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University of Macau / Institute of Chinese Medical Sciences

by Grant Richardson Stenton. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 259-287). / Abstract --- p.i / Acknowledgements --- p.iii / Publications --- p.iv / Abbreviations --- p.v / Contents --- p.vii / Chapter Chapter 1 --- Introduction / Chapter 1 1.1. --- Historical Background --- p.2 / Chapter 1.2. --- Origin and distribution of mast cells --- p.2 / Chapter 1.3. --- Mast cell heterogeneity --- p.3 / Chapter 1.4. --- Mast cell mediators --- p.5 / Chapter 1.4.1. --- Preformed mast cell mediators --- p.6 / Chapter 1.4.2. --- Newly synthesised mast cell mediators --- p.7 / Chapter 1.5. --- Mast cell activation --- p.11 / Chapter 1.5.1. --- Antigenic pathway of mast cell activation --- p.11 / Chapter 1.5.1.1. --- Antigen binding and receptor aggregation --- p.12 / Chapter 1.5.1.2. --- Early events following FcεRI aggregation --- p.13 / Chapter 1.5.1.3. --- Antigenic induction of mast cell second messenger production --- p.15 / Chapter 1.5.1.4. --- Phospholipase C activation and mast cells --- p.16 / Chapter 1.5.1.5. --- Phospholipase A2 activation and mast cells --- p.17 / Chapter 1.5.1.6. --- Intracellular calcium and mast cells --- p.18 / Chapter 1.5.1.7. --- Calcium and calmodulin --- p.21 / Chapter 1.5.1.8. --- Adenylate cyclase activation and mast cells --- p.21 / Chapter 1.5.2. --- Non-antigenic pathway of mast cell activation --- p.22 / Chapter 1.6. --- Aims of the study --- p.25 / Chapter 1.6.1. --- Diuretics --- p.26 / Chapter 1.6.2. --- Histamine receptor directed compounds --- p.27 / Chapter 1.6.3. --- Cyclo-oxygenase inhibitors --- p.28 / Chapter 1.6.4. --- Immunosuppressive compounds --- p.29 / Chapter Chapter 2 --- Materials and Methods --- p.31 / Chapter 2.1. --- Materials and methods --- p.32 / Chapter 2.1.1. --- Secretagogues --- p.32 / Chapter 2.1.2. --- Anti-allergic compounds --- p.32 / Chapter 2.1.3. --- Diuretics --- p.32 / Chapter 2.1.4. --- Immunosuppressants --- p.33 / Chapter 2.1.5. --- Histamine agonists and antagonists --- p.33 / Chapter 2.1.6. --- Cyclo-oxygenase inhibitors --- p.33 / Chapter 2.1.7. --- Materials for buffers --- p.34 / Chapter 2.1.8. --- Materials for rat sensitization --- p.34 / Chapter 2.1.9. --- Materials for histamine assay --- p.35 / Chapter 2.1.10. --- Materials for calcium measurement --- p.35 / Chapter 2.1.11. --- Materials for prostaglandin D2 measurement --- p.35 / Chapter 2.1.12. --- Materials for leukotriene C4 measurement --- p.36 / Chapter 2.1.13. --- Materials for cyclic AMP measurement --- p.36 / Chapter 2.1.14. --- Miscellaneous --- p.36 / Chapter 2.2. --- Buffers and stock solutions --- p.37 / Chapter 2.2.1. --- Buffer ingredients --- p.37 / Chapter 2.2.2. --- Stock solutions --- p.38 / Chapter 2.3. --- Animals and cell isolation --- p.39 / Chapter 2.3.1. --- Animals --- p.39 / Chapter 2.3.2. --- Sensitization of animals --- p.39 / Chapter 2.3.3. --- Cell isolation --- p.40 / Chapter 2.3.4. --- Cell washing and purification --- p.41 / Chapter 2.3.5. --- Preparation of cells for counting --- p.42 / Chapter 2.3.6. --- Cell counting on a haemocytometer --- p.42 / Chapter 2.4. --- General protocol for histamine release and histamine measurement --- p.43 / Chapter 2.4.1. --- Histamine release --- p.43 / Chapter 2.4.2. --- Spectroflurometric determination of histamine contents --- p.44 / Chapter 2.4.3. --- Calculation of histamine levels --- p.45 / Chapter 2.5. --- Protocol for cellular calcium measurement --- p.47 / Chapter 2.5.1. --- 45Ca2+ influx measurement --- p.47 / Chapter 2.5.2. --- Calculation of 45Ca2+ influx --- p.48 / Chapter 2.5.3. --- Fura-2 fluorescence measurement of intracellular calcium --- p.48 / Chapter 2.5.4. --- Fura-2 cell loading --- p.48 / Chapter 2.5.5. --- Fura-2 fluorescence parameters --- p.49 / Chapter 2.5.6. --- Calculation of basal calcium levels --- p.50 / Chapter 2.6. --- Protocol for prostaglandin D2 (PGD2) measurement --- p.52 / Chapter 2.6.1. --- PGD2 production --- p.52 / Chapter 2.6.2. --- Enzyme Immunosorbent Assay (EIA) method of PGD2 measurement --- p.52 / Chapter 2.6.3. --- Calculation of (EIA) PGD2 production --- p.53 / Chapter 2.6.4. --- Radio Immunosorbent Assay (RIA) method of PGD2 measurement --- p.53 / Chapter 2.6.5. --- Calculation of (RIA) PGD2 concentration --- p.54 / Chapter 2.7. --- Protocol for leukotriene C4 (LTC4) measurement --- p.54 / Chapter 2.7.1. --- LTC4 production --- p.54 / Chapter 2.7.2. --- Enzyme Immunosorbent Assay (EIA) method of LTC4 measurement --- p.55 / Chapter 2.7.3. --- Calculation of (EIA) LTC4 concentration --- p.55 / Chapter 2.8. --- Protocol for cyclic adenosine monophosphate (cAMP) measurement --- p.56 / Chapter 2.8.1. --- cAMP production --- p.56 / Chapter 2.8.2. --- Radio Immunosorbent Assay (RIA) method of cAMP measurement --- p.56 / Chapter 2.8.3. --- Calculation of cAMP concentration --- p.57 / Chapter 2.9. --- Statistical analysis --- p.57 / Chapter Chapter 3 --- "Frusemide, Bumetanide and DSCG" --- p.58 / Chapter 3.1. --- Introduction --- p.59 / Chapter 3.1.1. --- Frusemide and bumetanide as loop diuretics --- p.59 / Chapter 3.1.2. --- Effects of frusemide and bumetanide on the airways --- p.59 / Chapter 3.1.3. --- Effects of frusemide on mast cells --- p.60 / Chapter 3.1.4. --- Experimental aims --- p.61 / Chapter 3.2. --- Materials and methods --- p.62 / Chapter 3.3. --- Results --- p.63 / Chapter 3.3.1 --- "Effects of frusemide, bumetanide and DSCG on immunologically induced histamine release from rat peritoneal mast cells" --- p.63 / Chapter 3.3.2. --- "Effects of frusemide, bumetanide and DSCG on compound 48/80 induced histamine release from rat peritoneal mast cells" --- p.64 / Chapter 3.3.3. --- "Effects of frusemide, bumetanide and DSCG on compound 48/80 induced histamine release from rat peritoneal mast cells suspended in calcium free buffer" --- p.65 / Chapter 3.3.4. --- "Effects of frusemide, bumetanide and DSCG on ionophore A23187 and thapsigargin induced histamine release from rat peritoneal mast cells" --- p.65 / Chapter 3.3.5. --- Cross-tachyphylaxis effects of frusemide and bumetanide --- p.66 / Chapter 3.3.6. --- Effects of DSCG on the inhibition of anaphylactic histamine release due to frusemide --- p.67 / Chapter 3.3.7. --- Effects of frusemide and DSCG on immunologically and non-immunologically induced 45Ca2+ uptake --- p.67 / Chapter 3.3.8. --- Effects of frusemide and DSCG on immunologically and non-immunologically induced changes in the free intracellular calcium concentration of rat peritoneal mast cells --- p.68 / Chapter 3.3.9. --- Effects of frusemide and bumetanide on the spontaneous and secretagogue induced PGD2 production from rat peritoneal mast cells --- p.69 / Chapter 3.3.10. --- Effects of frusemide and DSCG on cellular cAMP levels --- p.70 / Chapter 3.4. --- Discussion --- p.101 / Chapter 3.5. --- Summary --- p.111 / Chapter 3.6. --- Conclusion --- p.114 / Chapter 3.7. --- Future studies --- p.114 / Chapter Chapter 4 --- Histamine Receptor Directed Compounds --- p.115 / Chapter 4.1. --- Introduction --- p.116 / Chapter 4.1.1. --- Histamine receptor subtypes --- p.116 / Chapter 4.1.2. --- Histamine effects on the airways --- p.117 / Chapter 4.2. --- Signal transduction mechanisms --- p.118 / Chapter 4.2.1. --- H1-receptors --- p.118 / Chapter 4.2.2. --- H2-receptors --- p.119 / Chapter 4.2.3. --- H3-receptors --- p.120 / Chapter 4.3. --- Histamine receptors and mast cells --- p.120 / Chapter 4.3.1. --- Effects of histamine agonists and antagonists on mast cells --- p.120 / Chapter 4.3.2. --- Experimental aims --- p.122 / Chapter 4.3.3. --- Materials and methods --- p.123 / Chapter 4.4. --- Results --- p.123 / Chapter 4.4.1. --- Effects of the test compounds on the spontaneous histamine release from rat peritoneal mast cells --- p.123 / Chapter 4.4.2. --- Effects of the test compounds on anti-IgE induced histamine release from rat peritoneal mast cells --- p.125 / Chapter 4.4.3. --- Effects of the test compounds on compound 48/80 induced histamine release from rat peritoneal mast cells --- p.126 / Chapter 4.4.4. --- Effects of the test compounds on anti-IgE and compound 48/80induced histamine release from rat peritoneal mast cells in calcium free buffer --- p.126 / Chapter 4.4.5. --- Effects of the test compounds on ionophore A23187 induced histamine release from rat peritoneal mast cells --- p.127 / Chapter 4.4.6. --- "Effects of histamine antagonists on dimaprit, imetit and impromidine induced histamine release from rat peritoneal mast cells" --- p.128 / Chapter 4.4.7. --- "Effects of anti-IgE, dimaprit and imetit on PGD2 production from rat peritoneal mast cells" --- p.128 / Chapter 4.4.8. --- "Effects of benzalkonium chloride (BAC) on dimaprit, imetit, compound 48/80 and anti-IgE induced histamine release from rat peritoneal mast cells" --- p.129 / Chapter 4.4.9. --- "Effects of pertussis toxin on dimaprit, imetit, compound 48/80and anti-IgE induced histamine release from rat peritoneal mast cells" --- p.129 / Chapter 4.4.10. --- "Effects of dimaprit, imetit, compound 48/80 and anti-IgE on the free intracellular calcium concentration of rat peritoneal mast cells" --- p.130 / Chapter 4.5. --- Discussion --- p.171 / Chapter 4.5.1. --- The possible existence of histamine receptors on rat peritoneal mast cells --- p.171 / Chapter 4.5.2. --- "Possible mechanism of action for the histamine releasing actions of dimaprit, imetit and impromidine on rat peritoneal mast cells" --- p.174 / Chapter 4.6. --- Conclusion --- p.181 / Chapter 4.7. --- Future studies --- p.182 / Chapter Chapter 5 --- Cyclo-oxygenase Inhibitors --- p.184 / Chapter 5.1. --- Introduction --- p.185 / Chapter 5.1.1. --- Cyclo-oxygenase isozymes --- p.185 / Chapter 5.1.2. --- Cyclo-oxygenase inhibitors and mast cells --- p.186 / Chapter 5.1.3. --- Experimental aims --- p.190 / Chapter 5.2. --- Materials and methods --- p.190 / Chapter 5.3. --- Results --- p.191 / Chapter 5.3.1. --- Effects of cyclo-oxygenase inhibitors on immunologically and non-immunologically induced histamine release from rat peritoneal mast cells - --- p.191 / Chapter 5.3.2. --- Effects of cyclo-oxygenase inhibitors on immunologically and non-immunologically induced PGD2 production from rat peritoneal mast cells --- p.192 / Chapter 5.3.3. --- Effects of cyclo-oxygenase inhibitors on immunologically and non-immunologically induced LTC4 production from rat peritoneal mast cells --- p.192 / Chapter 5.3.4. --- Effects of cyclo-oxygenase inhibitors on immunologically and non-immunologically induced 45Ca uptake by rat peritoneal mast cells --- p.193 / Chapter 5.4. --- Discussion --- p.221 / Chapter 5.5. --- Summary and Conclusion --- p.225 / Chapter Chapter 6 --- Immunosuppressive Drugs --- p.228 / Chapter 6.1. --- Introduction --- p.229 / Chapter 6.1.1. --- CsA and FK506 binding proteins --- p.230 / Chapter 6.1.2. --- Distribution of CyPA and FKBP12 --- p.231 / Chapter 6.1.3 --- Mechanism of immunosuppression --- p.232 / Chapter 6.1.4. --- The role of calcineurin in IL-2 promoter induction --- p.233 / Chapter 6.2. --- Immunosuppressive agents and mast cells --- p.234 / Chapter 6.2.1. --- Introduction --- p.234 / Chapter 6.2.2. --- CsA and FK506 inhibit mast cell cytokine production --- p.235 / Chapter 6.2.3. --- "CsA mediated inhibition of mediator release from, and calcium uptake by mast cells and basophils" --- p.236 / Chapter 6.2.4. --- Inhibition of mediator release from mast cells and basophils by FK506 --- p.239 / Chapter 6.2.5. --- Aim of this study --- p.240 / Chapter 6.2.6. --- Materials and methods --- p.241 / Chapter 6.3. --- Results --- p.241 / Chapter 6.3.1. --- Effects of CsA and FK506 on immunologically and non-immunologically induced histamine release from rat peritoneal mast cells --- p.241 / Chapter 6.3.2. --- Effects of CsA and FK506 on immunologically and non-immunologically induced PGD2 production from rat peritoneal mast cells --- p.242 / Chapter 6.3.3. --- Effects of CsA and FK506 on immunologically and non-immunologically induced 45Ca uptake by rat peritoneal mast cells --- p.243 / Chapter 6.4. --- Discussion --- p.254 / Chapter 6.4.1. --- "Effects of CsA on histamine release from, and 45Ca uptake by rat peritoneal mast cells, following immunological and non-immunological activation" --- p.254 / Chapter 6.4.2. --- Effects of CsA on PGD2 production from rat peritoneal mast cells --- p.256 / Chapter 6.4.3. --- "Effects of FK506 on histamine release from, and 45Ca uptake by rat peritoneal mast cells, following immunological and non-immunological activation" --- p.256 / Chapter 6.4.4. --- Effects of FK506 on immunological PGD2 production from rat peritoneal mast cells --- p.257 / Chapter 6.5. --- Summary --- p.257' / Chapter 6.6. --- Future work --- p.258 / References

Pharmacokinetic parameters for theophylline and dyphylline were evaluated in horse cerebrospinal fluid (csf) and plasma. Pharmacokinetic parameters did not differ significantly (p > 0.05) at the same dose for either drug when administered alone or concomitantly. Theophylline and dyphylline penetrate horse csf to produce approximately 1/2 the concentrations found in plasma. Doubling the theophylline dose from 10 mg/Kg to 20 mg/Kg doubled both csf and plasma theophylline concentrations. However, doubling the dyphylline dose from 20 mg/Kg to 40 mg/Kg tripled both csf and plasma dyphylline concentrations. Simultaneous fitting between plasma and csf drug concentrations indicates that plasma is a good indicator for predicting csf concentrations for both theophylline and dyphylline. The influence of ibuprofen input rate on antipyresis was studied in rats with yeast induced fever. In addition, a data analysis comparison was made between rat data collected from this present study and literature data from fevered children. Counterclockwise hysteresis curves (ibuprofen plasma concentration versus temperature decrement) were observed following ibuprofen oral suspension when administered to rats and children. When the collapsed hysteresis curves were plotted (mean predicted total ibuprofen effect compartment concentration versus mean predicted temperature decrement effect) the rat and children's curves were not superimposable. However, the collapsed hysteresis curves of mean predicted ibuprofen unbound effect concentration versus mean predicted temperature decrement effect were superimposable for data from the rats and children. Based on mean unbound ibuprofen effect compartment concentration versus mean predicted temperature decrement effect, the antipyretic response to ibuprofen appears to be comparable between rats and children. The apparent qualitative trend in temperature decrement, although not statistically significant, perhaps due to variability, appears to be different among ibuprofen input regimens in rats. Maximum temperature decrement appears to relate not just to the concentration of ibuprofen obtained at steady-state, but the rate at which it is obtained. / Graduation date: 1993

Thesis (M.S.)--University of North Texas, Aug., 2009. / Title from title page display. Includes bibliographical references.

Thesis (M.Tech.: Chiropractic)- Dept. of Chiropractic, Durban Institute of Technology, 2002 xii, 90 leaves / The purpose of this study was to determine the relative efficacy of topical flurbiprofen in the form of a local action transcutaneous patch (LAT), in the treatment of lateral epicondylitis.

Thesis (PhDPharmacy)--University of South Australia, 2003.

Bibliography: leaves 159-164. / iv, 158 leaves ; 30cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This thesis examines routes for the asymmetric synthesis of three members of the nonsteroidal anti-inflammatory class of drugs (NSAIDs) The aryl propanoic acid ibuprofen is synthesized in 96% e.e. Control of stereochemistry is achieved by use of the Sharpless epoxidation reaction, followed by reduction of the product epoxide by complex hydride with assistance by titanium tetraisopropoxide acting as a Lewis acid. The final step is the coupling of an optically active carboxylic acid intermediate with the iso-butyl side chain to give (S)-ibuprofen. / Thesis (Ph.D.)--University of Adelaide, Dept. of Organic Chemistry, 1997?

Thesis (Ph. D.)--Rutgers University, 2007. / "Graduate Program in Food Science." Includes bibliographical references (p. 73-80).

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.