The purpose of this investigation was to redesign, construct, and operate a two-inch experimental pulse liquid-liquid extractor, and to determine the effects of the pulse amplitude, the number of plates, and the plate-free-area on the stage efficiency of the column. The optimum liquid flow rates were also determined. An examination of the literature was conducted for a review of the available information on pulse extractors. Although a great deal of literature was available on the topic of liquid-liquid extraction, detailed information on only two pulse extractors could be found. The results obtained during this investigation compare favorably with those reported in the literature. A two-inch experimental pulse-type extractor was constructed. The liquids were pulsed by means of a sylphon-type bellows operated by a push rod which was driven by an eccentric cam. For the satisfactory operation of the extractor various auxiliary apparatus was required; important among these were the supporting framework, the push-rod bearing, the reduction train for the can, the storage tanks, and the tubing and fittings. Twenty-seven individual experimental tests were conducted, extracting acetone from carbon tetrachloride with water, to determine the effects of the various operating parameters on the stage efficiency of the pulse column. During the experimental tests the following variables were studied: pulse amplitude at one, two, and three inches of vertical liquid displacement; number of plates with four, eight, and twelve plates; and plate-free-area with eight, sixteen, and thirty-two per cent free area. It was found that the pulse amplitude, the number of plates, and the plate-free-area each have an independent significant effect on the stage efficiency of the pulse column; the plate-free-area has the largest relative effect, while the pulse amplitude has the smallest relative effect. It was further proven by this investigation that the interactions between the pulse amplitude and number of plates, the pulse amplitude and plate-free-area, and the number of plates and plate-free-area have no significant effect on the stage efficiency of the pulse column. The flow rates for satisfactory column operation are 1807, 2211, 1478, and 2299 pounds per hour-square foot of column cross-section for the feed, solvent, raffinate, and extract, respectively. / Master of Science

Throughout the United States, there are a large number of groundwater systems contaminated by chlorinated organic compounds. Of these compounds, carbon tetrachloride (CT) is one of the most frequently encountered due to its past, widespread industrial use. In anaerobic groundwater environments, CT has been shown to be susceptible to degradation by both biotic and abiotic processes. One abiotic process that has been researched extensively is the reduction of CT by iron metal and associated iron oxides and hydroxides. Magnetite, an iron oxide, is a ubiquitous component of many subsurface environments and has been investigated as a potential groundwater remediation technology. One beneficial characteristic of magnetite is the capability to be synthetically produced in various sizes and shapes - including particles within the nanoscale range. Nanoscale particles have been shown to be more reactive towards contaminants than larger sized particles due to their large surface areas and high surface reactivity. This project was designed to characterize the behavior of synthetic magnetite in the presence of carbon tetrachloride under anaerobic conditions. / Master of Science

no abstract provided by author / Master of Science

Dissertation (Ph.D.)--University of South Florida, 2007. / Title from PDF of title page. Document formatted into pages; contains 141 pages. Includes vita. Includes bibliographical references.

by Wong Wing-yee, Felice. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 144-166). / Abstract also in Chinese. / Acknowledgements --- p.i / List of Abbreviations --- p.ii / Abstract --- p.iv / Abstract (Chinese Version) --- p.vi / Table of Contents --- p.viii / List of Tables --- p.xii / List of Figures --- p.xiv / List of Appendices --- p.xvi / Chapter Chapter I --- Literature Review / Chapter 1. --- Introduction --- p.1 / Chapter 2. --- Background of Cytochrome P450 --- p.3 / Chapter 2.1 --- Discovery --- p.3 / Chapter 2.2 --- Tissue Distribution --- p.3 / Chapter 2.3 --- Structure and Functions --- p.7 / Chapter 2.4 --- Nomenclature of the P450 Superfamily --- p.10 / Chapter 3. --- Cytochrome P450 2E1 (CYP2E1) --- p.11 / Chapter 3.1 --- Discovery --- p.11 / Chapter 3.2 --- Tissue Distribution --- p.12 / Chapter 3.3 --- Substrates and Inducers --- p.13 / Chapter 3.4 --- Toxicological Role of CYP2E1 --- p.15 / Chapter 4. --- CYP2E1-knockout Mouse Model --- p.17 / Chapter Chapter II --- Carbon Tetrachloride (CC14) Study / Chapter 1. --- Introduction --- p.19 / Chapter 1.1 --- General Properties and Usage of CC14 --- p.19 / Chapter 1.2 --- Toxicological Aspects of CC14 --- p.19 / Chapter 1.3 --- Mechanism of CCl4-induced Hepatotoxicity --- p.20 / Chapter 1.4 --- Role of CYP2E1 in CCl4-induced Hepatotoxicity --- p.23 / Chapter 1.5 --- Objectives of the Study --- p.27 / Chapter 2. --- Materials and Methods --- p.29 / Chapter 2.1 --- Chemicals and Materials --- p.29 / Chapter 2.2 --- Animals --- p.29 / Chapter 2.3 --- Acute CC14 Treatment --- p.29 / Chapter 2.4 --- Preparation of Microsomal Fractions --- p.30 / Chapter 2.5 --- Determination of Microsomal Protein Concentration --- p.31 / Chapter 2.6 --- Determination of Serum Aminotransferase Activities --- p.31 / Chapter 2.7 --- Liver Histology --- p.32 / Chapter 2.8 --- Hepatic Microsomal CYP2E1 Activity -p-nitrophenol Assay --- p.34 / Chapter 2.9 --- SDS-PAGE and Western Blot Analysis --- p.35 / Chapter 2.10 --- Detection of Lipid Peroxidation in vitro and in vivo --- p.35 / Chapter 2.10.1 --- In vitro Lipid Peroxidation - 2-Thiobarbituric Acid (TBA) assay --- p.35 / Chapter 2.10.2 --- In vivo Lipid Peroxidation - Microsomal Conjugated Dienes Detection --- p.36 / Chapter 2.11 --- Hepatic Lipid Fatty Acid Composition Analysis --- p.39 / Chapter 2.11.1 --- Lipid Extraction --- p.39 / Chapter 2.11.2 --- Thin Layer Chromatography --- p.39 / Chapter 2.11.3 --- Methylation --- p.40 / Chapter 2.11.4 --- Gas Chromatography --- p.40 / Chapter 2.12 --- Statistical Analysis --- p.41 / Chapter 3. --- Results --- p.42 / Chapter 3.1 --- "Mortality, Liver Weight and Liver Color" --- p.42 / Chapter 3.2 --- Hepatotoxicity --- p.42 / Chapter 3.2.1 --- Serum ALT and AST activities --- p.42 / Chapter 3.2.2 --- Liver Histology --- p.45 / Chapter 3.3 --- CYP2E1-catalysed PNP Activities and CYP2E1 Protein Levels --- p.49 / Chapter 3.3.1 --- CYP2El-catalyzed PNP Activities --- p.49 / Chapter 3.3.2 --- CYP2E1 Protein Levels --- p.52 / Chapter 3.4 --- Lipid Peroxidation --- p.52 / Chapter 3.4.1 --- In vitro Lipid Peroxidation --- p.52 / Chapter 3.4.2 --- In vivo Lipid Peroxidation --- p.54 / Chapter 3.5 --- Hepatic Lipid Fatty Acid Composition --- p.56 / Chapter 3.5.1 --- Fatty Acid Composition in Hepatic Phospholipid --- p.56 / Chapter 3.5.2 --- Fatty Acid Composition in Hepatic Microsomal Phospholipid --- p.59 / Chapter 3.5.3 --- Fatty Acid Composition in Hepatic Triglyceride --- p.61 / Chapter 4. --- Discussion --- p.63 / Chapter 4.1 --- CYP2E1 is Required in CCl4-mediated Hepatotoxicity --- p.63 / Chapter 4.2 --- CYP2E1 is Degraded following CC14 Exposure --- p.65 / Chapter 4.3 --- CYP2E1 is Required in CCl4-induced Lipid Peroxidation --- p.67 / Chapter 4.4 --- CYP2E1 is Required in CCl4-induced Hepatic Phospholipid Depletion --- p.70 / Chapter 4.5 --- CYP2E1 is Required in CCl4-induced Hepatic Triglyceride Accumulation --- p.72 / Chapter 5. --- Conclusion --- p.76 / Chapter Chapter III --- Chronic Ethanol Consumption Study / Chapter 1. --- Introduction --- p.77 / Chapter 1.1 --- Multiple Metabolic Pathways for Ethanol Metabolism --- p.77 / Chapter 1.2 --- Metabolism of Ethanol by the Microsomal Ethanol Oxidizing System --- p.79 / Chapter 1.3 --- Role of CYP2E1 in Ethanol Metabolism --- p.82 / Chapter 1.4 --- Role of CYP2E1 in Alcoholic Liver Disease and Associated Oxidative Stress --- p.84 / Chapter 1.5 --- Objectives of the Study --- p.89 / Chapter 2. --- Materials and Methods --- p.90 / Chapter 2.1 --- Chemicals and Materials --- p.90 / Chapter 2.2 --- Animals --- p.90 / Chapter 2.3 --- Chronic Ethanol Treatment --- p.90 / Chapter 2.3.1 --- Ethanol Diet Composition --- p.90 / Chapter 2.3.2 --- Ethanol Feeding --- p.90 / Chapter 2.4 --- Monitoring of Blood Ethanol Levels --- p.96 / Chapter 2.5 --- Preparation of Microsomal Fractions --- p.96 / Chapter 2.6 --- Determination of Microsomal Protein Concentration --- p.97 / Chapter 2.7 --- Determination of Serum Aminotransferase Activities --- p.98 / Chapter 2.8 --- Liver Histology --- p.98 / Chapter 2.9 --- SDS-PAGE and Western Blot Analysis --- p.99 / Chapter 2.10 --- Hepatic Fatty Acid Composition Analysis --- p.100 / Chapter 2.10.1 --- Lipid Extraction --- p.100 / Chapter 2.10.2 --- Thin Layer Chromatography --- p.101 / Chapter 2.10.3 --- Methylation --- p.101 / Chapter 2.10.4 --- Gas Chromatography --- p.102 / Chapter 2.11 --- Statistical Analysis --- p.103 / Chapter 3. --- Results --- p.104 / Chapter 3.1 --- Average Food Consumption --- p.104 / Chapter 3.2 --- Average Ethanol Consumption for Ethanol Liquid Diet Feeding Group --- p.104 / Chapter 3.3 --- Body Weight Gain --- p.104 / Chapter 3.4 --- Blood Ethanol Levels --- p.108 / Chapter 3.5 --- "Mortality, Liver Weight and Liver Color" --- p.108 / Chapter 3.6 --- Serum ALT and AST Activities --- p.110 / Chapter 3.7 --- Liver Histology --- p.114 / Chapter 3.8 --- Western Blot Analysis --- p.119 / Chapter 3.9 --- Hepatic Lipid Fatty Acid Composition --- p.119 / Chapter 3.9.1 --- Fatty Acid Composition in Hepatic Phospholipid --- p.119 / Chapter 3.9.2 --- Fatty Acid Composition in Hepatic Triglyceride --- p.123 / Chapter 4. --- Discussion --- p.126 / Chapter 4.1 --- Nutrients Displacement after Chronic Ethanol Consumption --- p.126 / Chapter 4.2 --- Varied Blood Ethanol Levels after Chronic Ethanol Consumption --- p.127 / Chapter 4.3 --- Increase in CYP2E1 Levels after Chronic Feeding of Ethanolin WT mice --- p.127 / Chapter 4.4 --- Lack of Evidence Indicating the Development of Ethanol- Induced Liver Injury --- p.129 / Chapter 4.4.1 --- No Elevations in Serum ALT and AST Activities --- p.129 / Chapter 4.4.2 --- Normal Liver Histology --- p.130 / Chapter 4.4.3 --- Lack of Triglyceride Accumulation --- p.131 / Chapter 4.4.4 --- Elevations in Hepatic PL --- p.132 / Chapter 4.5 --- Possible Reasons for the Absence of Liver Damage after Chronic Ethanol Consumption in our Mouse Model --- p.134 / Chapter 5. --- Conclusion --- p.137 / Chapter Chapter IV --- Concluding Remarks / Chapter 1. --- A Comparison between Acute CC14 Study and Chronic Ethanol Consumption Study --- p.139 / Chapter 1.1 --- Regulation of CYP2E1 Expression --- p.139 / Chapter 1.2 --- Free Radical Production Involved in CC14- and Chronic Ethanol Consumption-Mediated Liver Injury --- p.140 / Chapter 1.3 --- An Overall Comparison between CC14 study and Chronic Ethanol Consumption Study --- p.140 / Chapter 2. --- Future Studies --- p.142 / Chapter 2.1 --- Acute CC14 Study --- p.142 / Chapter 2.1.1 --- Calcium Homeostasis Studies --- p.142 / Chapter 2.1.2 --- Spin Trapping Studies --- p.142 / Chapter 2.2 --- Chronic Ethanol Study --- p.142 / Chapter 2.2.1 --- "Generation of a Heterozygous ""Ethanol-Sensitive"" Mouse Strain (SV/129/ter x C57BL/6)" --- p.143 / Chapter 3. --- Concluding Remarks --- p.143 / References --- p.144 / Appendix --- p.167

Avasarala Sreedevi. / "December 2004." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2004. / Includes bibliographical references (p. 253-272) / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

published_or_final_version / Physics / Doctoral / Doctor of Philosophy

Abstract: Suppressor of cytokine signaling 1 (SOCS1) is an indispensable regulator of IFN-γ signaling and has been implicated in the regulation of liver fibrosis. However, it is not known whether SOCS1 mediates its anti-fibrotic functions in the liver directly, or via modulating IFN-γ, which has been implicated in attenuating hepatic fibrosis. Additionally, it is possible that SOCS1 controls liver fibrosis by regulating hepatic stellate cells (HSC), a key player in fibrogenic response. While the activation pathways of HSCs have been well characterized, the regulatory mechanisms are not yet clear. The goals of this study were to dissociate IFN-γ-dependent and SOCS1-mediated regulation of hepatic fibrogenic response, and to elucidate the regulatory functions of SOCS1 in H SC activation. Liver fibrosis was induced in Socs1[superscript -/-]Ifng[superscript -/-] mice with dimethylnitrosamine or carbon tetrachloride. Ifng[superscript -/-] and C57BL/6 mice served as controls. Following fibrogenic treatments, Socs1[superscript -/-]Ifng[superscript -/-] mice showed elevated serum ALT levels and increased liver fibrosis com-pared to mice Ifng[superscript -/-]. The latter group showed higher alanine aminotransferase (ALT) levels and fibrosis than C57BL/6 controls. The livers of Socs1-deficient mice showed bridging fibrosis, which was associated with increased accumulation of myofibroblasts and abundant collagen deposition. Socs1-deficient livers showed increased expression of genes coding for smooth muscle actin, collagen, and enzymes involved in remodeling the extracellular matrix, namely matrix metalloproteinases and tissue inhibitor of metalloproteinases. Primary HSCs from Socs1-deficient mice showed increased proliferation in response to growth factors such as HGF, EGF and PDGF, and the fibrotic livers of Socs1-deficient mice showed increased expression of the Pdgfb gene. Taken together, these data indicate that SOCS1 controls liver fibrosis independently of IFN-γ and that part of this regulation may occur via regulating HSC proliferation and limiting growth factor availability. / Résumé: Le suppresseur de la signalisation des cytokines 1 (SOCS1) est un régulateur indispensable de la signalisation de l'IFN-γ et a été aussi impliqué dans la régulation de la fibrose hépatique. Cependant, on ne sait pas si les fonctions anti-fibrotiques sont médiées directement dans le foie par SOCS1 ou par la modulation de l'IFN-γ, qui est connu pour son effet atténuateur de la fibrose hépatique. En outre, il est possible que SOCS1 contrôle la fibrose hépatique par la régulation des cellules stellaires hépatiques (CSH), un acteur clé dans la réponse fibrogénique. Alors que les voies d'activation des CSH ont été bien caractérisées, les mécanismes de régulation ne sont pas encore clairs. Les buts de cette étude étaient de dissocier la régulation de la réponse fibrogénique hépatique médiée par SOCS1 et celle dépendante de IFN-γ et d'élucider les fonctions régulatrices de SOCS1 dans l'activation des CSH. La fibrose hépatique a été induite chez des souris Socs1[indice supérieur -/-]Ifng[indice supérieur -/-] par la diméthylnitrosamine ou le tétrachlorure de carbone. Les souris Ifng[indice supérieur -/-] et C57BL6 ont servi comme contrôles. Après les traitements fibrogéniques, les souris Socs1[indice supérieur -/-]Ifng[indice supérieur -/-] ont montré des niveaux sériques élevés d'alanine aminotransférase (ALT) ainsi que l'augmentation de la fibrose du foie par rapport à des souris Ifng[indice supérieur -/-]. Le dernier groupe a montré des niveaux plus élevés d'ALT et de fibrose par rapport aux souris C57BL6 contrôles. Les foies des souris déficientes en Socs1 ont montré une fibrose septale, qui a été associée à une augmentation de l'accumulation des myofibroblastes et à un dépôt abondant du collagène. Les foies déficients en SOCS1 ont montré une expression accrue de gènes codant pour l'actine musculaire lisse, le collagène et les enzymes impliquées dans le remodelage de la matrice extracellulaire, à savoir les métalloprotéinases de la matrice et l'inhibiteur tissulaire des métalloprotéinases. Les CSH primaires de souris déficientes en Socs1 ont montré une prolifération accrue en réponse à des facteurs de croissance tels que le HGF, EGF et le PDGF. Aussi, les foies fibrotiques de souris déficientes en Socs1 ont montré une expression élevée du gène PDGFB. Pris ensemble, ces données indiquent que SOCS1 contrôle la fibrose hépatique indépendamment de l'IFN-γ et qu'une partie de cette régulation peut se produire en régulant la prolifération des HSC et en limitant la disponibilité des facteurs de croissance.

O uso de tetracloreto de carbono (CCl4) em ratos é um modelo experimental de dano ao tecido hepático, desencadeando fibrose e, a longo prazo, cirrose. Seu metabolismo ocorre no fígado pelo citocromo P450, resultando na produção de radicais livres e estimulação da lipoperoxidação, que induz um processo de necrose, inflamação e maior progressão da fibrose. Vários antioxidantes, entre eles os flavonoides, têm sido referidos como eficazes para diminuir a fibrose em modelos animais. Este estudo pretende avaliar a ação antioxidante da quercetina (Q) em um modelo experimental de cirrose induzida por CCl4 inalatório. Foram utilizados 25 ratos Wistar machos, com peso médio de 250g, divididos em 3 grupos: Controle (CO), CCl4 e CCl4+Q. Os ratos foram submetidos a inalações de CCl4 (2x/semana), durante 16 semanas, recebendo fenobarbital na água de beber na dose de 0,3g/dl, como indutor enzimático. A Q (50mg/Kg) via intraperitoneal foi iniciada na 10ª semana de inalação, perdurando até o final do experimento. A análise estatística foi ANOVA, seguida de Student Newmann Keuls (Média±SEM), considerando-se diferença estatisticamente significativa quando p<0,05. Após o tratamento com quercetina, observamos uma melhora na integridade hepática, diminuição da fibrose, do conteúdo de colágeno e re-estabelecimento nos níveis dos metabólitos do óxido nítrico, comparado ao grupo CCl4. Constatou-se também redução do dano oxidativo, verificada pela diminuição das substâncias que reagem ao ácido tiobarbitúrico (TBA-RS), assim como aumento na atividade das enzimas antioxidantes e da relação GSH/GSSG. A partir desses dados, sugerimos que o emprego da quercetina possa ser promissor como terapia antioxidante nas complicações hepáticas. / Carbon tetrachloride (CCl4) is a classic experimental model of oxidative damage to liver tissue, causing long-term fibrosis and cirrhosis. Metabolism in the liver via cytochrome P450 results in the stimulation of lipid peroxidation and production of free radicals, which induce a process of necrosis, inflammation and greater progression of fibrogenesis. Various antioxidants and flavonoids have been identified as effective in reducing fibrosis in animal models. This study aimed to assess the antioxidant activity of quercetin (Q) in an experimental model of cirrhosis induced by CCl4 inhalation. We used 25 male Wistar rats (250g) that were divided into 3 groups: control (CO), CCl4 and CCl4 + Q. The rats were subjected to CCl4 inhalation (2x/week) for 16 weeks, and they received phenobarbital in their drinking water at a dose of 0.3 g/dl as a P450 enzyme inducer. Q (50 mg/Kg) was initiated intraperitoneally at 10 weeks of inhalation and lasted until the end of the experiment. Statistical analysis was by ANOVA Student-Newman Keuls (mean ± SEM), and differences were considered statistically significant when p <0.05. After treatment with quercetin, we observed an improvement in liver integrity, decreased fibrosis, as analyzed by picrosirius for the quantification of collagen, and restored levels of nitric oxide metabolites compared with the CCl4 group. It also reduced oxidative stress, as confirmed by the decrease of substances reacting to thiobarbituric acid (TBARS), the increased activity of antioxidant enzymes and the reduced glutathione ratio and glutathione disulfide (GSH/GSSG). From these data, we suggest that the use of quercetin might be promising as an antioxidant therapy in liver complications.

Thesis (M.S.)--Indiana University, 2008. / Title from screen (viewed on January 26, 2010). Department of Cellular & Integrative Physiology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Navin Bansal, Andriy M. Babsky, Stephen A. Kempson, David P. Basile. Includes vitae. Includes bibliographical references (leaves 33-36).