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GaN RF switches are widely used in today’s communication systems. With digital communications getting more and more popular nowadays, the need for improving the performance of involved RF switches is inevitable. Designing low ON-state resistance GaN switches are exceedingly important to improve the switch insertion loss, isolation and power loss. Moreover, considerations need to be taken into account to improve the switching speed of the involved GaN HEMTs. In this dissertation, a new GaN HEMT structure called “Tunnel MOS Heterostructure FET (TMOSHFET)” is introduced which has lower ON-state resistance and faster switching speed compared to conventional AlGaN/GaN HEMTs. In the switch ON process, the channel of this device is charged up by electron tunneling from a layer underneath the channel as opposed to typical AlGaN/GaN HEMTs in which electron injection from the source is charging up the channel. The tunneling nature of this process together with the shorter travel distance of electrons in TMOSHFET provide for a faster switching speed. In order to understand the tunneling mechanisms in TMOSHFET, the fabrication of AlGaN/GaN Schottky Barrier Diodes (SBDs) with various AlGaN thicknesses is demonstrated on Si (111) substrate. The impacts of SF6 dry etching on the trap density and trap state energy of AlGaN surface are investigated using the GP/w- w method. Various tunneling mechanisms at different biases are then characterized in samples and compared with each other. To improve the source and drain resistances in TMOSHFET, a model is generated to optimize the 2DEG density and electric field in AlGaN/GaN heterostructure based on Al mole fraction, AlGaN thickness and the thickness of SiN passivation layer and it is experimentally verified by non-contact Hall 2DEG density measurements. The spontaneous and piezoelectric polarizations together with strain relaxation have been implemented into the model, taking into account the annealing effects. From the experimental data on obtained parameters, the operation and device parameterization of the TMOSHFET is outlined and design considerations to improve the device R_(ON)-V_(BR) figure of merit are discussed.

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In dieser Arbeit wird ein System entwickelt, welches die Zeit in das World Wide Web integriert, um einerseits die Evolution der Web-Seiten nachvollziehen und jeden vergangenen Stand wieder herstellen zu können und das andererseits eine Möglichkeit schafft, Ressourcen mit zusätzlichen temporalen Informationen auszustatten. Nach einer kurzen, den Fokus der Arbeit beschreibenden Einleitung, widmet sich das zweite Kapitel den grundsätzlichen Fragen der Zeitdimensionen im Web. Es werden Darstellungsformen von Datum und Zeit sowie die Möglichkeiten, Zeitinformationen mit bestehenden Webtechnologien zu integrieren, vorgestellt. Dazu werden Konzepte der temporalen Datenbanken auf das Web übertragen und gezeigt, dass durch Unterstützung der Transaktionszeit eine Versionierung von Web-Dokumenten ermöglicht wird. Kapitel 3 geht dann auf weiterführende Konzepte zur Darstellung von Zeit im World Wide Web ein. Es wird die Dublin Core Metadata Inititative vorgestellt und anhand von Beispielen gezeigt, wie derartige Daten in HTML-Dokumente eingebaut werden können. Im vierten Kapitel werden generelle Anforderungen an temporales Content-Management formuliert und eine Reihe von Ansätzen zur Erfüllung der Entwicklungsspezifikation beschrieben. Es wird gezeigt, dass keines der bisherigen Systeme eine wirklich zufriedenstellende Lösung anbietet. Deshalb wird in Kapitel 5 ein Prototyp eines temporalen Web-Informationssystems vorgestellt, der im Rahmen dieser Arbeit entwickelt wurde und somit deren Kernstück darstellt. (Autorenref.)

Thesis (MBusiness-Research)--University of South Australia, 2003.

Plasma lipid, lipoprotein and apolipoprotein levels are considered as important and well-established intermediate quantitative phenotypes of Cardiovascular Disease (CVD) risk. Both the mean values and the phenotypic variance vary over the human lifespan. However, it is not known whether there is a genetic basis for this age variability. For example, might different genes act, or different gene interactions occur, as a person ages? If so, how might this be influenced by both environment and phenotype? An understanding of traits at different ages will not only provide insight into the genetic components involved in CHD development, but may also identify additional genetic factors that predispose an individual or population to premature (and later-onset) CHD. By identifying genetic factors that account for variation in important intermediate traits (i.e. lipid levels), we hope to gain a better understanding of disease mechanisms and thus a better chance of developing clinical strategies for preventing or possibly treating abnormal lipid levels and, by association, CHD. The aim of this thesis was to better identify and explain the genetic basis of CHD by focusing on the use of lipid traits as intermediate quantitative phenotypes of CHD. First, phenotypic analyses using structural equation modeling were performed to estimate the relative importance of genetic and environmental factors, and also to investigate whether these traits are influenced by the same gene(s) across time or whether they are age-specific genetic effects. Then, genome-wide linkage analysis was performed to localize cardiovascular susceptibility loci. Finally, a small genome-wide association scan (GWAS) was performed on a subset of the data to identify the relevant variants, in particular those showing associations across time. Phenotypes and marker data were collected in two Australian samples: an adolescent and adult twin pair samples. The adult sample consisted of 1453 twin pairs (968 monozygotic and 485 dizygotic), measured for lipid traits. 415 adult twins provided blood on two to five occasions. The adolescent dataset consisted of 965 twin families (397 monozygotic and 568 dizygotic) measured longitudinally at ages twelve, fourteen and sixteen, and their siblings tested once for the same lipid variables. Results from both the adult and adolescent cohorts indicated that there is more than one genetic factor influencing total cholesterol, HDL, LDL and triglycerides over time (i.e. from different measurement occasions). Common environmental factors did not contribute to variances (except for HDL in adolescents). There were no sex differences in the heritabilities of these intermediate phenotypes. Non-shared environmental factors did not have significant long-term effects. Overall, these two cohorts confirmed that genetic variation contributes substantially to variation in these traits, and suggested there are changes in the genes affecting plasma lipid concentration at different periods of life. Thus, there are age-dependent gene effects influencing HDL, LDL, total cholesterol, or triglycerides at different ages. In the adult genome data, there were 485 adult dizygotic twin pairs typed on average 595 markers, at an average inter-marker distance of 5.0 cM. The genome-wide linkage analysis revealed evidence for linkage in the 7p13 region for triglycerides. Possible candidate genes included NPC1L1 and GSBS. Other regions of “suggestive” linkage identified were chromosome 4p13 (at 62 cM) and Xq26.2-28 (81 cM). Adolescent twins and their siblings from 760 families were typed for linkage using 16,781 markers spaced across the genome at an average distance of 6.25 cM. The adolescent data revealed evidence for linkage to region 6p24.3 for triglycerides (–log10p = 6.81; equivalent LOD = 6.13; p = 0.00000016) and to region 2q31.1 for HDL (–log10p = 3.22, equivalent LOD = 2.27; p = 0.00061). No obvious candidate gene is known in this 6p region. Possible candidate genes in the 2q region include LRP2 and ABCB11. A significant region of linkage was also found on 2q35 for LDL (–log10p = 5.59; equivalent LOD score = 4.53). Other interesting regions of linkage included chromosomes 1q32.1, 4p15.1, 5q13.2, 11p14.3 and 18q11.2. Thus, regions were identified by linkage analyses that are likely to harbour genetic risk factors for cardiovascular disease in the analysed Australian population: chromosomes 7p13 (in adults), 6p24 (adolescents), 2q31.1 and 2q35 (in adolescents). Other regions included 1q32.1, 4p15.1, 5q13.2, 11p14.3 and 18q11.2 in adolescents and chromosome 4p13 and Xq26.2–28 in adults. Genome-wide association results for adolescents showed significant evidence of association between total cholesterol at age 14 (p = 8.24x10-7) and rs10503840 on 8p21.1. Such association has not previously been reported. Evidence of differential association across time was also found between HDL and variant rs10492859, located in the intron of the CDH13 gene, consistent with earlier studies on larger datasets. Significant association (p = 2.25x10-6) was also found between rs10507266 on 12q24.21 in an intron of THRAP2, a gene involved in early development of heart and brain, with triglycerides at age 12. Evidence of association was also found between HDL across time and variant rs10492859 on 16q23. Several other “suggestive” potential loci associated with lipid traits at one time point as well as across time were also found. In conclusion, the work described in this thesis establishes the importance of age-specific genetic effects on plasma lipids and lipoproteins, and identifies several regions of highly significant genetic linkage with these phenotypes in either adolescence or adulthood. It is clear that, as well as cross-sectional studies to identify genes affecting CVD risk factors, longitudinal genetic linkage and association studies are needed to assess relative contributions to risk across the lifespan.

Thesis (MBusiness-Research)--University of South Australia, 2003.