Inaug.-Diss.--München. / At head of title: Aus dem Hygienischen institut der Universität München ... Lebenslauf. "Schrifttum": p. 33-34.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1970. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Bead count rate (BCR) monitoring successfully identifies pipetting error during single platform enumeration. Enumeration beads are a stable constant in each patient’s sample and if these can be multitasked to monitor overall flow cytometer operation in a model of continuous quality control (CQC), they could reveal further details of flow cytometer operation and fulfill more quality assurance functions than identify pipetting error alone. Methods The CQC model used manufacturer recommended quality control procedures daily. In addition, methods were developed to monitor flow cytometer fluidics and electronics as well as sample preparation to standardise and extended quality monitoring. Sample-to-sample CQC included monitoring BCR, selected time, optical and fluorescence histograms as well as FPCV and MCN. This model also incorporated diligent monitoring of BCR patterns to detect instrument malfunctions. Post standardisation and implementation of the CQC model, an extended EQA exercise assessed bias between standardised CD4 counting methods and determined a ‘near true’ CD4 count to use as a calibrator. Conclusion The proposed CQC model standardised overall flow cytometer and automated sample preparation systems and, established imprecision reference intervals for each aspect of testing (fluidics <3%, sample preparation 2-4% and protocol and electronics <2%). Further BCR pattern recognition was used to identify instrument malfunctions in real-time and, longitudinally for pro-actively identifying imminent breakdowns. CD4 counts were calibrated to consensus mean ‘near true’ counts on two flow cytometers in the Reference Laboratory.

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Smokers incur a sustained free radical load which may increase their vitamin E requirement. However, in the present study this was not apparent from plasma and red blood cells (RBC) vitamin E concentrations which were similar in both smokers and non-smokers. However, RBC from smokers were more susceptible to hydrogen peroxide-stimulated peroxidation than those from non-smokers (p<0.001). Furthermore, plasma concentrations of lipid peroxides, thiobarbituric acid reactive substances and conjugated dienes were also elevated in smokers compared with the non-smokers (p<0.05). These indices of oxidative stress were markedly decreased (p<0.001) in both the smokers, and non-smokers, following consumption of 280 mg dl- tocopherol acetate/day for ten weeks. Plasma and RBC vitamin E concentration increased substantially following supplementation, but the % increase in vitamin E required to improve resistance to in vitro RBC peroxidation was significantly greater in non-smokers (p<0.01). This may reflect an endogenous adaptive response to oxidant stress in RBC of smokers. Erythrocyte vitamin E concentrations increased in a dose dependent manner during 20 weeks of supplementation with either 70,140,560 or 1050mg d--tocopherol per day. In smokers each dose was associated with a significant decrease in susceptibility of erythrocytes to peroxidation (p<0.001). However, red cells of non-smokers on the 1050mg supplement demonstrated an increased susceptibility to peroxidation (p<0.001). Thus, vitamin E may demonstrate prooxidant activity in non-smokers at high and prolonged intakes. Moreover, prolonged supplementation with d--tocopherol in non-smokers induced a decline in plasma ascorbate concentration (p<0.02) in association with an increasing erythrocyte vitamin E uptake (p<0,001). Both smokers and non-smokers may benefit from increased vitamin E intakes, although their requirements may be very different. However pharmacological doses may not be required since it appears that doses as low as 70mg are equally effective.

Thesis (M.Sc. Biological Sciences)--University of Waikato, 2009. / Title from PDF cover (viewed October 2, 2009) Includes bibliographical references.

The arterial vasodilation seen in human septic shock is conventionally attributed to increased nitric oxide (NO) production, primarily by extrapolation of animal and cellular studies. Little is known of the cellular source of NO in human septic shock. Other mediators, such as carbon monoxide (CO), may modulate NO production, and could also directly contribute to vasodilation. This study has examined the NO and CO synthetic pathways in peripheral blood mononuclear cells and mesenteric arterial smooth muscle from patients with septic shock, and from non-septic controls. Peripheral blood mononuclear cells from septic patients had increased NO production, though this was perhaps more modest than expected. The transport of arginine, the substrate for NO synthase, into these cells was increased; this was due to an increase in the activity of one transporter system, y⁺. mRNA for a protein encoding y⁺ activity, CAT2B, was increased in these cells. However, mRNA and protein for inducible and endothelial NO synthase was decreased in sepsis, while inducible heme oxygenase (the enzyme responsible for CO production) mRNA and protein was increased. NO production in arterial smooth muscle from septic patients was reduced, as was mRNA for inducible and endothelial NO synthase, and the arginine transporter CAT1. There was no increase in inducible NO synthase protein, though there were small increases in endothelial NO synthase protein and NO synthase activity. In contrast, both mRNA and protein for inducible heme oxygenase were increased. These results challenge the assumption that NO is central to the pathogenesis of human sepsis. Negative feedback systems for NO production have been demonstrated in cell models. These may be relatively more important in human sepsis. In addition to forming one of these feedback systems, it may be that CO, more than NO, is responsible for the hypotension observed in these patients.