First principles study of point-like defects and impurities in silicon, carbon, and oxide materials

textSince materials properties are determined by the interactions between the constituent atoms, an accurate description of the inter-atomic interactions is crucial to characterize and control material properties. Particularly, a quantitative understanding of the formation and nature of defects and impurities becomes increasingly important in the era of nanotechnology, as the imperfections largely influence many properties of nanoscale materials. Indeed, due to its technological importance and scientific interest, there have been significant efforts to better understand their behavior in semiconductors and oxides, and their interfaces, yet many fundamental aspects are still ambiguous due largely to the difficulty of direct characterization. Hence, our study has focused on developing a better understanding of atomic-scale defects and impurities using first principles quantum mechanical calculations. In addition, based on the improved understanding, we have attempted to address some engineering problems encountered in the current technology. The first part of this thesis focuses on mechanisms underlying the transient enhanced diffusion of arsenic (As) during post-implantation annealing by examining the interaction of As with vacancies in silicon. In the second part, we address some fundamental features related to plasma-assisted nitridation of silicon dioxide; this study shows that oxygen vacancy related defects play an important role in (experimentally observed) peculiar nitridation at the Si/SiO2 interface during post O2 annealing. In the third part, we examine the interaction between vacancies and dopants in sp2–bonded carbon such as graphene and nanotube, specifically the formation and dynamics of boron-vacancy complexes and their influence on the electrical properties of host materials. In the fourth part, we study the interfacial interaction between amorphous silica (a-SiO2) and graphene in the presence of surface defects in a-SiO2; this study shows possible modifications in the electronic structure of graphene upon the surface defect assisted chemical binding onto the a-SiO2 surface. In the last part, we examine the structural and electronic properties of bismuth vanadate (BiVO4) which is a promising photocatalyst for water splitting to produce hydrogen; this study successfully explains the underlying mechanism of the interesting photocatalytic performance of BiVO4 that has been experimentally found to strongly depend on structural phase and doping.Electrical and Computer Engineerin

First principle determination of dopant ionization levels

Since CMOS (Complementary metal-oxide-semiconductor) circuits were invented in 1963, CMOS technology has made rapid advancements while keeping pace with the so-called Moore's law. With continued scaling, the size of transistors shrinks to the nanometer scale. In order to achieve the desired electronic properties of nanometer transistors, abrupt and high-concentration doping is a critical issue, but extremely challenging because of relatively large surfaces and interfaces as well as complex defect- dopant interactions. Therefore, a deeper understanding of the fundamental behavior and properties of dopants and their interactions with defects in various process conditions is essential in fabrication of nanotechnology-based CMOS devices. In this research, we use first principle quantum mechanical calculations to determine the structure, dynamics and electronic properties of dopants in crystalline silicon (Si). The first part of this thesis focuses on finding methods capable of predicting the ionization levels of dopants, such as P, As, B, and Al, as well as defect-dopant complexes. Since the ionization levels are closely related to doping conditions, it is worthwhile to understand the relationship. We first check carefully the convergence of total energy for the pure and doped systems with respect to calculation conditions, such as k-point mesh size, plane wave cutoff energy, supercell size, and so on. Then, based on the total energy calculations we evaluate the ionization levels of dopants with comparisons to experimental data available in literature. The second part of this thesis examines the structure and dynamics of phosphorus (P) near the Si(100) surface. First, P diffusion in bulk Si is presented as the reference to clarify the surface effect. Then, the relative stability and diffusion of P near the surface are calculated. The results show that surface P is far more energetically favorable than bulk P. Also, our calculations show that with a moderate barrier, bulk P will undergo out-diffusion to the surface, and surface P will migrate along a dimer row. The fundamental findings provide valuable guidance on how to control doping of silicon nanostructures.Electrical and Computer Engineerin

Docosahexaenoic acid suppresses breast cancer cell metastasis by targeting matrix-metalloproteinases

Breast cancer is one of the most prevalent cancers in women, and nearly half of breast cancer patients develop distant metastatic disease after therapy. Despite the significant advances that have been achieved in understanding breast cancer metastasis in the past decades, metastatic cancer is still hard to cure. Here, we demonstrated an anti-cancer mechanism of docosahexaenoic acid (DHA) that suppressed lung metastasis in breast cancer. DHA could inhibit proliferation and invasion of breast cancer cells in vitro, and this was mainly through blocking Cox-2-PGE 2 -NF-kappa B-MMPs cascades. DHA treatment significantly decreased Cox-2 and NF-kappa B expression as well as nuclear translocation of NF-kappa B in MDA-MB-231 cells. In addition, DHA also reduced NF-kappa B binding to DNA which may lead to inactivation of MMPs. Moreover, in vivo studies using Fat-1 transgenic mice showed remarkable decrease of tumor growth and metastasis to EO771 cells to lung in DHA-rich environment. In conclusion, DHA attenuated breast cancer progression and lung metastasis in part through suppressing MMPs, and these findings suggest chemoprevention and potential therapeutic strategy to overcome malignant breast cancer.119sciescopu

PMA synergistically enhances apicularen A-induced cytotoxicity by disrupting microtubule networks in HeLa cells

Background: Combination therapy is key to improving cancer treatment efficacy. Phorbol 12-myristate 13-acetate (PMA), a well-known PKC activator, increases the cytotoxicity of several anticancer drugs. Apicularen A induces cytotoxicity in tumor cells through disrupting microtubule networks by tubulin down-regulation. In this study, we examined whether PMA increases apicularen A-induced cytotoxicity in HeLa cells. Methods: Cell viability was examined by thiazolyl blue tetrazolium (MTT) assays. To investigate apoptotic potential of apicularen A, DNA fragmentation assays were performed followed by extracting genomic DNA, and caspase-3 activity assays were performed by fluorescence assays using fluorogenic substrate. The cell cycle distribution induced by combination with PMA and apicularen A was examined by flow cytometry after staining with propidium iodide (PI). The expression levels of target proteins were measured by Western blotting analysis using specific antibodies, and alpha-tubulin mRNA levels were assessed by reverse transcription polymerase chain reaction (RT-PCR). To examine the effect of combination of PMA and apicularen A on the microtubule architecture, alpha-tubulin protein and nuclei were visualized by immunofluorescence staining using an anti-alpha-tubulin antibody and PI, respectively. Results: We found that apicularen A induced caspase-dependent apoptosis in HeLa cells. PMA synergistically increased cytotoxicity and apoptotic sub-G1 population induced by apicularen A. These effects were completely blocked by the PKC inhibitors Ro31-8220 and Go6983, while caspase inhibition by Z-VAD-fmk did not prevent cytotoxicity. RNA interference using siRNA against PKC alpha, but not PKC beta and PKC gamma, inhibited cytotoxicity induced by combination PMA and apicularen A. PMA increased the apicularen A-induced disruption of microtubule networks by further decreasing alpha- and beta-tubulin protein levels in a PKC-dependent manner. Conclusions: These results suggest that the synergy between PMA and apicularen A is involved by PKC alpha activation and microtubule disruption, and that may inform the development of novel approaches to treat cancer.112sciescopu

Apicularen A acetate induced cell death via AIF translocation and disrupts the microtubule network by down-regulating tubulin in HM7 human colon cancer cells

Apicularen A is a novel antitumor agent and strongly induces death in tumor cells. In this study, we synthesized apicularen A acetate, an acetyl derivative of apicularen A, and investigated its antitumor effect and mechanism in HM7 colon cancer cells. Apicularen A acetate induced apoptotic cell death and caspase-3 activation; however, the pan-caspase inhibitor Z-VAD-fmk could not prevent this cell death. Apicularen A acetate induced the loss of mitochondrial membrane potential and the translocation of apoptosis-inducing factor (AIF) from mitochondria. In addition, apicularen A acetate significantly decreased tubulin mRNA and protein levels and induced disruption of microtubule networks. Taken together, these results indicate that the mechanism of apicularen A acetate involves caspase-independent apoptotic cell death and disruption of microtubule architecture. (C) 2013 Elsevier Inc. All rights reserved.112sciescopu