Master of Engineering by Research / Service-level-agreement (SLA) monitoring measures network Quality-of-Service (QoS) parameters to evaluate whether the service performance complies with the SLAs. It is becoming increasingly important for both Internet service providers (ISPs) and their customers. However, the rapid expansion of the Internet makes SLA monitoring a challenging task. As an efficient method to reduce both complexity and overheads for QoS measurements, sampling techniques have been used in SLA monitoring systems. In this thesis, I conduct a comprehensive study of sampling methods for network QoS measurements. I develop an efficient sampling strategy, which makes the measurements less intrusive and more efficient, and I design a network performance monitoring software, which monitors such QoS parameters as packet delay, packet loss and jitter for SLA monitoring and verification. The thesis starts with a discussion on the characteristics of QoS metrics related to the design of the monitoring system and the challenges in monitoring these metrics. Major measurement methodologies for monitoring these metrics are introduced. Existing monitoring systems can be broadly classified into two categories: active and passive measurements. The advantages and disadvantages of both methodologies are discussed and an active measurement methodology is chosen to realise the monitoring system. Secondly, the thesis describes the most common sampling techniques, such as systematic sampling, Poisson sampling and stratified random sampling. Theoretical analysis is performed on the fundamental limits of sampling accuracy. Theoretical analysis is also conducted on the performance of the sampling techniques, which is validated using simulation with real traffic. Both theoretical analysis and simulation results show that the stratified random sampling with optimum allocation achieves the best performance, compared with the other sampling methods. However, stratified sampling with optimum allocation requires extra statistics from the parent traffic traces, which cannot be obtained in real applications. In order to overcome this shortcoming, a novel adaptive stratified sampling strategy is proposed, based on stratified sampling with optimum allocation. A least-mean-square (LMS) linear prediction algorithm is employed to predict the required statistics from the past observations. Simulation results show that the proposed adaptive stratified sampling method closely approaches the performance of the stratified sampling with optimum allocation. Finally, a detailed introduction to the SLA monitoring software design is presented. Measurement results are displayed which calibrate systematic error in the measurements. Measurements between various remote sites have demonstrated impressively good QoS provided by Australian ISPs for premium services.

[Truncated abstract] Dyslipidaemia in obesity and the metabolic syndrome is typically characterized by elevated plasma concentrations of apolipoprotein (apo) B and chylomicron remnants, and low apoA-I levels. This may account for the increased risk of cardiovascularrelated diseases. Although the precise mechanisms whereby visceral obesity confers the onset of dyslipidaemia have not been fully established, it may relate chiefly to insulin resistance. Insulin resistance leads to increased hepatic secretion of very low density lipoprotein (VLDL) apoB, as well as impaired catabolism of VLDL, intermediate density lipoprotein (IDL), low-density lipoprotein (LDL) and chylomicron remnants, and high density lipoprotein (HDL) apoA-I. This thesis tests the unifying hypothesis that lipoprotein metabolism, in particular apoB, chylomicron remnants and apoA-I, is abnormal in the metabolic syndrome, and that medical intervention can correct for these abnormalities. The primary objectives were to examine firstly, the kinetics of apoB and apoA-I by stable isotope technology and secondly, chylomicron remnant kinetics by using an indirect assessment of a new breath test. Six observational statements and related hypotheses were constructed and derived from the unifying hypothesis that examine the kinetics of lipoprotein metabolism, adipose tissue mass compartments and liver fat accumulation, as well as the impact of plasma adipocytokines in subjects with visceral adiposity and features of the metabolic syndrome. The first four observational statements related to cross-sectional studies of lipoprotein kinetics, adipose tissue mass distribution and liver fat accumulation as well as plasma adipocytokines in both obese and non-obese men. The latter two observational statements related to the effect of statin therapy and dietary weight loss on the improvement of lipoprotein kinetics in obesity. The findings from these studies collectively support the unifying hypothesis. The kinetics of apoB in VLDL, IDL and LDL, and apoA-I in HDL were assessed by gas-chromatography mass spectrometry following either a primed-constant infusion of 13C-leucine or an intravenous bolus injection of d3-leucine. ... This is the first study to examine the effects of dietary weight loss on LDL and HDL metabolism and the relationships with adipocytokines in men with the metabolic syndrome. The data support the unifying hypothesis that medical intervention with dietary weight loss could correct the kinetic abnormalities in VLDL, LDL and HDL. The aforementioned studies showed that plasma lipid and lipoprotein abnormalities in visceral obesity are chiefly regulated by the combination of hepatic over-secretion of VLDL particles, and catabolic defects in apoB and chylomicron remnants as well as apoA-I-containing lipoprotein particles. These kinetic defects may also relate to low and high plasma adiponectin and RBP-4 levels, respectively. The data arising from the thesis are consistent with the unifying hypothesis and support the role of dietary intervention and pharmacotherapy as a recommended treatment in correcting the abnormalities in lipoprotein metabolism within the metabolic syndrome.

This thesis examines the relationship between tax-loss selling (TLS), where investors with taxable gains sell stocks that have declined in value just before the fiscal year-end to generate offsetting tax losses, and managers?? incentives to influence stock prices, either through increased disclosure or by engaging in upwards earnings management. Firms whose stock prices represent greater potential tax losses in investors?? portfolios at year-end are predicted to increase their disclosure level in June to prevent further share price falls due to TLS, and have higher levels of accruals. Using the number of discretionary, market-sensitive news releases in the Signal G announcement database to measure disclosure frequency, this thesis finds that, for a sample of 14,713 firm-year observations drawn from all ASX firms for the years 1994 to 2007, stocks with larger negative returns have higher disclosure in June, after controlling for size, performance, risk and external financing dependence. This is particularly true of small mining and exploration companies that are more reliant on voluntary disclosure as a vehicle for lowering information asymmetry. This increased disclosure does not appear to contribute to the higher July returns earned by stocks that experienced significant TLS in June. Disclosure frequency is negatively associated with the magnitude of operating and total accruals, suggesting that earnings management is less likely for firms with higher disclosure. There is also evidence that smaller firms with poor stock price performance have higher levels of operating accruals and thus may be more likely to engage in earnings management.

Loss of heterozygosity (LOH) on the long arm of chromosome 16 is frequently observed during the onset of breast cancer. Our laboratory has recently identified both ANKRD11 and FBXO31 as candidate tumour suppressor genes in the chromosome band 16q24.3, which is the smallest region of overlap for breast cancer LOH. This thesis focuses on the functional analysis of these two novel genes and implicates a role for them as breast cancer tumour suppressors. ANKRD11: a novel p53 coactivator involved in the rescue of mutant p53. The ability of p53 to act as a transcription factor is critical for its function as a tumour suppressor. Ankyrin repeat domain 11 (ANKRD11) was found to be a novel p53-interacting protein which enhanced the transcriptional activity of p53. ANKRD11 expression in breast cancer cell lines was shown to be down-regulated when compared to ANKRD11 expression in finite life-span HMECs and non-malignant immortalized breast epithelial cells. Restoration of ANKRD11 expression in MCF-7 (p53 wild-type) and MDA-MB-468 (p53[superscript R273H] mutant) cells suppressed the oncogenic properties of these breast cancer cell lines through enhancement of p21[superscript waf1] expression. ShRNA-mediated silencing of ANKRD11 reduced the ability of p53 to activate p21[superscript waf1] expression in response to DNA damage. ANKRD11 was shown to associate with the p53 acetyltransferase, P/CAF, and exogenous ANKRD11 expression increased the levels of acetylated p53. Exogenous ANKRD11 expression enhanced the DNA-binding properties of the p53[superscript R273H] mutant to the CDKN1A promoter, implicating a role for ANKRD11 in the restoration of mutant p53[superscript R273H] function. These findings demonstrate a role for ANKRD11 as a p53 coactivator and illustrate the potential of ANKRD11 in the restoration of mutant p53[superscript R273H] function. ANKRD11 has roles beyond that of p53 coactivation. This thesis also presents preliminary findings to suggest that ANKRD11 may be involved in the regulation of eukaryotic cell division. Furthermore, ANKRD11 was shown to function as an estrogen receptor coactivator. Taken together, these finding suggest that ANKRD11 is a multi-functional cancer-related protein. FBXO31: the 16q24.3 senescence gene. A BAC located in the 16q24.3 breast cancer loss of heterozygosity region was previously shown to restore cellular senescence when transferred into breast tumour cell lines. We have shown that FBXO31, although located just distal to this BAC, can induce cellular senescence in the breast cancer cell line MCF-7 and is the likely candidate senescence gene. Exogenous FBXO31 expression inhibited the oncogenic properties of the MCF-7 breast cancer cell line. In addition, compared to the relative expression in normal breast, levels of FBXO31 were down-regulated in breast tumour cell lines and primary tumours. FBXO31 protein levels were cell cycle regulated, with maximal expression from late G2 to early G1 phase. Ectopic expression of FBXO31 in the breast cancer cell line MDA-MB-468 resulted in the accumulation of cells at the G1 phase of the cell cycle. FBXO31 was also shown to be a component of a SCF ubiquitination complex. We propose that FBXO31 functions as a tumour suppressor by generating SCF[superscript FBXO31] complexes that target particular substrates, critical for the normal execution of the cell cycle, for ubiquitination and subsequent degradation. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1325445 / Thesis (Ph.D.) -- University of Adelaide, School of Medicine, Discipline of Medicine, 2008

Loss of heterozygosity (LOH) on the long arm of chromosome 16 is frequently observed during the onset of breast cancer. Our laboratory has recently identified both ANKRD11 and FBXO31 as candidate tumour suppressor genes in the chromosome band 16q24.3, which is the smallest region of overlap for breast cancer LOH. This thesis focuses on the functional analysis of these two novel genes and implicates a role for them as breast cancer tumour suppressors. ANKRD11: a novel p53 coactivator involved in the rescue of mutant p53. The ability of p53 to act as a transcription factor is critical for its function as a tumour suppressor. Ankyrin repeat domain 11 (ANKRD11) was found to be a novel p53-interacting protein which enhanced the transcriptional activity of p53. ANKRD11 expression in breast cancer cell lines was shown to be down-regulated when compared to ANKRD11 expression in finite life-span HMECs and non-malignant immortalized breast epithelial cells. Restoration of ANKRD11 expression in MCF-7 (p53 wild-type) and MDA-MB-468 (p53[superscript R273H] mutant) cells suppressed the oncogenic properties of these breast cancer cell lines through enhancement of p21[superscript waf1] expression. ShRNA-mediated silencing of ANKRD11 reduced the ability of p53 to activate p21[superscript waf1] expression in response to DNA damage. ANKRD11 was shown to associate with the p53 acetyltransferase, P/CAF, and exogenous ANKRD11 expression increased the levels of acetylated p53. Exogenous ANKRD11 expression enhanced the DNA-binding properties of the p53[superscript R273H] mutant to the CDKN1A promoter, implicating a role for ANKRD11 in the restoration of mutant p53[superscript R273H] function. These findings demonstrate a role for ANKRD11 as a p53 coactivator and illustrate the potential of ANKRD11 in the restoration of mutant p53[superscript R273H] function. ANKRD11 has roles beyond that of p53 coactivation. This thesis also presents preliminary findings to suggest that ANKRD11 may be involved in the regulation of eukaryotic cell division. Furthermore, ANKRD11 was shown to function as an estrogen receptor coactivator. Taken together, these finding suggest that ANKRD11 is a multi-functional cancer-related protein. FBXO31: the 16q24.3 senescence gene. A BAC located in the 16q24.3 breast cancer loss of heterozygosity region was previously shown to restore cellular senescence when transferred into breast tumour cell lines. We have shown that FBXO31, although located just distal to this BAC, can induce cellular senescence in the breast cancer cell line MCF-7 and is the likely candidate senescence gene. Exogenous FBXO31 expression inhibited the oncogenic properties of the MCF-7 breast cancer cell line. In addition, compared to the relative expression in normal breast, levels of FBXO31 were down-regulated in breast tumour cell lines and primary tumours. FBXO31 protein levels were cell cycle regulated, with maximal expression from late G2 to early G1 phase. Ectopic expression of FBXO31 in the breast cancer cell line MDA-MB-468 resulted in the accumulation of cells at the G1 phase of the cell cycle. FBXO31 was also shown to be a component of a SCF ubiquitination complex. We propose that FBXO31 functions as a tumour suppressor by generating SCF[superscript FBXO31] complexes that target particular substrates, critical for the normal execution of the cell cycle, for ubiquitination and subsequent degradation. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1325445 / Thesis (Ph.D.) -- University of Adelaide, School of Medicine, Discipline of Medicine, 2008

This paper describes the successful implementation of a prototype software application that independently and proactively detects whether a mobile phone is lost or misused. When the mobile phone is detected as being lost or misused, the application takes steps to mitigate the impact of loss and to gather evidence. The goal is to aid in the recovery of the mobile phone. The prototype works regardless of the cellular infrastructure the mobile phone is operating in and makes minimum demands on the owner of the mobile phone. The prototype was developed on Nokia 6600 mobile phones that run Symbian Operating System 7.0s. Development was done using Nokia’s Series 60 Developer’s Platform 2.0. / Singapore-MIT Alliance (SMA)

Thesis (Ph. D.)--West Virginia University, 2007. / Title from document title page. Document formatted into pages; contains vi, 75 p. Includes abstract. Includes bibliographical references (p. 48-54).

Using an existing data set comprised of 368 individuals newly diagnosed with cancers of the head and neck, we investigated the predictive validity of the Head and Neck Patient Symptom Checklist (HNSC) by comparing scores on the HNSC to scores on the Patient-Generated Symptom Global Assessment (PG-SGA), and by examining the ability of HNSC scores and four demographic variables to predict dietary intake, weight loss, and functional capacity. HNSC sensitivity (0.79 0.98), specificity (0.99 1.00), positive predictive value (92% 100%), and negative predictive value (94% - 100%) were excellent. Pain, loss of appetite and difficulty swallowing predicted 82% of reduced dietary intake. Advanced tumor stage, loss of appetite and difficulty swallowing predicted 79% of weight loss. Loss of appetite, difficulty swallowing, feeling full and lack of energy predicted 78% of reduced functional capacity. The HNSC appears to be valid and could aid with early symptom identification, intervention and improved outcomes.

Thesis (Ph. D.)--University of Rhode Island, 2005. / Typescript. Includes bibliographical references (leaves 135-142).

Wetlands are among the most ecologically productive lands in the world, but every year they continue to be lost due to increasing pressures from agriculture, industrial development, urbanization and the lack of effective mitigation to deal with such pressures. Despite environmental assessment processes, policies, and regulations to ensure the mitigation of affected wetlands, wetlands continue to experience a loss in areal extent, but more importantly, a functional net-loss. This is attributed, in large part, to the lack of incorporating cumulative effects principles into project-based wetland impact assessment and mitigation. The majority of activities that affect wetlands are either assessed at the screening level, where cumulative effects are rarely considered, or are deemed insignificant and do not trigger any formal environmental assessment process. As a result, the mitigation of cumulative effects on wetlands is often insufficient or completely lacking in development planning and decision-making. Part of the challenge is that there currently does not exist methodological guidance as to how to identify wetland cumulative effects and corresponding mitigation needs early in the project design process. This research presents a methodological framework and guidance for the integration of cumulative effects in decision-making for project-based, wetland impact mitigation. The framework provides a means for the early indication, assessment, and mitigation of the potential cumulative effects of project developments on the wetland environment, with the objective of ensuring a no-net-loss of wetland functions.