"A one dimensional, multiple reaction pathway model of the dechlorination reactions of trichloroethylene (TCE) and tetrachloroethylene (PCE) as these species pass through a zero valent iron permeable reactive barrier (PRB) was produced. Three different types of rate equations were tested; first order, surface controlled with interspecies competition, and surface controlled with inter and intra species competition. The first order rate equations predicted the most accurate results when compared to actual data from permeable reactive barriers. Sensitivity analysis shows that the most important variable in determining TCE concentration in the barrier is the first order rate constant for the degradation of TCE. The velocity of the water through the barrier is the second most important variable determining TCE concentration. For PCE the concentration in the barrier is most sensitive to the velocity of the water and to the first order degradation rate constant for the PCE to dichloroacetylene reaction. Overall, zero valent iron barriers are more effective for the treatment of TCE than PCE. "

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Philosophiae Doctor - PhD / Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain. Although the etiology of PD is not completely known, it is believed to involve an association of various genetic, cellular, and environmental factors that individually or simultaneously advance neuronal degeneration. Neurotoxins such as 1-methyl-4-phenylpyridinium (MPP+) and 6-hydroxydopamine (6-OHDA) have been widely used to investigate distinct underlying mechanisms involved in the pathogenesis of PD. Presently, treatment options for PD are limited, as the available drugs are mainly focused on alleviating symptoms with limited ability to prevent disease progression. Accordingly, there is an increase in the use of natural compounds/products as potential neuroprotective agents. These neuroprotective treatments are believed to intervene in some stages in the pathogenesis of PD to suppress possible mechanisms of dopaminergic neuronal death such as apoptosis, mitochondrial dysfunction, oxidative stress, disturbances of calcium homeostasis, inflammation and autophagy. Thus, novel protective strategies for PD may be designed by targeting these mechanisms or intracellular signaling cascades that participate in PD pathogenesis.

Ge, Tianfang. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 87-93). / Abstract also in Chinese. / EXAMINATION COMMITTEE LIST --- p.ii / DECLARATION --- p.iii / ACKNOWLEDGEMENTS --- p.iv / ABSTRACT --- p.v / ABSTRACT IN CHINESE --- p.vii / ABBREVIATIONS --- p.ix / TABLE OF CONTENTS --- p.xiii / Chapter 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Erythropoiesis --- p.2 / Chapter 1.2 --- The TF-1 model --- p.3 / Chapter 1.3 --- The erythroid marker glycophorin A (GPA) --- p.4 / Chapter 1.4 --- Reactive oxygen species (ROS) --- p.4 / Chapter 1.5 --- Oxidative stress in human erythrocytes --- p.6 / Chapter 1.6 --- Antioxidant defense systems --- p.6 / Chapter 1.7 --- Glucose provides the majority of reducing equivalents in human erythrocytes --- p.9 / Chapter 1.8 --- Glucose transporter type 1 (Glut l) transports glucose and vitamin C into human erythrocytes --- p.10 / Chapter 1.9 --- Hypothesis and objectives --- p.11 / Chapter 1.10 --- Long-term significance --- p.12 / Figure 1.1 Stages of mammalian erythropoiesis. Adapted from (Koury et al.，2002) --- p.13 / "Figure 1.2 Conversion of major ROS. Adapted from (Ghaffari," --- p.14 / Figure 1.3 Major oxidative defense in human erythrocytes --- p.15 / "Figure 1.4 Peroxide scavenging systems. Adapted from (Day," --- p.16 / Chapter 2 --- MATERIALS AND METHODS --- p.17 / Chapter 2.1 --- Cell culture --- p.18 / Chapter 2.1.1 --- Culture media --- p.18 / Chapter 2.1.2 --- Cell maintenance --- p.19 / Chapter 2.1.3 --- Cell cryopreservation --- p.19 / Chapter 2.1.4 --- Cell differentiation --- p.20 / Chapter 2.1.5 --- Cell treatments --- p.20 / Chapter 2.1.5.1 --- Antioxidant treatments --- p.21 / Chapter 2.1.5.2 --- H2O2 challenging --- p.22 / Chapter 2.1.5.3 --- Antibiotic treatment --- p.22 / Chapter 2.2 --- Flow cytometry --- p.23 / Chapter 2.2.1 --- Flow cytometers --- p.23 / Chapter 2.2.2 --- Analysis of erythroid differentiation --- p.23 / Chapter 2.2.3 --- Analysis of cell lineage --- p.24 / Chapter 2.2.4 --- Analysis of intracellular ROS --- p.24 / Chapter 2.2.5 --- Analysis of mitochondrial transmembrane potential (Δψm) --- p.25 / Chapter 2.2.6 --- Analysis of mitochondrial mass --- p.25 / Chapter 2.2.7 --- Analysis of cell death --- p.26 / Chapter 2.2.8 --- Analysis of caspase-3 activity --- p.27 / Chapter 2.2.9 --- FACS cell sorting --- p.27 / Chapter 2.2.10 --- Two-variant flow cytometric experiments --- p.28 / Chapter 2.2.11 --- Analysis of flow cytometry data --- p.28 / Chapter 2.2.12 --- Compensation --- p.29 / Chapter 2.2.12.1 --- Compensation matrix for Annexin V-PI double-staining --- p.29 / Chapter 2.2.12.2 --- Compensation matrix for Annexin V-TMRM double-staining --- p.30 / Chapter 2.2.12.3 --- Compensation matrix for CFSE- GPA double-staining --- p.31 / Chapter 2.2.12.4 --- Compensation matrix for CFSE- TMRM double-staining --- p.31 / Chapter 2.2.12.5 --- Compensation matrix for CM- H2DCFDA-GPA double-staining --- p.32 / Chapter 2.2.12.6 --- Compensation matrix for GPA- TMRM double-staining --- p.33 / Chapter 2.3 --- Western blot --- p.35 / Chapter 2.4 --- Statistical analysis --- p.37 / Chapter 3 --- RESULTS AND DISCUSSION --- p.38 / Chapter 3.1 --- The cells with high GPA staining were younger in cell lineage --- p.39 / Chapter 3.2 --- ROS was produced during TF-1 erythropoiesis --- p.40 / Chapter 3.3 --- ROS production was not essential for TF-1 erythropoiesis --- p.41 / Chapter 3.4 --- ROS production was not the cause of cell proliferation during TF-1 erythropoiesis --- p.41 / Chapter 3.5 --- ROS production was not the cause of sub-lethal mitochondrial depolarization in TF-1 erythropoiesis --- p.42 / Chapter 3.6 --- The cells showing mitochondrial depolarization were mother cells that gave rise to differentiating cells --- p.44 / Chapter 3.7 --- ROS production was not the cause of cell death in TF-1 erythropoiesis --- p.45 / Chapter 3.8 --- ROS production confers oxidative defense during TF-1 erythropoiesis --- p.47 / Chapter 3.8.1 --- Glut l inhibition partially blocked TF-1 erythropoiesis without affecting cell viability --- p.47 / Chapter 3.8.2 --- Antioxidant defense systems were established during TF-1 erythropoiesis --- p.48 / Chapter 3.8.3 --- Antioxidant treatments blocked the establishment of antioxidant defense systems during TF-1 erythropoiesis --- p.51 / Chapter 3.9 --- Conclusion --- p.55 / Chapter 3.10 --- Future work --- p.56 / Figure 3.1 Cell lineage versus erythroid marker during erythropoiesis under vitamin E treatment --- p.59 / Figure 3.2 ROS production during erythropoiesis --- p.60 / Figure 3.3 ROS production versus erythroid marker during erythropoiesis under vitamin E treatment --- p.61 / Figure 3.4 Percentage of ROS+ cells in vitamin E-treated TF-1 erythropoiesis as compared to control --- p.63 / Figure 3.5 Percentage of GPA+ cells in vitamin E-treated TF-1 erythropoiesis as compared to control --- p.64 / Figure 3.6 Cell death versus mitochondrial transmembrane potential (Δψm) during erythropoiesis under vitamin E treatment --- p.65 / Figure 3.7 Erythroid marker versus mitochondrial transmembrane potential (Δψm) during erythropoiesis under vitamin E treatment --- p.67 / Figure 3.8 Cell lineage versus mitochondrial transmembrane potential (Δψm) during erythropoiesis under vitamin E treatment --- p.69 / Figure 3.9 Change of mitochondrial mass during erythropoiesis --- p.71 / Figure 3.10 ROS production versus erythroid marker during erythropoiesis under levofloxacin treatment --- p.72 / Figure 3.11 Percentage of GPA+ cells in levofloxacin-treated TF-1 erythropoiesis as compared to control --- p.73 / Figure 3.12 Cell death versus mitochondrial transmembrane potential (Δψm) during erythropoiesis under levofloxac in treatment --- p.74 / Figure 3.13 Expression level of antioxidant enzymes during erythropoiesis --- p.75 / Figure 3.14 Expression level of Glut l during erythropoiesis --- p.76 / Figure 3.15 Expression level of Glut l in GPA positive and GPA negative populations --- p.77 / Figure 3.16 Cell death under oxidative stress challenging during erythropoiesis --- p.78 / Figure 3.17 Expression level of antioxidant enzymes and Glutl during erythropoiesis under EUK-134 treatment --- p.79 / Figure 3.18 Expression level of antioxidant enzymes and Glutl during erythropoiesis under vitamin E treatment --- p.80 / Figure 3.19 Cell death under oxidative stress challenging during erythropoiesis under vitamin E treatment --- p.82 / Figure 3.20 Expression level of antioxidant enzymes during erythropoiesis under vitamin C treatment --- p.83 / Figure 3.21 Cell death under oxidative stress challenging during erythropoiesis under vitamin C treatment --- p.84 / Figure 3.22 Cell death under oxidative stress challenging during erythropoiesis under NAC treatment --- p.85 / Figure 3.23 Summary of oxidative stress challenging during erythropoiesis --- p.86 / REFERENCES --- p.87

abstract: In order to meet climate targets, the solar photovoltaic industry must increase photovoltaic (PV) deployment and cost competitiveness over its business-as-usual trajectory. This requires more efficient PV modules that use less expensive materials, and longer operational lifetime. The work presented here approaches this challenge with a novel metallization method for solar PV and electronic devices. This document outlines work completed to this end. Chapter 1 introduces the areas for cost reductions and improvements in efficiency to drive down the cost per watt of solar modules. Next, in Chapter 2, conventional and advanced metallization methods are reviewed, and our proposed solution of dispense printed reactive inks is introduced. Chapter 3 details a proof of concept study for reactive silver ink as front metallization for solar cells. Furthermore, Chapter 3 details characterization of the optical and electrical properties of reactive silver ink metallization, which is important to understanding the origins of problems related to metallization, enabling approaches to minimize power losses in full devices. Chapter 4 describes adhesion and specific contact resistance of reactive ink metallizations on silicon heterojunction solar cells. Chapter 5 compares performance of silicon heterojunction solar cells with front grids formed from reactive ink metallization and conventional, commercially available metallization. Performance and degradation throughout 1000 h of accelerated environmental exposure are described before detailing an isolated corrosion experiment for different silver-based metallizations. Finally, Chapter 6 summarizes the main contributions of this work. The major goal of this project is to evaluate potential of a new metallization technique –high-precision dispense printing of reactive inks–to become a high efficiency replacement for solar cell metallization through optical and electrical characterization, evaluation of durability and reliability, and commercialization research. Although this work primarily describes the application of reactive silver inks as front-metallization for silicon heterojunction solar cells, the work presented here provides a framework for evaluation of reactive inks as metallization for various solar cell architectures and electronic devices. / Dissertation/Thesis / Doctoral Dissertation Materials Science and Engineering 2019

Permeable reactive barriers (PRBs) are one of the leading technologies being developed in the search for alternatives to the pump-and-treat method for the remediation of contaminated groundwater. A new optimising design methodology is proposed to aid decision-makers in finding minimum cost PRB designs for remediation problems in the presence of input uncertainty. The unique aspects of the proposed methodology are considered to be: design enhancements to improve the hydraulic performance of PRB systems; elimination of a time-consuming simulation model by determination of approximating functions relating design variables and performance measures for fully penetrating PRB systems; a versatile, spreadsheet-based optimisation model that locates minimum cost PRB designs using Excel's standard non-linear solver; and the incorporation of realistic input variability and uncertainty into the optimisation process via sensitivity analysis, scenario analysis and factorial analysis. The design methodology is developed in the context of the remediation of nitrate contamination due to current concerns with nitrate in New Zealand. Three-dimensional computer modelling identified significant variation in capture and residence time, caused by up-gradient funnels and/or a gate hydraulic conductivity that is significantly different from the surrounding aquifer. The unique design enhancements to control this variation are considered to be the customised down-gradient gate face and emplacement of funnels and side walls deeper than the gate. The use of velocity equalisation walls and manipulation of a PRB's hydraulic conductivity within certain bounds were also found to provide some control over variation in capture and residence time. Accurate functional relationships between PRB design variables and PRB performance measures were shown to be achievable for fully penetrating systems. The chosen design variables were gate length, gate width, funnel width and the reactive material proportion. The chosen performance measures were edge residence, centreline residence and capture width. A method for laboratory characterisation of reactive and non-reactive material combinations was shown to produce data points that could realistically be part of smooth polynomial interpolation functions. The use of smooth approximating functions to characterise PRB inputs and determine PRB performance enabled the creation of an efficient spreadsheet model that ran more quickly and accurately with Excel's standard non-linear solver than with the LGO global solver or Evolver genetic-algorithm based solver. The PRB optimisation model will run on a standard computer and only takes a couple of minutes per optimisation run. Significant variation is expected in inputs to PRB design, particularly in aquifer and plume characteristics. Not all of this variation is quantifiable without significant expenditure. Stochastic models that include parameter variability have historically been difficult to apply to realistic remediation design due to their size and complexity. Scenario and factorial analysis are proposed as an efficient alternative for quantifying the effects of input variability on optimal PRB design. Scenario analysis is especially recommended when high quality input information is available and variation is not expected in many input parameters. Factorial analysis is recommended for most other situations as it separates out the effects of multiple input parameters at multiple levels without an excessive number of experimental runs.

<p>Until just a few years ago wind farms where excluded from many of the requirementsthat can be found in grid codes. But as the numbers of wind farms have grown as wellas the sizes of them, the requirements to connect them to the grid have becomemore stringent. In this thesis it has been investigated if it’s possible to design a controlsystem that controls the reactive power from an offshore wind farm, so that the gridcode requirements regarding reactive power are fulfilled. By controlling the reactivepower the dynamic variations in the voltage are decreased. The regulator should alsobe able to help the wind farm to handle the fault conditions that are described in thegrid code.An offshore wind farm outside the coast of Western Europe is now being planned.Data from this wind farm has been used in this thesis. The wind farm has a total of 54wind turbines with more than 300 MW all together. The reactive power is controlledvia the generators and also by disconnecting and connecting four shunt reactors.A model of the wind farm has been built in Simpow, as well as design of the regulator.Simpow is a simulation program developed by ABB that enables simulations of powersystems. Different scenarios have been simulated to see if it is possible to control thewind farm in the desired way. The results show that the wind farm manages to handlefault conditions as described in the grid, and it is also possible to control the reactivepower in a desirable way.</p>

Protein-energy malnutrition (PEM) has been found in up to 16.3% of acute stroke patients upon admission to hospital. Our laboratory has previously shown that PEM impairs functional outcome in a gerbil model of global ischemia, but the mechanism has not been established. The purpose of the current study was to characterize the marked reactive gliosis apparent in a subset of these animals that could represent an increased inflammatory response. A second objective was to validate a screening protocol for assessing completeness of ischemia in this model. Male Mongolian gerbils, aged 11-12 weeks, were randomized to PEM (2% protein) or control diet (12.5% protein) for 28d. PEM animals lost 12.2% of their initial body weight, and feed intake and serum albumin concentration were 12.3% and 17.8% lower than controls, respectively. At day 28, animals underwent 5 min bilateral common carotid artery occlusion (ischemia) or sham surgery. Activity was monitored using infrared beam interruptions for 20h post-surgery to screen for complete ischemia on the basis of persistent hyperactivity. Brain sections were stained with hematoxylin & eosin, and viable hippocampal CA1 neurons were counted at 10d post-ischemia. Immunohistochemistry for glial-fibrillary acidic protein (GFAP) and ricinus communis agglutinin -120 (RCA-120), markers for astrocytes and microglia, respectively, and the inflammatory cytokine TNF-alpha was performed on brain sections at 6h, 24h, 3d and 10d post-surgery (Ischemic, n=8; Sham, n=3). The activity monitoring procedure for detecting complete ischemia validated against hippocampal CA1 neuronal loss at 10d demonstrated an accuracy of 84.6%. Temporal changes in GFAP and RCA-120 immunoreactivity characteristic of reactive gliosis were demonstrated following ischemia, but this was not exacerbated by PEM. TNF-alpha immunoreactivity following ischemia was also unaltered by PEM. Ischemia significantly reduced surviving CA1 neurons at 10 days post-ischemia (two-way ANOVA; p<0.05), but this was not influenced by PEM. Impaired functional outcome in PEM animals following global ischemia can not be accounted for by increased hippocampal CA1 neuron death or by altered glial response.

Until just a few years ago wind farms where excluded from many of the requirementsthat can be found in grid codes. But as the numbers of wind farms have grown as wellas the sizes of them, the requirements to connect them to the grid have becomemore stringent. In this thesis it has been investigated if it’s possible to design a controlsystem that controls the reactive power from an offshore wind farm, so that the gridcode requirements regarding reactive power are fulfilled. By controlling the reactivepower the dynamic variations in the voltage are decreased. The regulator should alsobe able to help the wind farm to handle the fault conditions that are described in thegrid code.An offshore wind farm outside the coast of Western Europe is now being planned.Data from this wind farm has been used in this thesis. The wind farm has a total of 54wind turbines with more than 300 MW all together. The reactive power is controlledvia the generators and also by disconnecting and connecting four shunt reactors.A model of the wind farm has been built in Simpow, as well as design of the regulator.Simpow is a simulation program developed by ABB that enables simulations of powersystems. Different scenarios have been simulated to see if it is possible to control thewind farm in the desired way. The results show that the wind farm manages to handlefault conditions as described in the grid, and it is also possible to control the reactivepower in a desirable way.

Protein-energy malnutrition (PEM) has been found in up to 16.3% of acute stroke patients upon admission to hospital. Our laboratory has previously shown that PEM impairs functional outcome in a gerbil model of global ischemia, but the mechanism has not been established. The purpose of the current study was to characterize the marked reactive gliosis apparent in a subset of these animals that could represent an increased inflammatory response. A second objective was to validate a screening protocol for assessing completeness of ischemia in this model. Male Mongolian gerbils, aged 11-12 weeks, were randomized to PEM (2% protein) or control diet (12.5% protein) for 28d. PEM animals lost 12.2% of their initial body weight, and feed intake and serum albumin concentration were 12.3% and 17.8% lower than controls, respectively. At day 28, animals underwent 5 min bilateral common carotid artery occlusion (ischemia) or sham surgery. Activity was monitored using infrared beam interruptions for 20h post-surgery to screen for complete ischemia on the basis of persistent hyperactivity. Brain sections were stained with hematoxylin & eosin, and viable hippocampal CA1 neurons were counted at 10d post-ischemia. Immunohistochemistry for glial-fibrillary acidic protein (GFAP) and ricinus communis agglutinin -120 (RCA-120), markers for astrocytes and microglia, respectively, and the inflammatory cytokine TNF-alpha was performed on brain sections at 6h, 24h, 3d and 10d post-surgery (Ischemic, n=8; Sham, n=3). The activity monitoring procedure for detecting complete ischemia validated against hippocampal CA1 neuronal loss at 10d demonstrated an accuracy of 84.6%. Temporal changes in GFAP and RCA-120 immunoreactivity characteristic of reactive gliosis were demonstrated following ischemia, but this was not exacerbated by PEM. TNF-alpha immunoreactivity following ischemia was also unaltered by PEM. Ischemia significantly reduced surviving CA1 neurons at 10 days post-ischemia (two-way ANOVA; p<0.05), but this was not influenced by PEM. Impaired functional outcome in PEM animals following global ischemia can not be accounted for by increased hippocampal CA1 neuron death or by altered glial response.