Thesis (MTech (Chemistry))--Cape Peninsula University of Technology, 2016. / Inclusion compounds of two hydroxyl hosts with a variety of guests have been investigated. These host compounds are bulky molecules and have the ability to interact with smaller organic guests to form new compounds. The host 9-(1-naphthyl)-9H-xanthen-9-ol (H1), forms inclusion compounds with pyridine (PYR), N,N-dimethylacetamide (DMA), morpholine (MORP) and N-methyl-2-pyrrolidinone (NMP). The crystal structures of H1•NMP, H1•DMA and H1•MORP1 were successfully solved in the triclinic space group PĪ, whereas the inclusion compound H1•PYR crystallised in the monoclinic space group P21/c. A different inclusion compound involving morpholine, H1•MORP2 resulted from dissolution of H1 in a 1:1 molar ratio of MORP: DMA. H1•MORP2 crystallised in the space group PĪ. All of the abovementioned inclusion compounds demonstrated a host: guest ratio of 1:1 except for H1•MORP1 (host: guest ratio = 1: ). H1 interacts with pyridine and morpholine guests via (Host)O-H•••N(Guest) hydrogen bonds and via (Host)OH•••O(Guest) hydrogen bonds with N-methyl-2-pyrrolidinone and N,N-dimethylacetamide.

No description available.

Endotoxin (lipopolysaccharide, LPS) a chemical component of cell wall of gram-negative bacteria, is an important mediator in pathogenesis of sepsis and acute respiratory distress syndrome. It causes production and release of a wide array of mediators including cytokines, chemokines, oxygen free radicals and nitric oxide from neutrophils, macrophages, endothelial cells and epithelial cells through the NF-£eB pathway. LPS increases the permeability of microcirculation, and causes the acute formation of numerous endothelial gaps among venular endothelial cells, resulting in extensive plasma leakage in the inflammatory tissue. Urethan is commonly used as an animal anesthetic for nonrecovery laboratory surgery. It is aslo an £\2-adrenoreceptor antagonist, which can suppress the activation of the cardiovascular system and reduce the angiotensin which increases the blood pressure. Urethan or its metabolites protect animals against LPS, in part, by reducing TNF-£\ release. The aims of the present study to investigate the time-course of vascular permeability in microcirculation of rat trachea, bronchus and esophagus after intravenous application of a high dose of LPS (15 mg/kg), and to reveal the role of urethan (1 g/¢V) and dimethylthiourea (DMTU, 0.375 g/¢V) in inhibition of LPS-induced plasma leakage and edema. India ink was used as a tracer dye to mark leaky microvessels after LPS application. Endothelial gaps were made visible for light microscopy by staining the borders of endothelial cells with silver nitrate. Tracheal sections were stained with toluidine blue to show the subendothelial edema formation. A high dose of LPS was administered intravenously to induce serious plasma leakage and edema and a large number of endothelial gaps formed in postcapillary and collecting venules in the rat trachea and esophagus. The peak values of plasma leakage and edema occurred 5 min after LPS (P<0.01). Urethan anesthesia significantly inhibited LPS-induced plasma leakage by 95 ¡Ó 1.7% in various parts of the respiratory tracts and inhibited edema ratio in the trachea by 57%. Urethan was also found to reduce leukocyte infiltration and the number of endothelial gaps by 46.8 ¡Ó 4.6%. DMTU pretreatment significantly inhibited plasma leakage by 88.5 ¡Ó 2.5% in the respiratory tract and inhibited edema ratio in the trachea by 89% at 5 min after LPS. It is concluded that LPS-induced increase in plasma leakage and edema correlated with the formation of endothelial gaps, and association with activation of alpha 2-adrenergic receptors and hydroxyl free radical production.

No description available.

Thesis (Ph. D.)--University of Missouri-Columbia, 2000. / Typescript. Vita. Includes bibliographical references. Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 2000. / Typescript. Vita. Includes bibliographical references. Also available on the Internet.

Thesis (Ph. D.)--Institute of Paper Chemistry, 1969. / Includes bibliographical references (p. 91-96).

Thesis (Ph. D.)--Institute of Paper Chemistry, 1980. / Includes bibliographical references (leaves 75-78).

Thesis (Ph. D.)--Institute of Paper Chemistry, 1967. / Bibliography: leaves 49-51.

The ubiquitous presence and chronic effect of pharmaceuticals is one of the emerging issues in environmental field. As a result of incomplete removal by sewage treatment plants, pharmaceuticals are released into the environment and drinking water sources. On the other hand, conventional drinking water treatment processes such as coagulation, filtration and sedimentation are reported to be ineffective at removing pharmaceuticals. Therefore, the potential presence of pharmaceuticals in finished drinking water poses a threat on public health. Antibiotics, as an important group of pharmaceuticals, are given special concerns because the potential development of bacteria-resistance. Ozonation and advanced oxidation processes are demonstrated to be quite effective at removing pharmaceuticals. The oxidation of pharmaceuticals is caused by ozone itself and hydroxyl radicals that are generated from ozone decomposition. Whether ozone or hydroxyl radicals are the primary oxidant depends on the specific pharmaceutical of interest and the background water matrix. In this research, erythromycin, a macrolide antibiotic, was chosen as the target compound because of its high detection frequency in the environment and its regulation status. The objective of this research was to investigate the removal performance of erythromycin by ozonation from the standpoint of kinetics. The effects of pH, carbonate and phosphate buffers, and initial ozone dose on ozonation of erythromycin were also studied. The second-order rate constant for the reaction between deprotonated erythromycin and ozone was determined to be 4.44x10⁹ M⁻¹·s⁻¹ while protonated erythromycin did not react with ozone. Ozone was determined to be the primary oxidant for erythromycin removal by ozonation. pH was found to have great positive impact on the degradation of erythromycin by ozonation due to the deprotonation of erythromycin at high pH. Carbonate and phosphate buffers were found to have negligible effects on the degradation of erythromycin by ozonation. Initial ozone dose showed a positive impact on the total erythromycin removal rate by ozonation. / text