Vol. 1 is the author's thesis, Tekniska högskolan, Stockholm.

Thesis--Catholic Univ. of America. / Includes bibliographical references.

Thesis (Ph.D.)--Memorial University of Newfoundland, 2004. / Bibliography: leaves 152-185.

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by Wan Sze Ping. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 172-185). / Abstracts in English and Chinese. / Abstract --- p.i / Acknowledgements --- p.v / Publications --- p.vi / Abbreviations --- p.vii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1. --- Historical Background --- p.2 / Chapter 1.2. --- Origin and heterogeneity of mast cells --- p.2 / Chapter 1.3. --- Mast cell mediators --- p.4 / Chapter 1.3.1. --- Preformed mediators --- p.5 / Chapter 1.3.2. --- Newly synthesised mediators --- p.6 / Chapter 1.4. --- Mast cell activation --- p.8 / Chapter 1.4.1. --- Antigenic/Immunological pathway --- p.8 / Chapter 1.4.1.1. --- Aggregation of IgE Receptors (FcsRI) --- p.9 / Chapter 1.4.1.2. --- Biochemical events following FcsRI aggregation --- p.10 / Chapter 1.4.1.3. --- Phospholipase C activation --- p.11 / Chapter 1.4.1.4. --- Phospholipase A2 activation --- p.12 / Chapter 1.4.1.5. --- Adenylate cyclase activation --- p.14 / Chapter 1.4.1.6. --- Role of calcium --- p.15 / Chapter 1.5. --- Roles of chloride channels in mast cell activation --- p.18 / Chapter 1.6. --- Aims of the study --- p.20 / Chapter Chapter 2 --- Materials and Methods --- p.23 / Chapter 2.1. --- Materials --- p.24 / Chapter 2.1.1. --- Secretagogues --- p.24 / Chapter 2.1.2. --- Anti-allergic compounds --- p.24 / Chapter 2.1.3. --- Chloride channel blockers --- p.24 / Chapter 2.1.4. --- Materials for buffers --- p.25 / Chapter 2.1.5. --- Materials for rat sensitisation --- p.25 / Chapter 2.1.6. --- Materials for histamine assay --- p.26 / Chapter 2.1.7. --- Materials for calcium measurement --- p.26 / Chapter 2.1.8. --- Miscellaneous --- p.27 / Chapter 2.2. --- Buffers --- p.28 / Chapter 2.3. --- Stock solutions of drugs --- p.30 / Chapter 2.4. --- Source of mast cells --- p.31 / Chapter 2.4.1. --- Animals --- p.31 / Chapter 2.4.2. --- Sensitization of animals --- p.31 / Chapter 2.4.3. --- Isolation of rat peritoneal mast cells --- p.32 / Chapter 2.4.4. --- Purification of rat peritoneal mast cells --- p.32 / Chapter 2.4.5. --- Cell counting --- p.33 / Chapter 2.5. --- General protocol for histamine release --- p.35 / Chapter 2.6. --- Histamine assay --- p.35 / Chapter 2.7. --- Protocol for fura-2 fluorescence measurement of intracellular calcium --- p.39 / Chapter 2.7.1. --- Fura-2 cell loading --- p.39 / Chapter 2.7.2. --- Fura-2 fluorescence measurement by fluorescence microscope --- p.39 / Chapter 2.7.3. --- Calculation of intracellular calcium --- p.41 / Chapter 2.8. --- Protocol for 45Ca2+ influx measurement --- p.44 / Chapter 2.9. --- Measurement of 43Ca2+ influx --- p.45 / Chapter 2.10. --- Statistical analysis --- p.45 / Chapter Chapter 3 --- Effects of chloride depletion on mast cell activation --- p.46 / Chapter 3.1. --- Introduction --- p.47 / Chapter 3.1.1. --- Mechanism of non-immunological stimuli --- p.48 / Chapter 3.2. --- Materials and methods --- p.50 / Chapter 3.3. --- Results --- p.51 / Chapter 3.3.1. --- Effects of anti-IgE induced histamine release in chloride free buffers --- p.51 / Chapter 3.3.2. --- Effects of compound 48/80 induced histamine releasein chloride free buffers --- p.52 / Chapter 3.3.3. --- Effects of calcium ionophore A23187 induced histamine release in chloride free buffers --- p.53 / Chapter 3.3.4. --- Effects of ionomycin induced histamine release in chloride free buffers --- p.53 / Chapter 3.3.5. --- Effects of thapsigargin induced histamine releasein chloride free buffers --- p.53 / Chapter 3.3.6. --- Effects of Triton-X 100 induced histamine releasein chloride free buffers --- p.54 / Chapter 3.3.7. --- Effects of anti-IgE on the free intracellular calcium concentration of rat peritoneal mast cells in chloride free buffers --- p.54 / Chapter 3.3.8. --- Effects of compound 48/80 on the free intracellular calcium concentration of rat peritoneal mast cellsin chloride free buffers --- p.56 / Chapter 3.3.9. --- Effects of ionomycin on the free intracellular calcium concentration of rat peritoneal mast cellsin chloride free buffers --- p.58 / Chapter 3.3.10. --- Effects of thapsigargin on the free intracellular calcium concentration of rat peritoneal mast cellsin chloride free buffers --- p.59 / Chapter 3.4. --- Discussion --- p.86 / Chapter 3.5. --- Conclusion --- p.96 / Chapter Chapter 4 --- "DSCG and Chloride channel blockers (NPPB, DIDS, SITS, DPC, IAA-94 & Flufenamic acid)" --- p.97 / Chapter 4.1. --- Introduction --- p.98 / Chapter 4.1.1. --- Role of chloride channels --- p.98 / Chapter 4.1.1.1. --- Chloride channel classification --- p.99 / Chapter 4.1.1.2. --- Chloride channel blockers --- p.101 / Chapter 4.1.2. --- Aims of study --- p.106 / Chapter 4.2. --- Materials and methods --- p.107 / Chapter 4.3. --- Results --- p.108 / Chapter 4.3.1. --- Effects of DSCG and the test blockers on immunologically induced histamine release from rat peritoneal mast cells --- p.108 / Chapter 4.3.2. --- Effects of DSCG and the test blockers on compound48/80 induced histamine release from rat peritoneal mast cells --- p.110 / Chapter 4.3.3. --- Effects of DSCG and the test blockers on ionophore A23187 induced histamine release from rat peritoneal mast cells --- p.112 / Chapter 4.3.4. --- Effects of DSCG and the test blockers on thapsigargin induced histamine release from rat peritoneal mast cells --- p.113 / Chapter 4.3.5. --- Effects of the test blockers on Triton-X 100 induced histamine release from rat peritoneal mast cells --- p.114 / Chapter 4.3.6. --- Effects of DSCG and the test blockers on immunologically and non-immunologically induced 45Ca2+ uptake --- p.115 / Chapter 4.4. --- Discussion --- p.160 / Chapter 4.5. --- Conclusion --- p.167 / References --- p.172

The penetration of chloride ions plays a crucial role in reinforcement corrosion and affects the durability and service life of marine structures. The problem is even more acute once cracking occurs in a concrete member. The presence of cracks is shown to have a significant impact on chloride penetration into concrete. It has been recognized, for concrete cracked in flexure, the chloride diffusion coefficient in the tension zone is higher than that in the compression zone. Even a single crack in the tensile zone could contribute to a higher diffusion coefficient compared to that of uncracked members. In this study, the influence of flexural cracks on chloride ion penetration into reinforced concrete beams has been investigated experimentally and a two-dimensional theoretical model is developed. The experimental study investigated the influence of multiple flexural cracks on the chloride diffusivity of reinforced concrete beams and on the corrosion rate of reinforcing bars. The size of the reinforced concrete beams tested is 200 x 250 x 2200 mm with 20mm concrete cover. The beams were pre-cracked using a compression testing machine and the crack widths induced were maintained between 0.1 mm to 0.2 mm. The chloride profile was determined after 1 month, 1 year and 2 years of immersion in 3.0% NaCl solution. The measured chloride profiles of the beams with multiple cracks are compared to those obtained from the uncracked (control) beam. An observation was also made on the effect of cracks on the corrosion development of steel bar after two years of immersion in salt solution. Chloride concentration varied linearly with the depth of crack (at crack planes). A twodimensional model using finite element analysis is developed to evaluate the chloride penetration into cracked concrete. This model was used to verify the chloride penetration data which is obtained from the experimental results. The prediction of chloride ingress, using the two dimensional model agrees well with the short-term and long-term chloride profiles.

Specimens of Citharichthys stigmaeus, the speckled sanddab, were taken from Yaquina Bay, Newport, Oregon and exposed for eight days to dissolved measured concentrations ranging from 2.9 μg/l to 190 μg/1 of the polychlorinated biphenyl, Aroclor® 1260. Oxygen consumption was measured to determine any change from routine levels of respiration. This research produced the following conclusions: 1) a relationship exists between oxygen consumption and measured concentrations of Aroclor® 1260 in the water as demonstrated by high negative partial correlations and subsequent significant water concentration terms in the regression equations for two of the four experiments: also, a relationship exists between oxygen consumption and tissue concentration of Aroclor® 1260 as demonstrated by high negative partial correlations and subsequent significant tissue concentration terms in the regression equations for three out of four experiments, (because of the inherent variability in oxygen consumption measurements and difficulties of predicting PCB concentrations in both water and tissue, the evidence is difficult to interprete); 2) acetone, used as a solvent for the toxicant, may change oxygen consumption levels and interfere with determining PCB effects; 3) after an eight day dosing period the concentration of Aroclor® 1260 in whole body tissue can be described by the equation: Y = 4.48(1 - e [superscript -.0365x]) where Y is the concentration of Aroclor® 1260 in the tissue and x is the measured Aroclor® concentration in the water; 4) after eight days a constant level of Aroclor® 1260 is present in the tissue if the animal is exposed to water levels of Aroclor® 1260 above approximately 25 μg/1. / Graduation date: 1976