A Classical Investigation of the Dynamics of MgO Grain Boundaries and an Ab Initio Study of Oxygen Vacancies in Amorphous SiO2

The arrangement of atoms in most ceramic materials is not perfect and point defects such as vacancies and interstitials, as well as extended defects like grain boundaries exist. In general these defects dominate the properties and processes that are important for the applications of the material. The capture and emission of charge at point defects can affect the stability of dielectrics such as those used in MOS devices. The presence of grain boundaries is also known to lower both the electric and thermal conductivity of a material. Collectively the diffusion of point defects at grain boundaries play a role in mechanisms such as creep and have also been suggested to be involved in the corrosion of metals. In this thesis simulation techniques were used to investigate properties of defects in amorphous silica and near grain boundaries in MgO. Atomistic methods were used to determine the migration barriers of defects at MgO grain boundaries, the effect of electric field on the stability of the defects, and also the effect of temperature on the structure and stability of the grain boundaries. The nudged elastic band method was used to determine the activation energy for vacancy and interstitial migration at the Σ17 {410}/[001] tilt and the Σ5 twist grain boundaries. At the tilt and the twist grain boundaries it was found that the activation energies for vacancy migration were up to 1.31 eV and 1.41 eV lower than those in bulk MgO respectively. A finite MgO film model was produced to investigate the effect of electric field on point defects at the tilt grain boundary. The electric field was added to the system by sandwiching the MgO between two layers of point charges. It was found that the field anisotropically lowers the activation energies for vacancy migration by up to 0.37 eV with respect to those determined in the absence of the field. Molecular dynamics simulations were used to investigate the effect of temperature on the stability of the tilt grain boundary and two of its metastable structures and also on the twist grain boundary. The twist grain boundary was found to have the highest entropy in the temperature range 300 - 3000 K which suggests that it may be the most commonly occurring grain boundary in MgO. An ab initio study was also carried out on the structure and electronic structure of the neutral oxygen vacancy in amorphous silica in order to investigate mechanisms associated with dielectric breakdown such as negative bias temperature instability. Contrary to published suggestions the positively charged and neutral vacancy defects studied were found to have one electron energy levels below the Si valence band which suggests that these defects do not contribute to threshold voltage shifts

Waste and decommissioning

This paper is the fifth in a series of 8 that make up the evidence base for SDC report 'The role of nuclear power in a low carbon economy'.This document is an extensive review of the nuclear waste issue, covering radioactive waste management in both practice and policy.Publisher PD

Safety and security

This paper is the sixth in a series of 8 that make up the evidence base for SDC report 'The role of nuclear power in a low carbon economy'.The document covers accident risk in plants (including a historical review of accidents), threats from design faults and terrorism, the implications of nuclear proliferation, and health impacts.Publisher PD

Dedifferentiation of stromal smooth muscle as a factor in prostate carcinogenesis

We had earlier established an animal model of prostate carcinogenesis using a combination of testosterone (T) and 17β-estradiol benzoate (E2) on Noble rats (Wang and Wong, 1998). In the present study we examined the changes in a number of smooth muscle differentiation markers including smooth muscle α-actin and myosin, vinculin, desmin, laminin and vimentin as well as changes in fine structure by electron microscopy. Our immunohistochemical (IHC) studies revealed that smooth muscle cells (SMCs) subjacent to dysplastic (precancerous) sites and carcinoma usually exhibited a preferential loss of myosin, desmin and laminin. However, the expression of α-actin and vinculin appeared to be more persistent in most dysplastic or neoplastic sites. The study reaffirmed our earlier observation that there was a concurrent dedifferentiation of surrounding SMCs during the development and progression of prostate carcinogenesis. The structural study revealed that SMC subjacent to epithelial dysplasia displayed a spectrum of derangements. These included the loosening of muscular layers with SMC characterized by their highly irregular external contours with numerous spine-like cytoplasmic projections. There was also a reduction in density of myofilaments and presence of many enlarged caveolae in muscle cells. Additionally, focal discontinuity or disruptions of muscular layer were often observed together with an increase in abundance of fibrous connective tissue. Moreover, the amount of smooth muscle appeared to be inversely correlated with the histologic grade of prostate tumors. In most instances, SMCs were totally absent in the moderately or poorly differentiated tumors and in metastatic tumors in the lung and the small intestine. Stromal muscular deformity was associated with concurrent changes in epithelial cells. Dysplastic epithelial cells were characterized by a reduction in abundance of secretory organelles such as reduction in size of Golgi apparatus, paucity of granular endoplasmic reticulum and secretory vesicles. The nuclei showed typical deformity characterized by deep nuclear membrane foldings. The basal lamina of dysplastic or tumor cells was present although focal structural abnormalities such as reduplication, disruption and smearing were sometimes observed. The present data indicate that derangements of epithelial cells during prostate carcinogenesis are associated with a reduction or dedifferentiation of stromal SMCs. Our results lend support to the hypothesis that transformed epithelium is incapable of maintaining normal differentiation of adjacent muscle. In turn, abnormal stromal, resulting from dedifferentiation or reduction of SMC, may lead to loss of stromal control over epithelial proliferation and differentiation. Consequently, a loss of differentiation in both epithelium and stromal SMCs may be critically involved in hormone-induced prostate carcinogenesis.link_to_subscribed_fulltex

Dedifferentiation of stromal smooth muscle as a factor in prostate carcinogenesis

We had earlier established an animal model of prostate carcinogenesis using a combination of testosterone (T) and 17β-estradiol benzoate (E2) on Noble rats (Wang and Wong, 1998). In the present study we examined the changes in a number of smooth muscle differentiation markers including smooth muscle α-actin and myosin, vinculin, desmin, laminin and vimentin as well as changes in fine structure by electron microscopy. Our immunohistochemical (IHC) studies revealed that smooth muscle cells (SMCs) subjacent to dysplastic (precancerous) sites and carcinoma usually exhibited a preferential loss of myosin, desmin and laminin. However, the expression of α-actin and vinculin appeared to be more persistent in most dysplastic or neoplastic sites. The study reaffirmed our earlier observation that there was a concurrent dedifferentiation of surrounding SMCs during the development and progression of prostate carcinogenesis. The structural study revealed that SMC subjacent to epithelial dysplasia displayed a spectrum of derangements. These included the loosening of muscular layers with SMC characterized by their highly irregular external contours with numerous spine-like cytoplasmic projections. There was also a reduction in density of myofilaments and presence of many enlarged caveolae in muscle cells. Additionally, focal discontinuity or disruptions of muscular layer were often observed together with an increase in abundance of fibrous connective tissue. Moreover, the amount of smooth muscle appeared to be inversely correlated with the histologic grade of prostate tumors. In most instances, SMCs were totally absent in the moderately or poorly differentiated tumors and in metastatic tumors in the lung and the small intestine. Stromal muscular deformity was associated with concurrent changes in epithelial cells. Dysplastic epithelial cells were characterized by a reduction in abundance of secretory organelles such as reduction in size of Golgi apparatus, paucity of granular endoplasmic reticulum and secretory vesicles. The nuclei showed typical deformity characterized by deep nuclear membrane foldings. The basal lamina of dysplastic or tumor cells was present although focal structural abnormalities such as reduplication, disruption and smearing were sometimes observed. The present data indicate that derangements of epithelial cells during prostate carcinogenesis are associated with a reduction or dedifferentiation of stromal SMCs. Our results lend support to the hypothesis that transformed epithelium is incapable of maintaining normal differentiation of adjacent muscle. In turn, abnormal stromal, resulting from dedifferentiation or reduction of SMC, may lead to loss of stromal control over epithelial proliferation and differentiation. Consequently, a loss of differentiation in both epithelium and stromal SMCs may be critically involved in hormone-induced prostate carcinogenesis.link_to_subscribed_fulltex