El texto completo de este trabajo no está disponible en el Repositorio Académico UPC por restricciones de la casa editorial donde ha sido publicado. / Chylothorax is defined as the accumulation of chyle within the pleural space. Originally described in 1917 by Pisek, it is the most common cause of pleural effusion in the neonatal period. The leading cause of chylothorax is laceration of the thoracic duct during surgery, which occurs in 0.85% to 6.6% of children undergoing cardiothoracic surgery. Few authors of reports in the literature have looked at etilefrine, a relatively unknown sympathomimetic, as an option for the medical treatment of chylothorax. In this case report, we review the clinical course of 2 infants with type III esophageal atresia who developed chylothorax after thoracic surgery and were successfully treated with intravenous etilefrine after failing initial dietary and pharmacological management. / Revisión por pares

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5-Nitrofurans are synthetic antibacterial agents. In general, nitrofurans have been shown to be toxic and mutagenic to cultured mammalian cells and carcinogenic in rodents. The possibility that human exposure to nitrofurans may be causing genetic damage or cancer has stimulated research directed towards elucidating the metabolism and mechanism of action of these compounds. A comprehensive understanding of the molecular basis of nitrofuran action may also be useful for comprehending the mechanism of action of other aryl and heterocyclic nitro compounds. It is known that enzymatic reduction of nitrofurans to reactive but uncharacterized metabolites that damage DNA constitutes an important "activation" step in both bacteria and hypoxic mammalian cells. However, since the known mammalian enzymes having nitroreductase activity are reported to be strongly inhibited by molecular oxygen, the relation of reductive activation to the DNA-damaging effects of nitrofurans in intact animals or in aerobic cultured cells is unclear. In rodents the liver is a major site of nitrofuran reduction in vivo. Net reduction of 5-nitro-2-furaldehyde semicarbazone (nitrofurazone) by rat liver homogenate was found to be relatively insensitive to oxygen when compared to net nitroreduction by milk xanthine oxidase. Intermediates generated in the aerobic nitroreduction bound tightly and probably covalently to protein. The nitroreductase in the rat liver preparation was identified as xanthine oxidoreductase by its apparent MW, substrate specificity and inhibition by allopurinol. Xanthine oxidoreductase is known to function in vivo as xanthine dehydrogenase (D form) which is converted to xanthine oxidase (0 form) during purification and storage. The 0 form is considered to be the major cytosolic nitroreductase and its activity is strongly inhibited by oxygen in vitro. Net nitroreduction by the D form has not been studied previously. In the rat liver preparation the bulk of the aerobic nitroreductase activity was associated with the D form of xanthine oxidoreductase during chromatography on CM cellulose, heat conversion of D form to 0 form and chemical interconversion of D form to 0 form and back to D form. Thus, net reduction of nitrofurazone by xanthine dehydrogenase is considerably less sensitive to inhibition by oxygen than is net nitroreduction by rat liver or milk xanthine oxidase. The ability of xanthine dehydrogenase to reduce nitrofurazone aerobically to highly reactive species in vitro suggests that this enzyme may play a role in a nitroreductive process which contributes to the mutagenic and carcinogenic action of nitrofurans and other nitroheterocyclic and nitroaromatic compounds in vivo. On the other hand, the nitroreductase activity of xanthine dehydrogenase in non-target tissues may, in some cases, decrease the amount of nitrocompound available in target tissues and hence play a "protective" role. / Thesis / Master of Science (MSc)

by Choy Ka-Fai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 107-125). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.I / 論文摘要 --- p.II / ABSTRACT --- p.III / ABBREVIATIONS --- p.V / TABLE OF CONTENTS --- p.VI / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter CHAPTER 2 --- PURIFICATION OF GRASS CARP ALDH FROM MITOCHONDRIA --- p.18 / Chapter CHAPTER 3 --- PURIFICATION & CHARACTERIZATION OF GRASS CARP ALDH --- p.49 / Chapter CHAPTER 4 --- CONCLUSION --- p.104 / REFERENCES --- p.107

Akademisk avhandling--Copenhagen. / Bibliography: p. 102-109.

Akademisk avhandling--Copenhagen. / Bibliography: p. 102-109.

<p>Gliomas are the most common tumors of the central nervous system. Our lab recently identified mutations in <italic>IDH1</italic> and <italic>IDH2</italic> as occurring frequently in progressive gliomas. We applied a series of biochemical and genetic approaches to explore the roles of the mutations in tumors and generate models for study. </p><p><italic>IDH1/2</italic> mutations have the potential to impact a number of metabolic pathways. IDH1/2 convert isocitrate to &#945;-ketoglutarate while simultaneously converting NADP+ to NADPH. To assess changes in metabolism, we completed metabolic profiling and complementary studies in cell lines with and without mutant <italic>IDH1</italic> or mutant <italic>IDH2</italic>. We identified a decrease in hypoxia signaling and a decrease in global 5-hydroxymethylcytosine in cell lines with mutant <italic>IDH1/2</italic> .</p><p>Having observed mutations in <italic>IDH1/2</italic> in a large fraction of progressive gliomas, we asked if the mutations were either 1) advantageous for growth in brain parenchyma, or 2) advantageous in a particular cell-of-origin. Sequencing of a series of metastases to the brain from non-central nervous system tumors identified no mutations in <italic>IDH1/2</italic>, lending less credence to the first hypothesis. To elucidate whether mutations in <italic>IDH1/2</italic> can initiate glioma progression and explore the potential cell-of-origin for progressive gliomas, we generated mice in which we induced expression of mutant <italic>IDH2</italic> in different populations of cells in the brain, either alone or in combination with <italic>TP53</italic> deletion, another frequently altered gene in progressive gliomas. Mice with broad expression of mutant <italic>IDH2</italic> developed hydrocephalus and encephalomalacia early in life, but did not develop tumors. Therefore, we restricted expression, and two brain tumors were identified in mice with both <italic>IDH2</italic> mutation and <italic>TP53</italic> deletion. While this suggests that both mutations might be required for the development of tumors, this is too small a number to draw significant conclusions. Further research with an expanded cohort of mice, utilization of additional drivers of expression, and further characterization of identified tumors will help in elucidating the role of mutant <italic>IDH2</italic> and the cell-of-origin for progressive gliomas.</p> / Dissertation