No description available.

No description available.

No description available.

A dissertation presented in partial compliance with the requirements for the Master's Degree in Technology: Chiropractic, Technikon Natal, 2000. / The literature shows neck pain, including cervical facet syndrome, to be a common problem. It also provides evidence that inflammation plays a role in cervical facet pathology. Prescription of nonsteroidal anti-inflammatory drugs (NSAIDs) is the first line treatment of allopathic physicians for neck pain. Traumeel S is a complex of homoeopathic remedies indicated in a variety of anti-inflammatory, traumatic and degenerative disorders. It has been clinically shown that Traumeel S is effective in the treatment of inflammation. There is a paucity of clinical research into the treatment of acute neck pain, including cervical facet syndrome, with antiinflammatory agents. The aim of this study was to compare the relative effectiveness of piroxicam, an NSAID, with Traumeel S in the treatment of acute cervical facet syndrome. The study was a double-blind, comparative, clinical trial. Fifty consecutive patients complying with all inclusion criteria were randomly assigned to either the Traumeel S group or the piroxicam group. Each patient in the NSAID group received 40 mg of piroxicam per day for the first two days and 20 mg per day for the following 5 days. The Traumeel S group received the same dosage of placebo piroxicam capsules and 3 Traumeel S tablets in crushed form, per day. Placebo Traumeel Stablets, also in crushed form, were taken 3 times a day by the NSAID group to facilitate blinding. III Patients were assessed on days 1, 3 and 7 of the trial. Subjective assessment involved two questionnaires: the CMCC Neck Disability Index, and the NRS-101 / M

A dissertation submitted to the Faculty of Health in partial compliance with the requirements for a Master's Degree in Technology: Chiropractic,Technikon Natal, 2001. / The purpose of this study was to evaluate Piroxicam versus Protease administration, in terms of subjective and objective clinical findings, in order to determine the effectiveness of each approach in the treatment of grade 1 and 2 acute ankle inversion sprains. The study was a prospective, randomized, double blinded, controlled study. The study involved 30 subjects, 15 in each group which were selected from the general population. One group received Protease and strapping while the other group two received Piroxicam and strapping. Patients received 3 treatments over a period of one week. Patients in the Protease group received 1200mg (3 x 400mg) of Protease daily before meals for seven days. Patients in the Piroxicam group received 40mg (2 x 20mg) of Piroxicam for the first two days, and then 20mg (1 x 20mg) for the following five days, administered with meals. All patients were taught how to apply an elastic crepe bandage to the ankle, which was to be used at all times, except during bathing for the duration of the study / M

No description available.

The benefits of fish oil supplementation for inflammation based disorders has been well-documented,[1] prompting investigations into the pathways through which these benefits are achieved. This led Serhan et al. to the discovery of a new class of pro-resolution lipid mediators, termed resolvins .[2][3] There has subsequently been much research into their being a potential treatment for chronic inflammatory diseases such as asthma,[4] diabetes,[5] and arthritis.[6] The aim of this research was to study the bioactivity of resolvin E1 (RvE1) and its analogues; to do this a flexible and versatile route towards the chemical synthesis of RvE1 had to be developed, which would allow for easy modification of the stereochemistry of the C-C double bonds and hydroxyl groups, as well as producing fragments containing key functional groups. The first proposed route synthesised RvE1 from two key fragments termed the lactone and epoxide fragments. RvE1 contains three stereogenic hydroxyl groups, one with S configuration and two with R configuration. The epoxide fragment was to be converted into two adjacent sections of the RvE1 chain. The S-stereocentre was introduced via hydrolytic kinetic resolution using a Jacobsen s catalyst.[7] The two R-stereocentres were introduced via the chiral pool originating from 1,2:5,6-di-O-isopropylidene-D-mannitol. Unfortunately, problems were encountered late on in the synthesis of both fragments and therefore a new synthetic route had to be devised. The second proposed route synthesised RvE1 from two key fragments termed the alkyne and halide fragments. The S-stereocentre and one R-stereocentre were proposed to be introduced via asymmetric reduction of a ketone group. The other R-stereocentre was proposed to be synthesised with the use of chiral additives during an indium-mediated coupling reaction.[8] As work progressed on the halide fragment, the Lewis acid catalysed thermodynamic conversion of a branched chain homoallylic alcohol to its linear counterpart was trialled in order to obtain one of the conjugated diene system in RvE1. Using literature conditions for a similar system[9] this reaction was unsuccessful. The reaction mechanism was studied and a hypothesis was put forward that adding a catalytic amount of the aldehyde that the branched chain homoallylic alcohol was synthesised from to the reaction mixture would promote the thermodynamic conversion to the linear chain. These conditions were trialled on a number of different starting materials, leading to either an improvement in yield for the thermodynamic conversion, or the success of a previously unsuccessful conversion.

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