A dissertation submitted to the Faculty of Science, University of the Witwatersrand, Johannesburg, South Africa, in ful lment of the requirements for the degree of Master of Science in Statistics November, 2017 / This study presents survival modelling and evaluation of risk factors of graft survival in the context of kidney transplant data generated in South Africa. Beyond the Kaplan-Meier estimator, the Cox proportional hazard (PH) model is the standard method used in identifying risk factors of graft survival after kidney transplant. The Cox PH model depends on the proportional hazard assumption, which is rarely met. Assessing and accounting for this assumption is necessary before using this model. When the PH assumption is not valid, modi cation of the Cox PH model could o er more insight into parameter estimates and the e ect of time-varying predictors at di erent time points. This study aims to identify the survival model that will e ectively describe the study data by employing the Cox PH and parametric accelerated failure time (AFT) models. To identify the risk factors that mediate graft survival after kidney transplant, secondary data involving 751 adults that received a single kidney transplant in Charlotte Maxeke Johannesburg Academic Hospital between 1984 and 2004 was analysed. The graft survival of these patients was analysed in three phases (overall, short-term and long-term) based on the follow-up times. The Cox PH and AFT models were employed to determine the signi cant risk factors. The purposeful method of variable selection based on the Cox PH model was used for model building. The performance of each model was assessed using the Cox-Snell residuals and the Akaike Information Criterion. The t of the appropriate model was evaluated using deviance residuals and the delta-beta statistics. In order to further assess how appropriately the best model t the study data for each time period, we simulated a right-censored survival data based on the model parameter-estimates. Overall, the PH assumption was violated in this study. By extending the standard Cox PH model, the resulting models out-performed the standard Cox PH model. The evaluation methods suggest that the Weibull model is the most appropriate in describing the overall graft survival, while the log-normal model is more reasonable in describing short-and long-term graft survival. Generally, the AFT models out-performed the standard Cox regression model in all the analyses. The simulation study resulted in parameter estimates comparable with the estimates from the real data. Factors that signi cantly in uenced graft survival are recipient age, donor type, diabetes, delayed graft function, ethnicity, no surgical complications, and interaction between recipient age and diabetes. Statistical inferences made from the appropriate survival model could impact on clinical practices with regards to kidney transplant in South Africa. Finally, limitations of the study are discussed in the context of further studies. / MT 2018

Artemisinin is a potent antimalarial sesquiterpene lactone produced and stored in the glandular trichomes (GLTs) of Artemisia annua. Although they produce no artemisinin, nor any of the precursor compounds, A. annua roots appear to have a regulatory effect on production of the terpene in leaves. However, more information is needed to define the role of the roots in artemisinin production in the plant. Grafting among three cultivars was used to measure phenotypic responses: SAM, and #15 cultivars both have GLTs, but produce artemisinin at 1.49% and 0.57% DW, respectively; GLS cultivar produces neither GLTs nor artemisinin. Compared to ungrafted plants, all self-grafts, e.g. SAM/SAM (scion/rootstock), increased scion artemisinin probably from grafting stress. SAM/#15 grafts yielded less artemisinin than SAM/SAM, but more than either #15/#15 or ungrafted #15 and SAM suggesting rootstock inhibition of the scion. SAM/SAM also had more artemisinin than #15/SAM, which was also greater than either #15/#15 or ungrafted #15 and SAM. The #15/SAM graft also produced more artemisinin than SAM/#15, and with the other grafting results suggested that SAM roots were stimulating artemisinin production in the #15 scion. There was no appearance of either GLTs or artemisinin when GLS scions were grafted to SAM indicating that GLTs had to be present to receive putative signals from SAM rootstocks. Furthermore, artemisinic acid and arteannuin B were only present in SAM scions and not scions of #15 suggesting a block in one of the side pathways of artemisinin biosynthesis. Other artemisinic metabolites, total flavonoids, and GLTs numbers were also measured. The various phenotypes were analyzed several months after grafting indicating a persistent change and suggesting a possible epigenetic alteration of the scion. This study will provide fundamental information regarding the role that roots play in the production of artemisinin in the shoots of A. annua.

No description available.

Thesis (M.S. in mechanical engineering)--Washington State University, December 2009. / Title from PDF title page (viewed on Jan. 22, 2010). "School of Mechanical and Materials Engineering." Includes bibliographical references (p. 123-128).

Not available / text

published_or_final_version / abstract / toc / Dentistry / Doctoral / Doctor of Philosophy

No description available.

This is research about apple trees grafted in winter.

No description available.

Cyclosporin A immunosuppression following organ transplantation is associated with a reversible nephrotoxicity as manifested by elevations in serum urea and creatinine concentrations and urinary N-acetyl-B-D-glucosaminidase activities. The metabolism of Cyclosporin A is primarily via the hepatic cytochrome P-450 mono-oxygenase system with previous studies having demonstrated that the short term co-administration of phenobarbitone, an inducer of this enzyme system, ameliorates this nephrotoxicity in the non-renal allografted rat. Initial studies demonstrated that the induction of Cyclosporin A nephrotoxicity in the Lewis rat followed by the co-administration of phenobarbitone in the long term abolished nephrotoxicity in the female whilst alleviating it in the male animal. In addition Cyclosporin A hepatotoxicity was also abolished in female rats co-treated with phenobarbitone. A rat renal transplantation model was successfully developed to allow the study of Cyclosporin A nephrotoxicity in the renal allografted animal. Initial studies demonstrated a protective effect of phenobarbitone against Cyclosporin A nephrotoxicity within the first 14 days of treatment in female, but not male allografted animals. These studies also demonstrated a greater susceptibility of the male renal allografted and surgically intact rat to Cyclosporin A induced nephrotoxicity. The effect of ischaemia and sympathetic nervous system denervation were investigated using a series of Lewis syngeneic renal transplanted animals. Histological examination revealed Cyclosporin A induced renal damage to be more marked in non-transplanted than transplanted kidneys. The results are discussed in relation to cold and warm ischaemia and also to the role of the sympathetic nervous and renin-angiotensin-aldosterone systems in the potentiation of Cyclosporin A induced nephrotoxicity. The effect of long term phenobarbitone treatment on Cyclosporin A induced deteriorations in renal and hepatic function was determined using the Lewis syngeneic transplant model. The effect of intraoperative liver ischaemia and diethyl ether anaesthesia on hepatic function and their potentiation of Cyclosporin A hepatotoxicity is also considered. Finally the role of surgical stress and reduction of renal mass by unilateral nephrectomy, on Cyclosporin A nephrotoxicity was studied revealing a protective effect of unilateral nephrectomy against nephrotoxicity in the female animal. Previous studies have demonstrated that reduction in renal mass results in glomerulosclerosis with a progressive impairment of renal function. The protective effect of unilateral nephrectomy reported here is discussed in relation to a Cyclosporin A induced reduction in glomerular filtration rate and subsequent protection against glomerulosclerosis.