The success of Solid Oxide Fuel Cells (S.O.F.C) rests heavily on material selection. The performances of several compounds were investigated as possible anode materials, starting with reduced titanates such as the magnesium titanate and zirconium titanate. These compositions, although possessing many qualities beneficial for use as an anode material, were found to be too unstable for practical use. For this reason further work concentrated on stable, zirconia based, compounds with exhibited mixed conduction under reducing atmospheres. The mobility of electronic carriers is considered to be much higher than that of ionic defects, therefore, promising mixed conductors can be formed by doping a good ionic conductor with a small concentration of transition metal ions. Zirconia based mixed conductors were studied for two reasons. Firstly, zirconia stabilised in the cubic defect fluorite structure, exhibits a high level of ionic conductivity. Secondly, it is the most common electrolyte material for an S.O.F.C. An anode based on zirconia would, therefore, be expected to offer a good physical compatibility with the electrolyte material and to exhibit a high ionic contribution to total conductivity. Large defect fluorite solid solutions in the systems Y<SUB>2</SUB>O<SUB>3</SUB>-ZrO<SUB>2</SUB>-Nb<SUB>2</SUB>O<SUB>5</SUB>, Yb<SUB>2</SUB>O<SUB>3</SUB>-ZrO<SUB>2</SUB>-Nb<SUB>2</SUB>O<SUB>5</SUB> and CaO-ZrO<SUB>2</SUB>-Nb<SUB>2</SUB>O<SUB>5</SUB> were established, which enabled the effects of composition, dopant size and charge on conduction to be investigated. These effects were shown to be linked to structure. From these results and comparisons with the Y<SUB>2</SUB>O<SUB>3</SUB>-ZrO<SUB>2</SUB>-TiO<SUB>2</SUB> system, optimum, mixed conducting, compositions were established. The sample Y<SUB>0.25</SUB>Ti<SUB>0.15</SUB>Zr<SUB>0.60</SUB>O<SUB>1.875</SUB> exhibited the best mixed conducting properties to date, obtained for compositions based on zirconia.

Current and future pollutant enussion legislation calls for decreased NOx emissions from combustion systems. A review of techniques used for NOx abatement led to the choice of combustor redesign to be the most cost effective method available. This led to the design, construction and development of a combustion system that utilised a Coanda ejector to generate recirculation of the exiting high temperature combustion products to mix with the air supply. Cooling of the burner was integrated into the design through the use of the air and fuel supplies. Computational fluid dynamics was used to model and aid development of the design. The model was used to predict NOx and CO emissions and the fuel-air mixing pattern. This, along with an analysis of experimental results and observations led to an understanding of the burner operation with respect to pollutant emissions and stability. NOx emissions from the Coanda burner were found to be lowest when using a 0.2 mm Coanda gap width, resulting in 16 ppm NOx being emitted at an air to fuel ratio of 1.5. However, the use ofa 0.2 mm Coanda gap width required an air supply pressure of up to 4 bar. The use of a 0.5 mm Coanda gap width enabled burner operation at lower air supply pressures. The resulting NOx emissions were measured as 23 ppm at an air to fuel ratio of 1.I, with a corresponding exit gas temperature of 2200 K. Flue gas recirculation quantity, flame stability, flame stabiliser shape and operational limits proved to be inter-linked in the reduction of NOx emissions. It was found that fuel-air mixing was controlled by the entrainment properties of the Coanda ejector and the flame stabiliser. The average oxygen concentration entering the combustion chamber when using a 0.2 mm and 0.5 mm Coanda gap width was 13.7 % and 16.6 %, respectively. Due to the position of the fuel injector, a fuel rich region formed behind the flame stabiliser. With a suitable flame stabiliser geometry and the use of 'fingers', low NOx combustion and flame stability was achieved near stoichiometric conditions. It was shown that the design of the burner enabled very low pollutant emissions near stoichiometric conditions, resulting in high exit gas temperatures. Conceivable applications of this type of burner could lie in small and intermediate furnaces where low NOx emissions are required. Additionally, very high temperature applications, such as glass furnaces could benefit in both cost and pollutant emissions from such a burner.

Spectrophotometric (including stopped-flow) techniques were used to examine the kinetics of NO-group transfer reactions (transnitrosation) between S-nitrosothiols (RSNO) and a wide range of sulfur/nitrogen nucleophiles in aqueous solution. A metal-ion chelator was added in all experiments to prevent RSNO decay and NO liberation catalysed by copper ions. In most cases reaction was envisaged as rate- determining attack of the nucleophile at the nitrogen atom of the -SNO moiety, and hence S-nitrosothiols essentially acted as electrophilic nitrosating agents. Sulfite, thiosulfate, thiourea, thiocyanate and thiomethoxide, were sufficiently nucleophilic to induce nitrosothiol decomposition at physiological pH. Reaction with sulfide (pH > 7.4) afforded the orange-yellow anion, SSNO, and embodies a potential quantitative test for RSNOs. S-Nitrosopenicillamine was reactive enough to allow a thorough investigation into its reaction at basic pH with primary, secondary (creating carcinogenic N-nitrosamines), and tertiary amines, as well as ambident (e.g. thiomorpholine) and alpha nucleophiles (e.g. azide ion). Parallels could be made with analogous studies using other nitroso compounds such as MNTS. The generality of the reaction of a S-nitrosothiol with a large excess of the corresponding or a different thiol was also assessed. Ammonia and not nitric oxide was confirmed as the primary nitrogenous product of this highly complicated process. Mechanistic details of the copper(I) catalysed decomposition of some novel S- nitroso derivatives (e.g. a synthesised S-nitroso-1 -thiosugar) are reported. The two- stage degradation pathway involved an initial Cu(^+) promoted component that halted at incomplete conversion, and was accompanied by a large thermal reaction. An explanation of this unique pattern has been offered in terms of the generation of a disulfide-Cu(^2+) complex, in which copper is/is not accessible to reduction.

Thesis (M.Sc.)--Chinese University of Hong Kong. / Bibliography: leaf [4].

Semiconductor photocatalysis degrades phenolic pollutants to carbon dioxide and water, but the mechanisms of this potentially attractive method of environmental remediation remain unclear. This study aimed to elucidate the primary molecular events by HPLC analysis of the initial products of degradation in water or aqueous acetonitrile. The position of substituents relative to the hydroxyl group were found to influence the reaction rate and also primary oxidation steps, and hence the intermediate profile. 2,6- Dialkylated phenols reacted fastest and showed high conversion to dehydrodimeric products as a prelude to degradation. In contrast, 3,5-dialkylated phenols and 4-tertbutylphenol reacted more slowly and appeared to degrade directly to small polar compounds with little accumulation of primary carbocyclic intermediates. The rate of photocatalytic degradation of two isomeric dibromohydroxybenzonitriles was also influenced by substitution pattern. 3,5-Dibromo-2-hydroxybenzonitrile, however, is itself photolabile in daylight giving 3-bromo-2,5-dihydroxybenzonitrile in aqueous solution. The analogous reaction does not occur for 3,5-dibromo-4-hydroxybenzonitrile, the difference in behaviour being attributed to differences in the electronic spectra of the two compounds. The mechanism of photocatalysis appears to be influenced by the orientation of the substrate on the catalyst surface. For the alkyl phenols, particularly those with tert-butyl substitution, minimisation of disturbance to the polar network of the solvent directs the more hydrophobic parts of the molecule towards the oxidising surface of the catalyst. In addition, this effect encourages clustering of molecules with the subsequent formation of aggregated products. While part of the behaviour observed may be attributable to the presence of acetonitrile in the solvent, the hydrophobic profile of a substrate undergoing heterogeneous photocatalytic oxidation in water would seem to be a significant determinant of the molecular pathway selected in the first phase of its degradation.

by To Ching Yuen. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references. / Abstracts in English and Chinese. / Abstract --- p.i / 摘要 --- p.iii / Acknowledgements --- p.iv / List of Tables --- p.v / List of Figures --- p.vi / Table of contents --- p.ix / Chapter Chapter 1. --- Introduction / Chapter 1.1. --- Introduction --- p.1-1 / Chapter 1.2. --- One-dimensional (1-D) nanomaterials --- p.1-1 / Chapter 1.3. --- Growth mechanisms --- p.1-2 / Chapter 1.3.1. --- The Vapor-liquid-solid mechanism --- p.1-2 / Chapter 1.3.2. --- The Vapor-Solid (VS) mechanism --- p.1-3 / Chapter 1.4. --- A1203 --- p.1-4 / Chapter 1.5. --- Recent works on 1-D alumina nanomaterials --- p.1-5 / Chapter 1.6. --- AlON --- p.1-6 / Chapter 1.7. --- Objectives and approaches --- p.1-8 / Chapter 1.8. --- Thesis layout --- p.1-9 / References --- p.1-10 / Tables --- p.1-14 / Chapter Chapter 2. --- Methodology and instrumentation / Chapter 2.1. --- Introduction --- p.2-1 / Chapter 2.2. --- Experimental setup --- p.2-1 / Chapter 2.3. --- Experimental conditions --- p.2-2 / Chapter 2.3.1. --- Fabrication of A12O3 nanobelts --- p.2-2 / Chapter 2.3.1.1. --- Heating environments --- p.2-3 / Chapter 2.3.1.2. --- Heating temperature --- p.2-3 / Chapter 2.3.1.3. --- Heating duration --- p.2-3 / Chapter 2.3.1.4. --- Substrates --- p.2-4 / Chapter 2.3.2. --- Nitridation of alumina --- p.2-4 / Chapter 2.3.2.1. --- Control experiments without residual A1 --- p.2-5 / Chapter 2.4. --- Methods of characterization --- p.2-6 / Chapter 2.4.1. --- Morphology --- p.2-6 / Chapter 2.4.2. --- Phase and micro structures --- p.2-7 / References --- p.2-8 / Figures --- p.2-9 / Chapter Chapter 3. --- Fabrication of alumina nanobelts / Chapter 3.1. --- Introduction --- p.3-1 / Chapter 3.2. --- General morphologies --- p.3-1 / Chapter 3.3. --- Microstructural analysis --- p.3-2 / Chapter 3.4. --- Effects of heating environments --- p.3-3 / Chapter 3.5. --- Effects of heating temperatures --- p.3-3 / Chapter 3.6. --- Effects of heating duration --- p.3-5 / Chapter 3.7. --- Effects of substrate orientation --- p.3-6 / Chapter 3.8. --- Proposed growth model --- p.3-7 / Chapter 3.8.1. --- Thermodynamic considerations --- p.3-7 / Chapter 3.8.2. --- Molecules impinging model --- p.3-9 / Chapter 3.8.3. --- 2-D nucleation model and surface diffusion --- p.3-11 / References --- p.3-14 / Figures --- p.3-16 / Chapter Chapter 4. --- Nitridation of alumina / Chapter 4.1. --- Introduction --- p.4-1 / Chapter 4.2. --- Effects of heating temperature in Nitrogen --- p.4-1 / Chapter 4.3. --- Nitridation with ammonia --- p.4-3 / Chapter 4.4. --- Removal of residual A1 powder --- p.4-4 / Chapter 4.5. --- Chemical reactions and the growth model --- p.4-6 / Chapter 4.5.1. --- Preferential nitridation --- p.4-6 / Chapter 4.5.2. --- Formation of γ-AlON nano-particles --- p.4-8 / References --- p.4-10 / Figures --- p.4-11 / Chapter Chapter 5. --- Conclusions and future works / Chapter 5.1. --- Conclusions --- p.5-1 / Chapter 5.2. --- Future works --- p.5-2

一氧化二氮，俗稱笑氣，是現代臨床麻醉最為常用的一種麻醉劑。然而，關於一氧化二氮效能及安全性的研究至今仍存在爭議。近來，一個稱為ENIGMA的臨床研究項目對2,050個施行大手術的病人接受麻醉情況及術後併發癥進行了研究。研究發現手術中施行一氧化二氮麻醉的病人術後傷口感染率較之對照組上升了35%。另一方面，對423個ENIGMA病人的長期隨訪研究發現，在術中接受一氧化二氮麻醉的病人中慢性術後痛的發病率相對對照組降低了56%。 對於這些臨床發現的分子機制，目前知之甚少。 因此我們進行了一系列實驗來研究一氧化二氮導致術後感染以及預防慢性痛的分子機制。 / 一氧化二氮對基因穩定性的影響 / 在對93個接受直腸結腸大型外科手術的病人進行的隨機對照試驗中，我們比較了接受一氧化二氮麻醉及其對照組病人的外周白細胞脫氧核糖核酸（DNA）損傷情況和術後傷口感染率。通過單細胞凝膠電泳（彗星實驗），我們發現術中一氧化二氮麻醉顯著增加了手術24小時后病人的DNA損傷情況 （p < 0.001）。且這種變化是劑量依賴的，r = 0.33; p = 0.03。並且，在DNA損傷程度及術後傷口感染率間存在顯著相關。術後DNA損傷程度每增加十個單位，傷口感染率則隨之增加17%。 / 一氧化二氮對DNA損傷應答及修復的影響 / 利用大鼠模型，我們對一氧化二氮導致基因不穩定的機制進行了研究。Sprague Dawley大鼠暴露於一氧化二氮中2小時後，我們對其DNA損傷應答及修復基因的轉錄情況進行了檢測。脂多糖（LPS）注射大鼠模擬了圍手術期的炎癥反應。我們發現LPS刺激的白細胞經一氧化二氮處理后，其編碼DNA連接酶IV的LIG4基因的轉錄量顯著降低（p < 0.05）。LIG4基因的下調導致了一氧化二氮麻醉後圍手術期的免疫抑制效應。 / NMDA受體抑制在一氧化二氮預防性鎮痛中的作用 / 在大鼠慢性神經痛模型中，我們檢測了一氧化二氮鎮痛作用的機制。我們發現一氧化二氮處理組的機械痛覺過敏相較對照組顯著降低（p = 0.001）。一氧化二氮處理后，神經痛大鼠脊髓背角中的c-Fos表達量也顯著降低，這表明了一氧化二氮對神經元活性的影響。該影響可能是NMDA受體抑制的結果。另外，我們還觀察到一氧化二氮的鎮痛特徵與NMDA受體非競爭性拮抗劑MK-801的鎮痛效果相似。 / 基因表達改變在一氧化二氮預防性鎮痛中的作用 / 一氧化二氮鎮痛效果的遲發性和延續性提示了除受體拮抗之外的其他作用機制的存在。我們發現在大鼠坐骨神經壓迫損傷模型中，一氧化二氮處理顯著降低了同側脊髓背角組織中LIG4基因的轉錄及表達（p = 0.006）。同時一氧化二氮處理降低了星形膠質細胞在同側脊髓背角中的活化。我們的研究表示一氧化二氮影響DNA修復， 抑制脊髓背角基因的表達，從而起到預防性鎮痛的作用。 / 總而言之，一氧化二氮通過抑制鉀硫氨酸合成酶，削弱DNA修復和基因組穩定性，從而成為導致術后傷口感染的危險因素。另一方面，這一機制也阻止了脊髓背角中異常突觸的建立，從而預防了神經損傷導致的慢性神經痛的建立。另外，一氧化二氮的鎮痛機制也和NMDA受體抑制作用有關。 / Nitrous oxide is a commonly administered anesthetic and analgesic agent in contemporary clinical anesthesia. However, the efficacy and safety of nitrous oxide delivery remains a subject of debate. The recent Evaluation of Nitrous oxide In a Gas Mixture for Anaesthesia (ENIGMA) Trial found that nitrous oxide administration, in 2,050 patients undergoing major surgery, increased the incidence of wound infection by 35%. On the other hand, in a long term follow-up study of 423 ENIGMA patients in Hong Kong, the risk of chronic postsurgical pain was reduced by 56% in patients who received nitrous oxide in the index surgery. Little is known about the mechanisms associated with these clinical observations; we therefore conducted a series of experiments to determine the molecular changes after nitrous oxide administration leading to postoperative wound infection and preventive analgesia. / Genomic Instability after Nitrous Oxide Administration / In a randomized controlled trial of 93 patients undergoing major colorectal surgery, we compared the changes of deoxyribonucleic acid (DNA) damage in circulating leukocytes and rates of wound infection in patients who were exposed to nitrous oxide or not. Using single cell gel electrophoresis (CometAssay), we found that intraoperative nitrous oxide administration produced significant DNA damage, 24 hours after surgery, compared with controls, p < 0.001. The changes were dose-dependent, r = 0.33; p = 0.03. In addition, there was a significant correlation between DNA damage and postoperative wound infection. For every 10 units increase in the percentage of DNA in tail after surgery compared with baseline, there was 17% increase in the risk of wound infection. / DNA Damage Response and Repair / In a rat model, we explored the mechanism of genomic instability after nitrous oxide administration. In Sprague Dawley rats exposed to nitrous oxide anesthesia for 2 hours, we tested the transcription of an array of DNA damage response and repair genes. Lipopolysaccharide (LPS) was added to mimic postoperative inflammation. In the mRNA that were extracted and analyzed by real-time polymerase chain reaction (RT-PCR), we found the transcription of gene encoding for DNA Ligase IV (LIG4 gene) was significantly reduced after nitrous oxide administration in LPS-stimulated leukocytes (p < 0.05). The down regulation of LIG4 gene contributed to perioperative immunosuppression following nitrous oxide exposure. / Role of N-methyl-D-aspartate receptor (NMDAR) Blockade for Preventive Analgesia with Nitrous Oxide / Using a rat model of chronic neuropathic pain, we tested the mechanisms underlying nitrous oxide analgesia. In Sprague Dawley rats undergoing unilateral constrictive injury to the sciatic nerve, we found that mechanical hyperalgesia was significantly reduced with nitrous oxide compared with controls (p = 0.01). In addition, c-Fos expression was decreased in spinal dorsal horn suggesting that neuron excitability was reduced after nitrous oxide administration which could be caused by blockade of the NMDA receptor. Interestingly, the characteristics of analgesia were similar to that provided by MK-801, a noncompetitive antagonist of NMDA receptors. / Transcriptional Changes for Nitrous Oxide Analgesia / The onset of nitrous oxide analgesia was delayed and outlasted actual receptor antagonism. We therefore explored mechanisms, other than NMDA receptor blockade, for nitrous oxide analgesia. Specifically, in rats undergoing sciatic nerve constrictive injury, we found that transcription of LIG4 gene was down-regulated in the ipsilateral spinal dorsal horn after nitrous oxide administration (p = 0.006). There was a decrease in DNA ligase IV expression and a reduction in the activation of astrocytes. Our data suggested that regulation of DNA repair and suppression spinal dorsal horn gene transcription is one of the alternative mechanisms for nitrous oxide analgesia. / In summary, nitrous oxide administration is a risk factor for postoperative wound infection. This is related to irreversible inhibition of the enzyme methionine synthase, impaired DNA repair and genomic instability. The same mechanism however prevented aberrations of synaptic regeneration in the spinal dorsal horn and could therefore prevent the development of chronic neuropathic pain after direct nerve injury. Nitrous oxide analgesia was also related to NMDA receptor blockade. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Chen, Yan. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 126-157). / Abstract also in Chinese. / Declaration of origination --- p.I / Abstract: --- p.II / Acknowledgements --- p.VIII / Table of Contents --- p.X / List of Tables --- p.XV / List of Figures --- p.XVI / List of Abbreviations --- p.XVIII / Chapter Part I: --- Literature Review --- p.1 / Chapter Chapter 1 --- A review of nitrous oxide: Historical, clinical and mechanistic Perspectives --- p.2 / Chapter 1.1 --- History of Nitrous Oxide --- p.2 / Chapter 1.2 --- Clinical Pharmacology of Nitrous Oxide --- p.4 / Chapter 1.3 --- Evaluation of Nitrous oxide In the Gas Mixture for Anesthesia (ENIGMA) Trial --- p.9 / Chapter 1.4 --- Efficacy and Toxicity of Nitrous Oxide: Biochemical and Molecular Mechanisms --- p.14 / Chapter 1.4.1 --- Immunosuppression Following Nitrous Oxide Administration --- p.14 / Chapter 1.4.2 --- Analgesia with Nitrous Oxide - Molecular Mechanisms --- p.17 / Chapter 1.4.2.1 --- Direct molecular target --- p.17 / Chapter 1.4.2.2 --- Interaction with γ aminobutyric acid type A (GABAA) receptors --- p.19 / Chapter 1.4.2.3 --- Regulation of opioid system --- p.20 / Chapter 1.4.2.4 --- Regulation of noradrenergic neurons --- p.21 / Chapter 1.4.2.5 --- N-methyl-d-aspartate (NMDA) receptor inhibition --- p.22 / Chapter 1.4.2.6 --- Long-term Preventive Analgesia with Nitrous Oxide --- p.23 / Chapter 1.4.3 --- Summary --- p.24 / Chapter Part II: --- Experiments --- p.26 / Chapter Chapter 2 --- Study Hypothesis and Objectives --- p.27 / Chapter 2.1 --- Genomic Instability after Nitrous Oxide Administration --- p.27 / Chapter 2.2 --- DNA Damage Response and Repair --- p.28 / Chapter 2.3 --- NMDA Receptor Blockade for Preventive Analgesia with Nitrous Oxide --- p.28 / Chapter 2.4 --- Transcriptional Changes for Nitrous Oxide Analgesia --- p.28 / Chapter Chapter 3 --- Genomic Instability After Nitrous Oxide Administration: A Randomized Controlled Trial --- p.32 / Chapter 3.1 --- Introduction --- p.32 / Chapter 3.2 --- Methods and Materials --- p.36 / Chapter 3.2.1 --- Study Participants --- p.36 / Chapter 3.2.2 --- Study Procedures --- p.36 / Chapter 3.2.3 --- Randomization --- p.37 / Chapter 3.2.4 --- Anesthetic Care --- p.37 / Chapter 3.2.5 --- Postoperative Care --- p.38 / Chapter 3.2.6 --- Measurement of Genomic Instability --- p.44 / Chapter 3.2.7 --- Statistical Analysis --- p.47 / Chapter 3.2.8 --- Sample Size Calculation --- p.47 / Chapter 3.3 --- Results --- p.48 / Chapter 3.4 --- Discussion --- p.61 / Chapter 3.4.1 --- Principal Findings --- p.61 / Chapter 3.4.2 --- Comparison to Other Studies --- p.61 / Chapter 3.4.3 --- Strengths and Limitations --- p.63 / Chapter 3.4.4 --- Implications --- p.64 / Chapter 3.4.5 --- Conclusions --- p.64 / Chapter Chapter 4 --- DNA Damage Response and Repair After Nitrous Oxide Administration / Chapter 4.1 --- Introduction --- p.65 / Chapter 4.1.1 --- DNA Damage Response and Repair Pathways --- p.65 / Chapter 4.1.2 --- Nitrous oxide and DNA Damage Response and Repair --- p.69 / Chapter 4.2 --- Materials and Methods --- p.70 / Chapter 4.2.1 --- Animals --- p.70 / Chapter 4.2.2 --- Nitrous Oxide Administration --- p.70 / Chapter 4.2.3 --- Lipopolysaccharide-Induced Infection Model --- p.72 / Chapter 4.2.4 --- Sample Collection and Preparation --- p.72 / Chapter 4.2.5 --- Single Cell Gel Electrophoresis (CometAssay) --- p.72 / Chapter 4.2.6 --- RNA Extraction for Gene Transcription Study --- p.72 / Chapter 4.2.7 --- Reverse Transcription Polymerase Chain Reaction (RT PCR) --- p.73 / Chapter 4.2.8 --- Quantitative RT PCR --- p.74 / Chapter 4.2.9 --- Statistical Analysis --- p.76 / Chapter 4.3 --- Results --- p.76 / Chapter 4.3.1. --- Genome Instability in Rat Leukocytes after Nitrous Oxide Administration --- p.76 / Chapter 4.3.2. --- Effect of Nitrous Oxide on the Transcription of DNA Damage Response Genes --- p.78 / Chapter 4.3.3. --- Effects of Nitrous Oxide on DNA Damage Response Genes in Animals Treated with Lipopolysaccharide --- p.80 / Chapter 4.4 --- Discussion --- p.84 / Chapter 4.4.1 --- Principal Findings --- p.84 / Chapter 4.4.2 --- Implications --- p.84 / Chapter 4.4.3 --- Limitation of our Study --- p.85 / Chapter 4.4.4 --- Conclusions --- p.87 / Chapter Chapter 5 --- Preventive Analgesia with Nitrous Oxide: Role of NMDA Receptor Blockade / Chapter 5.1. --- Introduction --- p.88 / Chapter 5.1.1. --- The ENIGMA Trial: Long Term Follow-up --- p.89 / Chapter 5.1.2. --- Nitrous oxide prevents chronic postsurgical pain: putative mechanisms --- p.89 / Chapter 5.1.3. --- Hypothesis --- p.90 / Chapter 5.2. --- Materials and methods --- p.91 / Chapter 5.2.1. --- Animals --- p.91 / Chapter 5.2.2. --- Chronic constriction injury (CCI) to induce neuropathic pain --- p.91 / Chapter 5.2.3. --- Behavioral test --- p.93 / Chapter 5.2.4. --- Nitrous oxide administration --- p.93 / Chapter 5.2.5. --- Dizocilpine (MK-801) pretreatment --- p.94 / Chapter 5.2.6. --- Tissue Collection, Preparation and Western Blot --- p.94 / Chapter 5.2.7. --- Statistical Analysis --- p.96 / Chapter 5.3. --- Results --- p.96 / Chapter 5.3.1. --- Preventive Analgesia with Nitrous oxide --- p.96 / Chapter 5.3.2. --- Nitrous oxide analgesia via NMDA receptors block --- p.99 / Chapter 5.3.3. --- Preventive analgesia with NMDA receptors Blockade --- p.101 / Chapter 5.4. --- Discussion --- p.103 / Chapter 5.4.1 --- Principal Findings --- p.103 / Chapter 5.4.2 --- Our Findings compared with Other Studies --- p.103 / Chapter 5.4.3 --- Limitations of the Study --- p.104 / Chapter 5.4.4 --- Conclusions --- p.105 / Chapter Chapter 6 --- Transcriptional Changes for Nitrous Oxide Analgesia --- p.106 / Chapter 6.1 --- Introduction --- p.106 / Chapter 6.1.1 --- Neuro-immune Interactions in the Development of Chronic Neuropathic Pain --- p.106 / Chapter 6.1.2 --- Nitrous Oxide Interferes Astrocytes and Glial Responses --- p.107 / Chapter 6.2 --- Materials and methods --- p.109 / Chapter 6.2.1 --- Chronic Constriction Injury Pain Model and Nitrous Oxide Administration --- p.109 / Chapter 6.2.2 --- Lumbar Dorsal Horn Tissue Collection, Preparation and Immunoflurescence --- p.109 / Chapter 6.2.3 --- RNA Extraction and Quantitative RT PCR for Gene Transcription Study --- p.110 / Chapter 6.2.4 --- Protein Extraction and Western Blot for protein Expression Study --- p.110 / Chapter 6.2.5 --- Statistical Analysis --- p.111 / Chapter 6.3 --- Results --- p.112 / Chapter 6.3.1 --- Time Course of LIG4 Gene Transcription after Constrictive Nerve Injury --- p.112 / Chapter 6.3.2 --- Nitrous oxide reduced DNA ligase IV expression in spinal dorsal horn --- p.114 / Chapter 6.3.3 --- Nitrous oxide Reduced Astrocytes Activation in Spinal Dorsal Horn --- p.116 / Chapter 6.4 --- Discussions --- p.119 / Chapter 6.4.1 --- Principal Findings --- p.119 / Chapter 6.4.2 --- Our Findings in Relation to Other Studies --- p.119 / Chapter 6.4.3 --- Limitations of Our Study --- p.120 / Chapter 6.4.4 --- Conclusions --- p.120 / Chapter Part III: --- Conclusions --- p.122 / Chapter Chapter 7 --- Conclusions and Future Perspectives --- p.123 / Chapter 7.1 --- Conclusions --- p.123 / Chapter 7.2 --- Future Perspectives --- p.124 / Chapter Part IV --- References --- p.126

nÃo hà / A Alpinia zerumbet à uma planta comumente encontrada na regiÃo do nordeste do Brasil. Essa planta à conhecida popularmente por colÃnia e à muito utilizada na medicina popular por suas propriedades diurÃticas e anti-hipertensivas. O objetivo do presente estudo foi investigar se o extrato aquoso das folhas de A. zerumbet (EAAz) apresentava atividade vasodilatadora em aorta de rato prÃ-contraÃda com fenilefrina e, elucidar o seu mecanismo de aÃÃo. Ratos machos Wistar (250 a 300 g), provenientes do biotÃrio da UFC, foram sacrificados por deslocamento cervical e a aorta torÃcica removida e dissecada. Os anÃis da aorta (4 a 5 mm) foram montados em cÃmeras orgÃnicas, contendo soluÃÃo de Krebs e aerados com carbogÃnio a 37ÂC, para as medidas de variaÃÃes na tensÃo isomÃtrica. O endotÃlio dos anÃis da aorta foi removido mecanicamente para estudar o seu envolvimento no efeito vasodilatador do EAAz. Para estudar o envolvimento do Ãxido nÃtrico (NO), GMPc, prostanÃides, canais de potÃssio ativados por Ca2+, espÃcies reativas do oxigÃnio e a ativaÃÃo das enzimas quinases Src e PI3 quinase, as preparaÃÃes foram tratadas, respectivamente, com L-NAME (100 ÂM), ODQ (10 ÂM), indometacina (10 ÂM), caribdotoxina (100 nM) mais apamina (100 nM), MnTMPyP (100 ÂM), catalase (500 U/ml), PEG-catalase (500 U/ml), SOD (500 U/ml) e PP2 (20 ÂM), Wortmannin (300 nM). O efeito vasodilatador do EAAz (0,05; 0,15; 0,5; 1,5; 15 e 50 Âg/mL), acetilcolina (10-8 - 10-5 M) e nitroprussiato de sÃdio (10-8 M) foram avaliados em aorta de ratos prÃ-contraÃda com fenilefrina (10-8 - 3x10-8 M), antes e apÃs tratamento com os inibidores especÃficos. A vasodilataÃÃo induzida pelo EAAz mostrou-se dependente do endotÃlio e mediada pelo NO via GMPc jà que o relaxamento vascular foi abolido na presenÃa do Ãster metÃlico de NG-nitro-l-arginina e do ODQ. A vasodilataÃÃo tambÃm foi reduzida pelo MnTMPyP (permeante celular mimÃtico da SOD), polietilenoglicol catalase, PP2 (inibidor da quinase Src) e Wortmannin (inibidor da fosfoinositideo 3-quinases). A via de produÃÃo de EROs induzida pelo EAAz foi inibida significativamente pela aÃÃo do MnTMPyP e PEG-catalase. Ocorreu tambÃm a inibiÃÃo da via EROs/PI3 quinase/Src quinase que estÃo envolvidas na ativaÃÃo da eNOS. O EAAz causou um relaxamento dependente do endotÃlio via NO/GMPc com o possÃvel envolvimento de EROs e das Src quinase e fosfoinositideo 3-quinase dependente de Akt. Dessa forma, pode-se concluir que o relaxamento vascular induzido pelo EAAz poderia explicar o tradicional uso do chà das folhas de A. zerumbet para o tratamento da hipertensÃo arterial. / The Alpinia zerumbet is a plant commonly found in the northeastern region of Brazil. This plant is popularly known as colony and is widely used in folk medicine for its diuretic and antihypertensive properties. The aim of this study was to investigate whether the aqueous extract of leaves of A. zerumbet (EAAz) had vasodilator activity in rat aorta pre-contracted with phenylephrine and to elucidate its mechanism of action. Male Wistar rats (250-300 g) from the vivarium of UFC, were killed by cervical dislocation and the thoracic aorta removed and dissected. The aortic rings (4-5 mm) were mounted in organ cameras, and containing Krebs solution aerated with carbogen at 37  C to measure changes in isometric tension. The endothelium of the aortic rings was removed mechanically to study their involvement in the vasodilator effect of EAAz. To study the involvement of nitric oxide (NO), cGMP, prostanoid, potassium channels activated by Ca2+, reactive oxygen species and activation of enzymes kinases Src and PI3 kinase, the preparations were treated respectively with L-NAME (100 ÂM ), ODQ (10 ÂM), indomethacin (10 ÂM), carybdotoxin (100 nM) plus apamin (100 nM), MnTMPyP (100 ÂM), catalase (500 U / ml), PEG-catalase (500 U/ ml), SOD (500 U / ml) and PP2 (20 ÂM), wortmannin (300 nM). The vasodilatory effect of EAAz (0.05, 0.15, 0.5, 1.5, 15 and 50 Âg / mL), acetylcholine (10-8 - 10-5 M) and sodium nitroprusside (10-8 M ) were evaluated in the aorta of rats pre-contracted with phenylephrine (10-8 - 3x10-8 M) before and after treatment with the specific inhibitors. EAAz induced vasodilation was dependent and endothelium mediated by NO via cGMP as the vascular relaxation was abolished in the presence of the methyl ester of NG-nitro-L-arginine and ODQ. Vasodilation was also reduced by MnTMPyP (mimetic cellular permeant SOD), catalase polyethylene glycol, PP2 (Src kinase inhibitor) and wortmannin (inhibitor of phosphoinositide 3-kinase). The route of production of ROS induced EAAz was significantly prevented by the action of MnTMPyP and PEG-catalase. There was also the inhibition of the kinase ROS/PI3 / Src kinase that are involved in the activation of the eNOS. The EAAz caused an endothelium-dependent relaxation via NO / cGMP with the possible involvement of ROS and Src kinase and phosphoinositide 3-kinase-dependent Akt. Taking us to the conclusion that the vascular relaxation induced by EAAz could explain the traditional use of the tea leaves of A. zerumbet for the treatment of hypertension.

The purpose of these studies was to determine if results similar to those of Fleischmann and Pons could be obtained using a titanium cathode instead of palladium in an electrolysis in a heavy water cell. The electrolyte consists of D20 and H2S04• Two experiments have been performed to examine the features of this electrolysis. As titanium shows the same properties to attract hydrogen, it seemed possible that excess heat could be produced. Radiation was monitored, and the surface of the titanium cathode was examined before and after electrolysis for any changes in the morphology and composition, hoping to discover new elements that can be created only by fusion reactions in the cell, i.e. by transmutation. The heat and radiation effects have been evaluated in comparison to a control cell, using the same electrolyte and current. The only difference was the cathode, which was of platinum. It appears that excess heat is produced during electrolyses of heavy water with a titanium cathode. The amount of this excess heat was 750 cal in a one hour period, an energy gain of 44%. No significant emission of any of the products associated with a "classical" deuterium-deuterium fusion was observed during either experiment, i.e. heat but no radiation. Unexpected elements were found in both experiments, i.e. K. Cr, Fe, Ni and Zn. Remarkable is the fact that the new elements always occur very close in the periodic table to an impurity element, i.e. Cu and Zn.

No description available.