content in females. Fibroblasts isolated from KO mice displayed decreased growth rate when compared with WT in respiratory media, and had decreased complex IV activity. Consistent with the above findings, we found that muscle, one of the tissues with high energy demands, showed abnormal mitochondrial function, displaying features characteristic of mitochondrial myopathy such as decreased muscle strength and endurance. Muscle mitochondria of the KO mice showed a significant decrease in the complex II +III and complex IV activity. The decrease in OXPHOS complexes activity was associated with increased citrate synthase activity, suggesting mitochondrial proliferation, a feature typical for mitochondrial disorders. Another important finding was a decrease in the muscle mitochondrial transcripts in the KO animals associated with decreased steady state levels of OXPHOS subunits. Together these data suggest that mTERFD3 is a mitochondrial protein involved in the regulation of mtDNA transcription. mTERFD3 KO is not embryonic lethal suggesting that it is involved in the fine tuning of mitochondrial transcription. We conclude that mTERFD3 is a mitochondrial protein that modulates oxidative phosphorylation function, probably by directed interactions with the mtDNA regulatory region. This work shows the importance of mTERFD3, an mTERF family member, in the mitochondrial gene expression regulation.

Pipelines are one of the safest forms of transportation for oil and gas. However, pipelines may experience some defects, such as cracks, corrosion and cracks in corrosion, during service period. In this thesis, the current defect assessment methods for crack, corrosion and crack in corrosion defects are reviewed. The aim of this study was to evaluate the effect of the crack in corrosion defects on the failure pressure of natural gas transmission pipelines. Consequently, a series of burst tests with varying defect depths were undertaken on end-capped, seam-welded API 5L Grade X60 (433 MPa yield stress) pipeline steel of external diameter 508 mm (20 inch), 5.7 mm wall thickness. Defects were created by pre-fatiguing the pipe to create a crack. The number of cycles required to create a fatigue crack were varied between 75000 to 150000 cycles based on the desired final defect depth. For the (CIC) defects, the pipe was pre-fatigued to create a sharp crack, and the artificial corrosion defect was simulated by machining a rectangular groove over the fatigue crack. The rupture tests were conducted by pressurizing the pipe until failure occurred. Results were analyzed using various assessment methods. For the artificial corrosion defects, the predicted failure pressures based on RSTRENG were more reliable than those based on Modified B31G. This study revealed that CorLAS provided the least conservative prediction for crack defects, whereas the other methods provided more conservative estimates of failure pressure. Moreover, the predicted failure pressure of the level 3 FAD for API 579 cylinder equations had better agreement with experimental results in comparison with the other methods, i.e. BS7910 and NG-18. The failure pressure for CIC defects for pipes tested fell between corrosion defects (lower bound) and crack defects (upper bound). The transition to crack defect behavior only occurs when the crack defect depth is significant or vice versa. It should be noted that the crack to corrosion ratio is not the only parameter to evaluate a CIC defect. There are other parameters such as total defect depth and defect profile, which affect the failure behavior of a CIC defect.

Pipelines are one of the safest forms of transportation for oil and gas. However, pipelines may experience some defects, such as cracks, corrosion and cracks in corrosion, during service period. In this thesis, the current defect assessment methods for crack, corrosion and crack in corrosion defects are reviewed. The aim of this study was to evaluate the effect of the crack in corrosion defects on the failure pressure of natural gas transmission pipelines. Consequently, a series of burst tests with varying defect depths were undertaken on end-capped, seam-welded API 5L Grade X60 (433 MPa yield stress) pipeline steel of external diameter 508 mm (20 inch), 5.7 mm wall thickness. Defects were created by pre-fatiguing the pipe to create a crack. The number of cycles required to create a fatigue crack were varied between 75000 to 150000 cycles based on the desired final defect depth. For the (CIC) defects, the pipe was pre-fatigued to create a sharp crack, and the artificial corrosion defect was simulated by machining a rectangular groove over the fatigue crack. The rupture tests were conducted by pressurizing the pipe until failure occurred. Results were analyzed using various assessment methods. For the artificial corrosion defects, the predicted failure pressures based on RSTRENG were more reliable than those based on Modified B31G. This study revealed that CorLAS provided the least conservative prediction for crack defects, whereas the other methods provided more conservative estimates of failure pressure. Moreover, the predicted failure pressure of the level 3 FAD for API 579 cylinder equations had better agreement with experimental results in comparison with the other methods, i.e. BS7910 and NG-18. The failure pressure for CIC defects for pipes tested fell between corrosion defects (lower bound) and crack defects (upper bound). The transition to crack defect behavior only occurs when the crack defect depth is significant or vice versa. It should be noted that the crack to corrosion ratio is not the only parameter to evaluate a CIC defect. There are other parameters such as total defect depth and defect profile, which affect the failure behavior of a CIC defect.

No description available.

published_or_final_version / Physics / Master / Master of Philosophy

published_or_final_version / Physics / Master / Master of Philosophy

No description available.

In this investigation, controlled thermal annealing and oxidation treatments were carried out on wafers obtained from seed-end and tang-end regions of (100)-oriented, 75 mm-diameter, Czochralski-grown, "typical" silicon single crystals. The radial variation of resistivity was characterized with four-point probe and spreading resistance probe measurements. The defects were studied by preferential etching and optical microscopy, using Wright etch for characterizing the individual etch figures, whereas the overall distribution of defects was obtained by using a modified form of Sirtl etch. The preferential etching was carried out in a Teflon barrel under controlled conditions. Transmission electron microscopy (TEM) was carried out on selected samples to study the defect structure in the as-grown crystal as well as after specific thermal treatments. In the p-type as well as n-type crystals studied in this work, the relative radial gradient as well as the magnitude of resistivity are greater at the seed-end than at the tang-end. An annealing treatment at 650°C for 100 min on seed-end wafers stabilized the resisitivity by destroying oxygen-donor complexes. Such an annealing treatment on tang-end wafers has a minor effect on the resistivity of the sample, which was uniform initially. The "swirl" patterns, as revealed by preferential etching, showed that they are more pronounced in seed-end wafers and are almost absent in tang-end wafers. A pre-annealing treatment at 650°C in argon for 100 min followed by a high-temperature (≥800°C) treatment precipitates the swirl pattern much more intensely, in comparison to just the high temperature treatment without any preanneal at 650°C. For comparable oxide thicknesses (0.5 μm) for thermal oxidation in steam at three different temperatures (900°C, 1050°C, 1200°C), it was found that the swirl pattern was most severe at 900°C and the dissolution of the defect structure progressively increased with increasing temperature. It was found in this investigation that bulk-type stacking faults are generated after argon annealing at 1050°C. This is in contrast to the generally prevailing confusion that thermal oxidation is essential for generation of stacking faults in silicon. It must be distinguished here that the formation of surface-type stacking faults requires thermal oxidation, whereas bulk-type stacking faults nucleate at individual swirl defects due to precipitation of dissolved oxygen. TEM work done in this investigation showed that as-grown CZ silicon defect structure consists of an assortment of precipitates, small dislocation lines, and a helical type of long (∼24 μm) dislocation line, and another long linear defect with periodically spaced nodes. The annealing treatment at 650°C as well as thermal oxidation at 900°C produce a spectrum of precipitates and small dislocations.