Thesis (Ph. D.)--University of Michigan, 1932. / Cover title. The first article is by C.R. Harte, jr., E.M. Baker, and H.H. Purcell; the second by C.R. Harte, jr., and E.M. Baker. "Reprinted from Industrial and engineering chemistry, vol. 25 ... May and October, 1933." "Literature cited": p. 10,12.

Thesis (Ph. D.)--University of Missouri-Columbia, 2006. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "August 2006" Includes bibliographical references.

Abstract The carbonic anhydrases (CAs) catalyze the reversible hydration of carbon dioxide. In mammals, there are 13 active isoenzymes, which clearly differ in their cell localisation, tissue distributions and functions. CA IX, a unique transmembrane member of the CA gene family, is a tumour-associated protein which is thought to be involved in malignant cell invasion, adhesion and the regulation of cell proliferation. The main focus in the present study was on elucidating the function and expression of CA IX in normal and malignant tissues, especially in the alimentary tract. The functional studies also included CA II, which is regarded as another important CA isoenzyme in the alimentary tract. CA IX immunostaining showed a decrease in the staining intensity of gastric adenomas with increasing dysplasia grade. Well differentiated carcinomas of the intestinal type showed expression comparable to that in the normal mucosa, while expression was decreased in the less differentiated tumours. CA IX deficiency (Car9-/-) genotype and C57/BL6 strain were the main factors which increased the susceptibility of CA IX deficient mice fed on either a normal or high-salt diet to histological abnormalities, including foveolar hyperplasia and glandular atrophy in the gastric body mucosa, while CA II deficiency was associated with only minor histological abnormalities. In a physiological analysis, CA IX played only a minor role in duodenal bicarbonate secretion (DBS), whereas absence of CA II in mice completely abolished the stimulatory effect of E-type prostaglandin 2 (PGE2) on duodenal alkalisation. The results demonstrate that CA IX expression is diminished in most gastric tumours. The variations observed in its expression support the concept that gastric adenomas and carcinomas do not emerge as progressive steps on a single pathway but may instead represent distinct entities with heterogenic genetic backgrounds. In the stomach, CA IX is mainly involved in the regulation of tissue morphogenesis in the body mucosa, while CA II has a major role in maintaining the gastroduodenal acid/base balance.

Abstract Glycans, as a part of glycoproteins, glycolipids and other glycoconjugates, are involved in many vital intra- and inter-cellular tasks, such as protein folding and sorting, protein quality control, vesicular trafficking, cell signalling, immunological defence, cell motility and adhesion. Therefore, their correct construction is crucial for the normal functioning of eukaryotic cells and organisms they form. Most cellular glycans are constructed in the Golgi, and abnormalities in their structure may derive, for instance, from alkalinization of the Golgi lumen. In this work we show that Golgi pH is generally higher and more variable in abnormally glycosylating, i.e. strongly T-antigen (Gal-β1,3-GalNAc-ser/thr) expressing cancer cells, than in non-T-antigen expressing cells. We also confirmed that the Golgi pH alterations detected in cancer cells have the potential to induce glycosylation changes. A mere 0.2 pH unit increase in Golgi pH is able to induce T-antigen expression and inhibit terminal N-glycosylation in normally glycosylating cells. The mechanism of inhibition involves mislocalization of the corresponding glycosyltransferases. We also studied potential factors that can promote Golgi pH misregulation in health and disease, and found that cultured cancer cells, despite variation and elevation in Golgi pH, are fully capable of acidifying the Golgi lumen under the normal Golgi pH. Moreover, we introduce a Golgi localized Cl-/HCO3- exchanger, AE2a, that participates in Golgi pH regulation by altering luminal bicarbonate concentration and thus also buffering capacity. Participation of AE2a in Golgi pH regulation is especially intriguing, because it also provides a novel mechanism for expelling protons from the Golgi lumen.

Release of uranium from Na-autunite, an artificial mineral created as a result of polyphosphate injection in the subsurface at the DOE Hanford Site, takes place during slow dissolution of the mineral structure. Stability information of the uranyl-phosphate phases is limited to conditions involving pH, temperature, and a few aqueous organic materials. The carbonate ion, which creates very strong complexes with uranium, is the predominant ion in the groundwater composition. The polyphosphate technology with the formation of autunite was identified as the most feasible remediation strategy to sequester uranium in contaminated groundwater and soil in situ. The objectives of the experimental work were (i) to quantify the effect of bicarbonate on the stability of synthetic sodium meta-autunite created as a result of uranium stabilization through polyphosphate injection, (ii) calculate the kinetic rate law parameters of the uranium release from Na-autunite during dissolution, and (iii) to compare the process parameters with those obtained for natural calcium meta-autunite. Experiments were conducted using SPTF apparatus, which consists of syringe pumps for controlling flow rate, Teflon reactors and a heating/cooling system. 0.25 grams of synthetic Na-autunite was placed in the reactor and buffer solutions with varying bicarbonate concentrations (0.0005 to 0.003 M) at different pH (6 - 11) were pumped through the reactors. Experiments were conducted at four different temperatures in the range of 5 - 60oC. It was concluded that the rate of release of uranium from synthetic Na-autunite is directly correlated to the bicarbonate concentration. The rate of release of uranium increased from 1.90 x 10-12 at pH 6 to 2.64 x 10-10 (mol m-2 s-1) at pH 11 at 23oC over the bicarbonate concentration range tested. The activation energy values were invariant with the change in the bicarbonate concentration; however, pH is shown to influence the activation energy values. Uranyl hydroxides and uranyl carbonates complexes helped accelerate the dissolution of autunite mineral.

Iron chlorosis has been a serious problem for many years. This physiological disease has occurred so frequently on calcareous soils that it has been called lime-induced chlorosis by many of the workers. Because the western United States has so many soils of this type, the chlorosis problem has been of primary concern. Untold economic losses have been the result of this physiological disease.

<p> Concretions in a zone about 4 m. below the Tichenor Limestone formed just below the sediment water interface. Their growth was initiated about an organic-rich fossil cluster and was probably completed before they were more than 5 to 8 m below the sediment surface. Chemical products of organic decay, notably bicarbonate ions and ammonia, diffused outward, raising the pH and precipitating calcite from connate waters already nearly saturated with respect to calcium carbonate. These conclusions derive from the shape of the concretions, from their relation to the enclosing shales, and from their overall structure , particularly the position of pyritic fossil clusters. The relative volumes of soluble material (calcite) in the concretions are consistent with relative pore volumes through the upper 5 m. of recent, fine-grained, clayey sediments. The postulated genetic sequence agrees with recent work on carbonate diagenesis. Restriction of the concretions to discrete layers was most probably due to a widespread comnbination of high rates of organic productivity, high rates ·of sedimentation, and low rates of water circulation, that lasted a short period of time and resulted in the rapid burial.of much undecomposed organic material. </p> / Thesis / Master of Science (MSc)

No description available.

No description available.

In seawater, drinking is a fundamental part of the osmoregulatory strategy for teleost fish, and presents a unique challenge. The intestine has an established role in osmoregulation, and its ability to effectively absorb fluid from imbibed seawater is crucial to compensating for water losses to the surrounding hyperosmotic environment. Alongside solute-linked water transport (driven by NaCl cotransport), intestinal bicarbonate (HCO3-) secretion also benefits fluid absorption directly (via apical Cl-/HCO3- exchange), and indirectly through the formation of calcium carbonate (CaCO3) thus removing the osmotic influence of Ca2+ within the gut fluid. For the European flounder (Platichthys flesus), elevated luminal Ca2+ has proven to be a specific, potent stimulator of HCO3- secretion both in vitro and in vivo where these actions are presumably modulated by an extracellular Ca2+-sensing receptor (CaR). The focus of this work was to learn more about how intestinal HCO3- secretion is regulated, the role of Ca2+, and more specifically the CaR. To achieve this, in vitro ‘gut sac’ experiments investigated how luminal Ca2+ influenced HCO3- secretion, and associated ion and fluid transport. Contrary to expectation, increasing Ca2+ from 5 to 20 mM did not stimulate HCO3- secretion. In an attempt to elucidate the role of CaCO3 precipitation in fluid absorption, and further explore the physiological implications of HCO3- secretion, the intestine was perfused in vivo with salines containing varying concentrations of Ca2+ (10, 40 and 90 mM). The production and secretion of HCO3-, in addition to CaCO3 formation increased accordingly with Ca2+, and was associated with a dramatic 25 % rise in the fraction of fluid absorbed by the gut. Additional in vitro experiments, utilising the Ussing chamber, helped establish some of the characteristics of intestinal HCO3- secretion by the euryhaline killifish (Fundulus heteroclitus), but was unresponsive to elevated mucosal Ca2+. Further attempts to potentiate the activity of the CaR, and application of the receptor agonists gadolinium (Gd3+) and neomycin, failed to produce responses consistent with the effect of Ca2+ observed previously, either in vitro or in vivo. With no evidence supporting a direct role for an extracellular, intestinal CaR in HCO3- secretion it was argued that secretion would be principally regulated by two factors, the ability of the epithelia to generate high levels of intracellular HCO3- and the rate of CaCO3 formation.