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This thesis offers an explanation of the statistical modelling of corporate financial indicators in the context where the life of a company is terminated. Whilst it is natural for companies to fail or close down, an excess of failure causes a reduction in the activity of the economy as a whole. Therefore, studies on business failure identification leading to models which may provide early warnings of impending financial crisis may make some contribution to improving economic welfare. This study considers a number of bankruptcy prediction models such as multiple discriminant analysis and logit, and then introduces survival analysis as a means of modelling corporate failure. Then, with a data set of UK companies which failed, or were taken over, or were still operating when the information was collected, we provide estimates of failure probabilities as a function of survival time, and we specify the significance of financial characteristics which are covariates of survival. Three innovative statistical methods are introduced. First, a likelihood solution is provided to the problem of takeovers and mergers in order to incorporate such events into the dichotomous outcome of failure and survival. Second, we move away from the more conventional matched pairs sampling framework to one that reflects the prior probabilities of failure and construct a sample of observations which are randomly censored, using stratified sampling to reflect the structure of the group of failed companies. The third innovation concerns the specification of survival models, which relate the hazard function to the length of survival time and to a set of financial ratios as predictors. These models also provide estimates of the rate of failure and of the parameters of the survival function. The overall adequacy of these models has been assessed using residual analysis and it has been found that the Weibull regression model fitted the data better than other parametric models. The proportional hazard model also fitted the data adequately and appears to provide a promising approach to the prediction of financial distress. Finally, the empirical analysis reported in this thesis suggests that survival models have lower classification error than discriminant and logit models.

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目的：收集及整理近5 年有失治疗卵巢早衰的中医和中西医结合文献，对该病的病因病机、治疗原则和方法，以及中医处方用药及临床疗效进行统计分析、归纳及总结，探寻卵巢早衷的证治方法和用药规律’为今后的中医药治疗提供系统化思路和文献学基础。方法：对收集到的符合标准的85 篇文献进行病因病机、证治方药和臨床疗效的归纳，并用Excel 软件建立数据库并进行数据统计分析。结果：通过对85 篇文献分析’卵巢早衰常见病因病机共有11 大类：肾精亏虚、肾虚肝郁、括子血阻滞、肾阳虚、肾阴虚、脾肾两虚、肝肾阴虚、气血不足、心肾不交、痰湿阻滞、以及其他。肾精亏虚所占比例最大，为29.26% 。将与“肾虚”相关的所有病机一起合计，所占比例为75.58% 。治疗药物出现总体频次为1292 味次，其中居第一位为补益药，共849 味矢，占65.71% ；居第二、第二位的分别为活血桔痕药， 165 味女，占12.77% ；清热药， 66 味矢，占5.11% 。高频药物：熟地、当归、莞丝子、山药、山英肉、构丰己子。结论：肾虚是卵巢早衰发病的根本病因病机，肝郁气滞和膝阻；中任是发病的主要环节。提出临床治疗该病的基本思路与方法为： (1 ）补肾为玉，佐以疏肝养肝、健脾养心是治本之法；（ 2 ）标本兼治，活血化插手是卵巢早衰主要的治标之法；（ 3)滋阴柔肝、清热凉血也是卵巢早衰常用的治疗方法之一；（ 4 ）中药周期疗法和辨证论治相结合；（ 5 ）身心同治，配合心理疏导。關键词：卵巢早衰；中医药治疗卵巢早衰；现代临床文献研究；病因病机；证治方药

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Acute Liver Failure (ALF) is a devastating ailment with a high mortality rate and limited treatment alternatives. This study presents a methodology for the design and development of a bio-artificial bioreactor to be used in a Bio-Artificial Liver Support System. The system will ultimately be used either to bridge a patient to orthotopic liver transplant (OLT), the only current cure for end stage ALF, or spontaneous recovery. Methods to optimize and visualize the flow and related mass transfer in the BR are presented. The use of magnetic resonance imaging (MRI), scanning electron microscopy (SEM) and simple testing methodology is applied with emphasis on modeling the flow conditions in the BR. The bioreactor (BR) used in the Bio-Artificial Liver Support System (BALSS), currently under-going animal trials at the University of Pretoria, was modeled and simulated for the flow conditions in the device. Two different perfusion steps were modeled including the seeding of hepatocyte cells and later the clinical perfusion step. It was found that the BR geometry was not optimal with “dead spots” and regions of retarded flow. This would restrict the effective transport of nutrients and oxygen to the cells. The different perfusion rates for the seeding and clinical perfusion steps allowed for different velocity contours with cells seeing inconsistent flow patterns and mass transfer gradients. An optimized BR design is suggested and simulated, that effectively reduces the areas of retarded flow (dead spots) and increases the flow speed uniformly through the BR to an order of magnitude similar to that found in the sinusoidal range. The scaffolding volume was also decreased to allow a larger local cell density promoting cell-cell interaction. Finally a summarized design table for the design of a hepatic BR is presented. / Dissertation (MEng (Mechanical))--University of Pretoria, 2008. / Mechanical and Aeronautical Engineering / unrestricted

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[No Abstract Available] / Applied Science, Faculty of / Mechanical Engineering, Department of / Graduate

Heart failure (HF) is one of the commonest complications of Diabetes Mellitus (DM) with the prevalence of DM reported at around 30% in many pivotal heart failure studies. However the pathophysiological mechanisms that contribute to HF development in diabetes are poorly understood. To investigate this we used a novel human relevant mouse model of DM (GENA348) in which there is a point mutation in the glucokinase (Gck) gene, the glucose sensor which regulates insulin secretion. A mutation in the same gene is known to underlie Maturity Onset Diabetes of the Young Type 2 (MODY 2) in humans. The mutant mice developed significant hyperglycaemia with normal insulin levels due to the altered glucose sensing. We examined the molecular mechanisms that contribute to the HF phenotype in DM. Mean random blood glucose was found to be increased in the GENA348 mutant(HO) mice compared to wild type (WT) litter mates (WT 6.9±0.3mmol/L vs HO20.6±0.8mmol/L, P<0.001). Serial echocardiography was performed, at 3, 6 and 12 months. No significant changes in echocardiographic parameters were observed at 3 months, although by 6 months development of significant cardiachypertrophy in HO mice was observed characterised by a 20% increase in the diastolic posterior wall thickness (dPW). At 12 months of age left ventricular dilatation was also evident. Systolic function was preserved although significant diastolic dysfunction was evident at 6 and 12 months. Histological staining illustrated significant cellular hypertrophy with real time PCR data demonstrating a relative 150% increase in the hypertrophic marker BNP. Hypertrophic pathways were examined through western blot analysis revealing an age dependent increase in Akt phosphorylation (6 months-140%, 12 months-460%). Serum levels of advanced glycation end products (AGEs) and expression of their receptors RAGE were also elevated. In vitro cellular experiments also revealed AGEs directly activate Akt through phosphorylation and increase levels of the receptor RAGE. AGE induced phosphorylation of Akt is inhibited in the presence of wortmannin, suggesting a PI3K dependent signalling mechanism. Wortmannin blocked the development of cardiac hypertrophy in the diabetic mice. In conclusion we demonstrate that the human relevant GENA348 mouse model of diabetes develops a progressive cardiac phenotype including cardiachypertrophy, LV dilatation and diastolic dysfunction similar to the clinical manifestations of diabetic cardiomyopathy. We propose a novel RAGE/PI3K/Akt pathway that for the first time provides insight into the molecular mechanisms that underlie the development of HF. Moreover, we show raised glucose alone is able to cause cardiotoxicity independently of insulin.